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Pharm 2024 > Diabetes and Dyslipidemia > Flashcards

Diabetes and Dyslipidemia Flashcards

Exam 4

1
Q

What are the 2 major types of secretory tissues of the pancreas?

A

Exocrine gland (digestive enzymes)
Endocrine gland (Islets of Langerhans)

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2
Q

What are the 5 cell types of islets of Langerhans?

A

Alpha, beta, delta, G cell, and F cell

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3
Q

What do the alpha Islets of Langerhans cells secrete?

A

glucagon and proglucagon

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4
Q

What do the beta Islets of Langerhans cells secrete?

A

insulin, C-peptide, proinsulin, amylin

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5
Q

What is the role of amylin?

A

suppressed the production of glucagon

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6
Q

_____ is the opposite of insulin

A

glucagon

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7
Q

What do the delta Islets of Langerhans cells secrete?

A

somatostatin

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8
Q

_______ blocks the release of glucagon and insulin

A

somatostatin

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9
Q

What is the main type of cells of the Islets of Langerhans?

A

Beta cells - 75%
Alpha cells - 20%

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10
Q

Insulin receptors are _____

A

RTKs - receptor tyrosine kinases

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11
Q

When insulin binds to insulin receptors, what occurs inside the cell?

A

Glucose transporters migrate to cell surface

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12
Q

What is the normal blood glucose?

A

90 mg/dL

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13
Q

Describe the homeostatic response to increased blood glucose

A

Increase in blood glucose → pancreatic beta cells release insulin → body cells take up more glucose and liver takes up glucose and stores it as glycogen → blood glucose levels decline to set point

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14
Q

Describe the homeostatic response to decreased blood glucose

A

Decrease in blood glucose → pancreatic alpha cells release glucagon → liver breaks down glycogen and releases glucose into the blood → blood glucose levels rises to set point

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15
Q

What are the 4 types of diabetes mellitus?

A

Type I - Insulin dependent
Type II - Non-insulin dependent
Type III - Other causes elevated blood glucose (pancreatitis, drug therapy, etc.)
Type IV - Gestational

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16
Q

The breakdown of glycogen is also known as _______

A

glycogenolysis

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17
Q

The creation of glycogen is also known as _______

A

glycogenesis

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18
Q

What is the most common cause of type 1 DM?

A

Immune
- idiopathic less common

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19
Q

How high does glucose need to be to be excreted in urine? What is this called?

A

160 mg/dL
- renal threshold

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20
Q

What are the 3 cardinal signs of all diabetes?

A

Polyuria, polydipsia, polyphagia

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21
Q

Mellitus means _____

A

sugar

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22
Q

Type I DM is caused by the destruction of ____, resulting in _____

A

beta cells
Severe or absolute insulin deficiency

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23
Q

What is the symptom of type 1 DM that differs from type 2?

A

weight loss

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24
Q

How is type 1 DM treated?

A

Require insulin replacement

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25
Q

If a patient with type 1 DM doesn’t take insulin, what happens?

A

Diabetic ketoacidosis (DKA)

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26
Q

Diabetic ketoacidosis causes a patient to have a _____ smelling breath

A

fruity

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27
Q

What is the patho behind type 2 DM?

A

Combination of relative deficiency of insulin secretion with tissue insulin resistance

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28
Q

What is the treatment for type 2 DM?

A

Exercise, treatment of obesity, medication

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29
Q

What are the clinical manifestations of type 2 DM?

A
  • Recurrent infections, vision problems, neuropathy
  • Dehydration – nonketotic hyperosmolar coma
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30
Q

What are the 4 chronic complications of type 2 DM?

A
  1. Hyperglycemia and nonenzymatic glycosylation - hemoglobin
  2. Hyperglycemia and the polyol pathway
    • Sorbitol and fructose increase intracellular osmotic pressure (attracts water, leading to cell injury)
    • Evident in the eye lens, nerves, RBCs
  3. Protein kinase C - Enzyme inappropriately activated by hyperglycemia
  4. Microvascular disease - Retinopathy
    and Diabetic nephropathy
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31
Q

Prediabetic fasting blood glucose is ____

A

100-110 mg/dL

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32
Q

What is the normal fasting blood glucose?

A

70 mg/dL

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33
Q

Gestational DM occurs in __% of US pregnancies

A

7%

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34
Q

Normal HA1C is __. Target for DM patients is __

A

4%, 7%

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35
Q

How does gestational DM work?

A

Hormones block → Insulin resistance

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36
Q

How is DM diagnosed?

A
  • Fasting Blood Glucose
  • Glucose Tolerance Test
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37
Q

How is DM monitored?

A
  • Self: Glucose POC
  • Hemoglobin A1C
  • Insulin
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38
Q

Insulin is a ____ hormone

A

peptide

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39
Q

The alpha and beta chains of insulin are held together via ______

A

disulfide linkages

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40
Q

Insulin is activated in the _____ before being released into the bloodstream

A

granules

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41
Q

The proform of insulin contains ______ which is _____ before entering the bloodstream

A

C-peptide
cleaved off

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42
Q

What is the function of C-peptide?

A

no known function

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43
Q

C-peptide is a measure of how much _____ function a patient has

A

beta cell

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44
Q

What is an insulin secretagogue? What are the different types?

A

increases release of insulin
- Glucose
- Amino acids
- Hormones
- Fatty acids
- Incretins
- Drugs – sulfonylureas, isoproterenol

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45
Q

The number one insulin secretagogue is _____

A

glucose

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46
Q

What are the transporters used to transport glucose into the beta cell?

A

GLUT2

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47
Q

Describe the effects of inward movement of glucose into pancreatic beta cells via GLUT2 transporters

A

excess glucose converted into ATP via metabolism → higher level of ATP binds to potassium channel - closing the channel → more positive Vrm → calcium channels open up → calcium enters beta cell → calcium triggers vesicle fusion and insulin exocytosis

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48
Q

How long does insulin last in the blood stream?

A

6 min

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49
Q

GLUT2 transporters have ____ affinity for glucose, meaning they have a ___ Km

A

low, high

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50
Q

Describe the pathway of insulin binding to its receptor

A

dimerization of units → insulin binds to receptor → beta units start internal signaling by becoming phosphorylated → IRS (insulin response substrates) activated → MAP kinase and IP3 pathways activated

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51
Q

Which glucose transporters have a high affinity for glucose?

A

GLUT1, 3, 5

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52
Q

Where are GLUT1 transporters located?

A

All tissues, especially RBCs and brain

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53
Q

GLUT4 transporters have a ____ affinity for glucose

A

medium

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54
Q

Where are GLUT2 transporters located?

A

Beta cells of pancrease
liver, kidney, gut

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55
Q

Where are GLUT3 transporters located?

A

Brain, kidney, placenta

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56
Q

Where are GLUT4 transporters located?

A

muscle and adipose

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57
Q

Where are GLUT5 transporters located?

A

gut, kidney

58
Q

What are the main 3 endocrine effects of insulin?

A
  1. inhibits glycogenolysis
  2. inhibits conversion of fatty acids and amino acids to keto acids (prevents DKA)
  3. Promotes glucose storage as glycogen
59
Q

What are the 5 inhibitors of insulin secretion?

A
  • Insulin
  • Leptin
  • SNS (alpha adrenergic)
  • Chronically high glucose
  • Drugs – diazoxide, phenytoin, vinblastine, colchicine
60
Q

What are the 4 types of insulin preparations?

A
  1. Rapid acting
  2. Short acting (regular)
  3. Intermediate acting
  4. Long acting
61
Q

What are the 3 rapid-acting insulin preparations?

A

Lispro, aspart, glulisine

62
Q

What are the 2 short-acting (regular) insulin preparations?

A

Novolin, humulin

63
Q

What is the 1 intermediate-acting insulin preparation?

A

Neutral protamine Hagedorn

64
Q

What are the 2 long-acting insulin preparations?

A

Glargine, detemir

65
Q

Why are there so many types of insulin preparations?

A

To mimic normal insulin secretion

66
Q

What are the different forms of insulin delivery?

A
  • SQ injection – hypodermic needle
  • Portable pen injectors
  • Continuous Subcutaneous Insulin Infusion Devices (CSIID) - pump
67
Q

Which type of insulin delivery is best for tight insulin control?

A

Continuous Subcutaneous Insulin Infusion Devices (CSIID)

68
Q

How is insulin calculated?

A
  1. Basal – 1 injection, long-acting
  2. Bolus – Carbohydrate coverage
    • 1 unit of RA insulin – disposes 12-15g of carbohydrate
  3. Correction – High glucose
    • 1 unit of RA insulin needed to drop 50 mg/dL
69
Q

Which type of insulin delivery is considered “okay” insulin control?

A

70:30 premixed

70
Q

We need ____ insulin when sick. Why?

A

more - metabolic rate increases

71
Q

What are the 6 symptoms of hypoglycemia?

A

Anxiety, blurred vision, palpitations, shakiness, slurred speech, sweating

72
Q

What is the treatment for hypoglycemia?

A
  • glucose/simple sugars: 3-4 glucose tablets, ½ can of soda
  • glucagon injection
73
Q

What are the 8 types of oral antidiabetic agents?

A
  1. Biguanides
  2. Insulin Secretagogues
  3. Thiazolidinediones (TZDs)
  4. α-glucosidase Inhibitors
  5. Bile Acid Binding Resins (BABR)
  6. Amylin Analogs
  7. Incretin-based Therapies
  8. SGLT2 Inhibitors - Gliflozins
74
Q

What is the MOA of Biguanides?

A

Reduction in hepatic glucose production
- gluconeogenesis: making glucose from other things

75
Q

What is the first-line therapy for type 2 DM or NIDDM?

A

Biguanides - metformin (Glucophage)

76
Q

What is the MOA of insulin secretagogues?

A

Bind to K+ channel
- Rectifier current
- Binding causes depolarization and additional release of insulin

77
Q

What are the 3 classes of Insulin Secretagogues?

A
  • Sulfonylureas
  • Meglitinide
  • Phenylalanine derivatives
78
Q

What is the difference between 1st generation vs 2nd generation sulfonylureas?

A

1st generation requires higher dose

79
Q

What is the main contraindication for taking Sulfonylureas?

A

CV disease - increases risk of CV mortality

80
Q

What is the MOA Thiazolidinediones (TZDs)?

A
  • Decrease insulin resistance (PPAR mediated)
  • Increase insulin signal transduction
81
Q

Meglitinides are _____ than Sulfonylureas

A

safer - half-life is shorter

82
Q

What is the risk of taking Thiazolidinediones (TZDs)?

A

Risk of MI - Increased with insulin, nitrates

83
Q

What is the MOA of α-glucosidase Inhibitors? What is the medication called?

A

Block digestion of complex carbohydrates - more beneficial for people have primary carbohydrate diet
Acarbose

84
Q

α-glucosidase Inhibitors are more beneficial in _______

A

Pre-diabetics

85
Q

What are the main side effects of α-glucosidase Inhibitors?

A

Prominent GI effects
- Flatulence, Diarrhea, Abdominal pain

86
Q

What is the MOA of Bile Acid Sequestrant?

A

Surrounds food, preventing absorption
- Large cation exchange resins – not absorbed
- Bind bile acids – prevent reabsorption

87
Q

Bile Acid Sequestrant can also be used to treat ______ because it surrounds ______

A

hyperlipidemia, cholesterol

88
Q

How must Bile Acid Sequestrants be taken?

A

with food

89
Q

What is the MOA of Amylin Analogs?

A

Suppresses glucagon release, decreases circulating glucose

90
Q

What is the MOA of Incretin-based Therapies?

A

Mimicking a substance normally produces by intestines

91
Q

What is the risk of Incretin-based Therapies?

A

Pancreatic cancer risk

92
Q

What are the 2 types of Incretin-based Therapies?

A
  • Glucagon-Like Polypeptide-1 (GLP-1) Agonists - Semaglutide
  • Dipeptidyl Peptidase-4 (DPP-4) Antagonists - Sitagliptin
93
Q

What is the MOA of SGLT2 Inhibitors (Gliflozins)?

A

Prevents glucose reabsorption in PCT
- specifically inhibits SGLT2
- increased glucosuria

94
Q

What are the side effects of SGLT2 Inhibitors?

A

Dehydration and necrosis in the genital region

95
Q

SGLT2 Inhibitors also acts as a _______

A

Osmotic diuretic

96
Q

What is the leading cause of death in the US?

A

Atherosclerosis

97
Q

Describe the cycle of atherosclerosis in LDLs

A

LDL entry and enlargement → foam cell formation → cholesterol crystallization in foam cells → apoptosis of foam cells and extracellular lipid deposit → plaque with lipid-rich necrotic core

98
Q

What are the 6 major lipids?

A
  • Free Fatty Acids
  • Phospholipids
  • Cholesterol (Free & Esterified)
  • Triglycerides
  • Glycolipids
  • Prostaglandins
99
Q

What are the 4 types of molecules that sterols are precursors to?

A
  • Steroid hormones
  • Cell membranes
  • Vitamin D
  • Bile salts
100
Q

______ is when the liver makes cholesterol from chronically high cholesterol

A

De novo synthesis

101
Q

HMG-CoA is converted to ______ via ______

A

mevalonate
HMG-CoA Reductase

102
Q

Statins reduce cholesterol by inhibiting ________

A

HMG-CoA Reductase

103
Q

What are the 4 types of lipoproteins?

A

chylomicrons, VLDLs, LDLs, and HDLs

104
Q

Which type of lipoproteins are formed in the intestine and end up in the liver?

A

Chylomicrons

105
Q

Which type of lipoproteins are secreted by the liver and travel to peripheral tissues?

A

VLDLs

106
Q

Which type of lipoproteins transport cholesterol from the liver to the cells, resulting in deposition in arteries in excess?

A

LDLs

107
Q

Which type of lipoproteins scavenge cholesterol from cells, resulting in decreased levels of atherosclerosis?

A

HDLs

108
Q

What does a lipid profile consist of?

A
  1. Total and LDL/HDL Ratio
  2. Triglyceride determination
  3. Lipoprotein electrophoresis
109
Q

There is a _________ relationship between HDL cholesterol and coronary risk

A

inverse

110
Q

What is the most common disease that causes high cholesterol?

A

Familial hypercholesterolemia

111
Q

What are the 6 classes of hyperlipidemia drugs?

A
  1. Statins
  2. Niacin
  3. Fibrates
  4. Binding Resins
  5. Absorption Inhibitors
  6. Monoclonal Antibodies
112
Q

What is the MOA of statins?

A

Structural analogs of HMG-CoA- decrease cellular cholesterol synthesis by inhibiting HMG-CoA reductase

113
Q

What are the effects of statins?

A
  • Mostly reduce LDL
  • Increase LDLR
  • Modest decrease of triglycerides
  • Small increase in HDL
114
Q

What is the toxicity of statins?

A
  • Elevated liver enzymes - Increased with liver damage, patients of Asian descent
  • CK elevations - Muscle pain or weakness
115
Q

Cholesterol is synthesized at ______ and is enhanced by ______

A

night, food

116
Q

When do you want to avoid statins?

A
  • Avoid in pregnant and lactating women
  • Restricted use in children
117
Q

The main reason patients stop taking statins is due to _______

A

muscle pain

118
Q

What are the effects of niacin?

A
  • Decreases VLDL, LDL - Reduces VLDL secretion from liver
  • Increases HDL
119
Q

What is the toxicity of niacin?

A

1 - Cutaneous vasodilation (flushing)

  • Pruritis, dry skin, rash
  • N, abdominal discomfort (rare)
  • Elevation of liver enzymes
120
Q

What is the name of the medication that is a fibrate?

A

Gemfibrozil (Lopid)

121
Q

What are the effects of fibrates?

A
  • Decrease VLDL
  • Modest decrease in LDL
  • Increase lipolysis in liver - PPAR
122
Q

What are the 2 drugs that are bile acid binding resins?

A

Colestipol, cholestyramine

123
Q

How do bile acid binding resins work to reduce cholesterol?

A
  • Large cation exchange resins – not absorbed
  • Bind bile acids – prevent reabsorption
  • May increase VLDL
  • Must be taken with meals
124
Q

What are the side effects of bile acid binding resins?

A
  • Constipation, bloating
  • Steatorrhea (lipid in stool)
125
Q

What is the medication considered an intestinal sterol absorption inhibitor?

A

Ezetimibe (Zetia)

126
Q

What is the MOA of Ezetimibe?

A

Blocks the NPC1L1 transporter that transports cholesterol transport from the lumen into the enterocyte

127
Q

What are the effects of Ezetimibe found in the ENHANCE trial?

A

ENHANCE trial
- Reduced LDL
- PROMOTED arterial wall thickening?

128
Q

Monoclonal antibodies used to treat hyperlipidemia are called ___________

A

PCSK9 Inhibitors

129
Q

PCSK9 Inhibitors are usually given with ______ to lower ______

A

statins, LDLs

130
Q

What is the PCSK9 inhibitor medication called?

A

Evolocumab (Repatha)

131
Q

How do PCSK9 inhibitors combined with statins lower LDLs? By how much?

A

Statin therapy upregulates PCSK9
PCSK9 inhibitors allow receptor recycling
65%

132
Q

What amount of LDL is considered too low aka hypocholesterolemia?

A

LDL <25 mg/dL

133
Q

What are the risks associated with hypocholesterolemia?

A
  • Cancer
  • Hemorrhagic stroke
  • Depression
  • Anxiety
  • Preterm birth and low birth weight
134
Q

Diagram a treatment algorithm for patients with Type II diabetes.

A

1st line - metformin
2nd line - sulfonylurea
3rd line - insulin or Thiazolidinediones (TZDs) or α-glucosidase Inhibitors or DPP-4 inhibitor
4th line - insulin

135
Q

Calculate coronary artery disease risk using the LDL/HDL ratio.

A
  • First Calculate LDL:
    • VLDL= Triglycerides/5
    • LDL = total cholesterol-VLDL-HDL
  • Figure LDL/HDL Ratio
136
Q

List target levels of total cholesterol, HDL, LDL, and triglycerides.

A

Total cholesterol < 200
HDL > 40 (men) and 50 (women)
LDL < 130
Triglycerides < 120

137
Q

Differentiate between primary hypercholesterolemias and secondary causes.

A

Primary - familial
Secondary - DM, estrogens, alcohol, nephrosis, cholestasis, corticosteroid excess

138
Q

Explain why dietary control of lipid intake may not be sufficient to lower cholesterol, and some dietary strategies.

A

Cholesterol is largely genetic, although some dietary changes can help

139
Q

What are the 2 sources of cholesterol?

A

the liver and the foods you eat

140
Q

Differentiate free and esterified cholesterol.

A

Free cholesterol is biologically active and found in the surface layer of lipoprotein particles, while esterified cholesterol is a protective form of cholesterol stored in cells and transported in plasma

141
Q

Describe the difference between triglycerides and cholesterol.

A

Triglycerides form adipose tissue and are the main storage form of fats in the human body
Cholesterol helps build cells, produce hormones, and digest food; produced in the liver

Pharm 2024 (32 decks)

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