Unit 2 Pharmacology 201

Front 1

Diuretics are drugs that

Back 1

increase the output of urine

Front 2

Diuretics have two major applications:

Back 2

(1) treatment of hypertension and
(2) mobilization of edematous fluid associated with heart failure, cirrhosis, or kidney disease.

Front 3

The nephron is...

Back 3

the basic functional unit of the kidney

Front 4

The kidney serves three basic functions:

Back 4

(1) cleansing of extracellular fluid (ECF) and maintenance of ECF volume and composition;
(2) maintenance of acid-base balance; and
(3) excretion of metabolic wastes and foreign substances.

Front 5

Diuretics most affect which function of the kidneys?

Back 5

Maintenance of ECF volume and composition is the function that diuretics affect most.

Front 6

Effects of the kidney on ECF are the net result of which three basic processes?

Back 6

(1) filtration, (2) reabsorption, and (3) active secretion.

Front 7

Where does filtration occur?

Back 7

Filtration occurs at the glomerulus.

Front 8

What is the first step in urine formation?

Back 8

filtration

Front 9

Virtually all small molecules present in plasma (electrolytes, amino acids, glucose, drugs, metabolic wastes) undergo filtration. Which elements remain behind in the blood?

Back 9

cells and large molecules (lipids, proteins)

Front 10

Filtration is a __________ process; therefore, it cannot regulate the __________ of urine.

Back 10

nonselective; composition

Front 11

How much of the water, electrolytes, and nutrients filtered at the glomerulus undergoes reabsorption?

Back 11

More than 99%

Front 12

Reabsorption of solutes (e.g., electrolytes, amino acids, glucose) takes place by way of __________ ; water then follows __________ along the osmotic gradient

Back 12

active transport; passively

Front 13

Most diuretics act by disrupting __________ .

Back 13

solute reabsorption

Front 14

Which ions are of greatest interest in kidney solute reabsorption?

Back 14

sodium and chloride ions

Front 15

What percentage of filtered sodium and chloride is reabsorbed at the proximal convoluted tubule?

Back 15

about 65%

Front 16

Which limb of the loop of Henle is freely permeable to water?

Back 16

The descending limb

Front 17

What is aldosterone and what does it do?

Back 17

It is the principal mineralocorticoid of the adrenal cortex, and it stimulates reabsorption of sodium from the distal nephron. At the same time, aldosterone causes potassium to be secreted.

Front 18

What basic mechanism of action do most diuretics share?

Back 18

blockade of sodium and chloride reabsorption

Front 19

Drugs that act ___________ in the nephron can block the ____________ amount of solute reabsorption. As a result, these agents produce the ___________ diuresis

Back 19

early; greatest; greatest

Front 20

diuretics that act at distal sites produce _____________ diuresis

Back 20

relatively scant

Front 21

What are the 3 major adverse effects diuretics can cause?

Back 21

hypovolemia, acid-base imbalance, and disturbance of electrolyte levels.

Front 22

What are the four major categories of diuretic drugs?

Back 22

(1) high-ceiling (loop) diuretics,
(2) thiazide diuretics,
(3) osmotic diuretics, and
(4) potassium-sparing diuretics.

Front 23

The high-ceiling diuretics are the _________ (most/least) effective diuretics available.

Back 23

most

Front 24

What is the high-ceiling diuretic's site of action?

Back 24

the loop of Henle

Front 25

What is the most frequently prescribed loop diuretic?

Back 25

Furosemide

Front 26

Lasix

Back 26

Brand name of furosemide

Front 27

By blocking solute reabsorption, what does furosemide prevent?

Back 27

passive reabsorption of water.

Front 28

Furosemide is a powerful drug. What is it generally reserved for?

Back 28

situations that require rapid or massive mobilization of fluid

Front 29

Name 3 conditions that justify the use of furosemide.

Back 29

(1) pulmonary edema associated with heart failure (HF);
(2) edema of hepatic, cardiac, or renal origin that has been unresponsive to less efficacious diuretics; and
(3) hypertension that cannot be controlled with other diuretics.

Front 30

Which diuretics are effective even when renal blood flow and the glomerular filtration rate (GFR) are low?

Back 30

high-ceiling diuretics (in contrast to thiazide diuretics)

Front 31

Adverse effects of furosemide:

Back 31

Furosemide can produce excessive loss of sodium, chloride, and water, and severe dehydration can result. Dehydration can promote thrombosis and embolism.
Furosemide can cause a substantial drop in blood pressure. It can also cause potassium loss and may cause hearing impairment.

Front 32

Loss of potassium is a special concern for patients taking which drug?

Back 32

digoxin

Front 33

The maximum diuresis produced by the thiazides is considerably ____________ (higher/lower) than the maximum diuresis produced by the high-ceiling agents.

Back 33

lower

Front 34

Which drug is the most widely used thiazide diuretic?

Back 34

Hydrochlorothiazide

Front 35

Hydrochlorothiazide promotes urine production by blocking the reabsorption of _____________ in the early segment of the _______________________.

Back 35

sodium and chloride; distal convoluted tubule

Front 36

The thiazides’ ability to promote diuresis depends on ____________________.

Back 36

adequate kidney function

Front 37

These drugs are ineffective when the GFR is low.

Back 37

thiazide diuretics

Front 38

The primary indication for hydrochlorothiazide is ________________, a condition for which thiazides are often drugs of first choice.

Back 38

hypertension

Front 39

Adverse effects of thiazide diuretics:

Back 39

Loss of sodium, chloride, and water can lead to hyponatremia, hypochloremia, and dehydration. The thiazides can cause hypokalemia from excessive potassium excretion. Thiazides can cross the placental barrier to produce fetal harm directly. Potential effects include electrolyte imbalance, hypoglycemia, jaundice, and hemolytic anemia.

Front 40

Two useful properties of the potassium-sparing diuretics:

Back 40

1. modest increase in urine production
2. substantial decrease in potassium excretion.

Front 41

These drugs are often used to counteract potassium loss caused by thiazide and loop diuretics.

Back 41

potassium-sparing diuretics

Front 42

Spironolactone blocks the actions of ____________ in the ______________.

Back 42

aldosterone; distal nephron

Front 43

What effect does the inhibition of aldosterone have on the nephron?

Back 43

retention of potassium and increased excretion of sodium

Front 44

How long does it take for the effects of spironolactone to develop.

Back 44

up to 48 hours

Front 45

Spironolactone is used primarily for:

Back 45

hypertension and edema

Front 46

What drug(s) is spironolactone used most commonly in combination with & for what purpose?

Back 46

with a thiazide or loop diuretic to counteract the potassium-wasting effects of these more powerful diuretics.

Front 47

Why does spironolactone greatly reduce mortality and hospital admissions in patients with severe heart failure?

Back 47

Benefits derive from protective effects of aldosterone blockade in the heart and blood vessels.

Front 48

What are the adverse effects of spironalactone?

Back 48

hyperkalemia;
a variety of endocrine effects, including gynecomastia, menstrual irregularities, impotence, hirsutism, and deepening of the voice.

Front 49

What can hyperkalemia result in?

Back 49

fatal dysrhythmias

Front 50

Why does spironolactone produce endocrine effects?

Back 50

It is a steroid derivative with a structure similar to that of steroid hormones.

Front 51

With what agents should spironolactone never be combined?

Back 51

potassium supplements, salt substitutes (which contain potassium chloride), or another potassium-sparing diuretic
[ACE inhibitors, ARBs, and direct renin inhibitors— should be combined with spironolactone only when clearly necessary.]

Front 52

Triamterene can be used alone or in combination with other diuretics to treat ________________.

Back 52

hypertension and edema

Front 53

When combined with other diuretics, _______________ augments diuresis and helps counteract the potassium-wasting effects of the more powerful diuretic.

Back 53

triamterene

Front 54

What is the most significant adverse effect of triamterene?

Back 54

excessive potassium accumulation

Front 55

Relatively common side effects of trimterene:

Back 55

nausea, vomiting, leg cramps, and dizziness

Front 56

Maintenance of fluid volume and osmolality is primarily the job of the _____________.

Back 56

kidneys

Front 57

In the clinical setting, changes in osmolality are described in terms of the ___________ content of plasma.

Back 57

sodium

Front 58

Causes of isotonic contraction include...

Back 58

vomiting, diarrhea, kidney disease, and misuse of diuretics.

Front 59

Hypertonic contraction is defined as volume contraction in which loss of water ________ loss of sodium.

Back 59

exceeds

Front 60

Causes of hypertonic contraction include...

Back 60

excessive sweating, osmotic diuresis, and feeding excessively concentrated foods to infants.

Front 61

Hypotonic contraction is defined as volume contraction in which loss of sodium exceeds loss of water. In this case, both the _____________ and____________ of extracellular fluid decrease.

Back 61

volume; osmolality

Front 62

The principal cause of hypotonic contraction is...

Back 62

excessive loss of sodium through the kidneys.

Front 63

Volume expansion may result from...

Back 63

- an overdose with therapeutic fluids
- disease states (such as heart failure, nephrotic syndrome, or cirrhosis of the liver with ascites)

Front 64

The principal drugs used to correct volume expansion:

Back 64

diuretics and the agents used for heart failure.

Front 65

Volume expansion

Back 65

an increase in the total volume of body fluid

Front 66

The respiratory system influences the pH through

Back 66

control of carbon dioxide (CO2) exhalation.

Front 67

The kidneys influence the pH by regulating __________. By retaining ________, the kidneys can raise the pH. Conversely, by increasing ____________, the kidneys can lower the pH and thereby compensate for alkalosis.

Back 67

bicarbonate excretion
bicarbonate
bicarbonate excretion

Front 68

Respiratory alkalosis is produced by ______________.

Back 68

hyperventilation

Front 69

Respiratory acidosis results from ______________________.

Back 69

retention of CO2 secondary to hypoventilation

Front 70

Primary causes of impaired ventilation:

Back 70

(1) depression of the medullary respiratory center
(2) pathologic changes in the lungs (e.g., status asthmaticus, airway obstruction)

Front 71

Primary treatment of respiratory acidosis:

Back 71

directed at correcting respiratory impairment

Front 72

Common causes of metabolic alkalosis include:

Back 72

- excessive loss of gastric acid (through vomiting or suctioning)
- administration of alkalinizing salts (e.g., sodium bicarbonate).

Front 73

In most cases, metabolic alkalosis can be corrected by infusing a solution of _____________________.

Back 73

sodium chloride plus potassium chloride

Front 74

Principal causes of metabolic acidosis are...

Back 74

1) chronic renal failure,
2) loss of bicarbonate during severe diarrhea
3) metabolic disorders that result in overproduction of lactic acid (lactic acidosis) or ketoacids (ketoacidosis).

Front 75

Treatment of metabolic acidosis:

Back 75

+ correcting the underlying cause of acidosis
+ if the acidosis is severe, administering an alkalinizing salt (sodium bicarbonate)

Front 76

Potassium is the most abundant ______________ cation.

Back 76

intracellular

Front 77

What role does potassium play in the body?

Back 77

Potassium plays a major role in conducting nerve impulses and maintaining the electrical excitability of muscle. Potassium also helps regulate acid-base balance.

Front 78

How are serum levels of potassium regulated?

Back 78

primarily by the kidneys

Front 79

What substance, produced by the body, increases renal excretion of potassium?

Back 79

aldosterone

Front 80

Extracellular acidosis promotes the ________ of potassium from cells, thereby causing extracellular _______________.

Back 80

exit
hyperkalemia

Front 81

What is the definition of hypokalemia, and what is its most common cause?

Back 81

Hypokalemia exists when the serum potassium level falls below 3.5 mEq/L.
Its most common cause is treatment with a thiazide or loop diuretic.

Front 82

Potassium depletion can be treated with ____________.

Back 82

potassium salts (The preferred salt is potassium chloride.)

Front 83

Hyperkalemia can result from:

Back 83

+ severe tissue trauma,
+ untreated Addison’s disease,
+ acute acidosis (which draws potassium out of cells), + misuse of potassium-sparing diuretics, and
+ overdose with IV potassium

Front 84

The most serious consequence of hyperkalemia is ___________.

Back 84

disruption of the electrical activity of the heart

Front 85

Treatment of hyperkalemia:

Back 85

1. withdrawal of potassium-containing foods and drugs that promote potassium accumulation
2. infusing a calcium salt to offset the cardiac effects of potassium
3. infusing glucose and insulin to promote potassium uptake by cells
4. infusing sodium bicarbonate if acidosis is present.

Front 86

Low levels of magnesium may result from...

Back 86

diarrhea,
hemodialysis,
kidney disease,
prolonged intravenous feeding with magnesium-free solutions

Front 87

Low levels of magnesium causes...

Back 87

increased muscle excitability (perhaps to the point of tetany)

Front 88

In the kidneys, hypomagnesemia may lead to

Back 88

nephrocalcinosis (formation of minuscule calcium stones within nephrons).

Front 89

Frank hypomagnesemia is treated with

Back 89

parenteral magnesium sulfate.

Front 90

Toxic elevation of magnesium levels is most common in patients with _________________.

Back 90

renal insufficiency

Front 91

Symptoms of mild intoxication:

Back 91

+ muscle weakness
+ hypotension
+ sedation
+ electrocardiographic (ECG) changes

Front 92

Higher magnesium concentrations pose a risk of ______________.

Back 92

cardiac arrest

Front 93

Drugs recommended for the treatment of HF include:

Back 93

diuretics, inhibitors of the renin-angiotensin-aldosterone system (RAAS), beta blockers, and digoxin

Front 94

Heart failure is a syndrome in which...

Back 94

the heart is unable to pump sufficient blood to meet the metabolic needs of tissues.

Front 95

Heart failure is characterized by...

Back 95

signs of inadequate tissue perfusion (fatigue, shortness of breath, exercise intolerance)
and/or signs of volume overload (venous distention, peripheral and pulmonary edema).

Front 96

The major underlying causes of HF are:

Back 96

chronic hypertension and myocardial infarction.

Front 97

Heart failure is a chronic disorder that requires _________________ treatment with drugs.

Back 97

continuous

Front 98

In the initial phase of failure, the heart undergoes _________ , a process in which the ventricles dilate (grow larger), hypertrophy (increase in wall thickness), and become more spherical (less cylindrical).

Back 98

remodeling

Front 99

The net result of the pathologic changes of heart failure is a progressive decline in _____________.

Back 99

cardiac output

Front 100

Water retention results from a reduction in renal blood flow, resulting in decreases in...

Back 100

the glomerular filtration rate (GFR), urine production, and activation of the RAAS.

Front 101

Levels of circulating _____________ are an important index of cardiac status in HF patients and thus can be a predictor of long-term survival.

Back 101

BNP

Front 102

In HF, if the cardiac output is insufficient to maintain adequate kidney function...

Back 102

renal retention of water progresses unabated.

Front 103

If cardiac output becomes too low to maintain sufficient production of urine, the resultant accumulation of water eventually is ___________.

Back 103

fatal

Front 104

The prominent signs and symptoms of HF are:

Back 104

Reduced exercise tolerance, fatigue, and shortness of breath
Tachycardia
Increased heart size
Pulmonary edema
Peripheral edema
Hepatomegaly (increased liver size)
Distention of the jugular veins
Weight gain resulting from fluid retention

Front 105

HF is routinely treated with what types of drugs?

Back 105

(1) diuretics
(2) agents that inhibit the RAAS
(3) beta blockers

Front 106

_____________ are first-line drugs for all HF patients with signs of volume overload or with a history of volume overload.

Back 106

Diuretics

Front 107

Do diuretics prolong survival for HF patients?

Back 107

No, for the most part, the benefits of diuretics are limited to symptom reduction.

Front 108

The principal adverse effect of the thiazides is __________.

Back 108

hypokalemia, which increases the risk of digoxin-induced dysrhythmias

Front 109

Why are loop diuretics drugs of choice for patients with severe HF?

Back 109

Because they can mobilize large volumes of water and because they work when the GFR is low,

Front 110

Adverse effects of loop diuretics?

Back 110

hypokalemia (increasing risk of digoxin toxicity)
hypotension (due to excessive volume reduction)

Front 111

Can agents that inhibit the RAAS prolong life in patients with HF?

Back 111

Yes, agents that inhibit the RAAS can be highly beneficial.
In the absence of specific contraindications, all patients with HF should receive one of these drugs.

Front 112

ACE inhibitors block production of angiotensin II, reduce the release of aldosterone, and suppress degradation of kinins. How does this help the patient with HF?

Back 112

These actions improve hemodynamics and favorably alter cardiac remodeling.

Front 113

By suppressing production of angiotensin II, ACE inhibitors cause ___________ of arterioles and veins and reduce the release of ____________. Arteriolar dilation improves regional blood flow in the __________ and other tissues and, by reducing afterload, it __________ the stroke volume and cardiac output. Increased renal blood flow promotes ___________ of sodium and water.

Back 113

dilation
aldosterone
kidneys
increases
excretion

Front 114

Diuretics in HF--
Venous dilation reduces venous pressure, thereby reducing what?

Back 114

Pulmonary congestion, peripheral edema, preload, and cardiac dilation.

Front 115

(in heart failure clients)
With continued use, ACE inhibitors have a favorable impact on _______________.

Back 115

cardiac remodeling.
(Elevation of kinins is largely responsible. )

Front 116

The principal adverse effects of the ACE inhibitors are:

Back 116

hypotension (secondary to arteriolar dilation), hyperkalemia (secondary to decreased aldosterone release),
intractable cough, and
angioedema.

Front 117

Because ARBs do not increase levels of ____________, their effects on cardiac remodeling are less favorable than those of ACE inhibitors.

Back 117

kinins

Front 118

How can beta blockers improve a HF patient’s status?

Back 118

improve the LV ejection fraction
increase exercise tolerance
slow progression of HF
reduce the need for hospitalization
prolong survival

Front 119

Adverse effects of beta blockers in HF patients:

Back 119

(1) fluid retention and worsening of HF, (2) fatigue, (3) hypotension, and (4) bradycardia or heart block.

Front 120

Digoxin belongs to a class of drugs known as ___________, agents best known for their positive ________ actions (i.e., their ability to increase the myocardial contractile force).

Back 120

cardiac glycosides
inotropic

Front 121

Does digoxin prolong life in patients with HF?

Back 121

Although digoxin can reduce symptoms of HF, it does not prolong life.

Front 122

Major risk of digoxin use?

Back 122

cardiac dysrhythmias

Front 123

When using digoxin, what levels need to be monitored closely?

Back 123

potassium

Front 124

Digoxin use--As a result of increased cardiac output, three major secondary responses occur:

Back 124

(1) sympathetic tone declines, (2) urine production increases, and (3) renin release declines.

Front 125

Some patients taking digoxin may require an antidysrhythmic drug, such as:

Back 125

phenytoin or lidocaine

Front 126

Patients who develop bradycardia or AV block while using digoxin can be treated with ___________.

Back 126

atropine

Front 127

In addition to dysrhythmias, digoxin can cause __________ effects and ___________ effects. These effects often precede dysrhythmias and therefore can provide advance warning of serious toxicity.

Back 127

gastrointestinal (GI)--(anorexia, nausea, vomiting)
central nervous system (CNS) -- (fatigue, visual disturbances

Front 128

Patients should be warned about digoxin-induced dysrhythmias and instructed to take their medication ______________.

Back 128

exactly as prescribed

Front 129

the process by which the body makes red blood cells, white blood cells, and platelets.

Back 129

hematopoiesis

Front 130

In all patients, erythropoiesis stimulating agents (ESAs) may increase the risk of ...

Back 130

stroke, heart failure, blood clots, myocardial infarction (MI), and death

Front 131

a growth factor produced by recombinant DNA technology

Back 131

Epoetin alfa

Front 132

Epoetin alfa is used to treat ______________-induced anemia in patients with nonmyeloid malignancies.

Back 132

chemotherapy

Front 133

Because ESAs can shorten survival time in all cancer patients, epoetin is indicated only when the goal of cancer therapy is ____________.

Back 133

palliation

Front 134

Epoetin may be given to increase ___________ levels in anemic patients scheduled for elective surgery. The drug should be used only when significant____________ is anticipated; however, it should not be used before ___________ or vascular surgery.

Back 134

erythrocyte
blood loss
cardiac

Front 135

The most significant adverse effect of epoetin alfa:

Back 135

hypertension

Front 136

When given to preoperative patients to reduce the need for RBC transfusion, ESAs have increased the risk of...

Back 136

deep vein thrombosis

Front 137

filgrastim, pegfilgrastim, and sargramostim are all...

Back 137

leukopoietic growth factor --stimulate production of leukocytes (white blood cells)

Front 138

Filgrastim has two principal uses:

Back 138

elevation of neutrophil counts in cancer patients and treatment of severe chronic neutropenia.

Front 139

Filgrastim is given to reduce the risk of infection in patients undergoing ______________. It does this by stimulating _______________________.

Back 139

cancer chemotherapy
neutrophil production

Front 140

The principal adverse effects of filgrastim are ____________ and ____________ .

Back 140

bone pain; leukocytosis

Front 141

Thrombopoietic growth factors are endogenous compounds that stimulate production of ______________.

Back 141

platelets

Front 142

At this time, ___________ is the only thrombopoietic growth factor available.

Back 142

oprelvekin

Front 143

Oprelvekin is given to stimulate ____________ production in patients undergoing myelosuppressive chemotherapy for _____________.

Back 143

platelet
nonmyeloid cancers

Front 144

Adverse effects of oprelvekin:

Back 144

retention of sodium and water by the kidneys;
anemia, due to expanded plasma volume;
tachycardia, atrial fibrillation, and atrial flutter;
severe allergic reactions, including anaphylaxis

Front 145

the cells responsible for insulin synthesis and release into the bloodstream

Back 145

pancreatic beta cells

Front 146

develops when hypoglycemia becomes severe and is allowed to persist

Back 146

Ketoacidosis

Front 147

Most long-term complications of diabetes occur secondary to disruption of blood flow because of ____________ or ______________ damage.

Back 147

macrovascular; microvascular

Front 148

Levels of ________ reflect average blood glucose levels over the previous 2 to 3 months.

Back 148

A1c

Front 149

Name some long-term complications of diabetes.

Back 149

CVD, retinopathy, kidney disease, and amputations

Front 150

4 elements of glycemic control (keeping blood glucose levels in normal range around the clock):

Back 150

diet modification,
self-monitoring of blood glucose (SMBG),
exercise, and
insulin replacement.

Front 151

Oral antidiabetic agents are helpful for patients with which type of diabetes?

Back 151

Type 2

Front 152

Which drugs are preferred agents for managing diabetic hypertension and can help protect against diabetic nephropathy?

Back 152

An ACE inhibitor or an ARB

Front 153

To reduce high levels of LDL cholesterol, ____________ are preferred drugs

Back 153

statins

Front 154

Clinical experience has shown that ______________, by themselves, often normalize insulin release and decrease insulin resistance.

Back 154

dietary measures

Front 155

Target values for blood glucose are ____________ mg/dL before meals and _________________ mg/dL at bedtime.

Back 155

90 to 130
100 to 140

Front 156

What is the principal stimulus for insulin release?

Back 156

a rise in blood glucose

Front 157

Insulin lispro, insulin aspart, and insulin glulisine are ___________ acting and ______ duration insulins.

Back 157

rapid; short

Front 158

Lispro insulin's effects begin within __________ minutes of subcutaneous injection and persist for_________ hours.

Back 158

15 to 30; 3 to 6

Front 159

Regular insulin is unmodified human insulin; its effects begin in ___________ minutes, peak in _________ hours, and last up to _____________ hours.

Back 159

30 to 60; 1 to 5; 10

Front 160

Neutral Protamine Hagedorn (NPH) insulin is injected ___________ daily to provide glycemic control between _____________ and during _________.

Back 160

twice;
meals;
the night

Front 161

These insulins are supplied as cloudy suspensions that must be gently agitated before administration.

Back 161

NPH

Front 162

Insulin glargine is a modified human insulin with a prolonged duration of action (at least ___ hours). Insulin glargine achieves blood levels that are relatively _______ over _____ hours.

Back 162

24;
steady;
24

Front 163

Only ______________ insulin is appropriate for mixing with short-acting insulins.

Back 163

NPH

Front 164

Why is insulin infusion employed to treat hyperkalemia?

Back 164

It can promote cellular uptake of potassium and lower plasma potassium levels.

Front 165

The principal indication for insulin is _____________.

Back 165

diabetes mellitus

Front 166

Responsibility for managing diabetes rests with the _____________.

Back 166

patient

Front 167

Main cause of insulin excess:

Back 167

overdose

Front 168

signs and symptoms of hypoglycemia

Back 168

Rapid fall in glucose levels--tachycardia, palpitations, sweating, and nervousness (SNS)
Gradual decline in glucose--headache, confusion, drowsiness, and fatigue (CNS)

Front 169

In conscious patients, glucose levels can be restored with __________. In cases of severe hypoglycemia, ___________ is the preferred treatment. Parenteral __________ is an alternative treatment.

Back 169

a fast-acting oral sugar
IV glucose
glucagon

Front 170

What can sulfonylureas, glinides, beta-adrenergic blocking agents, and alcohol do when combined with insulin?

Back 170

Drugs that lower blood glucose levels can intensify hypoglycemia induced by insulin.

Front 171

When combined with insulin, what is the effect of thiazide diuretics, glucocorticoids, and sympathomimetics.

Back 171

Drugs that raise blood glucose can counteract the desired effects of insulin.

Front 172

What is the diabetic patient's concern when taking beta blockers?

Back 172

Can delay awareness of and response to hypoglycemia by masking signs that are associated with stimulation of the sympathetic nervous system.

Front 173

How do sulfonylureas, glitazones, and glinides work?

Back 173

These drugs actively drive blood glucose down.

Front 174

How does metformin work?

Back 174

It doesn’t drive blood glucose down, but modulates the rise in glucose that happens after a meal.

Front 175

What is the drug of choice for initial therapy in most patients with type 2 diabetes?

Back 175

metformin

Front 176

Metformin lowers blood glucose and improves glucose tolerance in three ways: It inhibits glucose production in the ______, it reduces glucose absorption in the ____ slightly, and it ________ insulin receptors in target tissues (fat and skeletal muscle), increasing glucose uptake in response to available insulin.

Back 176

liver; gut; sensitizes

Front 177

Why does metformin not pose a risk of hypoglycemia when used alone?

Back 177

It does not stimulate insulin release from the pancreas.

Front 178

Metformin is used to lower blood sugar in patients with type 2 diabetes who have not responded adequately to __________________.

Back 178

diet modification and exercise

Front 179

What are the most common side effects of metformin?

Back 179

decreased appetite, nausea, and diarrhea

Front 180

Metforminin must never be used by patients with ______________.

Back 180

renal insufficiency

Front 181

The thiazolidinediones, also known as glitazones or TZDs, reduce glucose levels primarily by __________________.

Back 181

decreasing insulin resistance

Front 182

Sulfonylureas act primarily by______________________ .

Back 182

stimulating the release of insulin from pancreatic islets

Front 183

The most common reactions to pioglitazone are:

Back 183

upper respiratory tract infection, headache, sinusitis, and myalgia

Front 184

Glinides—also known as meglitinides—are hypoglycemic agents that have the same mechanism as the sulfonylureas: ______________________________.

Back 184

stimulation of pancreatic insulin release

Front 185

Over time, repaglinide can lower _____ by about 1.7%. The drug is approved for ______ diabetes only.
Repaglinide is approved for monotherapy or combined therapy with ______ or ______.

Back 185

A1c;
type 2;
metformin;
a glitazone

Front 186

The alpha-glucosidase inhibitors—acarbose and miglitol—act in the ______ to delay ______.

Back 186

intestine;
absorption of carbohydrates

Front 187

Acarbose frequently causes ___________. These responses result from bacterial fermentation of unabsorbed carbohydrates in the _________.

Back 187

flatulence, cramps, abdominal distention, diarrhea, and borborygmus;
colon

Front 188

Acarbose can decrease absorption of ______, posing a risk of ______. Long-term, high-dose therapy may cause ______ dysfunction.

Back 188

iron; anemia; liver

Front 189

The combination of _______ and acarbose should probably be avoided. Both drugs cause significant ______ side effects, and the combination could be very unpleasant.

Back 189

metformin
GI

Front 190

Gliptins promote glycemic control by...

Back 190

suppressing postprandial release of glucagon.

Front 191

Sitagliptin's most common side effects are

Back 191

respiratory tract infection, headache, and inflammation of the nasal passages and throat

Front 192

There are three other injectable drugs for diabetes.

Back 192

Pramlintide, exenatide and liraglutide

Front 193

Exenatide was the first ______.

Back 193

incretin mimetic

Front 194

Adverse effects of exenatide:

Back 194

nausea and hypoglycemia

Front 195

Risks of exenatide--

Back 195

pancreatitis; renal impairment

Front 196

The most severe manifestation of insulin deficiency

Back 196

DKA

Front 197

Treatment of DKA--

Back 197

Correct hyperglycemia and acidosis,
replace lost water and sodium,
and normalize potassium balance.
Begin with IV fluids and electrolytes, followed as soon as possible by IV insulin.

Front 198

What do thyroid hormones affect?

Back 198

metabolism, cardiac function, growth, and development

Front 199

Thyrotropin-releasing hormone (TRH) from the ______ causes the ______ to release thyroid-stimulating hormone (thyrotropin, TSH), which causes the ______ to make and release T3 and T4, which then act on the ______ to suppress further release of TSH.

Back 199

hypothalamus; pituitary; thyroid ; pituitary

Front 200

Hypothyroidism in adults requires ______ with thyroid hormones. In almost all cases, treatment must continue ______.

Back 200

replacement therapy
lifelong

Front 201

What is the most common cause of excessive thyroid hormone secretion?

Back 201

Graves’ disease

Front 202

How is hyperthyroidism treated?

Back 202

Reducing the production of thyroid hormones by
(1) surgical removal of thyroid tissue, (2) destruction of thyroid tissue with radioactive iodine, and (3) suppression of thyroid hormone synthesis with an antithyroid drug (methimazole or propylthiouracil).

Front 203

Symptoms & treatment of thyrotoxic crisis:

Back 203

Profound hyperthermia (105°F or even higher), severe tachycardia, restlessness, agitation, and tremor
High doses of potassium iodide to suppress thyroid hormone release, beta blocker to slow the heart rate, sedation, cooling, glucocorticoids and IV fluids.

Front 204

Levothyroxine

Back 204

a synthetic preparation of thyroxine (T4) & the drug of choice for most patients who require thyroid hormone replacement

Front 205

When should levothyroxine be taken?

Back 205

in the morning, at least 30 to 60 minutes before breakfast, on an empty stomach

Front 206

Levothyroxine has a _______ therapeutic range

Back 206

narrow

Front 207

How is therapy with levothyroxine evaluated?

Back 207

via measurement of the serum TSH

Front 208

What condition do methimazole and propylthiouracil (PTU) treat & what do they do?

Back 208

hyperthyroidism; suppress synthesis of thyroid hormones.

Front 209

Name a first-line drug for hyperthyroidism.

Back 209

Methimazole

Front 210

Once therapy with methimazole has begun, why may it take 3 to 12 weeks to produce a euthyroid state?

Back 210

Methimazole prevents thyroid hormone synthesis, but does not destroy existing stores of thyroid hormone.

Front 211

Who should avoid takine methimazole?

Back 211

women who are pregnant or breast feeding

Front 212

What conditions can methimazole cause?

Back 212

Methimazole can cause neonatal hypothyroidism, goiter, and even cretinism.

Front 213

What is Iodine-131 (131I) used for?

Back 213

destroying thyroid tissue in patients with hyperthyroidism

Front 214

What is the objective in Iodine-131 therapy?

Back 214

to produce clinical remission without causing complete destruction of the gland

Front 215

Advantages of Iodine-131 therapy:

Back 215

(1) low cost; (2) patients are spared the risks, discomfort, and expense of thyroid surgery; (3) death from 131I treatment is extremely rare; and (4) no tissue other than the thyroid is injured.

Front 216

Who is a candidate for 131I therapy?

Back 216

patients over age 30,
patients who have not responded adequately to antithyroid drugs or to subtotal thyroidectomy

Front 217

Who should not undergo 131I therapy?

Back 217

young children; women who are pregnant or breastfeeding

Front 218

Working together, the _____________ and _____________ help regulate practically all bodily processes.

Back 218

hypothalamus; pituitary

Front 219

The anterior pituitary produces six major hormones:

Back 219

growth hormone, corticotropin, thyrotropin, follicle-stimulating hormone, luteinizing hormone, and prolactin.

Front 220

The posterior pituitary produces only two hormones,

Back 220

oxytocin and antidiuretic hormone.

Front 221

The _____________ is primarily responsible for regulating the release of hormones from the anterior pituitary.

Back 221

hypothalamus

Front 222

The only treatment for GH deficiency is replacement therapy with...

Back 222

human GH itself.

Front 223

Treatment of gigantism requires...

Back 223

surgical removal of the pituitary.

Front 224

Antidiuretic hormone (ADH), also known as_______________, acts on the kidneys to cause reabsorption (conservation) of __________.

Back 224

vasopressin
water

Front 225

When ADH replacement therapy is started, the patient must be warned to reduce _________, because failure to do so can cause _______________.

Back 225

water intake
water intoxication

Front 226

Vasopressin can cause what side effects?

Back 226

adverse cardiovasculareffects; vasoconstriction.

Front 227

Diabetes insipidus may be treated with...

Back 227

desmopressin

Front 228

The two most familiar forms of adrenocortical dysfunction are __________, caused by adrenal hormone excess, and ______________, caused by adrenal hormone deficiency.

Back 228

Cushing’s syndrome
Addison’s disease

Front 229

The adrenal cortex produces three classes of steroid hormones:

Back 229

glucocorticoids, mineralocorticoids, and androgens

Front 230

Glucocorticoids influence...

Back 230

carbohydrate metabolism and other processes

Front 231

Mineralocorticoids modulate ...

Back 231

salt and water balance

Front 232

Adrenal androgens contribute to...

Back 232

expression of sexual characteristics.

Front 233

Of the several glucocorticoids produced by the adrenal cortex, _______ is the most important.

Back 233

cortisol

Front 234

The mineralocorticoids influence renal processing of sodium, potassium, and hydrogen; ____________ is the most important.

Back 234

aldosterone

Front 235

In the absence of aldosterone, renal excretion of sodium and water is greatly _____________, whereas excretion of potassium and hydrogen is _______________.

Back 235

increased
reduced

Front 236

Secretion of aldosterone is regulated by _____________.

Back 236

the renin-angiotensin-aldosterone system (RAAS)

Front 237

The treatment of choice for adrenal adenoma and carcinoma is __________________.

Back 237

surgical removal of the diseased adrenal gland

Front 238

The role of drugs in treating Cushing’s syndrome is limited; benefits derive from suppression of corticosteroid synthesis. The most effective agent is ____________, an antifungal drug that also blocks glucocorticoid synthesis.

Back 238

ketoconazole

Front 239

_______________ causes hypokalemia, metabolic alkalosis, and hypertension and can increase the risk of heart failure

Back 239

Hyperaldosteronism

Front 240

Chronic adrenal insufficiency requires lifelong replacement therapy with appropriate _____________. All patients require a ________________. Some may require a ____________ as well.

Back 240

corticosteroids
glucocorticoid
mineralocorticoid

Front 241

_______________ is a drug of choice among the glucocorticoids available to treat Addison's disease.

Back 241

Hydrocortisone

Front 242

At times of ___________, patients must increase their glucocorticoid dosage.

Back 242

stress

Front 243

If additional mineralocorticoid activity is needed for treatment of Addison's, ___________ can be added to the regimen.

Back 243

fludrocortisone

Front 244

What are the symptoms of adrenal crisis (acute corticosteroid deficiency)?

Back 244

hypotension, dehydration, weakness, lethargy, and gastrointestinal (GI) symptoms

Front 245

Hydrocortisone, a synthetic steroid, has a structure identical to that of _______, the principal glucocorticoid produced by the adrenal cortex.

Back 245

cortisol

Front 246

Hydrocortisone is a preferred drug for all forms of __________________.

Back 246

adrenocortical insufficiency

Front 247

______________ is the only mineralocorticoid available and is the drug of choice for chronic mineralocorticoid replacement.

Back 247

Fludrocortisone

Front 248

Patients taking fludrocortisone should be monitored for ...

Back 248

weight gain, elevation of blood pressure, and hypokalemia.

Front 249

Why is calcium important?

Back 249

Calcium is critical to blood coagulation and to the functional integrity of bone, nerve, muscle, and the heart.

Front 250

Absorption of calcium takes place in the ______________. Absorption is increased by ____________________.

Back 250

small intestine
parathyroid hormone (PTH) and vitamin D

Front 251

Calcium excretion is primarily ___________.

Back 251

renal

Front 252

How does PTH increase serum calcium levels?

Back 252

PTH (1) promotes calcium resorption from bone, (2) promotes tubular reabsorption of calcium that had been filtered by the kidney glomerulus, and (3) promotes activation of vitamin D and thereby promotes increased absorption of calcium from the intestine.

Front 253

Both vitamin D and PTH __________ plasma calcium levels. Vitamin D differs from PTH in that vitamin D _________ plasma levels of phosphate, whereas PTH __________ levels of phosphate.

Back 253

increase
elevates
reduces

Front 254

Calcitonin, a hormone produced by the thyroid gland, ________ plasma levels of calcium. Hence, calcitonin acts _________ PTH and vitamin D.

Back 254

decreases
in opposition to

Front 255

Oral calcium preparations are used to treat ___________. In addition, calcium salts are taken as________________.

Back 255

mild hypocalcemia
dietary supplements

Front 256

People who may need supplemental calcium:

Back 256

adolescents, the elderly, and postmenopausal women

Front 257

Hypercalcemia is most likely in patients who are receiving large doses of calcium and____________.

Back 257

vitamin D

Front 258

Signs and symptoms of hypercalcemia:

Back 258

GI disturbances, renal dysfunction, and CNS effects
may also cause cardiac dysrhythmias and deposition of calcium in soft tissue

Front 259

Vitamin D is an important regulator of ___________ and _____________ homeostasis.

Back 259

calcium
phosphorus

Front 260

Vitamin D is obtained through...

Back 260

food, supplements, and exposure to sunlight.

Front 261

Calcitonin has two principal actions:

Back 261

(1) it inhibits the activity of osteoclasts, thereby reducing bone resorption, and (2) it inhibits tubular resorption of calcium, thereby increasing calcium excretion.

Front 262

Calcitonin-salmon, given by nasal spray or injection, is indicated for treatment of _____________________—but not for prevention.

Back 262

established postmenopausal osteoporosis

Front 263

Benefits of calcitonin-salmon derive from suppressing ___________. The treatment program should include supplemental ____________ and adequate intake of vitamin D.

Back 263

bone resorption
calcium

Front 264

carvedilol's trade name

Back 264

Coreg

Front 265

Carvedilol is a _______________ used as an adjunct to treat ____________.

Back 265

beta blocker
heart failure

Front 266

carvedilol's MOA

Back 266

reduces cardiac output and tachycardia, causes vasodilation, reduces blood pressure and cardiac workload

Front 267

carvedilol's contraindications

Back 267

asthma; severe bradycardia

Front 268

D/D interactions for carvedilol

Back 268

amiodarone; beta blockers; digoxin; CCBs

Front 269

If giving carvedilol to a HF patient, also expect to give ____________.

Back 269

digoxin, a diuretic, & an ACE inhibitor

Front 270

Abrupt stoppage of carvedilol in hyperthyroid patients could precipitate ______________.

Back 270

thyroid storm

Front 271

Desmopressin (DDAVP) is an ______________ given to treat ______________.

Back 271

antidiuretic; diabetes insipidus

available as a nasal spray

Front 272

desmopressin's MOA

Back 272

increases permeability of renal collecting ducts, thus enhancing water reabsorption

Front 273

Contraindications for desmopressin

Back 273

renal impairment; hyponatremia

Front 274

Nursing consideration when giving desmopressin--

Back 274

Monitor pt closely for signs of hyponatremia (headache, N/V, restlessness, fatigue, changes in mental status)

Front 275

digoxin

Back 275

Lanoxin

Front 276

Digoxin is an ________________.

Back 276

antiarrhythmic

Front 277

Digoxin is given to treat:

Back 277

heart failure, atrial flutter, a-fib

Front 278

digoxin's MOA

Back 278

increases force and velocity of myocardial contraction (positive inotropic effect)
decreases conduction rate (antiarrhythmic effect); slows heartrate

Front 279

Patient teaching for digoxin:

Back 279

take as prescribed, same time each day, take pulse before administration, watch drug/drug, notify Dr. of GI distress or pulse changes

Front 280

Enalapril

Back 280

Vasotec

Front 281

Enalapril is an _____________ used to control _______________ and to treat ________________.

Back 281

ACE inhibitor
hypertension
heart failure

Front 282

Enalapril's MOA

Back 282

Decreases vascular tone & pressure (inhibits aldosterone release, reducing sodium & water reabsorption-->lower BP)

Front 283

Drug/Drug for enalapril

Back 283

potassium-containing salt substitutes (risk of hyperkalemia)
alcohol (added hypotensive effect)

Front 284

Nursing considerations--enalapril

Back 284

use caution in pts with impaired renal function; watch for hypotension; watch for angioedema of face, lips, tongue

Front 285

exenatide

Back 285

Byetta

Front 286

exenatide is an ________________ drug

Back 286

antidiabetic

Front 287

route for exenatide

Back 287

subQ

Front 288

D/D exenatide

Back 288

oral antidiabetics (hypoglycemia); warfarin (bleeding)

Front 289

exenatide MOA

Back 289

spurs insulin synthesis; suppresses glucacon secretion

Front 290

Nursing considerations for exenatide

Back 290

monitor for pancreatitis; monitor blood glucose levels; administer within 60 min before morning & evening meals

Front 291

epoetin alfa

Back 291

Epogen

Front 292

Epoetin alfa is an ________________ drug.

Back 292

antianemic

Front 293

Who takes epoetin alfa?

Back 293

renal failure, HIV, and chemo patients (in danger of anemia)
also pre-surgery

Front 294

D/D for epoetin alfa

Back 294

don't mix with any other drug
antihypertensives; heparin; iron supplements

Front 295

contraindications for epoetin alfa

Back 295

uncontrolled HTN

Front 296

Nursing implications for epoetin alfa

Back 296

don't shake--denatures protein & inactivates drug
target hemoglobin not to exceed 12 g/dl
take seizure precautions

Front 297

filgastrim

Back 297

Neupogen

Front 298

Filgastrim is an ________________ given to prevent ________________ and ________________.

Back 298

antineutropenic, hematopoietic stimulator
neutropenia
infection

Front 299

Patients who might receive filgastrim:

Back 299

chemotherapy, bone marrow transplant patients

Front 300

Nursing implications for filgastrim

Back 300

monitor CBC, hematocrit, & platelet count
don't shake

Front 301

fludrocortisone

Back 301

Florinef

Front 302

Fludrocortisone is given to treat ________________

Back 302

chronic adrenocortical insufficiency

Front 303

fludrocortisone MOA

Back 303

similar to aldosterone--enhances sodium reabsorption, hydrogen & potassium excretion, and water retention

Front 304

nursing implications--fludrocortisone

Back 304

monitor for signs of heart failure, monitor BP & fluid status, weight
Don't stop taking abruptly

Front 305

furosemide

Back 305

Lasix

Front 306

glipizide

Back 306

Glucotrol

Front 307

Glipizide is a ________________ used to control blood glucose levels in ________________.

Back 307

sulfonylurea
type 2 diabetes

Front 308

glipizide MOA

Back 308

stimulates insulin release from beta cells in pancreas
increases peripheral tissue sensitivity to insulin

Front 309

Glipizide--Increased risk of hypoglycemia in patient with ________________

Back 309

renal, hepatic, pituitary, or adrenal insufficiency

Front 310

Hydrocortisone is a ________________ used to treat ________________.

Back 310

glucocorticoid
severe inflammation or acute adrenal insufficiency

Front 311

hydrocortisone's MOA

Back 311

suppresses inflammatory & immune responses

Front 312

Nursing considerations for hydrocortisone

Back 312

Avoid sudden withdrawal after long-term therapy--could precipitate adrenal crisis. Reduce dosage gradually.
Client should avoid people with infections.

Front 313

Kayexalate is an ________________ drug given to treat ________________.

Back 313

antihyperkalemic
hyperkalemia

Front 314

Nursing considerations--Kayexalate

Back 314

Use cautiously in pts with HF, hypertension, or marked edema. Not for treatment of acute, life-threatening hyperkalemia (takes hours to work). Monitor for hypokalemia. Watch for cramps, N/V.

Front 315

levothyroxine

Back 315

Synthroid

Front 316

Levothyroxine teachings

Back 316

separate iron & calcium supplements from levothyroxine with 4 hours or more; may need weeks to take effect

Front 317

Signs of hypermagnesemia

Back 317

bradycaria; dyspnea; decreased deep tendon reflexes; hypotension; vomiting; weakness

Front 318

metformin

Back 318

Glucophage

Front 319

Metformin reduces ________________ in ________________.

Back 319

blood glucose levels; type 2 DM

Front 320

Nursing considerations--metformin

Back 320

Give with food (reduces GI upset).
Withhold if pt has diarrhea, GI obstruction, or vomiting.
Monitor blood glucose levels.
Report signs of lactic acidosis.

Front 321

Methimazole is an ________________ drug used to treat ________________.

Back 321

antithyroid; hyperthyroidism

Front 322

octreotide

Back 322

Sandostatin

Front 323

Octreotide is a ________________ used to treat ________________.

Back 323

hormone suppressant;
symptoms of acromegaly

Front 324

route for octreotide

Back 324

injection only

Front 325

Considerations for octreotide

Back 325

orthostatic hypotension; possible pancreatitis; diabetic--take extra care of blood glucose levels

Front 326

hydrochlorothiazide

Back 326

HydroDIURIL

Front 327

Nursing considerations for hydrocholrothiazide

Back 327

Give in morning & early evening to avoid nocturia.
Monitor I&O, daily weight, BP, and serum electrolye levels (esp. K+).
Advise pt to eat foods rich in potassium.

Front 328

Why take morphine sulfate to relieve HF?

Back 328

as an adjunct to treat pulmonary edema caused by left-sided heart failure

Front 329

repaglinide

Back 329

Prandin

Front 330

Repaglinide is an ________________ used to achieve ________________ in type 2 DM.

Back 330

antidiabetic; glucose control

Front 331

repaglinide MOA

Back 331

Stimulates release of insulin from functioning pancreatic beta cells.

Front 332

Contraindications for repalinide

Back 332

gemfibrozil therapy; DKA; severe hepatic or renal impairment

Front 333

Nursing considerations for repaglinide

Back 333

Shouldn't be used with NPH insulin--risk of angina

Front 334

sitagliptin

Back 334

Januvia

Front 335

sitagliptin MOA

Back 335

slows inactivation of incretin hormones (which stimulates work of insulin)

Front 336

Somatropin is a ________________ used to treat ________________ caused by ________________.

Back 336

growth hormone; growth failure; hormone deficiency

Front 337

Adverse effects to watch for with somatropin

Back 337

Although uncommon, intracranial hypertension is possible. (headache, nausea, vision changes)

Front 338

Spironolactone (Aldactone) is an ________________ used to treat ________________ caused by ________________.

Back 338

aldosterone antagonist/diuretic
edema
heart failure

Front 339

spironolactone's MOA

Back 339

competes with aldosterone in nephron, causing sodium and water excretion (reducing blood volume and BP)