Final Exam Review Flashcards
Issues with inhalation technique–___% delivered to the lungs, the rest to the mouth, pharynx, and larynx
12% delivered to the lungs
Issues with inhalation technique–presence of an ETT decreases the amount of drug delivered by a MDI to the trachea by ___-___%
presence of an ETT decreases the amount of drug delivered by a MDI to the trachea by 50-70%
Dose delivered by a nebulizer requires ___-___x that of a MDI dose to produce the same degree of bronchodilation
Dose delivered by a nebulizer requires 6-10x that of a MDI dose to produce the same degree of bronchodilation
What should be administered first, bronchodilators or corticosteroids?
Bronchodilators should be administered before corticosteroids
^ because the bronchodilator will open up the lungs and increase the surface area that the corticosteroid can work on
What are the (6) classes of respiratory medications?–anti___; ___ agonists; membrane ___; ___thines; ___lytics; cortico___
- Anticholinergics
- Adrenergic agonists
- Membrane stabilizers
- Xanthines
- Tocolytics (related drug)
- Corticosteroids
What (3) muscarinic receptors are stimulatory?
M1, M3, M5
Odd = stimulatory
What (2) muscarinic receptors are inhibitory?
M2, M4
Even = inhibitory
Antimuscarinic = anti___
anticholinergic
Antimuscarinic/anticholinergic both mean that we are blocking ___ from binding to ___ receptors
we are blocking ACH from binding to muscarinic receptors
Atropine antagonizes ___ effects on airway smooth muscle in large and medium sized airways; it affects airways that respond to vagal stimulation; it ___ (increases/decreases) airway resistance; ___ (increases/decreases) dead space
Atropine antagonizes ACH effects on airway smooth muscle in large and medium sized airways; it affects airways that respond to vagal stimulation; it decreases airway resistance; increases dead space
What is the main issue with nebulized atropine?–a lot of ___ complications, ___arrhythmias
A lot of CV complications, tachyarrhythmias
Atropine is ___ (more/less) lipophilic than glycopyrrolate
atropine is more lipophilic than glyocpyrrolate
Atropine is a ___ amine
tertiary amine
Atropine ___ (can/cannot) cross the BBB
can cross the BBB (because it’s a tertiary amine and more lipophilic)
Glycopyrrolate is a ___ ammonium; it ___ (does/does not) absorb systemically as much as atropine
glycopyrrolate is a quaternary ammonium; it does not absorb systemically as much as atropine
Ipratropium is most effective in treating bronchospasm due to ___
treating bronchospasm due to beta antagonists (i.e.: propranolol which has non-selective beta blockade)
Compared to beta agonists, ipratropium has a ___ (slower/faster) onset and is ___ (more/less) effective in treating bronchial asthma
ipratropium has a slower onset (30-90 minutes) and is less effective in treating bronchial asthma than beta agonists
Albuterol is better than ipratropium for acute asthma attacks because it has a faster onset of action–T/F?
True
Tiotropium (Spiriva) is a ___ (short/long) acting anticholinergic bronchodilator
long-acting anticholinergic bronchodilator
Tiotropium (Spiriva) is used as maintenance treatment of bronchospasm associated with COPD, including chronic ___ and ___
chronic bronchitis and emphysema
Long-acting bronchodilators ___ (should/should not) be used to treat acute anything
should NOT be used to treat acute anything
Warnings for inhaled anticholinergics–can cause ___ and severe ___
narrow angle glaucoma and severe urinary retention
Beta 2 agonists ___ (relax/contract) bronchial smooth muscle
relax bronchial smooth muscle
Newer beta 2 agonists lack stimulating effects on the heart at therapeutic doses–T/F?
True
Beta 2 agonists ___ (do/do not) have a catecholamine structure
do NOT have a catecholamine structure
The non-catecholamine structure of beta 2 agonists makes them resistant to what enzyme? What effect does this have on their duration of action?
Beta 2 agonists are resistant to COMT (because they are non-catecholamines); this contributes to their LONGER duration of action
Beta 2 agonists have a longer duration of action because they are __, NOT ___…do NOT have a ___ structure
Beta 2 agonists have a longer duration of action because they are sympathomimetics, NOT catecholamines…do NOT have a catecholamine structure
Uses of beta 2 agonists–preferred treatment for ___ (acute/chronic) episodes of asthma; prevention of ___-induced asthma; improve airflow and exercise tolerance in patients with ___; tocolytic to stop premature ___ contractions; treatment of ___kalemia
preferred treatment for acute episodes of asthma; prevention of exercise-induced asthma; improve airflow and exercise tolerance in patients with COPD; tocolytic to stop premature uterine contractions; treatment of hyperkalemia
Classes of beta 2 agonists–short acting = ___-___ hours; long acting = > ___ hours
short acting = 3-6 hours; long acting = > 12 hours
In spite of their non-respiratory side effects, ephedrine and epinephrine do have ___ effects from activation of beta 2 receptors
bronchodilating effects from activation of beta 2 receptors
Isoproterenol is a ___ (selective/non-selective) sympathomimetic that acts at ___ and ___ receptors
non-selective sympathomimetic that acts at beta 1 and beta 2 receptors
Isoproterenol is highly pro-
pro-arrhythmic
What medication is the preferred beta 2 agonist for acute bronchospasm?
Albuterol
Albuterol is a ___ (short/long) acting beta agonist
short acting beta agonist
Levoalbuterol (Xopenex) is the (___)-enantiomer of racemic albuterol
(R)-enantiomer of racemic albuterol
What was the main point of levoalbuterol (xopenex) for being marketed?
Because it is an (R)-enantiomer, it was expected to have little to no cardiac effects
Studies have shown that there is little or no clinically significant difference in adverse effects of levoalbuterol (xopenex) compared to albuterol–T/F?
True
Beta 2 ___ (relaxes/contracts) the uterus
Beta 2 relaxes the uterus
Ritodrine was removed from the market d/t ___ complications and 24 maternal ___
d/t CV complications and 24 maternal deaths
Side effects of ritodrine–crosses the ___; causes ___ and ___ effects in both the mother and fetus; dose-related ___cardia (because it’s slightly non-selective, beta1 and beta 2 agonism), ___ (increased/decreased) cardiac output; increased ___ secretion d/t beta1 stimulation; exaggerated systemic BP ___ (increase/decrease); ___glycemia in the mother (from beta2 effects) may cause reactive ___glycemia in the fetus
crosses the placenta; causes CV and metabolic effects in both the mother and fetus; dose-related tachycardia (because it’s slightly non-selective, beta1 and beta2 agonism), increased cardiac output; increased renin secretion d/t beta1 stimulation; exaggerated systemic BP decrease; hyperglycemia in the mother (from beta2 effects) may cause reactive hypoglycemia in the fetus
Side effects of ritodrine–increased renin secretion from beta1 stimulation causes ___ (increased/decreased) sodium; water ___ (reabsorption/secretion); ___ (increased/decreased) K+ and H+; pulmonary ___ may occur
increased renin secretion from beta1 stimulation causes increased sodium; water reabsorption; decreased K+ and H+; pulmonary edema may occur
Long acting beta agonists ___ (are/are not) used for acute effect
are NOT used for acute effect–used for long-term management
Salmeterol (serevent) and vilanterol are both ___ (short/long) acting beta agonists
long acting beta agonists
Formoterol and aformoterol are two other ___ (short/long) acting beta agonists
long acting beta agonists
Side effects of beta 2 agonists–___ usually occurs with overdose/systemic absorption due to stimulation of beta 2 receptors on ___ muscle; ___cardia from direct stimulation of receptors on the heart; metabolic response–___glycemia, ___kalemia, ___magnesemia
tremor usually occurs with overdose/systemic absorption due to stimulation of beta 2 receptors on skeletal muscle; tachycardia from direct stimulation of receptors on the heart; metabolic response–hyperglycemia, hypokalemia, hypomagnesemia
Why do you see hypokalemia/hypomagnesemia with beta 2 agonists?
When you give a beta 2 agonist, potassium is pulled into the cell in exchange for sodium; magnesium follows potassium into the cell
Black box warning for LABAs–increased risk of ___; ___ (should/should not) be used alone
increased risk of asthma related death; should not be used alone
How can LABAs (when used alone) lead to asthma related death?–LABAs have no ___ action
LABAs have no anti-inflammatory action–so if someone is having an asthma attack and you only give them an LABA, their lungs won’t react to the inflammatory response that is going on, leading to death
Cromolyn sodium is a ___; it inhibits antigen-induced release of ___ and other mediators from pulmonary mast cells during antibody mediated allergic responses
membrane stabilizer; it inhibits antigen-induced release of histamine and other mediators from pulmonary mast cells during antibody mediated allergic responses
Cromolyn sodium ___ (does/does not) relax bronchial or vascular smooth muscle
does NOT relax bronchial or vascular smooth muscle
Cromolyn sodium is used for ___ (acute/chronic) management; has no use in ___
used for chronic management; has no use in an acute asthma attack
What are (3) types of methylxanthines?
- Theophylline/aminophylline
- Caffeine
- Theobromine
Methylxanthines ___ (stimulate/inhibit) the CNS; ___ (increase/decrease) BP; ___ (increase/decrease) myocardial contractility and heart rate; ___ (contract/relax) smooth muscle in the airways
stimulate the CNS; increase BP; increase myocardial contractility and heart rate; relax smooth muscle in the airways
Methylxanthines are non-selective ___ inhibitors
non-selective phosphodiesterase inhibitors–inhibit all fractions of PDE isoenzymes [PDE breaks down cAMP/cGMP]
Methylxanthines are also competitive antagonists of ___ receptors
competitive antagonists of adenosine receptors
Theophylline has more competitive antagonism for adenosine receptors than caffeine and theobromine–T/F?
True
Theophylline is used to treat ___ in infants
apnea of prematurity in infants (because it is a CNS stimulant)
Theophylline toxicities–___-___ mcg/ml = GI upset, nausea/vomiting, tremor
15-25 mcg/ml = GI upset, nausea/vomiting, tremor
Theophylline toxicities–___-___ mcg/ml = tachycardia, PVCs
25-35 mcg/ml = tachycardia, PVCs
Theophylline toxicities– >___ mcg/ml = fatal VTach, seizures
> 35 mcg/ml = fatal VTach, seizures
Caffeine effects–CNS ___ (stimulant/inhibitor); cerebral vaso___ (dilator/constrictor); secretion of ___
CNS stimulant; cerebral vasoconstrictor; secretion of gastric acid
Caffeine uses–apnea of ___; ___ headache; ___ remedies (to offset sedation from antihistamines)
apnea of prematurity; post-dural puncture headache; cold remedies (to offset sedation from antihistamines)
Histamine ___ (does/does not) easily cross the blood-brain barrier
does not easily cross the blood-brain barrier
Through H1 and H2 receptors, histamine causes ___ (increased/decreased) capillary permeability; ___tension; ___cardia; ___ing; ___ache
increased capillary permeability; hypotension; tachycardia; flushing; headache
What receptor(s) need to be blocked in order to completely block the vasodilatory effects of histamine release?
Both H1 and H2 receptors need to be blocked in order to completely block the vasodilatory effects of histamine release
So–if someone is having a severe allergic reaction, give Benadryl and pepcid to block H1 and H2 receptors
H1 = broncho___ (constriction/dilation)
H1 = bronchoconstriction
H2 = broncho___ (constriction/dilation)
H2 = bronchodilation
Histamine triple response (wheal and flare)–___ due to increased permeability; ___ (dilated/constricted) arteries around the edema (flare); ___ due to histamine in the superficial layers of the skin
edema due to increased permeability; dilated arteries around the edema (flare); pruritus due to histamine in the superficial layers of the skin
Histamine stimulates gastric ___ ion secretion (d/t H__ receptor stimulation)
Histamine stimulates gastric hydrogen ion secretion (d/t H2 receptor stimulation)
Histamine receptor antagonists are ___ (competitive/noncompetitive) and ___ (reversible/irreversible) antagonists of histamine receptors
competitive and reversible antagonists of histamine receptors
Histamine receptor antagonists ___ (do/do not) inhibit the release of histamine
do NOT inhibit the release of histamine–histamine is still released from the mast cells, but it is unable to bind to its receptor
Histamine receptor antagonists attach to receptors and prevent the responses mediated by histamine–T/F?
True–competitive antagonism
Histamine receptor antagonists stabilize the receptor in the ___ (active/inactive) form, making them ___ agonists
stabilize the receptor in the inactive form, making them inverse agonists
Two generations of H1 receptor antagonists–first generation = ___; second generation = ___
first generation = sedating; second generation = non-sedating
First generation H1 receptor antagonists are ___; they may also activate ___ or ___-adrenergic receptors; they block ___ receptors
First generation H1 receptor antagonists are sedating; they may also activate serotonin or alpha-adrenergic receptors; they block muscarinic receptors
Benadryl is a ___ (1st/2nd) generation H1 receptor antagonist; can cause ___/___ in the very young and very old; used as a ___ative, anti___, anti___, and used to treat type ___ allergic reactions (___)
Benadryl is a 1st generation H1 receptor antagonist; can cause agitation/restlessness in the very young and very old; used as a sedative, antipruritic, antiemetic, and used to treat type 1 allergic reactions (anaphylaxis)
Second generation H1 antagonists are unlikely to produce CNS side effects unless recommended doses are exceeded–T/F?
True
(3) second generation H1 antagonists
- Zyrtec (cetirizine)
- Claritin (loratidine)
- Allegra (fexofenadine)
HPA axis–hypothalamus releases ___, anterior pituitary releases ___, adrenal cortex releases ___
hypothalamus releases corticotropin releasing hormone (CRH), anterior pituitary releases adrenocorticotropic hormone (ACTH), adrenal cortex releases cortisol
Adrenal cortex–zona glomerulosa = ___ layer; releases ___
outer layer; releases mineralocorticoids
Adrenal cortex–zona fasciculata = ___ layer; releases ___
middle layer; releases glucocorticoids
Adrenal cortex–zona reticularis = ___ layer; releases ___
inner layer; releases weak androgens
What hormone is produced in the adrenal cortex in response to stress?
Cortisol (hydrocortisone)
What is the major mineralocorticoid?
Aldosterone
Aldosterone is secreted secondary to ___ (increased/decreased) K+; ___ (increased/decreased) sodium; ___ (increased/decreased) BP/fluid volume
aldosterone is secreted secondary to increased K+; decreased sodium; decreased BP/fluid volume
Review of RAAS
renin is released by the kidneys in response to low BP –> angiotensinogen (released by the liver) converts renin to angiotensin I –> angiotensin I is converted to angiotensin II by ACE (released from the lungs) –> angiotensin II is potent vasoconstrictor, stimulates release of aldosterone from the adrenal cortex
Aldosterone ___ (increases/decreases) K+ excretion; ___ (increases/decreases) Na+ retention; ___ (increases/decreases) water retention; ___ (increases/decreases) blood volume
Aldosterone increases K+ excretion; increases Na+ retention; increases water retention; increases blood volume
Circadian rhythm–secretory rates of CRH, ACTH, and cortisol are ___ (low/high) in the early morning; ___ (low/high) in the late evening
high in the early morning; low in the late evening
Primary adrenocortical insufficiency is AKA ___ disease
Addison’s disease
Addison’s disease–the adrenals do not secrete ___ or ___; replacement therapy must include ___corticoid and ___corticoid
the adrenals do not secrete cortisol or aldosterone; replacement therapy must include glucocorticoid and mineralocorticoid
Secondary adrenocortical insufficiency is due to chronic ___ use and suppression of the ___ axis
due to chronic steroid use and suppression of the HPA axis
In secondary adrenocortical insufficiency, ___ secretion is maintained
aldosterone secretion is maintained
Replacement therapy for secondary adrenocortical insufficiency usually requires only ___corticoid
glucocorticoid
Glucocorticoid effect = anti-___ response
glucocorticoid effect = anti-inflammatory response
Mineralocorticoid effect = evoke distal renal tubular reabsorption of ___ in exchange for ___
mineralocorticoid effect = evoke distal renal tubular reabsorption of Na+ in exchange for K+
Which (2) corticosteroid medications have the greatest anti-inflammatory potency?
- Betamethasone
- Dexamethasone
^ Both are synthetic glucocorticoids
What corticosteroid medication has the greatest sodium-retaining potency?
Fludrocortisone–synthetic mineralocorticoid
Corticosteroids ___ (are/are not) able to cross the placenta
Corticosteroids are able to cross the placenta
Corticosteroid use can lead to ___kalemic metabolic ___osis due to ___corticoid effect of cortisol on distal renal tubules, leading to enhanced absorption of ___ and loss of ___; also leads to ___ and weight ___
corticosteroid use can lead to hypokalemic metabolic alkalosis due to mineralocorticoid effect of cortisol on distal renal tubules, leading to enhanced absorption of Na+ and loss of K+; also leads to edema and weight gain
Aldosterone secretion remains intact in ___ (primary/secondary) adrenal insufficiency
secondary adrenal insufficiency
Prednisone 5 mg/day or less or 10 mg every other day is ___ (likely/unlikely) to suppress the HPA axis
unlikely to suppress the HPA axis
Glucocorticoids any dose < ___ weeks does not clinically suppress the HPA axis
any dose < 3 weeks
Prednisone or dexamethasone (even physiologic doses) given as a single daily dose at bedtime is associated more commonly with HPA axis suppression–T/F?
True
Therapies assumed to suppress HPA axis–prednisone 20 mg/day (or equivalent) for > ___ weeks within the previous year; patient with clinical signs of ___ syndrome from any steroid dose
> 3 weeks; patient with clinical signs of Cushing syndrome
After cessation of steroid therapy, recovery of the HPA function can take ___ months or longer
12 months or longer
Patients at high risk of HPA suppression, including those treated with at least 20mg/day of prednisone for > 3 weeks or who have signs and symptoms of Cushings–unless data states otherwise, supplementation ___ (is/is not) recommended
supplementation is recommended
Patients at low risk of HPA suppression–any dose of steroid for < 3 weeks, less than 5 mg/day of prednisone (or 10 mg every other day)–steroids ___ (are/are not) required unless signs and symptoms of HPA suppression are observed
are not required unless signs and symptoms of HPA suppression are observed
What two conditions could exaggerate the need for exogenous corticosteroid supplementation?
Burns or sepsis
Signs and symptoms of acute adrenal crisis–___tension unresponsive to ___; ___dynamic circulation; ___glycemia; ___kalemia; ___natremia; ___volemia; metabolic ___osis; ___ (increased/decreased) level of consciousness
hypotension unresponsive to vasopressors; hyper dynamic circulation; hypoglycemia; hyperkalemia; hyponatremia; hypovolemia; metabolic acidosis; decreased level of consciousness
(4) medication classes that can cause hyperglycemia–gluco___; anti___; ___ medications; ___
glucocorticoids; antipsychotics; HIV medications; octreotide
Diagnosis of diabetes–fasting blood glucose ___ mg/dl or greater; random blood glucose > ___ mg/dl
fasting blood glucose 126 mg/dl or greater; random blood glucose > 200 mg/dl
Normal HgA1C = ___-___%
4-6%
ADA recommends HgA1C < ___-___%, depending on the age of the diabetic patient
< 7-8.5%
HgA1C gives an idea of the degree of control of blood glucose levels over the past ___ months
3 months
What does PI-3K do?–It moves a ___ into the cell wall of cells
It moves a glucose transporter into the cell wall of cells
Insulin MOA–binds to plasma membrane ___ receptors; translocation of ___ to plasma membranes
binds to plasma membrane insulin receptors; translocation of glucose transporters to plasma membranes
Glucose transporters facilitate ___ diffusion into cells; shift intracellular glucose metabolism toward ___ (glyco___); stimulate cellular uptake of ___ acids, ___ate, ___ium, and ___ium; stimulate protein ___ and inhibit proteo___; regulate ___ expression via insulin regulatory elements in target DNA
Glucose transporters facilitate glucose diffusion into cells; shift intracellular glucose metabolism toward storage (glycogenesis); stimulate cellular uptake of amino acids, phosphate, potassium, and magnesium; stimulate protein synthesis and inhibit proteolysis; regulate gene expression via insulin regulatory elements in target DNA
___ occurs when there is an impaired intracellular insulin signal that results in decreased recruitment of glucose transport proteins to the plasma membrane and subsequent decreased glucose uptake
Insulin resistance
Compensatory ___insulinemia occurs to overcome insulin resistance
Compensatory hyperinsulinemia occurs to overcome insulin resistance
Cells send signals to the CNS that they’re starving (because insulin signal is messed up and isn’t bringing glucose into the cells); body sends signals to the pancreas to make more glucose/release more insulin, resulting in hyperinsulinemia; hyperinsulinemia leads to eventual burnout of the pancreas and worsening of diabetes
Insulin receptor saturation occurs with ___ (low/high) circulating concentrations of insulin; ___ (more/less) insulin receptors are popped into the cell walls as a result
Insulin receptor saturation occurs with low circulating concentrations of insulin; more insulin receptors are popped into the cell walls as a result
The number of insulin receptors in a cell wall is ___ (inversely/directly) related to the plasma concentration of insulin
The number of insulin receptors in a cell wall is inversely related to the plasma concentration of insulin
The higher the plasma concentration of insulin, the ___ (less/more) insulin receptors in the cell wall
The higher the plasma concentration of insulin, the less insulin receptors in the cell wall
The lower the plasma concentration of insulin, the ___ (less/more) insulin receptors in the cell wall
The lower the plasma concentration of insulin, the more insulin receptors in the cell wall
Elimination half-life of insulin is ___-___ minutes
5-10 minutes
Insulin is metabolized by the ___ and ___
kidneys and liver
What prolongs the elimination half-life of insulin more–kidney or liver disease?
Kidney disease prolongs the elimination half-life of insulin more than liver disease
Despite rapid clearance from the plasma, there is a sustained pharmacologic effect of insulin for ___-___ minutes because insulin is tightly bound to ___ receptors
Despite rapid clearance from the plasma, there is a sustained pharmacologic effect of insulin for 30-90 minutes because insulin is tightly bound to tissue receptors
Basal rate of insulin secretion by the pancreas is ___ unit/hr
Basal rate of insulin secretion by the pancreas is 1 unit/hr
Food prompts a ___-___ fold increase in insulin secretion
Food prompts a 5-10 fold increase in insulin secretion
Total daily secretion of insulin is approximately ___ units/day
Total daily secretion of insulin is approximately 40 units/day
Insulin response to glucose is greater for IV infusion than oral ingestion–T/F?
FALSE–insulin response to glucose is greater for oral ingestion than IV infusion
Long acting insulins should be used for acute diabetic attacks–T/F?
FALSE–long acting insulins should NOT be used for acute diabetic attacks
What long acting insulin acts just like basal rate insulin; is sgiven once a day; good for people who have very brittle diabetes/lots of swings in glucose levels; also good for patients who are not good at keeping a schedule for giving themselves insulin?
Degludec (Tresiba)
What insulin is given at bedtime and helps to counteract the morning burst of hormones?
Glargine (Lantus)
Side effects of insulin–___glycemia; ___kalemia; ___magnesemia; ___phosphatemia; ___ reactions; ___dystrophy; insulin ___; drug ___
hypoglycemia; hypokalemia; hypomagnesemia; hypophosphatemia; allergic reactions; lipodystrophy; insulin resistance; drug interactions
Hypokalemia/hypomagnesemia that may occur with insulin administration puts patients at risk for ___
arrhythmias
Hypophosphatemia that may occur with insulin administration puts patients at risk for respiratory ___
respiratory depression
___ syndrome can occur in patients who have been NPO for awhile; get ___ (up/down) regulation of insulin receptors because the cells are hungry and waiting for more glucose to be introduced into the body
Refeeding syndrome can occur in patients who have been NPO for awhile; get up regulation of insulin receptors because the cells are hungry and waiting for more glucose to be introduced into the body
What happens if you give someone who has been NPO for so long 100% of their caloric requirements for the day?
Refeeding syndrome–they will get massive rush of insulin release from the pancreas; insulin will bind to all of the up regulated receptors; and there will be a rush of potassium, magnesium, and phosphate into the cells
Symptoms of hypoglycemia reflect the compensatory effects of increased ___–___esis, ___cardia, ___tension
increased epinephrine–diaphoresis, tachycardia, hypertension
Epi is released in response to hypoglycemia because it kickstarts gluconeogenesis/glycogenolysis to increase blood glucose levels
Rebound ___glycemia caused by ___ (sympathetic/parasympathetic) nervous system activity in response to hypoglycemia may mask the correct diagnosis–this is known as the ___ Effect
Rebound hyperglycemia caused by sympathetic nervous system activity in response to hypoglycemia may mask the correct diagnosis–this is known as the Somogyi Effect
Chronic NPH administration may lead to the development of antibodies to ___
protamine
Insulin resistance occurs in patients requiring > ___ units/day (remember avg daily insulin release from the body is ~___ units/day)
Insulin resistance occurs in patients requiring > 100 units/day (remember the avg daily insulin release from the body is ~40 units/day)
Insulin drug interactions–epinephrine ___ (inhibits/stimulates) the secretion of insulin; ___ (inhibits/stimulates) glycogenolysis
epinephrine inhibits the secretion of insulin; stimulates glycogenolysis
Perioperative management of blood glucose–optimal blood glucose levels ___-___ mg/dl; < ___ mg/dl for total joints; glucose infusion if blood glucose decreases to < ___ mg/dl
optimal blood glucose levels 110-180 mg/dl; < 150 mg/dl for total joints; glucose infusion if blood glucose decreases to < 80 mg/dl
What are the (8) classes of oral hypoglycemics?–___ureas; ___ inhibitors; ___nides; ___nides; ___diones; ___ inhibitors; ___ mimetics; ___inhibitor
- Sulfonylureas
- Alpha-glucosidase inhibitors
- Meglitanides
- Biguanides
- Thiazolidinediones
- DPP4 inhibitors
- Incretin mimetics
- SLGT2 inhibitor
Sulfonylureas MOA–act at ___ cells to stimulate release of ___
act at pancreatic beta cells to stimulate release of insulin
In order for sulfonylureas to work, you need to have a functioning ___
pancreas
Sulfonylureas have high ___ rates
high failure rates
20% primary failures (1 in 5 patients they won’t work for at all); each year 10-15% secondary failures
Sulfonylureas should be avoided in patients with allergy to ___ drugs
sulfa drugs
If patient took their sulfonylurea the morning of surgery, he/she will be at high risk for ___glycemia; have ___ or ___ available
he/she will be at high risk for hypoglycemia; have D50 or glucagon available
___ patients are at high risk of hypoglycemia from sulfonylureas
Renal failure patients are at high risk of hypoglycemia from sulfonylureas (because they are renally eliminated…renal failure prolongs their duration of action)
Most common severe complication of sulfonylureas is ___
hypoglycemia
Risk of hypoglycemia from sulfonylureas is highest with ___ and ___
glyburide and chlorpropamide (because they have the longest elimination half-life)
Duration of action of a sulfonylurea is up to ___ days
up to 7 days
Hypoglycemia from sulfonylureas is ___ (more/less) frequent than with insulin; it is often ___ and more ___ than hypoglycemia due to insulin
Hypoglycemia from sulfonlyureas is less frequent than with insulin; it is often prolonged and more dangerous than hypoglycemia due to insulin
Do sulfonylureas cross the placenta?
Yes–can cause fetal hypoglycemia
Contraindications/precautions for sulfonylurea use–hypersensitivity to ___; patients with ___glycemic unawareness; poor ___ function
hypersensitivity to sulfonamides; patients with hypoglycemic unawareness; poor renal function
What sulfonylurea is safest to use in patients with poor kidney function?
Glipizide (Glucotrol)
If CrCl is above 10, it ___ (is/is not) safe for the patient to take glipizide
it is safe for the patient to take glipizide
If someone took a sulfonylurea the morning of surgery, they are at risk for ___, especially if they took ___
they are at risk for hypoglycemia, especially if they took glyburide
Which 1st generation sulfonylurea is the longest acting?
Chlorpropamide (Diabinese)
Chlorpropamide (Diabinese) duration of action may approach ___ hours; 20% of the drug is excreted unchanged by the ___; it is associated with ___-like reactions; can cause severe ___natremia
duration of action may approach 72 hours; 20% of the drug is excreted unchanged by the kidneys; it is associated with disulfiram-like reactions; can cause severe hyponatremia (< 129)
Disulfiram = drug that causes an adverse reaction to alcohol, leading to nausea, vomiting, flushing, dizziness, throbbing headache, chest/abdominal discomfort, and general hangover-like symptoms
(2) meglitinides = ___ and ___
Repaglinide (Prandin) Nateglinide (Starlix)
Meglitinides MOA–increase ___ secretion from islet cells like ___ (what other drug class?)
increase insulin secretion from islet cells like sulfonylureas
Meglitinides have a ___ (slower/faster) onset and ___ (shorter/longer) duration of action than sulfonylureas
faster onset (1 hour) and shorter duration of action (4 hours)
Meglitinides can be administered while fasting–T/F?
FALSE–NEVER administer while fasting
Meglitinides are active only in the presence of ___; this decreases the risk of prolonged ___glycemic episodes
active only in the presence of glucose; this decreases the risk of prolonged hypoglycemic episodes
What is the name of (1) biguanide that is the #1 medication in type 2 diabetes treatment guidelines?
Metformin (Glucophage)
Metformin (Glucophage) decreases blood glucose concentrations with a very ___ (low/high) risk of hypoglycemia; has a positive effect on ___ concentrations; and leads to mild weight ___ in obese patients
very low risk of hypoglycemia; has a positive effect on lipid concentrations; and leads to mild weight loss in obese patients (unlike sulfonlyureas and meglitinides, which both cause weight gain)
Metformin MOA–___ (increased/decreased) hepatic glucose production [gluconeogenesis]; ___ (increases/decreases) glucose absorption from the intestine [similar to acarbose]; and ___ (increases/decreases) insulin sensitivity at the skeletal muscle cells
decreased hepatic glucose production [gluconeogenesis]; decreases glucose absorption from the intestine [similar to acarbose]; and increases insulin sensitivity at the skeletal muscle cells
Why should type 2 diabetics continue their metformin even if they are started on insulin?
Because metformin enhances the action of insulin at skeletal muscle cells
Rare side effect of metformin/black box warning for metformin = ___
lactic acidosis
Signs of lactic acidosis from metformin–___/___; ___ (increased/decreased) RR, HR; ___ pain; ___
nausea/vomiting; increased RR, HR; abdominal pain; shock
Metformin can exaggerate post-op nausea/vomiting–T/F?
True
Starting regular dose of metformin post-op can make patient very sick after surgery
Discontinue metformin ___ hours prior to elective surgery d/t risk of lactic acidosis in the intraoperative period
48 hours prior to elective surgery
Metformin and IV contrast = increased risk of ___toxicity; hold ___ hours prior to and after dye, check ___ levels
increased risk of nephrotoxicity; hold 48 hours prior to and after dye, check creatinine levels
Metformin contraindications/precautions–new recommendations for renal impairment–contraindicated in patients with eGFR < ___ ml/min; do not initiate or re-evaluate patients with eGFR < ___ ml/min
contraindicated in patients with eGFR < 30 ml/min; do not initiate or re-evaluate patients with eGFR < 45 ml/min
Metformin contraindications/precautions–age > ___ years old; ___ impairment; ___
age > 80 years old; hepatic impairment; CHF
(2) thiazolidinediones–___ and ___
rosiglitazone (Avandia) and pioglitazone (actos)
Thiazolidinediones MOA–___ (increase/decrease) insulin resistance; ___ (increase/decrease) hepatic glucose output
decrease insulin resistance; decrease hepatic glucose output
Thiazolidinediones require the presence of ___ and are especially effective in ___ patients
require the presence of insulin and are especially effective in obese patients
Thiazolidinediones side effects–weight ___ (loss/gain); ___toxicity; peripheral ___; ___ exacerbations; risk of ___
weight gain; hepatotoxicity; peripheral edema; CHF exacerbations; risk of bone fractures
Why was rosiglitazone (avandia) pulled from the market?
Controversial increase in MI and CV death
(4) DPP4 inhibitors
- Sitagliptin (Januvia)
- Saxagliptin (Onglyza)
- Linagliptin (Tradjenta)
- Alogliptin (Nesina)
DPP4 inhibitors MOA–___ (increase/decrease) pancreatic insulin secretion; ___ (limit/enhance) glucagon secretion; ___ (slow/speed up) gastric emptying; ___ (promote/inhibit) satiety
increase pancreatic insulin secretion; limit glucagon secretion; slow gastric emptying; promote satiety
How do DPP4 inhibitors specifically work though? They slow down metabolism of what protein?
slow down metabolism of GLP-1
Post-marketing, DPP4 inhibitors were found to cause ___titis, ___edema, ___ syndrome, ___laxis
pancreatitis, angioedema, Stevens Johnson syndrome, anaphylaxis
DPP4 inhibitors 08/2015 FDA safety warning for ___
joint pain
Incretin mimetics are also known as ___ analogs and ___ analogs
GLP-1 analogs and amylin analogs
(4) incretin mimetics–GLP-1 analogs
- Exanatide (Byetta, Bydureon)
- Liraglutide (Victoza)
- Albiglutide (Tanzeum)
- Dulaglutide (Trulicity)
^ These are injectables
GLP-1 analogs ___ (slow/speed up) gastric emptying; ___ (reduce/enhance) postprandial glucagon secretion
slow gastric emptying; reduce postprandial glucagon secretion
Amylin analogs ___ (increase/decrease) insulin secretion; ___ (slow/speed up) gastric emptying; ___ (increase/decrease) beta cell growth; ___ (suppress/stimulate) central appetite
increase insulin secretion; slow gastric emptying; increase beta cell growth; suppress central appetite
What is a risk postoperatively if the patient takes a GLP-1 analog?
Postop nausea/vomiting because GLP-1 analogs slow down the GI tract
Specific GLP-1 analog precautions–avoid Byetta in ___ failure; avoid Victoza in ___ carcinoma
avoid Byetta in renal failure; avoid Victoza in thyroid carcinoma
Side effects of amylin analogs–black box warning: ___glycemia, especially in type ___ diabetics; ___/___; ___rexia; ___ache; gastro___
black box warning: hypoglycemia, especially in type I diabetics; nausea/vomiting; anorexia; headache; gastroparesis
(3) SGLT2 inhibitors
- Canagliflozin (Invokana)
- Dapagliflozin (Farxiga)
- Empagliflozin (Jardiance)
SGLT2 inhibitors MOA–___ (increased/decreased) urinary glucose excretion from the ___ tubule
increased urinary glucose excretion from the proximal tubule
Contraindications for SGLT2 inhibitors–CrCl < ___ ml/min, end stage ___ disease, patients on hemo___
CrCl < 30 ml/min, end stage renal disease, patients on hemodialysis
Warnings for SGLT2 inhibitors–___tension, ___ side effects
hypotension, urinary side effects
Increased risk of ___ and ___ with SGLT2 inhibitors
gangrene and amputations, primarily toe
What does SGLT2 inhibitor mean?
sodium glucose transporter 2 inhibitor
SGLT2 inhibitors–increased risk of perioperative ___glycemic keto___
euglycemic ketoacidosis
Thyroid gland hormones review–hypothalamus releases ___; pituitary releases ___; thyroid releases ___ and ___
hypothalamus releases thyroid releasing hormone (TRH); pituitary releases thyroid stimulating hormone (TSH); thyroid releases T3 ad T4
Clinical presentation of HYPOthyroid (Hashimoto disease)–___ (cold/heat) intolerance; ___ (moist/dry) skin; ___ness; weight ___ (loss/gain); ___cardia; ___ (slow/fast) reflexes; ___ (coarse/fine) skin and hair; periorbital ___; painful/heavy ___; ___ coma
cold intolerance; dry skin; weakness; weight gain; bradycardia; slow reflexes; coarse skin and hair; periorbital swelling; painful/heavy menstruation; myxedema coma
Clinical presentation of HYPERthyroid (Graves disease)–weight ___ (loss/gain); ___ (increased/decreased) appetite; ___ (cold/heat) intolerance; ___er; ___ (coarse/fine) hair; ___cardia; ___iety; ___nia; ___ (lighter/heavier) periods/___menorrhea; ___ (cold/warm) skin; ___thalmos; ___ storm
weight loss; increased appetite; heat intolerance; goiter; fine hair; tachycardia; anxiety; insomnia; lighter periods/amenorrhea; warm skin; exophthalmos; thyroid storm
Armour thyroid composition ratio of T4 to T3 is ___:___
4:1
T4 = ___ (active/inactive)
T4 = inactive
T3 = ___ (active/inactive)
T3 = active
What is the most frequently administered drug for the treatment of diseases requiring thyroid hormone replacement (i.e.: hypothyroidism)?
Levothyroxine (T4) (Synthroid)
If a patient is on PO Synthroid and is unable to take oral meds for several days, do they need immediate IV replacement of Synthroid? Why?
No because Synthroid has a long elimination half-life (7 days)
After 7 days, if patient is still not able to take PO, you can administer half the oral dose IV
The elimination half-life of Synthroid is ___ days
7 days
In the body, Synthroid is deiodinated and converted to ___
T3
Liothyronine (Cytomel) is a levorotatory isomer of ___
T3
Liothyronine (T3) (Cytomel) is __-__x as potent as levothyroxine
2.5-3x as potent as levothyroxine
Liothyronine (T3) (Cytomel) is usually added on if someone is on a max dose of Synthroid and their body isn’t responding appropriately to it–T/F?
True
Hypothyroidism anesthetic implications–___ (increased/decreased) sensitivity to depressant drugs, including inhaled anesthetics; ___dynamic (hyper/hypo) CV system; ___ (increased/decreased) CO d/t ___ (increased/decreased) HR and SV; ___ (slow/fast) metabolism of drugs, particularly opioids; unresponsive ___ reflexes; ___ (increased/decreased) intravascular fluid volume; impaired ventilatory response to ___ (low/high) PaO2 and/or ___ (increased/decreased) PaCO2; ___ (delayed/enhanced) gastric emptying; ___natremic; ___thermic; ___nemic; ___glycemic; primary ___ insufficiency
increased sensitivity to depressant drugs, including inhaled anesthetics; hypodynamic CV system; decreased CO d/t decreased HR and SV; slow metabolism of drugs, particularly opioids; unresponsive baroreceptor reflexes; decreased intravascular fluid volume; impaired ventilatory response to low PaO2 and/or increased PaCO2; delayed gastric emptying; hyponatremic; hypothermic; anemic; hypoglycemic; primary adrenal insufficiency
Two antithyroid drugs to treat hyperthyroidism–___ and ___
propylthiouracil (PTU) and methimazole (tapazole)
Methimazole MOA–inhibit the formation of ___ hormone
thyroid hormone
PTU blocks the peripheral deiodination of ___ to ___
T4 to T3
PTU and methimazole are useful in treating ___thyroidism (including thyroid ___) before elective ___
useful in treating hyperthyroidism (including thyroid storm) before elective thyroidectomy
PTU and methimazole are only available ___
orally
PTU and methimazole require several days for full effect because pre-formed hormone must be depleted–T/F?
True
What is the oldest effective treatment for hyperthyroidism?
Iodines–Lugol’s solution, saturated KI (potassium iodide) solution
Iodines inhibit the release of ___ hormone into the circulation
inhibit the release of thyroid hormone into the circulation
Iodines are combined with ___olol to treat hyperthyroidism before thyroidectomy
propranolol
Signs of thyroid storm–___thermia, ___cardia, ___, ___hydration, and ___
hyperthermia, tachycardia, CHF, dehydration, and shock
Thyroid storm resembles ___
malignant hyperthermia
Thyroid storm is more likely to occur in the first ___-___ hours postop than intraop
first 6-19 hours postop
Treatment of thyroid storm–IV infusion of ___ (warm/cold) crystalloid solutions; sodium ___ IV to reduce the release of active hormones from the thyroid gland; ___ IV to treat acute primary adrenal insufficiency from increased metabolism and use of corticosteroids; ___ IV to alleviate the CV effects of thyroid hormones; ___ PO to reduce synthesis of new thyroid hormone
IV infusion of cold crystalloid solutions; sodium iodide IV to reduce the release of active hormones from the thyroid gland; cortisol IV to treat acute primary adrenal insufficiency from increased metabolism and use of corticosteroids; propranolol IV to alleviate the CV effects of thyroid hormones; PTU PO to reduce synthesis of new thyroid hormone
Avoid ___ for elevated temperature because it may displace thyroxine from carrier proteins
Avoid aspirin for elevated temperature because it may displace thyroxine from carrier proteins (so then there will be more circulating thyroxine)
The lowest concentration of antibiotic required to prevent growth is the ___
minimum inhibitory concentration (MIC)
The lowest concentration of antibiotic required to kill bacteria is the ___
minimum bactericidal concentration (MBC)
You can compare MICs of different antibiotics to each other–T/F?
False–cannot compare MICs of different antibiotics to each other
You can, however, compare MIC of one single antibiotic to different organisms (i.e.: MIC of cipro for klebsiella vs. pseudomonas)
What is the difference between bactericidal and bacteriostatic?
Bactericidal = kills the bacteria
Bacteriostatic = stops the bacteria from replicating (but does not kill the existing bacteria)
Penicillins, cephalosporins, aminoglycosides, vancomycin, quinolone, aztreonam, imipenem, bacitracin, and polymyxins are all bacteri___
bactericidal
Tetracyclines, chloramphenicol, eryrthromycin, clindamycin, sulfonamides, and trimethoprim are all bacteri___
bacteriostatic
Time-dependent killing–greater concentrations ___ (do/do not) kill bacteria faster or in greater numbers
greater concentrations do NOT kill bacteria faster or in greater numbers
Time-dependent killing–clinical efficacy is related to the duration for which these levels are maintained–T/F?
True
What (3) antibiotic classes demonstrate time-dependent killing?
- Beta-lactams
- Monobactams (aztreonam)
- Macrolides (erythromycin, clindamycin)
Continuous infusion of time-dependent killing antibiotics ___ (has/has not) shown to be more effective than intermittent boluses
continuous infusion of time-dependent killing antibiotics has NOT shown to be more effective than intermittent boluses
What term describes the following?–some antibiotics continue to suppress the growth of bacteria even after the antibiotic is no longer detectable
Post Antibiotic Effect (PAE)
PAE is demonstrated virtually for all antimicrobials–T/F?
True
PAE can be ___ (increased/decreased) in acidic, infected media
decreased
During the PAE phase, bacteria are ___ (more/less) susceptible to killing by leukocytes–this is known as what?
During the PAE phase, bacteria are MORE susceptible to killing by leukocytes–this is known post antibiotic leukocyte effect
(2) types of antibiotic resistance–___ and ___
intrinsic and acquired
___ (intrinsic/acquired) resistance is natural resistance to the antimicrobial
Intrinsic resistance is natural resistance to the antimicrobial
___ (intrinsic/acquired) resistance reflects a genetic alteration in the bacteria that renders a once effective antimicrobial ineffective
Acquired resistance reflects a genetic alteration in the bacteria that renders a once effective antimicrobial ineffective
The majority of nosocomial (hospital-acquired) infections are ___, ___, and ___ infections
urinary, respiratory, and blood infections
Rate of central line related infections (from highest risk location to lowest risk location)
Femoral > IJ > Subclavian
Clostridium difficile is now known as ___
Clostridioides difficile
What provokes C. difficile disease? How?
Antibiotic therapy, including prophylaxis…it alters normal bowel flora
Pathogenesis of C. diff–typically ___-mediated; bacteremia with C. diff is extremely ___ (rare/common)
toxin-mediated–enterotoxin A, cytotoxin B; bacteremia with C. diff is extremely rare
Diagnosis of C. diff is confirmed by detection of one of the ___
toxins
C. diff spores are extremely hearty and impervious to antibiotic therapy, resulting in a 10% relapse rate in successfully treated patients–T/F?
True
Treatment of C. diff = oral ___
oral vancomycin
Dificid (fidaxomicin) is another antibiotic that can be used to treat C. diff with similar cure rates as Vancomycin and reduced recurrence for moderate to severe infection–T/F?
True
In patients with ongoing original infection [the infection that they had before getting C. diff]…treat the infection with appropriate ___-spectrum antibiotics; continue C. diff therapy also and extend the C. diff therapy course for ___ to ___ days after the completion of the other antibiotics
In patients with ongoing original infection [the infection that they had before getting C. diff]…treat the infection with appropriate broad-spectrum antibiotics; continue C. diff therapy also and extend the C. diff therapy course for 5 to 10 days after the completion of the other antibiotics
Treatment course of C. diff is usually ___ to ___ days
Treatment course of C. diff is usually 10 to 14 days
In the future, C. diff ___ (can/cannot) be provoked with subsequent antibiotic courses because of the presence of latent ___
In the future, C. diff can be provoked with subsequent antibiotic courses because of the presence of latent spores
Surgical antibiotic prophylaxis ___ (is/is not) usually necessary to continue past the 1st post-op day
Surgical antibiotic prophylaxis is NOT usually necessary to continue past the 1st post-op day
For surgical antibiotic prophylaxis, usually use what antibiotic class?
1st generation cephalosporin–cefazolin
Low cost, broad spectrum, low incidence of allergic reactions
Wound classification–classes __-__
classes I-IV
Class I = ___; ___traumatic, no break in ___ technique; ___, ___, and ___ tracts not entered
Class I = clean
- atraumatic
- no break in sterile technique
- respiratory, GI, and GU tracts not entered
Class II = ___; surgery in areas known to harbor ___; ___ spillage of contents
Class II = clean-contaminated
- surgery in areas known to harbor bacteria
- no spillage of contents
Class III = ___; major break in ___ technique; surgery on ___ wounds; gross ___ spillage; entrance into an infected ___ or ___ tract
Class III = contaminated
- major break in sterile technique
- surgery on traumatic wounds
- gross GI spillage
- entrance into an infected biliary or GU tract
Class IV = ___; infection existed ___ the surgery, i.e.: old wound with devitalized tissue, perforated viscera
Class IV = dirty-infected; infection existed before the surgery, i.e.: old wound with devitalized tissue, perforated viscera
Prophylactic antibiotic administration is initiated within ___ minutes prior to the surgical incision
120 minutes prior to the surgical incision
Ancef is initiated within ___ minutes prior to the surgical incision
Ancef is initiated within 60 minutes prior to the surgical incision
Vanco is initiated within ___ minutes prior to the surgical incision
Vanco is initiated within 120 minutes prior to the surgical incision
JAMA surgery 2019–increasing duration of antimicrobial prophylaxis was associated with higher odds of acute ___ injury and ___ infection in a duration-dependent fashion
increasing duration of antimicrobial prophylaxis was associated with higher odds of acute kidney injury and C. diff infection in a duration-dependent fashion
JAMA surgery 2019–extended duration of antibiotic prophylaxis (3 days, 5 days post-op) ___ (did/did not) lead to additional SSI reduction
extended duration (3 days, 5 days post-op) did NOT lead to additional SSI reduction
Antibiotic medications by class–beta-___; ___sporins; ___bactams, ___penems; ___lides; ___quinolones; ___cyclines; ___glycosides
- beta-lactams
- cephalosporins
- monobactams, carbapenems
- macrolides
- fluoroquinolones
- tetracyclines
- aminoglycosides
What (4) antibiotic classes are beta-lactams?
- Penicillin
- Cephalosporins
- Carbapenem
- Monobactam
Beta-lactams bind to the ___; they are ___ inhibitors
Beta-lactams bind to the penicillin binding protein (PBP); they are cell wall synthesis inhibitors
What enzyme causes penicillin resistance?
B-lactamase–breaks a bond in the B-lactam ring of penicillin to disable the molecule
Bacteria with B-lactamase can resist the effects of ___ and other ___ antibiotics
can resist the effects of penicillin and other B-lactam antibiotics (cephalosporins, carbapenem, monobactam)
What can be added to penicillin antibiotics to prevent resistance?
A beta-lactamase inhibitor
(3) beta-lactamase inhibitors = ___bactam, ___bactam, ___ acid
sulbactam, tazobactam, clavulanic acid
Penicillins end in -___
-cillin
Examples = penicillin ampicillin, amoxicillin, piperacillin, ticarcillin, oxacillin, nafcillin, dicloxacillin, methicillin
Zosyn = ___ + ___
piperacillin + tazobactam
Penicillin ___ (is/is not) stable to beta lactamase
Penicillin is NOT stable to beta lactamase (have to add a beta-lactamase inhibitor to it)
What is Jarisch-Herxheimer reaction? What antibiotic may cause it?
high fevers, rash, similar to Rocky Mountain spotted fever; penicillin may cause it
If someone has a penicillin allergy, what are the next antibiotic choices? ___ or ___
vancomycin or cleocin
Clinical Infectious Diseases October 2017–patients with a reported penicillin allergy had a 50% increased odds of SSI, attributable to the receipt of ___-line perioperative antibiotics
attributable to the receipt of second-line perioperative antibiotics
Because people with penicillin allergy will often receive vancomycin or cleocin instead–vanco only covers gram positive infections (staph, strep); cleocin has some broad spectrum coverage but doesn’t really cover some of the common bacteria that cause SSIs
MRSA and C. diff rates are ___ (lower/higher) in patients with a reported penicillin allergy because they have higher use of ___-spectrum antibiotics
MRSA and C. diff rates are higher in patients with a reported penicillin allergy because they have higher use of broad spectrum antibiotics
What antibiotic has the highest rates of resultant C. Diff infection?
Cleocin
Pencillins, when given alone, ___ (are/are not) stable to beta-lactamase
Penicillins, when given alone, are NOT stable to beta-lactamase
Penicillins with beta lactamase inhibitors ___ (do/do not) cover MRSA
Penicillins with beta lactamase inhibitors do NOT cover MRSA
Ticarcillin +/- Clavulanate (Timentin) causes what electrolyte abnormalities?–___natremia, ___kalemia
hypernatremia, hypokalemia
Piperacillin +/- Tazobactam (Zosyn) side effects–prolonged ___ time; ___kalemia; ___penia at high doses
prolonged bleeding time; hypokalemia; neutropenia at high doses
Spectrum of action of cephalosporins is based on ___
generation
As you go up in generation of cephalosporins, you lose gram ___ coverage and gain gram ___ coverage
As you go up in generation of cephalosporins, you lose gram positive coverage and gain gram negative coverage
___ generation cephalosporins = cefazolin, cephalexin
1st generation
Half-life of ancef is ___ hours
1.8 hours
If procedure is going beyond ___ hours, need to redose ancef
If procedure is going beyond 4 hours, need to redose ancef
Cephalexin (keflex) and cefazolin (ancef) are both ___ eliminated
renally eliminated
Which 3rd generation cephalosporins cross the BBB and can be used to treat meningitis?
Ceftriaxone (rocephin); cefotaxime (claforan)
Ceftazidime (Fortaz) is a ___ generation cephalosporin; it covers most gram ___ with good ___ coverage
Ceftazidime (Fortaz) is a 3rd generation cephalosporin; it covers most gram negatives with good pseudomonas coverage
Ceftazidime (Fortaz) [3rd gen cephalosporin] + avibactam (beta lactamase inhibitor) offers significant gram ___ coverage and is usually reserved to treat ___
Ceftazidime (Fortaz) + avibactam offers significant gram negative coverage and is usually reserved to treat MDROs–multidrug resistant organisms
Ceftriaxone (Rocephin) is a ___ generation cephalosporin; it covers ___ better than most 3rd gens and most ___; covers most gram ___; ___ (does/does not) cover pseudomonas
Ceftriaxone (Rocephin) is a 3rd generation cephalosporin; it covers staph better than most 3rd gens and most strep; covers most gram negatives; does NOT cover pseudomonas
Side effects of ceftriaxone (rocephin) = ___ and biliary ___, particularly in young children; precipitates with ___ if running in the same IV line
diarrhea and biliary sludging, particularly in young children; precipitates with calcium if running in the same IV line
Main differences between ceftazidime (fortaz) and ceftriaxone (rocephin)–fortaz covers more gram ___, better ___ coverage; rocephin has more gram ___ coverage (not as good as 1st and 2nd generation cephalosporins), ___ (does/does not) cover pseudomonas
fortaz covers more gram negatives, better pseudomonas coverage; rocephin has more gram positive coverage (not as good as 1st and 2nd generation cephalosporins), does not cover pseudomonas
Ceftaroline (Teflaro) is a ___ generation cephalosporin; covers ___; gram ___ bacteria; has broad-spectrum activity against gram ___ bacteria
Ceftaroline (Teflaro) is a 5th generation cephalosporin; covers MRSA; gram positive bacteria; has broad-spectrum activity against gram negative bacteria
Cefiderocol (Fetroja) is a ___ generation cephalosporin; it is the first cephalosporin to cover ___
Cefiderocol (Fetroja) is a 5th generation cephalosporin (just came out in 2020); it is the first cephalosporin to cover Acinetobacter baumannii complex
Carbapenems–imipenem/cilastatin (primaxin) … cilastatin ___ (is/is not) a beta-lactamase inhibitor
cilastatin is NOT a beta-lactamase inhibitor
What does cilastatin do?–it inhibits ___ enzyme from breaking down imipenem
Cilastatin inhibits dihydropeptidase enzyme from breaking down imipenem
Imipenem/cilastatin (primaxin) has a high risk of ___
seizures
Primaxin [imipenem/cilastatin] + relebactam = ___, reserved for ___ gram negative infections in the ___ and ___
Primaxin [imipenem/cilastatin] + relebactam = recarbrio, reserved for MDRO gram negative infections in the urine and abdomen
Meropenem is a ___; it has a ___ (lower/higher) incidence of seizures than imipenem
Meropenem is a carbapenem; it has a lower incidence of seizures than imipenem
Primaxin vs. meropenem–primaxin has ___ (better/worse) coverage, ___ (lower/higher) risk of seizures; meropenem has (better/worse) coverage, ___ (lower/higher) risk of seizures
Primaxin has better coverage, higher risk of seizures; meropenem has worse coverage, lower risk of seizures
Ertapenem (Invanz) has a ___ (low/high) seizure risk
low seizure risk
Vancomycin inhibits ___ formation; disrupts cell wall ___; bacteri___; ___ (concentration/time) dependent
Vancomycin inhibits peptidoglycan formation; disrupts cell wall synthesis; bactericidal; concentration dependent
Vanco is given PO to treat ___ only; usually is given IV for treatment of other infections
Vanco is given PO to treat C. diff only; usually is given IV for treatment of other infections
If you take vanco orally, it does not leave the GI tract–T/F?
True
Vancomycin ___ (is/is not) a beta lactam
Vancomycin is not a beta lactam
Beta lactams are ___ (time/concentration) dependent
Beta lactams are time dependent
Vancomycin is ___ (time/concentration) dependent
Vancomycin is concentration dependent
Vancomycin offers ___ (broad/narrow) spectrum gram ___ (positive/negative) coverage
Vancomycin offers broad spectrum gram positive coverage
Treats staph, strep, enterococci, C. diff
Side effects of vanco = ___ syndrome; ___toxicity; ___toxicity; ___penia
Red-Man syndrome; nephrotoxicity; ototoxicity; thrombocytopenia
Vanco weight based dosing–___mg/kg
15 mg/kg
1 g usually does not cut it as a loading dose
Linezolid (Zyvox) inhibits protein synthesis by binding ___S ribosomal subunit of the ___S ribosome to prevent the formation of a functional ___S initiation complex
Linezolid (Zyvox) inhibits protein synthesis by binding 23S ribosomal subunit of the 50S ribosome to prevent the formation of a functional 70S initiation complex
Side effects of linezolid (Zyvox)–___suppression–___emia, ___penia, ___penia, ___penia…check CBC; drug interaction with ___, potential for ___ syndrome
myelosuppression–anemia, leukopenia, pancytopenia, thrombocytopenia…check CBC; drug interaction with MAO (monoamine oxidase), potential for serotonin syndrome
What should you do if a person is on an SSRI and is going to be started on linezolid (Zyvox)?
Hold SSRI to prevent the development of serotonin syndrome because linezolid is a MAOI
Azithromycin (Zithromax) is a ___; half-life is ___ hours, only dose ___ per day; may prolong ___ interval
Azithromycin (Zithromax) is a macrolide; half-life is 68 hours, only dose once per day; may prolong QT interval
Azithromycin (Zithromax) has drug interactions with ___phylline, ___sporine, ___toin, ___mazepine, ___vudine; interactions ___ (are/are not) a CYP3A4 mechanism
theophylline, ciclosporine, phenytoin, carbamazepine, zidovudine (AZT–azidothymidine…drug used to prevent/treat HIV/AIDS); interactions are NOT a CYP3A4 mechanism (so it’s not an inhibitor or inducer of these medications)
Macrolides end in -___
-thromycin
Clarithromycin (Biaxin) may prolong ___ interval, has significant ___ toxicity, same drug interactions as azithromycin but is a potent ___ (inhibitor/inducer) of CYP3A4
Clarithromycin (Biaxin) may prolong QT interval, has significant GI toxicity, same drug interactions as azithromycin but is a potent inhibitor of CYP3A4
Erythromycin is the drug of choice for ___ disease; also used to treat gastro___, alternative to reglan
drug of choice for Legionnaires’ disease; also used to treat gastroparesis, alternative to reglan (because reglan has extrapyramidal side effects)
Which macrolide has the most drug interactions?
Clarithromycin (Biaxin) because it is a CYP3A4 inhibitor
But all macrolides have CYP3A4 drug interactions
Fluoroquinolones have many drug interactions–___s, ___, ant___, ___, pro___
NSAIDs, warfarin, antacids, amiodarone, probenecid–used to treat gout
How do fluoroquinolone work?–inhibit ___ synthesis
inhibit DNA synthesis
FDA safety communication for fluoroquinolones–black box warning for patients > ___ years
black box warning for patients > 65 years
Avoid in elderly patients > 65 years when other antibiotics are appropriate
High risk of side effects with fluoroquinolones–___itis/___ tendon rupture; ___logic effects; ___glycemia (fatal); ___idity/___ality; ___ prolongation
tendonitis/Achilles tendon rupture; neurologic effects; hypoglycemia (fatal); morbidity/mortality; QT prolongation
Fluoroquinolones end in -___
-floxacin
Examples = ciprofloxacin, levofloxacin, ofloxacin, moxifloxacin
Main things to know for FQ antibiotics–they can cause ___ prolongation; they cover a lot of gram ___; black box warning for elderly > age ___
they can cause QT prolongation; they cover a lot of gram negatives; black box warning for elderly > age 65
Delafloxacin (Baxdela) is the first fluoroquinolone antibiotic with activity against ___; unlike other FQs, it is not associated with ___ prolongation or ___sensitivity
Delafloxacin (Baxdela) is the first fluoroquinolone antibiotic with activity against MRSA; unlike other FQs, it is not associated with QT prolongation or photosensitivity
Side effects of tetracycline antibiotics–___ upset; ___sensitivity; inhibition of ___ growth; ___toxicity; tooth dis___ and enamel ___plasia
Side effects of tetracycline antibiotics–GI upset, photosensitivity; inhibition of bone growth; hepatotoxicity; tooth discoloration (yellow teeth) and enamel hypoplasia
Tetracycline antibiotics inhibit bone growth during ___ and ___ trimesters through the age of ___
inhibit bone growth during 2nd and 3rd trimesters through the age of 8
Doxycycline (Vibramycin) has excellent tissue ___, including into the ___; causes permanent tooth ___; rare but fatal ___toxicity; drug interactions with ___farin, ___toin, ___pine, oral ___
Doxycycline (Vibramycin) has excellent tissue distribution, including into the CNS; causes permanent tooth discoloration; rare but fatal hepatotoxicity; drug interactions with warfarin, phenytoin, carbamazepine, oral contraceptives
Aminoglycosides are ___ and ___toxic, prolong ___ blockade
Aminoglycosides are oto and nephrotoxic, prolong neuromuscular blockade
Amikacin is an aminoglycoside used to treat ___
tuberculosis
Need to check ___ of aminoglycosides; want to prevent ___toxicity and ___toxicity
Need to check levels of aminoglycosides; want to prevent nephrotoxicity and ototoxicity
Bactrim affects ___ synthesis to starve out bacteria so that it can’t create new DNA
Bactrim affects folic acid synthesis to starve out bacteria so that it can’t create new DNA
Side effects of Bactrim–___cytopenia, ___penia, ___penia, ___ syndrome
pancytopenia, neutropenia, thrombocytopenia, Stevens Johnson Syndrome
Bactrim is a ___ antibiotic, so take ___ allergies seriously
Bactrim is a sulfonamide antibiotic, so take sulfa allergies seriously
Nitrofurantoin (Macrobid, Macrodantin) is used to treat ___ pathogens
urinary pathogens
Clindamycin (Cleocin) is used to treat ___ (aerobes/anaerobes), specifically ___ bacteria
Clindamycin (Cleocin) is used to treat anaerobes, specifically gut bacteria
Clindamycin (Cleocin) has the highest ___ risk; and can cause prolonged ___ blockade
Clindamycin (Cleocin) has the highest C. diff risk; and can cause prolonged neuromuscular blockade
What happens if you drink alcohol while taking flagyl?
Disulfiram like reaction–alcohol withdrawal symptoms
Flagyl interacts with what blood thinner?
Coumadin
Quinupristin/Dalfopristin (Synercid) (30/70) should be given via ___ due to significant phlebitis
should be given via central line due to significant phlebitis
Rifampin and Rifabutin are potent ___ (inhibitors/inducers) of the CYP 450 system with significant interactions
Rifampin and Rifabutin are potent inducers of the CYP 450 system with significant interactions
Rifampin and Rifabutin can rarely cause ___toxicity, ___ body fluids
Rifampin and Rifabutin can rarely cause hepatotoxicity, orange-red body fluids
What (3) antibiotics are OK to use in pregnant patients?
- Penicillins
- Cephalosporins
- Erythromycin
What (2) antibiotics should only be used in pregnancy if necessary?
- Aminoglycosides
- Isoniazid–usually only used to prevent or treat TB
What antibiotics should be avoided completely in pregnancy?–___dazole, ___cillin, ___fampin, ___prim, ___lones, ___cyclines
metronidazole, ticarcillin, rifampin, trimethoprim, fluoroquinolones, tetracyclines
Tetracycline in pregnant women is associated with acute ___ of the liver, ___titis, and possible ___ injury
Tetracycline in pregnant women is associated with acute fatty necrosis of the liver, pancreatitis, and possible renal injury
Canadian Population Study 11/2017–cleocin, doxycycline, FQs, macrolides, phenyoxymetylPCN = ___ (increased/decreased) risk of congenital malformations, risk of organ specific malfunctions; ___ (higher/lower) risk if used first trimester
increased risk of congenital malformations, risk of organ specific malfunctions; higher risk if used first trimester
Canadian Population Study 11/2017–___cillin, ___sporins, ___bid = no increased risk of congenital malformations/organ specific malfunctions
amoxicillin, cephalosporins, Macrobid = no increased risk of congenital malformations/organ specific malfunctions
Besides amphoteracin B, what other antibiotics cause hypokalemia?
penicillins–Piperacillin +/- tazobactam (zosyn), Ticarcillin +/- Clavulanate (Timentin)
First line treatment for status epilepticus = ___
benzos
Anticonvulsants MOA–___ channel blockade, ___ channel blockade
sodium channel blockade, calcium channel blockade
Anticonvulsants calcium channel blockade–particularly the ___-type channels located in the ___ which act as ‘pacemakers’ of normal rhythmic brain function
Anticonvulsants calcium channel blockade–particularly the T-type channels located in the thalamus which act as ‘pacemakers’ of normal rhythmic brain function
Anticonvulsants other MOAs–GABA ___ (enhancers/inhibitors); glutamate ___ (enhancers/blockers); carbonic anhydrase ___ (enhancers/inhibitors); ___ hormones; synaptic vesicle protein ___
GABA enhancers [remember GABA is inhibitory]; glutamate blockers [remember glutamate is excitatory]; carbonic anhydrase inhibitors; sex hormones; synaptic vesicle protein 2A (SV2A)
Carbamazepine is a ___ channel blocker
Carbamazepine is a sodium channel blocker
Carbamazepine ___ (induces/inhibits) its own metabolism
Carbamazepine induces its own metabolism
Carbamazepine is a CYP3A4 ___ (inducer/inhibitor)
Carbamazepine is a CYP3A4 inducer
What is the most important thing to consider about carbamazepine?
Drug interactions–because it is a CYP inducer/substrate, it ramps up the metabolism of other drugs and itself, clears medications from the bloodstream faster, and shortens the duration of action of other drugs
If patient is on carbamazepine, check ___ levels
sodium levels
Why was oxcarbazepine created?–to eliminate the auto-___ of carbamazepine
to eliminate the auto-induction of carbamazepine
As a person takes carbamazepine for a longer period of time, it loses its effectiveness because it’s an inducer and substrate–T/F?
True
Main concerns for the -carbazepine anticonvulsants–check ___ levels, check for drug ___, check ___/___s
check sodium levels, check for drug interactions, check CBC/LFTs
Phenytoin is a ___ channel blocker; has ___ (linear/non-linear) pharmacokinetics; CYP enzyme ___ and ___
Phenytoin is a sodium channel blocker; has non-linear pharmacokinetics; CYP inducer and substrate
What is the therapeutic range for phenytoin?
10-20
Dose adjustments for phenytoin are ___ (small/large)
Small because it has non-linear pharmacokinetics
Example: Patient is on 300 mg phenytoin. You check a level and it comes back at 5. You increase the dose to 300 mg bid. You re-check the level and it is 28, and patient is dizzy, nauseous, and having vision changes. You may just add 30-50 mg at a time to get to desired therapeutic levels for phenytoin.
Fosphenytoin = ___drug for ___ (oral/parenteral) administration
prodrug for parenteral administration
Side effects of phenytoin/fosphenytoin–gingival ___plasia; ___mias, CV ___, ___tension mostly at toxic levels; ___mus; vitamin ___ and ___ deficiencies; if given during pregnancy–cleft ___/___, congenital ___ disease, slowed ___ rate, mental ___
Side effects of phenytoin/fosphenytoin–gingival hyperplasia; arrhythmias, CV depression, hypotension mostly at toxic levels; nystagmus; vitamin K and folate deficiencies; if given during pregnancy–cleft lip/palate, congenital heart disease, slowed growth rate, mental deficiency
Lamotrigine is a ___ channel blocker
sodium channel blocker
If patient is on depakote/lamictal and stops taking both prior to surgery, if they are both not restarted in 3-4 days and you have to reinitiate, there is a long cross-taper period of 4-8 weeks where you can only make minor incremental increases in the dosages–T/F?
True
What happens if you reinitiate a person’s regular doses of depakote/lamictal after having stopped both drugs for 3-4 days or more?What happens if you reinitiate a person’s regular doses of depakote/lamictal after having stopped both drugs for 3-4 days or more?
Steven Johnsons syndrome–very high rates, can cause devastating skin reactions
Lamotrigine drug interaction with depakote = high risk of ___
high risk of SJS
Zonisamide side effects–can cause renal ___ in 1.5% of patients
can cause renal stones in 1.5% of patients
Lacosamide (Vimpat) has a ___ (low/high) side effect profile; pregnancy category ___
Lacosamide has a low side effect profile; pregnancy category C–still unsure of what the true risk is in pregnancy
Benzodiazepines should be restarted as soon as possible if held before/after a surgical procedure to avoid withdrawal–T/F?
True–continue Benzos as long as possible, restart ASAP
Higher lipophilicity for benzos = ___ (slower/faster) onset of action, ___ (shorter/longer) duration of action
higher lipophilicity for benzos = faster onset of action, longer duration of action
i.e.: diazepam (Valium), clonazepam (Klonopin)
Lower lipophilicity for benzos = ___ (slower/faster) onset of action, ___ (shorter/longer) duration of action
lower lipophilicity for benzos = slower onset of action, shorter duration of action
i.e.: alprazolam (xanax), temazepam (restoril)
Which benzodiazepine is only used for seizures and is not appropriate to use for anxiety/sleep? If this medication is discontinued, it needs to be restarted ASAP otherwise patient will experience wild withdrawal symptoms and will start seizing really quick. This medication has a long taper if you want to get a person off of it.
Clobazam (Onfi)
Vigabatrin has a risk of permanent ___, and for this reason is only available through a very specific program with REMS monitoring
Vigabatrin has a risk of permanent vision loss, and for this reason is only available through a very specific program with REMS monitoring
Gabapentin is more often used for ___ than ___ control
Gabapentin is more often used for neuropathic pain than seizure control
Gabapentin ___ (is/is not) protein bound, ___ (is/is not) metabolized, is excreted completely ___ (changed/unchanged) by the ___, ___ (has/has no) PK drug interactions
Gabapentin is not protein bound, is not metabolized, is excreted completely unchanged by the kidneys, has no PK drug interactions
A meta analysis of RCTs suggests that gabapentin given 1x 30 minutes pre-operatively in regional anesthesia for multiple procedures ___ (improves/worsens) post-op pain and ___ (increases/reduces) opiate requirements with increased post op ___ being the highest safety risk
A meta analysis of RCTs suggests that gabapentin given 1x 30 minutes pre-operatively in regional anesthesia for multiple procedures improves post-op pain and reduces opiate requirements with increased post op sedation being the highest safety risk
You may see increased side effects of gabapentin in patients with poor kidney function–T/F?
True–because it is completely eliminated by the kidneys
Gabapentin is very well tolerated–T/F?
True
December 2019 FDA safety communication–gabapentinoids in combo with opiates may lead to severe ___ distress
gabapentinoids in combo with opiates may lead to severe respiratory distress
Lots of people taking pregabalin complain of difficulty ___
Lots of people taking pregabalin complain of difficulty walking
Valproic acid drug interactions occur through ___ (stimulation/inhibition) of oxidation and glucuronidation pathways
Valproic acid drug interactions occur through inhibition of oxidation and glucuronidation pathways
In utero exposure to valproic acid leads to lower ___ in children compared to other anti-epileptics
In utero exposure to valproic acid leads to lower IQ in children compared to other anti-epileptics
Valproic acid is pregnancy category ___-___
Valproic acid is pregnancy category D-X
Valproic acid may cause ___penia
thrombocytopenia–just like carbamazepine family, heparin, H2 receptor antagonists, SSRIs
Valproic acid may cause ___ammonemia
Valproic acid may cause hyperammonemia
If someone is on depakote and becomes confused, what should you do?
Check ammonia level because depakote increases ammonia levels
What labs should be routinely checked if patient is on valproic acid?
Ammonia, LFTs, CBC
If patient is pregnant and in status epilepticus, you can give valproic acid–T/F?
False–never use depakote in pregnancy, even if patient is in status epilepticus
What are (3) glutamate blockers?–___bamate, ___ramate, ___ampanel
Felbamate (felbatol), topiramate (topamax), perampanel (fycompa)
Felbamate (felbatol) is very rarely used in the US because it has high risk of ___ anemia and fatal ___ failure
Felbamate (felbatol) is very rarely used in the US because it has high risk of aplastic anemia and fatal hepatic failure
What is one common side effect of topiramate (topamax)? ___ slowing
Psychomotor slowing–want to do something, but can’t make it happen
Perampanel black box warning–serious or life threatening ___ and ___ adverse effects
Perampanel black box warning–serious or life threatening psychiatric and behavioral adverse effects–aggression, hostility, irritability, anger, homicidal ideation, threats
Common side effect of perampanel (in 43% of patients) = ___
dizziness
Levetiracetam MOA is possibly related to synaptic vesicle protein ___, which appears to be important for the availability of __-dependent neurotransmitter vesicles ready to release their content
Levetiracetam MOA is possibly related to synaptic vesicle protein 2A, which appears to be important for the availability of calcium-dependent neurotransmitter vesicles ready to release their content
Keppra–without SV2A, reduced action potential-___ (independent/dependent) neurotransmission, while action potential-___ (independent/dependent) neurotransmission remains normal
Keppra–without SV2A, reduced action-potential dependent neurotransmission, while action potential-independent neurotransmission remains normal
Keppra also inhibits ___ release from IP3-sensitive stores
Keppra also inhibits calcium release from IP3-sensitive stores
A significant side effect of keppra is ___ impairment
A significant side effect of keppra is cognitive impairment–have a convo and don’t even remember having it
Baclofen is a ___ analog
Baclofen is a GABA analog
Substance ___ is released in response to pain impulses
Substance P is released in response to pain impulses
How does baclofen work?–it inhibits substance ___ release into the spinal cord to reduce pain
Baclofen inhibits substance P release into the spinal cord to reduce pain
If baclofen is abruptly discontinued, patients will experience ___ symptoms–i.e.: ___nations, ___er, ___tation, ___or, ___cardia, ___ure
If baclofen is abruptly discontinued, patients will experience withdrawal symptoms–i.e.: hallucinations, fever, agitation, tremor, tachycardia, seizure
Tizanidine is a centrally acting alpha ___–slows down ___ release using negative feedback
Tizanidine is a centrally acting alpha 2 agonist–slows down NE release using negative feedback
Withdrawal is possible with abrupt discontinuation of tizanidine–T/F?
True
Side effects of tizanidine–___ mouth, ___ation, anti___ effects
Side effects of tizanidine–dry mouth, sedation, anticholinergic effects
Dantrolene blocks ___ channel, reduces ___ release from the ___
Dantrolene blocks ryanodine channel, reduces calcium release from the sarcoplasmic reticulum
___ mutations are associated with malignant hyperthermia
RyR1 mutations are associated with malignant hyperthermia
Dantrolene has dose dependent ___rrhea and ___toxicity (BB warning > ___mg/day with long term use)
Dantrolene has dose dependent diarrhea and hepatotoxicity (BB warning > 800 mg/day with long term use)
Other side effects of dantrolene–___nea, ___phagia, ___lence
Other side effects of dantrolene–dyspnea, dysphagia, somnolence
Skeletal muscle relaxants have risks of ___ sedation and ___
Skeletal muscle relaxants have risks of over sedation and withdrawal
Zolpidem (Ambien), Zaleplon (Sonata), and Eszopiclone (Lunesta) are all ___, AKA ___-drugs
Zolpidem (Ambien), Zaleplon (Sonata), and Eszopiclone (Lunesta) are all sedative hypnotics, AKA Z-drugs
Ramelteon (Rozerem) is a ___ receptor agonist
Ramelteon (Rozarem) is a melatonin receptor agonist
Suvorexant (Belsomra) is a ___ antagonist; is associated with significant sleep ___
Suvorexant (Belsomra) is a norexin 2 antagonist; is associated with significant sleep activities
Sedative hypnotics ___ (should/should not) be used regularly in the hospital to help patients sleep
Sedative hypnotics should NOT be used regularly in the hospital to help patients sleep
Sedative hypnotics like Zolpidem (Ambien) are benzodiazepine like drugs–T/F?
True
Patients can go through withdrawal when they stop taking sedative hypnotics like ambien, sonata, and Lunesta–T/F?
True–withdrawal symptoms include insomnia and anxiety
Sedative hypnotics help people fall asleep and provide restorative REM sleep–T/F?
FALSE–sedative hypnotics DO help people fall asleep, but they DO NOT provide restorative REM sleep
“Sleep behaviors” are very common with Z drugs, i.e.: sleep eating, sleep fighting, sleep walking; patients can hurt themselves when they take these medications–T/F?
True
Ramelteon and melatonin help you fall asleep–T/F?
True
Ramelteon and melatonin will help if you have difficulty staying asleep–T/F?
False–do not help you stay asleep, just help you fall asleep
(6) classes of antidepressant medications
- TCAs
- SSRIs
- SNRIs
- DNRIs
- 5HT2A antagonists
- Nuedexta
TCAs MOA–___ and ___ reuptake inhibition, anti___, ___ antiarrhythmic
TCAs MOA–serotonin and norepinephrine reuptake inhibition, anticholinergic, 1A antiarrhythmic
TCAs are not typically used to treat depression anymore, but may still be used to treat neuropathic pain/migraines–T/F?
True–have fallen out of favor to treat depression since prozac came out
Side effects of TCAs–anticholinergic side effects–___pation, ___fusion, ___tation in elderly/children, urinary ___, ___ vision, ___ mouth; CV effects–QT ___, ___mias
Side effects of TCAs–anticholinergic side effects–constipation, confusion, agitation in elderly/children, urinary retention, blurred vision, dry mouth; CV–QT prolongation, arrhythmias
TCA overdose–administer ___ d/t metabolic ___osis, supportive therapy
TCA overdose–administer NaHCO3 d/t metabolic acidosis, supportive therapy
Serotonin excitatory receptors
2, 3, 4, 6, 7
Increase cAMP
Serotonin inhibitory receptors
1, 5
Decrease cAMP
Side effects of SSRIs–___natremia, ___cytopenia, ___ality, ___mias, ___ syndrome, ___/___/___, weight ___
Side effects of SSRIs–hyponatremia, thrombocytopenia, suicidality, arrhythmias, serotonin syndrome, nausea/vomiting/diarrhea, weight fluctuations
All antidepressants, most anticonvulsant mood stabilizers, and most psychiatric medications have a black box warning for ___
suicidality
Neuroleptic malignant syndrome is precipitated by ___ antagonists; onset is ___-___ days
Neuroleptic malignant syndrome is precipitated by dopamine antagonists; onset is 1-3 days
Serotonin syndrome is precipitated by ___ agents; onset is < ___ hours
Serotonin syndrome is precipitated by serotonergic agents; onset is < 12 hours
NMS and SS identical features–___tension, ___cardia, ___pnea, ___thermia, ___salivation, ___phoresis
NMS and SS identical features–hypertension, tachycardia, tachypnea, hyperthermia (> 40 C), hypersalivation, diaphoresis
NMS demonstrates ‘___’ rigidity in all muscle groups
NMS demonstrates ‘lead-pipe’ rigidity in all muscle groups
SS has ___ (increased/decreased) muscle tone, especially in ___ (upper/lower) extremities
SS has increased muscle tone, especially in lower extremities
NMS distinct features–___reflexia, pupils ___ (normal/dilated), bowel sounds ___ (normal/increased/decreased)
NMS distinct features–hyporeflexia, pupils normal, normal bowel sounds
SS distinct features–___reflexia, ___ unless masked by increased muscle tone, pupils ___ (normal/dilated), bowel sounds ___active
SS distinct features–hyperreflexia, clonus unless masked by increased muscle tone, pupils dilated, bowel sounds hyperractive
What antibiotic can cause serotonin syndrome?
Linezolid (because it is an MAOI)
Opioids can cause serotonin syndrome–T/F?
True
Serotonin syndrome has a slower onset than neuroleptic malignant syndrome–T/F?
False–serotonin syndrome has a faster onset (<12 hours) than neuroleptic malignant syndrome (1-3 days)
Neuroleptic malignant syndrome has ___reflexia, whereas serotonin syndrome has ___reflexia
Neuroleptic malignant syndrome has hyporeflexia, whereas serotonin syndrome has hyperreflexia
Neuroleptic malignant syndrome pupils are ___, serotonin syndrome pupils are ___
Neuroleptic malignant syndrome pupils are normal, serotonin syndrome pupils are dilated
How do SNRIs like duloxetine, venlafaxine, desvenlafaxine, and levomilnacipran work?–___ and ___ reuptake inhibition
serotonin and norepinephrine reuptake inhibition
SRNIs side effects–___ syndrome, ___toxicity, ___tension, ___nia, abnormal ___, ___somnolence throughout the day d/t sleep interruptions throughout the night, ___/___/___, weight ___ (loss/gain), ___or, ___tation
SNRIs side effects–serotonin syndrome, hepatotoxicity, hypertension, insomnia, abnormal dreams, hypersomnolence throughout the day d/t sleep interruptions throughout the night, nausea/vomiting/diarrhea, weight loss, tremor, agitation
SNRIs can also cause ___natremia and ___cytopenia just like SSRIs
SNRIs can also cause hyponatremia and thrombocytopenia just like SSRIs
Mirtazepine (Remeron) and Trazodone (Desryl) are ___ antagonists
Mirtazepine (Remeron) and Trazodone (Desryl) are 5HT2A antagonists
Think ___ with mirtazepine (remeron) and trazodone (desryl)
sedation
Nuedexta is a combination of ___ and ___
Nuedexta is a combination of dextromethorphan and quinidine
Nuedexta is the only medication approved by the FDA to treat ___
Nuedexta is the only medication approved by the FDA to treat pseudobulbar affect
Pseudobulbar affect is inappropriate ___ or ___, seen in patients with ___
Pseudobulbar affect is inappropriate crying or laughing, seen in patients with TBI
Check ___ if someone is on a neuropsychiatric medication
platelets…many of these meds cause thrombocytopenia
Lithium is a mood ___
Lithium is a mood stabilizer
Side effects of lithium–diabetes ___, ___uria, ___dipsia
diabetes insipidus, polyuria, polydipsia
It is important to check ___ levels and ___ levels in patients on lithium
It is important to check sodium levels and lithium levels in patients on lithium
What is the difference between first and second generation antipsychotics?
First generation = mostly dopamine (D2) blockers; second generation = S2, D2 blockers
Chlorpromazine (thorazine); prochlorperazine (compazine); and haloperidol (haldol) are all ___ (first/second) generation antipsychotics
first generation antipsychotics
Aripiprazole (Abilify); clozapine (clozaril); olanzapine (zyprexa); quetiapine (Seroquel); risperidone (risperdal) are all ___ (first/second) generation antipsychotics
second generation antipsychotics
Dopamine pathways in the CNS–meso___ = positive symptoms of schizophrenia and psychosis
Dopamine pathways in the CNS–mesolimbic = positive symptoms of schizophrenia and psychosis
Dopamine pathways in the CNS–meso___ = negative symptoms, cognitive and affective symptoms
Dopamine pathways in the CNS–mesocortical = negative symptoms, cognitive and affective symptoms
Dopamine pathways in the CNS–___ = Parkinsonian effects, i.e.: extrapyramidal symptoms, tardive dyskinesias
Dopamine pathways in the CNS–nigrostriatal = Parkinsonian effects, i.e.: extrapyramidal symptoms, tardive dyskinesias
Dopamine pathways in the CNS–___ = hyperprolactinemia
Dopamine pathways in the CNS–tuberohypophyseal = hyperprolactinemia
Side effects of antipsychotics–___ symptoms, ___ dyskinesias; metabolic side effects–weight ___ (gain/loss), ___glycemia; CNS side effects–___gy, ___ation, ___fusion; CV–QT ___, especially with ___
Side effects of antipsychotics–extrapyramidal symptoms, tardive dyskinesias; metabolic side effects–weight gain, hyperglycemia; CNS side effects–lethargy, sedation, confusion; CV–QT prolongation, especially with haldol
Black box warning for clozaril 2008–___ related death, ___cytosis
Black box warning for clozaril 2008–dementia (CV/stroke) related death, agranulocytosis
Antipsychotics should be used as a last resort when a patient is a risk to others and/or themselves–T/F?
True
Carbidopa/Levodopa (Sinemet) and Carbidopa/Levodopa/Entacapone (Stalevo) are ___ analogs
dopamine analogs
___ = dopamine precursor, looks and acts like dopamine
Levodopa = dopamine precursor, looks and acts like dopamine
___ = false dopamine; confuses the enzymes MAO and COMT to prevent breakdown of levodopa
Carbidopa = false dopamine; confuses the enzymes MAO and COMT to prevent breakdown of levodopa
___ = COMT inhibitor, has no effect on dopamine
Entacapone (Comtan) = COMT inhibitor, has no effect on dopamine
Benztropine (Cogentin) and trihexyphenidyl (Artane) are anti___ used to treat ___ associated with antipsychotic administration
Benztropine (Cogentin) and trihexyphenidyl (Artane) are anticholinergics used to treat EPS associated with antipsychotic administration
MAOB inhibitors rasaligine (azilect) and selegiline (eldepryl) ___ (increase/decrease) dopamine availability via enzyme inhibition
MAOB inhibitors rasaligine (azilect) and selegiline (eldepryl) increase dopamine availability via enzyme inhibition
If you have a patient on MAOB inhibitors, you may see exaggerated effects of epi, NE, or ephedrine–T/F?
True
Two classes of Alzheimer’s medications–___ inhibitors, ___ receptor antagonist
acetylcholinesterase inhibitors, NMDA receptor antagonist
Side effects of acetylcholinesterase inhibitors–‘___’ side effects–___cardia, ___ stools, ___ bladder
‘rest and digest’ side effects–bradycardia, loose stools, overactive bladder
Acetylcholinesterase inhibitors drug interactions–anti___, ___choline, ___ neuromuscular blockers
anticholinergics, succinylcholine, non depolarizing neuromuscular blockers
Acetylcholinesterase inhibitors ___ (potentiate/reduce) the effects of succinylcholine
Acetylcholinesterase inhibitors potentiate the effects of succinylcholine (because you’re flooding the receptors with acetylcholine)
Acetylcholinesterase inhibitors ___ (potentiate/reduce) the effects of nondepolarizing neuromuscular blockers
Acetylcholinesterase inhibitors reduce the effects of nondepolarizing neuromuscular blockers
What benzodiazepine has risk of wild withdrawal when stopped abruptly?
ONFI
Delirium and dementia are two different things–T/F?
True
Post op delirium may be fatal and is preventable in up to 40% of cases–T/F?
True
Almost 50% of cases of delirium are not reported–T/F?
True
Post op delirium may occur in up to 75% of cases–T/F?
True
JAMA Surgery 2018 STRIDE Trial–hip fracture repair, reducing sedation levels to reduce post op delirium–in the primary analysis, limiting the level of sedation provided no significant benefit in reducing incident delirium–T/F?
True
JAMA Surgery 2018 STRIDE Trial–hip fracture repair, reducing sedation levels to reduce post op delirium–in a prespecified subgroup analysis, lighter sedation levels reduced postoperative delirium for persons with a Charlson Comorbidity Index of 0 (less sick patients)–T/F?
True
Antipsychotics should not be used unless patient is at risk of harm to self or others–T/F?
True
If using antipsychotics, use the ___ (lowest/highest) dose for the ___ (shortest/longest) duration
If using antipsychotics, use the lowest dose for the shortest duration
Prophylactic low dose PO haloperidol did reduce delirium incidence in acutely hospitalized older patients–T/F?
FALSE–DID NOT reduce delirium incidence in acutely hospitalized older patients
Prophylactic haldol reduces mortality in critically ill adults at high risk of delirium–T/F?
FALSE–prophylactic haldol DOES NOT reduce mortality in critically ill adults at high risk of delirium
Benzos exacerbate delirium–T/F?
True
The ___ sets up the final concentration of urine
The nephron sets up the final concentration of urine
___ inside Bowman’s capsule is responsible for filtration; ___% of plasma that arrives here passes through the filtration barrier to become filtrate
Glomerulus inside Bowman’s capsule is responsible for filtration; 25% of plasma that arrives here passes through the filtration barrier to become filtrate
Carbonic anhydrase inhibitors and osmotic diuretics work on the ___ tubule
Carbonic anhydrase inhibitors and osmotic diuretics work on the PROXIMAL tubule
Loop diuretics work on the ___
Loop diuretics work on the LOOP OF HENLE
___ (ascending/descending) loop of Henle is responsible for water reabsorption, sodium diffuses in
Descending loop of Henle is responsible for water reabsorption, sodium diffuses in
___ (ascending/descending) loop of Henle is responsible for active reabsorption of sodium, water stays in
Ascending loop of Henle is responsible for active reabsorption of sodium, water stays in
Thiazide diuretics work on the ___ (proximal/distal) tubule
Thiazide diuretics work on the DISTAL tubule
Reabsorption of water in the distal tubule requires ___
ADH
Reabsorption of water in the collecting duct requires ___
ADH
The final concentration of urine is determined in the ___
collecting duct
Chronic kidney disease = kidney damage for > ___ months defined by structural or functional abnormalities with or without decreased GFR
kidney damage for > 3 months defined by structural or functional abnormalities with or without decreased GFR
Chronic kidney disease = GFR < ___ ml/min for > ___ months with or without structural kidney damage
Chronic kidney disease = GFR < 60 ml/min for > 3 months with or without structural kidney damage
Stages of chronic kidney disease = stages ___-___
Stages 1-6
Stage 1 CKD = damage with normal or increased GFR–GFR > ___ ml/min
GFR > 90 ml/min
Stage 2 CKD = damage with mildly deceased GFR–GFR __-__ ml/min
GFR 60-89 ml/min
Stage 3 CKD = moderately deceased GFR–GFR __-__ ml/min
GFR 30-59 ml/min
Stage 4 CKD = severely deceased GFR–GFR __-__ ml/min
GFR 15-29 ml/min
Stage 5 CKD = kidney failure–GFR < ___ ml/min
GFR < 15 ml/min
Stage 6 CKD = ___
dialysis
Acute kidney disease is kidney damage for < ___ months
< 3 months
RIFLE criteria for acute kidney disease stands for ___
- Risk
- Injury
- Failure
- Loss of kidney function
- ESRD
Risk = increased Cr x ___ or decreased GFR by ___%; UO < 0.5 ml/kg/hr for ___ hours
Risk = increased Cr x 1.5 or decreased GFR by 25%; UO < 0.5 ml/kg/hr for 6 hours
Injury = increased Cr x ___ or decreased GFR by ___%; UO < 0.5 ml/kg/hr for ___ hours
Injury = increased Cr x 2 or decreased GFR by 50%; UO < 0.5 ml/kg/hr for 12 hours
Failure = increased Cr x ___ OR Cr > ___ mg/dl or decreased GFR by ___%; UO < 0.5 ml/kg/hr for ___ hours
Failure = increased Cr x 3 OR Cr > 4 mg/dl or decreased GFR by 75%; UO < 0.5 ml/kg/hr for 24 hours
Loss of kidney function = persistent acute kidney disease, complete loss of kidney function > ___ weeks
Loss of kidney function = persistent acute kidney disease, complete loss of kidney function > 4 weeks
ESRD = end stage > ___ months
ESRD = end stage > 3 months
Pre-renal kidney disease = ___
dehydration
Intrinsic kidney disease = ___
drug damage, i.e.: NSAIDs
Post-renal kidney disease = ___
blockage preventing urine from freely flowing, causing a back up
What are (6) classes of diuretics?
- Carbonic anhydrase inhibitors
- Osmotic diuretics
- Loop diuretics
- Thiazide diuretics
- Potassium sparing diuretics
- Aldosterone antagonists
What is most commonly used carbonic anhydrase inhibitor?
Acetazolamide (Diamox)
How do carbonic anhydrase inhibitors work?–inhibit ___, which inhibits ___ secretion in the ___ (proximal/distal) tubule; ___ and ___ are blocked from reabsorption
inhibit carbonic anhydrase, which inhibits H+ secretion in the proximal tubule; bicarb and sodium are blocked from reabsorption
Carbonic anhydrase inhibitors cause ___ to be lost in the urine
Carbonic anhydrase inhibitors cause bicarb to be lost in the urine [water follows into the urine]
Carbonic anhydrase inhibitors cause ___kalemic metabolic ___osis as an effect
Carbonic anhydrase inhibitors cause hypokalemic metabolic acidosis as an effect
Tolerance to carbonic anhydrase inhibitors may develop after ___-___ days; why?
Tolerance to carbonic anhydrase inhibitors may develop after 2-3 days
Because they work very early on in the nephron (at the proximal tubule)–there is still a lot of time/traveling left in the nephron, still a lot of opportunities for water to be reabsorbed; even though we are holding water in the urine at the front of the nephron, it can still be reabsorbed later
REVIEW–carbonic anhydrase inhibitors work at the ___ tubule; cause a loss of ___ to the urine; can lead to ___kalemic metabolic ___osis; tolerance may develop after __-__ days
carbonic anhydrase inhibitors work at the proximal tubule; cause a loss of bicarb to the urine; can lead to hypokalemic metabolic acidosis; tolerance may develop after 2-3 days
Common side effects of carbonic anhydrase inhibitors–___ vision; changes in ___; ___/___/___/___ [all GI effects]; ___siness; frequent ___; loss of ___
blurred vision; changes in taste; nausea/vomiting/constipation/diarrhea; drowsiness; frequent urination; loss of appetite
Two osmotic diuretics = ___ and ___
Two osmotic diuretics = mannitol and urea
Where do osmotic diuretics work?
Proximal tubule
How do osmotic diuretics work?–increase the ___ gradient in the ___ (proximal/distal) tubule
increase the osmotic gradient in the proximal tubule
Basically create a big bulky molecule [a concentration gradient] that begins to pull water in through osmosis
Mannitol results in a significant loss of ___; reduced ___ (intra/extra)cellular volume; ___natremia risk
Mannitol results in a significant loss of water; reduced intracellular volume; hypernatremia risk
Why is hypernatremia a risk with mannitol?
Because the sodium reabsorption cannot keep up with the loss of water
Mannitol has an osmotic diuretic effect in the renal tubules that results in the urinary excretion of ___, ___, ___, and ___
urinary excretion of water, sodium, chloride, and bicarbonate ion
Urinary pH ___ (is/is not) altered by mannitol-induced osmotic diuresis
Urinary pH is NOT altered by mannitol-induced osmotic diuresis
IV mannitol ___ (increases/decreases) the plasma osmolarity; it draws fluid from ___cellular to ___cellular spaces; it acutely expands the ___ fluid volume
IV mannitol increases the plasma osmolarity; it draws fluid from intracellular to extracellular spaces; it acutely expands the intravascular fluid volume
Detrimental effects of redistribution from mannitol = ___ in patients with poor myocardial function
Detrimental effects of redistribution from mannitol = CHF in patients with poor myocardial function
Clinical uses of mannitol–prophylaxis against acute ___ failure; differential diagnosis of acute ___ria; treatment of increase in ___; decreasing ___ pressure
Clinical uses of mannitol–prophylaxis against acute renal failure; differential diagnosis of acute oliguria; treatment of increase in ICP; decreasing intraocular pressure
Mannitol ARF prophylaxis–there ___ (is/is not) true evidence that mannitol is nephroprotective
There is NOT true evidence that mannitol is nephroprotective
Mannitol ARF prophylaxis–mannitol ___ (is/is not) better than plain saline pre-radiocontrast dye
Mannitol is NOT better than plain saline pre-radiocontrast dye
Mannitol ARF prophylaxis–mannitol is only shown to be nephroprotective in what type of surgery?
Mannitol is only shown to be nephroprotective in renal transplant surgery–less incidence of ARF
Mannitol will increase urine output when the cause of acute oliguria is decreased intravascular fluid volume–T/F?
True
If glomerular or renal tubular function is severely compromised, mannitol will increase urine output–T/F?
FALSE–mannitol will NOT increase urine output if glomerular or renal tubular function is severely compromised
If mannitol is being used to treat increased ICP, it is important that the person has an intact blood-brain barrier–T/F?
True
Without intact blood-brain barrier, osmosis won’t be able to occur and you won’t get any benefit from using mannitol. Can lead to cerebral edema if BBB is not intact.
Mannitol ___ (increases/decreases) plasma osmolarity; ___ (increases/decreases) CSF volume by ___ (increasing/decreasing) the rate of CSF formation
Mannitol increases plasma osmolarity; decreases CSF volume by decreasing the rate of CSF formation
Chronic mannitol use reduces its effectiveness-T/F?
True
Mannitol can cause vaso___ (dilation/constriction) of vascular smooth muscle; this can ___ (increase/decrease) cerebral blood volume and ICP, ___ (increase/decrease) systemic blood pressure
Mannitol can cause vasodilation of vascular smooth muscle; this can increase cerebral blood volume and ICP, decrease systemic blood pressure
Because mannitol may initially increase ICP, you should infuse the selected dose over about ___ minutes; administer the dose in conjunction with treatments that decrease ICP, i.e.: ___ and ___ventilation
Because mannitol may initially increase ICP, you should infuse the selected dose over about 10 minutes; administer the dose in conjunction with treatments that decrease ICP, i.e.: corticosteroids and hyperventilation
Side effects of mannitol–may precipitate pulmonary ___; ___volemia; electrolyte ___; plasma ___osmolarity d/t water and NaCl secretion
may precipitate pulmonary edema; hypovolemia; electrolyte disturbances; plasma hyperosmolarity d/t water and NaCl secretion
Urea is another osmotic diuretic that has fallen out of favor because it has greater rebound increase in ___ than mannitol
Urea is another osmotic diuretic that has fallen out of favor because it has greater rebound increase in ICP than mannitol
Urea also has high incidence of venous ___ and tissue ___ after extravasation
Urea also has high incidence of venous thrombosis and tissue necrosis after extravasation (not seen with mannitol)
(3) loop diuretics =
- Furosemide (Lasix)
- Bumetanide (Bumex)
- Torsemide (Demedex)
What is (1) non-sulfa loop diuretic?
Ethacrynic acid (Edecrin)
Caution using lasix, bumex, and demedex in patients with ___ allergy
sulfa allergy
How do loop diuretics work?–inhibit ___ and ___ reabsorption in the ___ (ascending/descending) loop
Inhibit Na and Cl reabsorption in the ascending loop [and to a lesser extent in the proximal tubule]
You get more significant and sustained diuretic effects with loop diuretics than with CAIs or osmotic diuretics–T/F?
True
Loop diuretics block reabsorption of ___, ___, and 2 ___ in the ___; also lose ___ and ___ secondarily
Loop diuretics block reabsorption of sodium, potassium, and 2 chloride in the loop of Henle; also lose calcium and magnesium secondarily
Loop diuretics as a class have the most significant electrolyte loss out of all other diuretics–T/F?
True
Loop diuretics may cause ___kalemic metabolic ___osis
Loop diuretics may cause hypokalemic metabolic alkalosis
CAIs may cause ___kalemic metabolic ___osis; loops may cause ___kalemic metabolic ___osis
CAIs may cause hypokalemic metabolic acidosis; loops may cause hypokalemic metabolic alkalosis
What labs should be checked frequently in patients on a loop diuretic?
BMP + Mg
Furosemide renovascular effect–furosemide induced production of prostaglandins results in renal vaso___ and ___ (increased/decreased) renal blood flow
Furosemide renovascular effect–furosemide induced production of prostaglandins results in renal vasodilation and increased renal blood flow
Furosemide induced increases in RBF are inhibited by ___ (what medication class?), resulting in an attenuated (lessened) diuretic effect
Furosemide induced increases in RBF are inhibited by NSAIDs, resulting in an attenuated (lessened) diuretic effect
Furosemide induced production of prostaglandins also leads to ___tension by causing vaso___
Furosemide induced production of prostaglandins also leads to hypotension by causing vasodilation
Clinical uses of loop diuretics = mobilization of ___ d/t renal, hepatic, or cardiac dysfunction; treatment of increased ___; treatment of ___calcemia; differential diagnosis of acute ___
mobilization of fluid d/t renal, hepatic, or cardiac dysfunction; treatment of increased ICP; treatment of hypercalcemia; differential diagnosis of acute oliguria
Combination of mannitol + lasix is greater than either drug alone–T/F?
True, synergistic effect when used together
Mannitol pulls as much fluid out of the extravascular space into the intravascular space; lasix keeps the fluid within the nephron through the movement of electrolytes and then all are excreted in the urine
Peripheral vasodilation precedes the onset of diuresis when lasix is given–T/F?
True
Decreased venous return from lasix administration provides prompt effects in the management of acute pulmonary ___
Decreased venous return from lasix administration provides prompt effects in the management of acute pulmonary edema
Lasix increases lymph flow through the ___ duct
Lasix increases lymph flow through the thoracic duct
Decreased ICP d/t lasix is NOT accompanied by changes in ___ blood flow or changes in plasma ___
Decreased ICP d/t lasix is NOT accompanied by changes in cerebral blood flow or changes in plasma osmolarity
Unlike mannitol–which causes [initially] increased cerebral blood volume/ICP and increases plasma osmolarity
Compared to mannitol, furosemide ___ (is/is not) as effective in decreasing ICP
Compared to mannitol, furosemide is NOT as effective in decreasing ICP
Mannitol may produce rebound intracranial ___tension if a disrupted BBB allows mannitol to enter the CNS
Mannitol may produce rebound intracranial hypertension if a disrupted BBB allows mannitol to enter the CNS
Combination of furosemide and mannitol is ___ (more/less) effective in decreasing ICP than either drug alone
Combination of furosemide and mannitol is more effective in decreasing ICP than either drug alone
Risk of severe dehydration and electrolyte imbalance is ___ (increased/decreased) when a combination of furosemide and mannitol is used
Risk of severe dehydration and electrolyte imbalance is increased when a combination of furosemide and mannitol is used
Side effects of loop diuretics–___kalemia, ___chloremia, ___natremia, ___magnesemia, ___calcemia, metabolic ___osis
hypokalemia, hypochloremia, hyponatremia, hypomagnesemia, hypocalcemia, metabolic alkalosis
What is this side effect of loop diuretics known as?–if someone is on a loop diuretic and does not have electrolytes replaced, the body won’t be able to maintain a gradient of electrolytes; as such, there is not enough electrolytes for water to follow anymore, so the loop diuretic loses its effectiveness
Acute Tolerance (Braking Phenomenon)
Loop diuretics + aminoglycoside given together can cause ___toxicity
ototoxicity
Allergic reaction cross-sensitivity may exist between loop diuretics and ___ drugs
Allergic reaction cross-sensitivity may exist between loop diuretics and sulfa drugs (i.e.: sulfa abx, sulfonylureas, thiazide diuretics)
Risks of nephrotoxicity may be increased when loop diuretics are administered with what (3) antibiotic classes?
- Aminoglycosides
- Cephalosporins
- Penicillin
(2) thiazide diuretics = ___ and ___
hydrochlorothiazide (hydrodiuril) and metolazone (zaroxolyn)
Thiazide diuretics work on the ___ (proximal/distal) convoluted tubule; they compete for the ___-___ cotransporter to inhibit reabsorption
Thiazide diuretics work on the distal convoluted tubule; they compete for the Na-Cl cotransporter to inhibit reabsorption
Thiazide diuretics cause loss of ___ and ___; ___kalemic metabolic ___osis; increased ___ reabsorption
Thiazide diuretics cause loss of sodium and water; hypokalemic metabolic alkalosis; increased Ca reabsorption
Loop diuretics cause ___ (loss/reabsorption) of calcium; thiazide diuretics cause ___ (loss/reabsorption) of calcium)
Loop diuretics cause loss of calcium; thiazide diuretics cause reabsorption of calcium
Loops = ___calcemia; thiazides = ___calcemia
Loops = hypocalcemia; thiazides = hypercalcemia
For patients without comorbidities, thiazides are recommended as first line treatment of ___
For patients without comorbidities, thiazides are recommended as first line treatment of hypertension
Side effects of thiazide diuretics–___kalemia, ___chloremia, ___calcemia, metabolic ___osis with chronic administration; ___ and ___ depletion may accompany kaliuresis; ___ may occur as a result of diuretic-induced hypokalemia or hypomagnesemia; increased likelihood of developing ___ toxicity (d/t hypokalemia); ___ (potentiation/inhibition) of non depolarizing neuromuscular blockers
Side effects of thiazide diuretics–hypokalemia, hypochloremia, HYPERcalcemia, metabolic alkalosis with chronic administration; sodium and magnesium depletion may accompany kaliuresis; dysrhythmias may occur as a result of diuretic-induced hypokalemia or hypomagnesemia; increased likelihood of developing digoxin toxicity (d/t hypokalemia); potentiation of non depolarizing neuromuscular blockers
Thiazide diuretics may also cause ___glycemia and ___uricemia, caution in patients with ___
Thiazide diuretics may also cause hyperglycemia and hyperuricemia, caution in patients with gout
Potassium sparing diuretics–amiloride and triamterene inhibit ___ reabsorption induced by ___; inhibit active counter transport of ___ and ___ in the collecting duct
Amiloride and triamterene inhibit sodium reabsorption induced by aldosterone; inhibit active counter transport of Na and K in the collecting duct
Potassium sparing diuretics–spironolactone and eplerenone compete for ___ receptor sites in the distal tubule to block ___ reabsorption and ___ secretion; they are also known as ___
Spironolactone and eplerenone compete for aldosterone receptor sites in the distal tubule to block sodium reabsorption and potassium secretion; they are also known as aldosterone receptor antagonists
Aldosterone antagonists cause loss of ___ and ___; ___kalemia; and some risk of ___osis
Aldosterone antagonists cause loss of sodium and water; hyperkalemia; and some risk of acidosis
K sparing diuretics have ___ (more/less) effective diuresis
K sparing diuretics have less effective diuresis, often used in combo with other diuretics
K sparing diuretics may be used for treatment of refractory edematous states due to ___ or ___ of the liver
K sparing diuretics may be used for treatment of refractory edematous states due to CHF or cirrhosis of the liver
Why are K sparing diuretics good to use in CHF and cirrhosis of the liver?–because decreased hepatic function and metabolism lead to increased plasma concentration of ___
Because decreased hepatic function and metabolism lead to increased plasma concentration of aldosterone
What is the principle side effect of K sparing diuretics?
HYPERKALEMIA
Patients are at increased risk of hyperkalemia if they are taking K sparing diuretic + ___s, ___s, and ___ blockers
NSAIDs, ACEIs, and beta blockers
K sparing diuretics ___ (do/do not) produce hyperuricemia or hyperglycemia
K sparing diuretics do NOT produce hyperuricemia or hyperglycemia (unlike thiazides)
Review–thiazide diuretics cause ___kalemic metabolic ___osis; ___glycemia; ___uricemia
Thiazide diuretics cause hypokalemic metabolic alkalosis; hyperglycemia; hyperuricemia
Review–loop diuretics cause ___kalemic metabolic ___osis
Loop diuretics cause hypokalemic metabolic alkalosis
Review–potassium-sparing diuretics cause ___kalemia
Potassium-sparing diuretics cause hyperkalemia
Hypoaldosteronism causes ___kalemia; hyperaldosteronism causes ___kalemia
Hypoaldosteronism causes hyperkalemia; hyperaldosteronism causes hypokalemia
ACEIs/ARBs cause ___kalemia
ACEIs/ARBs cause hyperkalemia
Digoxin causes ___kalemia
Digoxin causes hyperkalemia
Mineralocorticoids (i.e.: aldosterone) causes ___kalemia
Mineralocorticoids (i.e.: aldosterone) causes hypokalemia
EKG changes with hyperkalemia that warrant emergent treatment–___, ___ T waves; loss of ___ wave; ___ (wide/narrow) QRS with ___ (tall/short) T wave
tall, peaked T waves; loss of P wave; wide QRS with tall T wave
Why is IV calcium given to treat hyperkalemia?
Calcium is given to reduce EKG changes–causes membrane stabilization of the myocardium and slows down the rate of arrhythmia development
IV calcium reduces potassium levels–T/F?
FALSE–calcium does NOT reduce potassium levels, it reduces EKG changes associated with high potassium levels
Caution giving IV calcium to patients who are on ___; calcium has been reported to worsen the myocardial effects of ___ toxicity; use ___ as an alternative to stabilize the myocardium
Caution giving IV calcium to patients who are on digoxin; calcium has been reported to worsen the myocardial effects of digoxin toxicity; use magnesium as an alternative to stabilize the myocardium
Calcium ___ is preferred, but calcium ___ is an option if central line is in place
Calcium gluconate is preferred, but calcium chloride is an option if central line is in place
Can give ___ and ___ to treat hyperkalemia
Insulin and dextrose to treat hyperkalemia
10 units regular insulin IV + 50 ml of 50% dextrose (if BG < 250)
What inhaled beta 2 agonist can be used to treat hyperkalemia because it helps with movement of K into cells?
Albuterol
Sodium bicarbonate is not recommended to lower potassium levels–T/F?
True–super unpredictable, may take several hours to work
Patiromer (Veltassa) and sodium zirconium cyclosilicate (Lokelma) are oral potassium binders that lower potassium levels through ___ elimination
Patiromer (Veltassa) and sodium zirconium cyclosilicate (Lokelma) are oral potassium binders that lower potassium levels through fecal elimination
Patiromer (Veltassa) and sodium zirconium cyclosilicate (Lokelma) should NOT be used for acute management of potassium levels–T/F?
True–should be used to manage potassium levels long-term
Osmotic diuretics can cause ___natremia
hypernatremia
Thiazides, loops, CHF, carbamazepine, lithium, SSRIs, and liver disease can all cause ___natremia
hyponatremia
If you correct sodium levels too quickly, it can cause ___
permanent brain damage–central pontine myelinolysis
Sodium correction rates–severe symptomatic hyponatremia–__-__ meq/L in the first 24 hours, __ meq/L or less in 48 hours
Severe symptomatic hyponatremia–6-12 meq/L in the first 24 hours, 18 meq/L or less in 48 hours
Sodium correction rates–chronic hyponatremia–__ meq/L/hr with max change of __-__ meq/L in a 24 hour period
Chronic hyponatremia–0.5 meq/L/hr with max change of 8-10 meq/L in a 24 hour period
You can correct sodium levels a little faster in patients with chronic vs. acute hyponatremia–T/F?
True
What are VAPTANS?–___ receptor blockers
Vasopressin receptor blockers
VAPTANS are used to treat ___volemic and ___volemic ___natremia
euvolemic and hypervolemic hyponatremia
Get rid of fluid to correct sodium levels
VAPTANS can be used in hypovolemic hyponatremia–T/F?
FALSE–cannot use VAPTANS in people who are hypovolemic because they will cause even further loss of fluid, leading to CV collapse
Calcium levels are dependent upon ___
albumin
Hypercalcemia may be caused by ___parathyroidism, ___ diuretics
Hypercalcemia may be caused by hyperparathyroidism, thiazide diuretics
Hypocalcemia may be caused by ___parathyroidism, ___ disease, ___ diuretics
Hypocalcemia may be cause by hyperparathyroidism, renal disease, loop diuretics
Can give ___ to correct hypercalcemia
NS–dilute high calcium levels
Can give ___ diuretics to treat hypercalcemia
LOOP, NOT thiazide!
Pamidronate, zoledronic acid, denosumab, and calcitonin are medications used to treat ___; they can also treat ___calcemia
osteoporosis; they can also treat hypercalcemia–slow down bone resorption/breakdown to reduce calcium coming into the circulation
