Exam 3

Question 1

How do counterregulatory hormones increase blood glucose levels?

Answer 1

(1) stimulating glucose production and release by the liver and (2) decreasing the movement of glucose into the cells.

Question 2

Insulin resistance

Answer 2

insulin resistance, a condition in which body tissues do not respond to the action of insulin because insulin receptors are unresponsive, are insufficient in number, or both

Question 3

second factor in the development of type 2 diabetes

Answer 3

A second factor in the development of type 2 diabetes is a marked decrease in the ability of the pancreas to make insulin, as the β cells become fatigued from the compensatory overproduction of insulin or when β-cell mass is lost.

Question 4

third factor in the development of Type 2 DM

Answer 4

This leads to a third factor, which is inappropriate glucose production by the liver. Instead of properly regulating the release of glucose in response to blood levels, the liver does so in a haphazard way that does not correspond to the body’s needs at the time.

Question 5

Fourth factor in the development of Type 2 DM

Answer 5

A fourth factor is altered production of hormones and cytokines by adipose tissue (adipokines). Adipokines secreted by adipose tissue appear to play a role in glucose and fat metabolism and are likely to contribute to the development of type 2 diabetes.4 We think adipokines cause chronic inflammation, a factor involved in insulin resistance, type 2 diabetes, and cardiovascular disease (CVD).

Question 6

Lipodystrophy (related to DM)

Answer 6

Lipodystrophy (loss of subcutaneous fatty tissue) may occur if the same injection sites are used frequently. The use of human insulin has significantly reduced the risk for lipodystrophy.

Question 7

Cloudy insulins

Answer 7

All insulins are clear solutions except NPH, lispro protamine, and aspart protamine

Question 8

Atrophy (related to DM)

Answer 8

Atrophy, which is uncommon, is the wasting of subcutaneous tissue and presents as indentations in injection sites

Question 9

Hypertrophy (related to DM)

Answer 9

Hypertrophy happens more often and is a thickening of the subcutaneous tissue. It eventually regresses if the patient does not use the site for at least 6 months. Injecting into a hypertrophied site may result in erratic insulin absorption.

Question 10

Somogyi effect.

Answer 10

Hyperglycemia in the morning may be due to the Somogyi effect. A high dose of insulin causes a decline in blood glucose levels during the night. As a result, counterregulatory hormones (e.g., glucagon, epinephrine, GH, cortisol) are released. They stimulate lipolysis, gluconeogenesis, and glycogenolysis, which in turn cause rebound hyperglycemia. The danger of this effect is that when blood glucose levels are measured in the morning, hyperglycemia is apparent and the patient (or the HCP) may increase the insulin dose

Treatment: The treatment for Somogyi effect is a bedtime snack, reducing the dose of insulin, or both.

Question 11

dawn phenomenon

Answer 11

The dawn phenomenon is also characterized by hyperglycemia that is present on awakening. Two counterregulatory hormones (GH and cortisol), which are excreted in increased amounts in the early morning hours, may be the cause of this phenomenon. The dawn phenomenon affects many people with diabetes and tends to be most severe when GH is at its peak in adolescence and young adulthood.

Treatment: The treatment for dawn phenomenon is an increase in insulin or an adjustment in administration time.

Question 12

DM drug therapy: Biguanides

Answer 12

most widely used OA is metformin. Forms of metformin include Glucophage (immediate release), Glucophage XR (extended release), Fortamet (extended release), and Riomet (liquid). The primary action of metformin is to reduce glucose production by the liver. It enhances insulin sensitivity at the tissue level and improves glucose transport into the cells. Lactic acidosis is a rare complication of metformin accumulation

Question 13

DM drug therapy: Sulfonylureas

Answer 13

Sulfonylureas include glimepiride (Amaryl), glipizide (Glucotrol, Glucotrol XL), and glyburide (DiaBeta, Glynase). The primary action of sulfonylureas is to increase insulin production by the pancreas. Therefore hypoglycemia is the major side effect.

Question 14

Meglitinides

Answer 14

Like sulfonylureas, nateglinide (Starlix) and repaglinide (Prandin) increase insulin production by the pancreas. However, because they are more rapidly absorbed and eliminated than sulfonylureas, they are less likely to cause hypoglycemia. When taken just before meals, pancreatic insulin production increases during and after the meal, mimicking the normal response to eating. Teach patients to take meglitinides any time from 30 minutes before each meal right up to the time of the meal. These drugs should not be taken if a meal is skipped.

Question 15

α-Glucosidase Inhibitors

Answer 15

These drugs, also known as “starch blockers,” work by slowing down carbohydrate absorption in the small intestine. Acarbose (Precose) and miglitol (Glyset) are the available drugs in this class. Taken with the first bite of each main meal, they are most effective in lowering postprandial blood glucose.

Question 16

Thiazolidinediones, sometimes called “insulin sensitizers,”

Answer 16

pioglitazone (Actos) and rosiglitazone (Avandia). They are most effective for people who have insulin resistance. These agents improve insulin sensitivity, transport, and use at target tissues. Because they do not increase insulin production, they do not cause hypoglycemia when used alone. However, these drugs are rarely used today because of their adverse effects. Rosiglitazone is associated with adverse cardiovascular events (e.g., myocardial infarction [MI]) and can be obtained only through restricted access programs. Pioglitazone can worsen heart failure (HF) and is associated with an increased risk for bladder cancer.

Question 17

Dipeptidyl Peptidase-4 (DPP-4) Inhibitors

Answer 17

DPP-4 inhibitors (also known as gliptins) come in pill form. They include alogliptin (Nesina), linagliptin (Tradjenta), saxagliptin (Onglyza), and sitagliptin (Januvia). DPP-4 inhibitors block the action of DPP-4, which inactivates incretin hormones. The result is an increase in insulin release, decrease in glucagon secretion, and decrease in hepatic glucose production. Since the DPP-4 inhibitors are glucose dependent, they lower the potential for hypoglycemia. The main benefit of these drugs over other medications with similar effects is the absence of weight gain as a side effect.

Question 18

Sodium-Glucose Co-Transporter 2 (SGLT2) Inhibitors

Answer 18

Normally, sodium glucose transporters reabsorb glucose from the kidneys back into the blood stream. Sodium-glucose co-transporter 2 (SGLT2) inhibitors work by blocking the reabsorption of glucose by the kidney, increasing urinary glucose excretion. Drugs in this class include canagliflozin (Invokana), dapagliflozin (Farxiga), and empagliflozin (Jardiance).

Question 19

Hypoglycemia

Answer 19

Altered mental function—“neuroglycopenia”
-Difficulty speaking
-Visual disturbances
-Stupor
-Confusion
-Coma
-Mimics alcohol intoxication
Untreated hypoglycemia can progress to loss of consciousness, seizures, coma, and death

Question 20

Manifestations of hypoglycemia

Answer 20

Common manifestations
-Shakiness
-Diaphoresis
-Anxiety
-Pallor
• Cold, clammy skin
• Numbness of fingers, toes, mouth
• Tachycardia, palpitations
• Emotional changes
• Headache
• Nervousness, tremors
• Faintness, dizziness
• Unsteady gait, slurred speech
• Hunger
• Changes in vision
• Seizures, coma

Question 21

Manifestation of hyperglycemia

Answer 21

• Elevated blood glucose
• Increase in urination
• Increase in appetite followed by lack of appetite
• Weakness, fatigue
• Blurred vision
• Headache
• Glycosuria
• Nausea and vomiting
• Abdominal cramps
• Progression to DKA or HHS
• Mood swings

Question 22

Progression of DKA

Answer 22

If not treated, the patient will develop severe depletion of sodium, potassium, chloride, magnesium, and phosphate. Vomiting caused by the acidosis results in more fluid and electrolyte losses. Eventually, hypovolemia, followed by shock, will ensue. Renal failure, which may eventually occur from hypovolemic shock, causes the retention of ketones and glucose, and the acidosis progresses. Untreated, the patient becomes comatose from dehydration, electrolyte imbalance, and acidosis. Ifthe condition is not treated, death is inevitable.

Question 23

Hyperosmolar hyperglycemia syndrome (HHS)

Answer 23

Hyperosmolar hyperglycemia syndrome (HHS) is a life-threatening syndrome that can occur in the patient with diabetes who is able to make enough insulin to prevent DKA, but not enough to prevent severe hyperglycemia, osmotic diuresis, and extracellular fluid depletion

Question 24

Theories as to how and why chronic hyperglycemia damages cells and tissues

Answer 24

Possible causes include (1) the accumulation of damaging by-products of glucose metabolism, such as sorbitol, which is associated with damage to nerve cells; (2) the formation of abnormal glucose molecules in the basement membrane of small blood vessels, such as those that circulate to the eyes and kidneys; and (3) a derangement in RBC function that leads to a decrease in oxygenation to the tissues.

Question 25

Diabetes-related retinopathy

Answer 25

refers to the process of microvascular damage to the retina because of chronic hyperglycemia, nephropathy, and hypertension in patients with diabetes. Diabetes-related retinopathy is the leading cause of new cases of adult blindness.

Question 26

nonproliferative retinopathy

Answer 26

In nonproliferative retinopathy, the most common form, partial occlusion of the small blood vessels in the retina causes microaneurysms to develop in the capillary walls. The walls of these microaneurysms are so weak that capillary fluid leaks out, causing retinal edema and eventually hard exudates or intraretinal hemorrhages. This may cause mild to severe vision loss, depending on which parts of the retina are affected

Question 27

Proliferative retinopathy

Answer 27

Proliferative retinopathy, the most severe form, involves the retina and vitreous. When retinal capillaries become occluded, the body compensates by forming new blood vessels to supply the retina with blood, a pathologic process known as neovascularization. These new vessels are extremely fragile and hemorrhage easily, producing vitreous contraction. Eventually light is prevented from reaching the retina as the vessels break and bleed into the vitreous cavity. The patient sees black or red spots or lines. If these new blood vessels pull the retina while the vitreous contracts, causing a tear, partial or complete retinal detachment will occur. If the macula is involved, vision is lost.

Question 28

Diabetes-related nephropathy

Answer 28

Diabetes-related nephropathy is a microvascular complication associated with damage to the small blood vessels that supply the glomeruli of the kidney

Question 29

Diabetes-related neuropathy

Answer 29

Diabetes-related neuropathy is nerve damage that occurs because of the metabolic imbalances associated with diabetes.

Question 30

Modifiable risk factors for CAD

Answer 30

Modifiable risk factors include
-high serum lipids levels (total serum cholesterol level greater than 200 mg/dL (5.2 mmol/L), an LDL greater than 130 mg/dL (3.4 mmol/L), a high-density lipoprotein (HDL) level less than 40 mg/dL (1.0 mmol/L) in men and less than 50 mg/dL (1.3 mmol/L) in women, and/or a fasting triglyceride level greater than 150 mg/dL (1.7 mmol/L))
-high BP,
-tobacco use,
-physical inactivity,
-obesity, diabetes,
-metabolic syndrome,
-psychologic states,
-high homocysteine level

Question 31

Nonmodifiable risk factors for CAD

Answer 31

Nonmodifiable risk factors are age, gender, ethnicity, family history, and genetics

Question 32

Homocysteine

Answer 32

High blood levels of homocysteine are linked to an increased risk for CAD and other CVDs. Homocysteine is made by the breakdown of the essential amino acid methionine, which is found in dietary protein. High homocysteine levels may contribute to atherosclerosis by (1) damaging the inner lining of blood vessels, (2) promoting plaque buildup, and (3) changing the clotting mechanism to make clots more likely to occur. Although folic acid lowers homocysteine levels, research has not shown that reducing homocysteine levels lowers the risk of CAD

Question 33

HMG-CoA Reductase Inhibitors (Statins)

Answer 33

The statin drugs are the most widely used lipid-lowering drugs (Table 33.6). These drugs inhibit the synthesis of cholesterol in the liver. An unexplained result of inhibiting cholesterol synthesis is an increase in hepatic LDL receptors. This allows the liver to remove more LDL from the blood. Rosuvastatin (Crestor) is the most potent statin currently available.

Question 34

Niacin

Answer 34

Niacin, a water-soluble B vitamin, is effective in lowering LDL and triglyceride levels by interfering with their synthesis. Niacin, at high doses, increases HDL levels better than many other lipid-lowering drugs. Unfortunately, side effects are common. They may include severe flushing, pruritus, gastrointestinal (GI) symptoms, and orthostatic hypotension.

Question 35

Fibric Acid Derivatives

Answer 35

The fibric acid derivatives (Table 33.6) work by aiding the removal of VLDLs. They are very effective for lowering triglycerides and increasing HDL levels. They have no effect on LDLs. GI irritability is common. should be used with caution when combined with statin medications due to increased risk for myopathy. E..g. fenofibrate (Tricor)
gemfibrozil (Lopid

Question 36

Bile Acid Sequestrants

Answer 36

Bile-acid sequestrants increase conversion of cholesterol to bile acids in the liver and decrease hepatic cholesterol (Table 33.6). The primary effect is a decrease in total cholesterol and LDL levels. These drugs have been associated with side effects related to taste and a variety of upper and lower GI symptoms. These include belching, heartburn, nausea, abdominal pain, and constipation. Bile-acid sequestrants decrease absorption of many other drugs. Separating the time of giving these drugs from that of other drugs by at least 2 hours decreases this adverse effect.
E.g. cholestyramine (Prevalite)
colesevelam (Welchol)
colestipol (Colestid)

Question 37

Proprotein Convertase Subtilisin/Kexin 9 (PCSK9) Inhibitors

Answer 37

PCSK9 reduces the number of receptors on the liver that remove LDL cholesterol from the blood. By blocking PCSK9’s ability to work, more receptors are available and can get rid of LDL, thus decreasing circulating LDL levels. Evolocumab (Repatha) and alirocumab (Praluent) are 2 PCSK9 inhibitors. They are given subcutaneously every 2 weeks. Evolocumab may be given every 4 weeks at a higher dose, depending on patient preference. They are not a first-line therapy. They are used in addition to diet and maximum statin therapy for adults with familial hypercholesterolemia and for patients intolerant of statin drugs.
E.g. alirocumab (Praluent)
evolocumab (Repatha)

Question 38

Ezetimibe (Zetia)

Answer 38

selectively inhibits the absorption of dietary and biliary cholesterol across the intestinal wall (Table 33.6). It serves as an adjunct to dietary changes, especially for patients with primary hypercholesterolemia. When it is combined with a statin, either as a combination drug (e.g., ezetimibe and simvastatin [Vytorin]) or as 2 separate drugs (ezetimibe and a statin), even greater reductions in LDLs occur.

Question 39

Angina

Answer 39

Angina, or chest pain, is the clinical manifestation of myocardial ischemia. It is caused by either an increased demand for O2 or a decreased supply of O2

Question 40

Chronic stable angina

Answer 40

Chronic stable angina refers to chest pain that occurs intermittently over a long period of time with a similar pattern of onset, duration, and intensity of symptoms. It is often provoked by physical exertion, stress, or emotional upset

Question 41

PQRST Assessment of Angina

Answer 41

P= Precipitating events
Q= Quality of pain
R= Region (location) and radiation of pain
S= Severity of pain
T= Timing

Question 42

The overall goals for a patient who presents with angina

Answer 42

The overall goals for a patient who presents with angina include (1) relief of pain, (2) immediate and appropriate treatment, (3) preservation of heart muscle if an MI is suspected, (4) effective coping with illness-associated anxiety, (5) participation in a rehabilitation plan, and (6) reduction of risk factors.

Question 43

Short-acting nitrates

Answer 43

Short-acting nitrates are first-line therapy for an acute episode of angina. Nitrates produce their principal effects by the following mechanisms:

Dilating peripheral blood vessels: This results in decreased SVR, venous pooling, and decreased venous blood return to the heart (preload). Therefore myocardial O2 demand is decreased because of the reduced cardiac workload.

Dilating coronary arteries and collateral vessels: This may increase blood flow to the ischemic areas of the heart. However, when the coronary arteries are severely atherosclerotic, coronary dilation is hard to achieve.

Question 44

Sublingual Nitroglycerin

Answer 44

SL NTG tablets or translingual spray (Nitrolingual) usually relieves pain in about 5 minutes and lasts about 30 to 40 minutes. Type of short acting nitrate

Question 45

Long-Acting Nitrates

Answer 45

Oral nitrates, such as isosorbide dinitrate (e.g., Isordil) and isosorbide mononitrate, are longer acting than SL or translingual NTG. They are used to reduce the frequency of angina attacks and to treat Prinzmetal’s angina. The main side effect is headache from the dilation of cerebral blood vessels

Question 46

Angiotensin-Converting Enzyme (ACE) Inhibitors and Angiotensin Receptor Blockers (ARBs)

Answer 46

These drugs result in vasodilation and reduced blood volume. Most important, they can prevent or reverse ventricular remodeling in patients who have had an MI (see p. 725). For patients who are intolerant of ACE inhibitors (e.g., cough, angioedema), angiotensin receptor blockers (ARBs) (e.g., losartan [Cozaar]) are used.

Patients with chronic stable angina who have an ejection fraction (EF) of 40% or less, diabetes, hypertension, or CKD should take an ACE inhibitor (e.g., lisinopril [Zestril]) indefinitely, unless contraindicated. Patients with chronic stable angina and a normal EF, diabetes, and 1 other CAD risk factor should also take an ACE inhibitor to decrease the risk for MI, stroke, and death

Question 47

β-Adrenergic Blockers

Answer 47

Patients who have LV dysfunction or elevated BP or had an MI should start and continue β-blockers indefinitely, unless contraindicated. These drugs decrease myocardial contractility, HR, SVR, and BP, all of which reduce the myocardial O2 demand and relieve angina symptoms. β-Blockers that reduce the risk for death in patients with LV dysfunction, HF, or MI include carvedilol (Coreg), metoprolol succinate (Toprol XL), and bisoprolol

Question 48

Calcium Channel Blockers

Answer 48

Their main effects are: (1) systemic vasodilation with decreased SVR, (2) decreased myocardial contractility, (3) coronary vasodilation, and (4) decreased HR. They are used to treat Prinzmetal’s angina.

Question 49

percutaneous coronary intervention (PCI)

Answer 49

PCI may be done at the same time as the cardiac catheterization. During PCI, a catheter with a deflated balloon tip is inserted into the blocked coronary artery. The deflated balloon is positioned inside the blockage and inflated. This compresses the plaque against the artery wall, resulting in vessel dilation and a larger vessel diameter. This procedure is called balloon angioplasty.

Question 50

The cause of ACS

Answer 50

ACS is caused by the decline of a once-stable atherosclerotic plaque. The previously stable plaque ruptures, releasing the lipid core into the vessel. This causes platelet aggregation and thrombus formation. The vessel may be partially blocked by a thrombus (manifesting as UA or NSTEMI) or totally blocked by a thrombus (manifesting as STEMI).

Question 51

Unstable Angina

Answer 51

Unstable angina (UA) is chest pain that is new in onset, occurs at rest, or occurs with increasing frequency, duration, or less effort than the patient’s chronic stable angina pattern. The pain usually lasts 10 minutes or more. occurs with increasing frequency and is easily provoked by minimal exertion, during sleep, or even at rest. ECG changes that may be seen with UA include ST depression and/or T wave inversion. These changes are referred as ischemic changes

Question 52

Myocardial infarction

Answer 52

myocardial infarction (MI) occurs because of an abrupt stoppage of blood flow through a coronary artery with a thrombus caused by platelet aggregation. This causes irreversible myocardial cell death (necrosis) in the heart muscle beyond the blockage (Figs. 33.10 and 33.11). Serum cardiac biomarkers are released into the blood. Most MIs occur in the setting of preexisting CAD.13

Question 53

STEMI ECG Changes

Answer 53

lowering of the initially elevated ST segments, T wave inversion and/or a pathologic Q wave

Question 54

Actions of water

Answer 54

Water
Transports nutrients and waste products
Provides a structure to large molecules
Promotes metabolic reactions
Serves as a solvent, lubricant, and cushion
Regulates body temperature
Maintains blood volume

Question 55

Short term feeding tubes

Answer 55

Nasally and orally placed tubes (orogastric, nasogastric [NG], nasoduodenal, nasojejunal) are appropriate for short-term feeding (less than 4 weeks)= feeding patient below pyloric sphincter

Question 56

Diverticulosis Sx

Answer 56

Diverticulosis—most asymptomatic
Abdominal pain, bloating, flatulence, changes in bowel habits; Serious: bleeding or diverticulitis

Question 57

Diverticulitis Sx

Answer 57

Acute pain in LLQ, distention, decreased or absent bowel sounds, nausea, vomiting, systemic symptoms of infection; Older adults—afebrile, normal WBC, possible abdominal tenderness

The most common signs and symptoms of diverticulitis are acute pain in the left lower quadrant, distention, decreased or absent bowel sounds, nausea, vomiting, and systemic symptoms of infection (fever, leukocytosis with a shift to the left)

Acute diverticulitis:
—Goal: bowel rest to reduce inflammation
—Clear liquids, bed rest, analgesia
Severe symptoms: systemic infection, comorbidities: hospitalization: NPO, NGT, bed rest, IV fluid and antibiotics; observe for signs of abscess, bleeding and peritonitis; advance diet as tolerated

Question 58

Dietary Intolerances for IBS

Answer 58

—Gluten
Fermentable oligo-, di-, and monosaccharides and polyols (FODMAPs)
—wheat& rye
—Onion
—garlic,
—Legumes
—Milk products
—Honey
—Artificial sweeteners

Question 59

What could cause Paralytic ileus?

Answer 59

Paralytic ileus—abdominal surgery, peritonitis, inflammatory disorders, electrolyte imbalances, thoracic, or lumbar spinal fractures

Question 60

4 hallmark clinical manifestations of an obstruction

Answer 60

abdominal pain, nausea and vomiting, distention, and constipation. Colicky abdominal pain is usually the first symptom. In SBO, the pain is often of sudden onset. It occurs at 4- to 5-minute intervals for proximal obstructions and less often for distal obstructions

Question 61

Inflammatory response

Answer 61

inflammatory response is a sequential reaction to cell injury.
It neutralizes and dilutes the inflammatory agent, removes necrotic materials, and establishes an environment suitable for healing and repair

Question 62

Inflammatory response 4 categories:

Answer 62

Vascular response
Cellular response
Formation of exudate
Healing

Question 63

Major functions of the complement system

Answer 63

Major functions of the complement system are enhanced phagocytosis, increased vascular permeability, chemotaxis, and cellular lysis.

Question 64

Prostaglandins

Answer 64

PGs are proinflammatory
Potent vasodilators contribute to increased blood flow and edema
Also: inhibit platelet and neutrophil aggregation, sensitize pain receptors, and stimulate fever