Mid-term Flashcards

1
Q

SNS & PNS: central nervous system

A

consists of the brain and the spinal cord

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2
Q

SNS & PNS: peripheral nervous system

A

consists of neurons outside the brain and spinal cord

it is made up of two sub-systems: autonomic nervous system and the somatic nervous system

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3
Q

SNS & PNS: autonomic nervous system

A

one of two systems of the peripheral nervous system
this sub-system is made of 2 of its own sub-systems: sympathetic and parasympathetic nervous systems
this system deals with our involuntary responses
responsible for:
- control of smooth muscle i.e. bronchi, blood vessels, GI tract
- cardiac muscle which functions whether the person is conscious or not
- exocrine glands i.e. gastric, sweat, salivary

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4
Q

SNS & PNS: synaptic transmission

A

this is the process that all activity in our autonomic nervous system occurs
involves the synthesis of neurotransmitters in the nerve terminal
includes storage of the neurotransmitter in the nerve terminal awaiting an action potential
involves release if the specific neurotransmitter
after release, the neurotransmitter diffuses across the synaptic gap and reversibly binds to a receptor on the post-synaptic cell
- reversibility is an ideal mechanism when it comes to drug administration when the effects of a drug ever need to be reversed
after binding and exerting an effect, the neurotransmitter [or drug, or chemical] is released and dissociated from its binding site by a variety of mechanisms
the neurotransmitter is now degraded for use

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5
Q

SNS & PNS: sympathetic nervous system

A

or S.N.S. or adrenergic
- it is termed adrenergic for the receptors found in this system
it is responsible for our fight or flight response
sympathoMIMEtics turn on or replicate “mime” responses by stimulating receptors
- occurs through adrenergic agonist’s: alpha-beta agonist’s
sympathoLYTICs turn off or “lysis” responses by blocking receptors
- occurs through adrenergic antagonists: alpha-beta blockers
sub-type receptors: alpha-1, alpha-2, beta-1, and beta-2
drugs that are agonist or “activate” this system are similar to the effects seen with antagonist in the P.N.S.

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6
Q

SNS & PNS: parasympathetic nervous system

A

or P.N.S. or cholinergic
- it is termed cholinergic for the receptors found in this system
it is responsible for our rest and digest response
parasympathoMIMEtics turn on or replicate “mime” responses by stimulating recceptors
parasympathoLYTICs turn off or block “lysis” responses by stimulating receptors
sub-type receptors: Nicotinic N, Nicotinic M, Muscarinic
- muscarinic sub-types: M1, M2, and M3
this system is solely mediated by acetylcholine [Ach]
drugs that are antagonist or “block” this system are similar to the effects seen with agonist of the S.N.S.

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7
Q

SNS & PNS: stimulation of alpha-1 receptors

A

therapeutic effects: vasoconstriction, hemostasis [leads to blood clotting], increased peripheral resistance [leads to increased B.P.], mydriasis or pupil dilation, closure of the internal sphincter of the bladder [to keep stores of fluid]
adverse effects: hypertension [2o to widespread vasoconstriction], necrosis [2o to vasoconstriction and hemostasis], tachycardia [2o to reflex slowing of the heart]

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8
Q

SNS & PNS: phenylephrine

A

brand name: neosynephrine IV
it is a potent vasoconstrictor that exclusively stimulates alpha-1
adverse effects: vascular failure, hypotension, shock states

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9
Q

SNS & PNS: prazosin

A

a vasodilator that block alpha-1
it decreases peripheral resistance and increases vasodilation
indications: hypertension

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10
Q

SNS & PNS: stimulation of alpha-2 receptors

A

alpha-2 [unlike-1, beta-1, and beta-2] block the sympathetic response
the activation of these receptors inhibits norepinephrine
there are no therapeutic applications r/t activation of peripheral alpha-2 receptors
effects: reduces sympathetic outflow from brain to heart and blood vessels, relief of severe pain

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11
Q

SNS & PNS: epineprhine

A

it is a non-selective adrenergic agonist meaning that it will activate all alpha-beta receptors

  • alpha-1, beta-1, and beta-2 will cause activation of the S.N.S.
  • alpha-2 will block activation of the S.N.S
    indication: cardiopulmonary arrest, ventricular fibrillation [the lethal dysrhythmia], anaphylactic shock, asthma [relived by beta-2 by causing bronchodilation]
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12
Q

SNS & PNS: what do alpha-1, beta-1, and beta-2 work on?

A

alpha-1 on blood vessels
beta-1 on the heart
beta-2 on the lungs and uterus

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13
Q

SNS & PNS: stimulation of beta-1 receptors

A

indications: cardiac arrest, heat failure, heart block [a conduction disturbance]
therapeutic effects: tachycardia, increase in myocardial contractility, increase in lipolysis [burning of fat for energy]
- an antagonist to beta-1 would cause the opposite effects which would be beneficial for pt.’s with hypertension

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14
Q

SNS & PNS: stimulation of beta-2 receptors

A

therapeutic applications limited to the lungs and uterus
indications: asthma, hypertension, delay pre-term labor
therapeutic effects: bronchodilation, vasodilation, slightly decreased peripheral resistance, increased muscle and liver glycolysis [monitor pt. for hyperglycemia], increased release of glucgon [breaks down to become glucose in the blood], relaxation of uterine smooth muscle
adverse effects: hyperglycemia, tremors [2o to activation of S.N.S]

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15
Q

SNS & PNS: isoproterenol

A

it is a non-selective beta-2 stimulant
- its non-selectiveness signifies that it can stimulate beta-1 as well, causing unwanted cardiac stimulation
indication: CHF, various types of shock, hypoperfusion, asthma, bronchitis, emphysema
adverse effects: primarily r/t cardiac stimulation

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16
Q

SNS & PNS: propranolol

A

it is a non-specific beta blocker therefore it block both beta-1 and beta-2 receptors
indication: cardiovascular disorders
adverse effects: r/t cardiac and respiratory effects
- discontinue administration of this drug slowly to prevent rebound tachycardia leading to angina and possibly myocardial infarction

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17
Q

SNS & PNS: what do muscarinic M1, M2, and M3 work on?

A

M1 works on the brain
M2 works on the heart
M3 works on every other organ

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18
Q

SNS & PNS: stimulation of P.N.S. effectss

A
SLUGBAM
salivation, secretions, sweat
lacrimation [eye moisture]
urination
GI upset [diarrhea]
bradycardia, bowel movement, bronchoconstriction
abdominal cramps, anorexia
miosis [pupillary constriction]
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19
Q

SNS & PNS: pilocarpine

A

binds solely to cholinergic receptors
indications: simple and acute glaucoma [for its miotic effects], preoperative and postoperative elevated intraocular pressure, drug induced mydriasis [pupil dilation]

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20
Q

SNS & PNS: neostigmine

A

brand name: prostigmin
indications: myasthenia gravis [a neuromuscular disorder] to minimize muscle fatigue
adverse effects: cholinergic crisis [an excess of Ach]
it has a cholinergic effect despite it not binding to a cholinergic receptor
- the drug inhibits the enzyme cholinesterase which breaks down Ach, if that action is inhibited there is more Ach which causes the cholinergic agonist effect

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21
Q

SNS & PNS: atropine

A

an anti-cholinergic drug, which acts as an antidote to a cholinergic crisis
indication: preoperative drying of secretions [facilitates intubation, if needed], acute cardiac emergencies, ophthalmic disorders, motion sickness, diarrhea [by slowing down gastric peristalsis

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22
Q

SNS & PNS: excessive blockage of P.N.S. effects

A
increased intraocular pressure
mydriasis [dilation of pupils]
photophobia
decreased sweating
dry mouth
decreased bronchial secretions
respiratory depression
decreased GI motility w/ possible constipation
decreased B.P. followed by increase B.P.
- these drugs will decrease B.P. causing the heart to compensate for the decrease by increasing the heart rate which causes the rise in B.P.
tachycardia and, possibly, palpitations
urinary retention
vasodilation
drowsiness, confusion, and agitation
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23
Q

SNS & PNS: anti-cholinergic poisoning

A
a lack of Ach
remember:
mad as a hatter
blind as a bat
red ass a beet
dry as a bone
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24
Q

diuretics: thiazides

A

the largest group of diuretics, structurally r/t the antibacterial sulfoamides [ask pt. for allergies to sulfa]
prototype: hydrochlorothiazide [HCTZ]
acts in the early tubules
- excretes Na and Cl by inhibiting the ion pumps that work in Na and Cl reabsorption
- furthermore, it increases excretion of water-soluble vit.’s, K, HCO3, and Mg and decreases the excretion of Ca
indications: hypertension, edema [resulting from CHF, hepatic cirrhosis, renal disease, long-term steroid or estrogen therapy]
nursing interventions: ID allergies to sulfa, determine renal and hepatic status, ID blood glucose and uric acid levels
decreases GFR and increases BUN, blood glucose, and uric acid

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25
diuretics: loop diuretics
or high-ceiling diuretics, is rapid-acting which takes effect in less than 10 minutes when administered IV prototype: furosemide [lasix] acts in the loop of Henle - inhibits the reabsorption of Na, Cl, and water - furthermore, it excretes K, Mg, and Ca [thiazides increases the levels of Ca] indications: reduces peripheral edema [from pulmonary edema, CHF, hepatic or renal disease], hypertension, pre-existing renal disease [loop preferred b/c it has no effect on the GFR, unlike thiazides adverse effects: F&E imbalance [may cause hypovoleia and dehydration], ototoxicity [occurs w/ rapid IV administration] can increase blood glucose, low-density lipoprotein, total cholesterol, uric acid and triglyceride levels
26
diuretics: [aldosterone-antagonist] potassium sparing diuretics
acts in the late distal tubules blocks the effect of aldosterone causing the body to excrete Na yet hold on to K prototype: spironolactone [aldactone] indications: hyperaldosteronism, minimizes K loss adverse effects: impotence, menstrual irregularities, gynecomastia, interacts w/ salicylates, hyperkalemia interferes w/ testosterone synthesis, which leads to altered estrogenic and androgenic activity; a major use is in diagnosisng and treating primary hyperaldosteronism
27
diuretics: [non-aldosterone antagonist] potassium sparing diuretic
acts in the late distal convoluted tubules inhibits the Na-K pump causing the body to excrete Na but hold on to K prototype: triamterene [dyrenium] decreases Na, Cl, water, HCO3, and Ca and promotes the retention of K and Mg indications: edema, hypertension, minimizes K loss adverse effects: electrolyte imbalance, esp. hyperkalemia increases serum uric acid levels
28
diuretics: osmotic diuretics
work by increasing osmotic pressure and pulling fluid into the vascular from the interstitial space prototype: mannitol [osmitrol] indications: preventing and treating acute renal failure, reduce intracranial pressure, reduce cerebral edema, reduce intraocular pressure, promote excretion of toxic substances in the urine adverse effects: edema - due to its osmotic properties, if the drug were to leave the intravascular and enter the interstitial space it would pull fluid to the space that it occupies
29
diuretics: foods w/ high K levels
avocados green, leafy vegetables bananas citrus fruits
30
electrolytes: sodium
cation, Na, 135-145 mEq/L most abundant [90%] cation in ECF functions: water balance via their effect on serum osmolality, nerve impulse transmission, regulation of acid-base balance, participation in cellular chemical reactions it is regulated by dietary intake and aldosterone secretions
31
electrolytes: potassium
cation, K, 3.5-5.0 mEq/L the major electrolyte and principle cation in the ICF functions: regulates metabolic activities, glycogen deposits in the liver and skeletal muscle, transmission and conduction of nerve impulses, normal cardiac conduction, skeletal and smooth muscle contraction it is regulated by dietary intake and renal excretion the body conserves K poorly, so any condition that increases urine output decreases the serum K concentration causing hypokalemia
32
electrolytes: hypokalemia
causes: treatment w/ diuretics, excessive insulin, alkalosis, vomiting, diarrhea, abuse of laxatives tx: IV or PO K chloride - adverse effects: GI irritation [give w/ meals of water], IV irritation [dilute infusion and infuse slowly], hyperkalemia
33
electrolytes: hyperkalemia
causes: severe tissue trauma, misuse of K spring diuretics, untreated Addison's disease, overdose of IV k Tx: stop all K foods and med.'s, infuse Ca salt, infuse insulin and glucose, infuse sodium bicarbonate, give kayexalate
34
electrolytes: calcium
cation, Ca, total Ca 8.4-10.2 mg/dL functions: bone and teeth formation, blood clotting, hormone secretion, cell membrane integrity, cardiac conduction, transmission nerve impulses, muscle contraction
35
electrolytes: hypocalcemia
causes: endocrine disorders that affect the thyroid and parathyroid glands
36
electrolytes: hypercalcemia
causes: frequently a symptom of an underlying disease resulting in excess bone resorption w/ release of Ca
37
electrolytes: magnesium
cation, Mg, 1.5-2.5 mEq/L functions: enzyme activities, neurochemical activities, cardiac and skeletal muscle excitability, membrane stabilizer it is regulated by dietary intake, renal mechanisms, and actions of the parathyroid hormone
38
electrolytes: hypermagnesemia
causes: renal failure, almost exclusively tx: discontinue PO and IV Mg, administer Mg free IV fluids, loop diuretics, Ca for cardiac effects
39
electrolytes: hypomagnesemia
causes: diarrhea, hemodialysis, kidney disease, prolonged IV feeding w/ Mg free solutions, chronic alcoholism, diabetes, pancreatitis, malnourishment tx: Mg gluconate/hydroxide/sulfate
40
electrolytes: chloride
anion, Cl, 96-106 mEq/L major anion in ECF it is regulated by dietary intake and the kidneys via elimination
41
electrolytes: hypochloremia
causes: vomiting, prolonged and excessive NG or fistula drainage due to the loss of hydrochloric acid, use of loop and thiazide diurtics
42
electrolytes: hyperchloremia
causes: serum bicarbonate falls, Na level rises
43
electrolytes: bicarbonate
anion, HCO3, 22-26 mEq/L functions: essential component for acid-base balance it is regulated by the kidneys
44
acid-base balance: chemical buffering system
the largest chemical buffer in ECF is the carbonic and bicarbonate buffer system it is the first buffering system to act and it does so in seconds when the CO2 is made, there is an increase in hydrogen ions produced, and wherever hydrogen ions are produced, there is more CO2 produced
45
acid-base balance: biological buffering system
occurs when hydrogen ions are absorbed or released by body cells it occurs after chemical buffering and take 2 to 4 hours after any major pH change is made
46
acid-base balance: physiological buffering system
the two buffers are lungs and kidneys when the concentration of hydrogen ions is altered the lungs react to correct the imbalance by altering the rate and depth of respiration - an increase in respiratory rate leads to a decrease in CO2 which leads to decrease in hydrogen ions the kidneys take from a few hours to several days to regulate acid-base imbalance - they absorb bicarbonate in cases of acid excess and excrete it in cases of acid deficit
47
acid-base balance: metabolic acidosis
it is a type of acid-base imbalance results b/c of the high acid content of the blood, which also causes a loss of Na bicarbonate, the alkaline half of the carbonate buffer system
48
acid-base balance: metabolic alkalosis
it is a type of acid-base imbalance | marked by the heavy loss of acid from the body or an increased level of bicarbonate
49
acid-base balance: respiratory acidosis
it is a type of acid-base imbalance | marked by an increased arterial PaCO@, excess HCO3, and a decreased pH
50
acid-base balance: respiratory alkalosis
it is a type of acid-base imbalance | marked by decreased PaCO2 and increased pH
51
acid-base balance: hypotonic IV solution
moves fluid into the cells causing them to enlarge | there is less solute diluted in the solution
52
acid-base balance: isotonic IV solution
expands the body's fluid volume having no effect on cell size there is an equivalent of solute or physiologic to the solute content in the body
53
acid-base balance: hypertonic IV solution
pulls fluid from the cells, causing them to shrink | there is more solute diluted in the solution
54
acid-base balance: hypervolemia
may result from excessive Na and water retention fluid shifts from the vascular into the interstitial spaces may occur w/ fluid volume excess causing edema peripheral edema increases the cardiac work load and decreases tissue perfusion when systemic edema is severe, the congestion will back up into the lungs, affecting breathing and gas exchange
55
diabetes mellitus: types of diabetes
type I, absolute insulin deficiency type II, relative insulin deficiency - causes: decreased insulin release from defective beta cells in pancreas, peripheral insulin resistance, increased glucose output by liver gestational - occurs during pregnancy and is resolved after labor
56
diabetes mellitus: rapid acting insulin
anaLOG insulin - i.e. lispro [humalog], aspart [novalog] onset: 15-30 minutes - imp. to administer right before a meal this insulin must be paired w/ an intermediate insulin to provide glycemic control can be given IV
57
diabetes mellitus: short-acting insulin
``` regular insulin [LIN] - i.e. novolin R, humalin R onset: 30-60 minutes - it is imp. to administer before a meal can be given IV ```
58
diabetes mellitus: intermediate-acting insulin
``` NPH [LIN] onset: 1-2 hours injected twice daily to provide glycemic control b/w meals and during the night can be mixed w/ short-acting insulin cannot be given IV ```
59
diabetes mellitus: long-acting insulin
``` determir [levemir] - 12 hour dosing - can NOT be mixed w/ other insulin - onset: 1-2 hours glargine [lantus] - 24 hour dosing - once daily at same time every day b/c of the plateau of concentration - can NOT be mixed w/ other insulin cannot be given IV ```
60
diabetes mellitus: sulfonylureas
``` an oral anti-diabetic drug that actively drives blood glucose down which can cause hypoglycemia prototype: glipizide [glucotrol] promotes insulin release may increase tissue reponse to insulin adverse effects: hypoglycemia ```
61
diabetes mellitus: glinides
an oral anti-diabetic drug that actively drives blood glucose down which can cause hypoglycemia prototype: repaglinide [prandin] increase the release of insulin from the pancreas adverse effect: hypoglycemia
62
diabetes mellitus: thiazolidinediones
an oral anti-diabetic drug that actively drives blood glucose down which can cause hypoglycemia decrease insulin resistance decrease glucose production by liver adverse effects: fluid retention , elevation of lipid levels, hypoglycemia
63
diabetes mellitus: biguanides
prototype: metformin [glucophage] drug choice for initial therapy started immediately upon diagnosis inhibits glucose production in liver slightly reduces glucose absorption in GI tract sensitizes insulin receptors in target tissues to increase the cells ability to take in glucose whenever insulin is present adverse effects: Gi disturbance, vit. B12 and folic acid deficiency, weight loss
64
diabetes mellitus: alpha-glucosidase inhibitors
prototype: arcabose [precise] delays absorption of dietary CHO by inhibiting enzyme that breaks down complex CHO to simple CHO decreases post-prandial [after eating] rise in blood glucose adverse effects: flatulence, cramps, abdominal distention, diarrhea, liver dysfunction
65
diabetes mellitus: gliptins
prototype: sitagliptin [januvia] enhances the activity of incretin hormones by inhibiting their breakdown increases insulin release reduces glucagon release decreases hepatic glucose production adverse effects: pancreatitis, hypersensitivity reactions
66
diabetes mellitus: complications of insulin therapy
hypoglycemia hyperglycemia lipohypertrophy - occurs in areas where fat accumulates after continuous injections of insulin