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PATHO/PHARM II > Conditions Effecting the Endocrine System and PharmacotherapyPart One: Pancreas & DM > Flashcards

Conditions Effecting the Endocrine System and PharmacotherapyPart One: Pancreas & DM Flashcards

Exam 2

1
Q

The Endocrine function of Pancreas:

Islets of Langerhans

A

The pancreatic islets or islets of Langerhans are the regions of the pancreas that contain its endocrine (hormone-producing) cells

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2
Q

The Endocrine function of Pancreas:

What cells make up the Islets of Langerhans?

A
  1. Beta cells
  2. Alpha cells
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3
Q

The Endocrine function of Pancreas:

What do beta cells do?

A

Beta cells—insulin and amylin

secrete the hormone insulin in response to a high concentration of glucose in the blood.

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4
Q

The Endocrine function of Pancreas:

What do alpha cells do?

A

Secrete glucagon in response to low blood glucose levels

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5
Q

The Endocrine function of Pancreas:

What is glucagon?

A

antagonistic to insulin

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6
Q

The Endocrine function of Pancreas:

What do alpha cells do to glucose stores?

A

Mobilize glucose stores from liver
to brain/heart & used for energy production

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7
Q

The Endocrine function of Pancreas:

What are the hormones of the pancreas?

A

Amylin

GLP-1 glucagon-like peptide 1 Incretin hormone

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8
Q

The Endocrine function of Pancreas:

What is Amylin?

A

Peptide hormone co-secreted with insulin by beta cells

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9
Q

The Endocrine function of Pancreas:

What does amylin do?

A

Delays gastric emptying,

suppresses glucagon secretion,

decreasing postprandial glucose

Satiety,

reduces food intake,

works with insulin,

prevents hyperglycemia

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10
Q

The Endocrine function of Pancreas:

What does GLP-1 glucagon-like peptide 1 Incretin hormone do?

A

Slows gastric emptying, stimulates insulin release

Suppresses postprandial glucose

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11
Q

The Endocrine function of Pancreas:

Where is GLP-1 glucagon-like peptide 1 Incretin hormone produced? What does it respond to?

A

Produced in gut, responds to nutrients in the gut - carbs and fats.

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12
Q

The Endocrine function of Pancreas:

What does GLP-1 glucagon-like peptide 1 Incretin hormone act on?

A

Acts via the vagus nerve to regulate appetite control

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13
Q

Glucose metabolism & the role of insulin:

How does the pancreas act on in the liver?

A

The pancreas releases insulin which stimulates the synthesis of glycogen &
↑’d uptake

Fat synthesis

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14
Q

Glucose metabolism & the role of insulin”

How does the pancreas’ insulin act on the liver?

A

Gluceose trigger pancreas to release insulin.

Insulin causes other stuff

Insulin tells liver to uptake the glucose and turn the glucose into storage form (glycogen)

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15
Q

Glucose metabolism & the role of insulin:

When food consumed, what does the pancreas do?

A

Stimulates release of insulin into blood

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16
Q

Glucose metabolism & the role of insulin:

How does insulin act on the muscle?

A

↑’d uptake glucose & AAs, glycogen synthesis, protein synthesis (anabolic)

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17
Q

Glucose metabolism & the role of insulin:

What does insulin do to K?

A

Insulin also ↑ K+ uptake by cells

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18
Q

Glucose metabolism & the role of insulin:

What does insulin do to fat storing cells?

A

Insulin causes an increase in glucose uptake

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19
Q

Glucose metabolism & the role of insulin:

What is role of insulin on the muscle?

A

Insulin stimulates increased glucose uptake by skeletal muscle and activates glycogen synthase, protein synthesis

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20
Q

What does insulin do to fat cells?

A

When glucose levels are high, the pancreas secretes insulin, which signals fat cells to take in glucose.

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21
Q

Glucose metabolism & the role of insulin:

What does fat cells do to glucose they uptake?

A

Cells can then use the glucose for energy or convert it into fat for long-term storage.

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22
Q

Glucose metabolism & the role of insulin:

What is the goal for insulin?

A

Blood glucose level declines and stimulus for insulin release diminishes

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23
Q

In basic terms, what does insulin do?

What does glucagon do?

A

Insulin drives glucose into cells

Glucagon is for when glucose is gone

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24
Q

Metabolic Consequences of Insulin Deficiency :

What mode is your body in when there is an insulin deficiency?

A

Insulin deficiency puts the body into catabolic mode

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25
Q

Metabolic Consequences of Insulin Deficiency

In the absence of insulin, what 3 things get changed/converted?

A

Glycogen

Proteins

Fats

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26
Q

Metabolic Consequences of Insulin Deficiency:

In the absence of insulin, what happens with glycogen?

A

Glycogen –> converted into glucose

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27
Q

Metabolic Consequences of Insulin Deficiency:

In the absence of insulin, what happens with proteins?

A

Proteins –> degraded into amino acids

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28
Q

Metabolic Consequences of Insulin Deficiency:

In the absence of insulin, what happens with fats?

A

Fats –> converted to glycerol & free fatty acids

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29
Q

What does insulin deficiency promote?

A

Insulin deficiency promotes hyperglycemia

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30
Q

Insulin deficiency promotes hyperglycemia via what?

A

Increased glycogenolysis (breakdown of glycogen)

Increased gluconeogenesis (generation of new glucose)

Reduced glucose utilization

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31
Q

Metabolic Consequences of Insulin Deficiency :

What does Increased glycogenolysis (breakdown of glycogen) mean?

A

Breakdown of glycogen into free glucose

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32
Q

Metabolic Consequences of Insulin Deficiency :

What does Increased gluconeogenesis (generation of new glucose) mean?

A

Amino acids & fatty acids produced from metabolic breakdown of proteins & fats

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33
Q

Amino acids & fatty acids produced from metabolic breakdown of proteins & fats

Lead to what?

A

Fat breakdown –> weight loss

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34
Q

Metabolic Consequences of Insulin Deficiency :

Reduced glucose utilization leads to what?

A

Decreased cellular uptake of glucose

Decreased conversion of glucose to glycogen

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35
Q

Diabetes mellitus -what is it characterized by?

A

Characterized by hyperglycemia resulting from defects in insulin production, insulin action, or both.

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36
Q

Diabetes mellitus -what is Impaired insulin production or action results?

A

Impaired insulin production or action results in abnormal carbohydrate, protein, and fat metabolism because of the glucose transportation issue.

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37
Q

What is the primary disorder of carb metabolism manifested as?

A

Primary disorder of CHO metabolism manifested as high blood glucose levels from the body’s inability to produce or properly use insulin.

Glucose cannot be moved into cells & utilized.

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38
Q

What is Type 1 Diabetes:

A

↓’d insulin secretion by Beta cells of islets of Langerhans (Type 1)

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39
Q

What is Type 2 Diabetes:

A

insensitivity to insulin (Type 2).

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40
Q

Without insulin’s effects, what can or can’t happen?

A

Without insulin’s effects, glucose cannot be moved into cells. Insulin is needed to maintain life!!!

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41
Q

T1DM overview:

What is T1DM formally known as?

A

Child-onset DM & Insulin-dependent DM (IDDM)

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42
Q

T1DM overview:

When does it typically develop? What percent of the population is affected?

A

Typically develops during childhood or adolescence

5%-10% of the population

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43
Q

T1DM overview :

What does T1DM cause destruction of?

A

Destruction of pancreatic beta cells (autoimmune)

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44
Q

T1DM overview:

What does T1DM require?

A

Insulin supplementation!!!

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45
Q

T1DM overview:

What are predisposing factors to T1DM?

A

Genetics
Family hx
Any physical condition that destroys pancreatic beta cells
Abnormal immune response
Envi: drugs, foods, viruses

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46
Q

What genetics would be a predisposing factor to T1DM?

A

major histocompatibility complex (MHC)

people with variant of this have higher chance of developing T1DM?

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47
Q

How do major complications of T1DM occur?

A

Occur early
Often severe

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48
Q

Patho of T1DM:

What kind of reaction is it?

A

Autoimmune reaction

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49
Q

What happens in the autoimmune reaction of T1DM?

A

Islet cell autoantibodies destroy beta cells

Reduces normal pancreatic functioning by 80% to 90%

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50
Q

Patho of T1DM

What causes a lack of insulin in T1DM?

How long does this occur before symptoms to occur?

A

Destroyed beta cells cause lack of insulin

Can occur for months/years before symptoms of diabetes.

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51
Q

Patho of T1DM:

How would hyperglycemia occur in T1DM?

A

No glucose enters the cells resulting in hyperglycemia

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52
Q

What is altered in T1DM?

A

Metabolism of protein, fat, and carbohydrates is altered

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53
Q

Patho of T1DM:

What acts on the liver in T1DM? What does this lead to?

A

Glucagon from alpha cells acts in the liver –> glycogenolysis and gluconeogenesis

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54
Q

Patho of T1DM:

What does lack of insulin and excess of glucagon lead to?

A

lack of insulin & excess of glucagon –> hyperglycemia

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55
Q

Patho of T1DM:

Why does increased thirst occur in T1DM?

A

Osmotic glucose –> thirst

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56
Q

Patho of T1DM:

What is elevated glucose greater than?

A

Elevated glucose > renal threshold

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57
Q

Patho of T1DM:

What are symptoms of T1DM?

A

thirst

weight loss

excessive hunger

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58
Q

Patho of T1DM:

Why does weight loss occur in T1DM?

A

Inappro utilization of carbs–> weight loss

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59
Q

What leads to excessive hunger in T1DM?

Why does excess hunger occur?

A

Breakdown of nutritional stores –> excessive hunger because inefficient use of glucose

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60
Q

Patho of T1DM:

What does elevated glucose do to blood?

A

Elevated glucose makes blood hypertonic

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61
Q

Patho of T1DM:

What is the honeymoon phase?

A

a period after an initial type 1 diabetes diagnosis when the remaining insulin-producing beta cells in the pancreas are still functioning well.

at first, giving insulin injections rejuvenates beta cells. But then over time, beta cells lose ability and die or whatever.

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62
Q

T2DM: What is it formally known as?

A

Adult-onset/Non-insulin-independent DM

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63
Q

T2DM: When does it typically develop?

A

Typically develops in adulthood

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64
Q

What percent of people with diabetes have type 2?

A

90% to 95% of people with diabetes have type 2

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65
Q

What are the causes of Type II Diabetes?

A

Insulin resistance, genetics, envi

Decreased effectiveness of the cells’ insulin receptors

Insulin deficit (body may not be producing enough insulin)

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66
Q

What is still produced in T2DM that isn’t produced in T1DM?

A

Insulin still produced

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67
Q

In T2DM, insulin is still produced, but what is the issue with it?

A

Reduced binding to receptors

Reduced # of receptors

Reduced receptor responsiveness

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68
Q

What are predisposing factors to T2DM?

A

Age
Obesity
Race/ethnicity
Metabolic syndrome
Prediabetes
Diet – simple carbs, sat fats, red meat

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69
Q

Patho of T2DM: Occurs in what two ways?

A

Insulin resistance:

Pancreatic islet cells dysfunctional

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70
Q

Patho of T2DM:

In T2DM, what does insulin resistance mean?

A

Insulin resistance: Cellular insulin receptors less sensitive

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71
Q

Patho of T2DM:

What does Pancreatic islet dysfunction lead to?

A

Pancreatic islet cells dysfunctional –> decreased synthesis of insulin and rise of glucagon —> glucose synthesis in liver.

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72
Q

Patho of T2DM

What leads to hyperglycemia?

A

Liver synthesis of glucose increases when the pancreatic islet cells malfunction –> hyperglycemia

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73
Q

Patho of T2DM:

Inflammation

A

adipocyte cells & cytokines induce insulin resistance/cytotoxic to beta cells

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74
Q

Patho of T2DM

Obesity and Insulin resistance lead to what specifically?

A

Adipokines, FFAs, inflammation, mitochondrial dysfunction

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75
Q

Patho of T2DM:

What prevents clinical appearance of DM for many years?

A

Compensatory hyperinsulinemia prevents clinical appearance of DM for many years

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76
Q

Patho of T2DM:

What happens to alpha cells in response to glucose inhibition, what does this lead to?

A

Pancreatic alpha cells become less responsive to glucose inhibition –> increase in glucagon secretion –> increase in glucagon secretion –> hyperglycemia

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77
Q

Clinical Manifestations of Diabetes:
The classic signs (3Ps) are mostly present in what kind of diabetes?

A

Classic Signs (3Ps) (mostly in Type 1)

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78
Q

Clinical Manifestations of Diabetes:

What are the classic signs (3Ps):

A

Polyuria

Polydipsia

Polyphagia

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79
Q

Clinical Manifestations of Diabetes:

Polyuria- Why does this occur?

A

Glucose in urine exerts osmotic pressure in the filtrate –> a large volume of urine excreted.

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80
Q

Clinical Manifestations of Diabetes:

Polyuria- the large volume of urine excreted leads to what?

A

The large excretion results in a subsequent loss of fluid and electrolytes.

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81
Q

Clinical Manifestations of Diabetes:

Polydipsia:

A

Thirst from fluid loss through the large volume of urine produced and high blood glucose, since both draw water from the cells

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82
Q

Clinical Manifestations of Diabetes:

Polydipsia- what does it lead to?

A

Thirst from fluid loss through the large volume of urine produced and high blood glucose, since both draw water from the cells

leads to dehydration, increased thirst.

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83
Q

Clinical Manifestations of Diabetes:

Polyphagia

A

The cells in a person with diabetes lack nutrients, stimulating and increasing the person’s appetite.

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84
Q

Additional Clinical Manifestations: T1DM

What are they?

A

Flushed skin, fruity breath

Listless, lethargic

Unusual thirst, ↑UO

Skin dry

Hyperventilate

Elevated sugar

Drowsiness

Skin hot and dry: sugar high

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85
Q

Additional Clinical Manifestations: T1DM:

Why does hyperglycemia occur?

A

Insulin allows glucose access into cells.

Without insulin, there are increased blood glucose levels, since glucose cannot enter cells.

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86
Q

Additional Clinical Manifestations: T1DM:

Why does glucosuria occur?

A

When glucose builds up in the blood, excess glucose spills into the urine. This is because the level of glucose in the filtrate exceeds the capacity of the renal tubular transport limits for reabsorption.

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87
Q

Additional Clinical Manifestations: T1DM

Why does fatigue and lethargy occur?

A

Without glucose being able to enter the cells in the body, there is no energy for cells to function.

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88
Q

Additional Clinical Manifestations: T1DM

Why does weight loss occur?

A

Glucose-starved cells must use protein and fats for energy, so the person loses weight.

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89
Q

Additional Clinical Manifestations: T2DM

What are symptoms:

A

Nonspecific

Fatigue

Recurrent infections

Recurrent vaginal or candida infections

prolonged healing

visual changes

weight gain

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90
Q

Additional Clinical Manifestations: T2DM

Are nonspecific symptoms always present? Why or why not?

A

The classic signs (polyuria, polydipsia, polyphasia) of diabetes may or may not be observed.

The body still has some insulin that functions properly, although it may not be enough or efficient.

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91
Q

Additional Clinical Manifestations: T2DM:

Why would fatigue occur?

A

Insulin resistance does not allow glucose to enter the cell efficiently.

This means the cells do not get the energy they need, and the person becomes tired.

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92
Q

Additional Clinical Manifestations: T2DM:

Why would recurrent infections occur?

A

Increased glucose in the blood impairs the immune system because immune cells do not function as well in high glucose environments & some pathogens proliferate rapidly, suppressed immune response from chronic hyperglycemia

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93
Q

Additional Clinical Manifestations: T2DM:

Why would recurrent vaginal or candida infections occur?

A

Increased glucose is an excellent source for yeast and fungal growth.

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94
Q

Additional Clinical Manifestations: T2DM

Why would prolonged healing occur?

A

Increased glucose impairs and slows the healing of wounds.

Glycosolated hgb in RBCS impedes release of O2 to tissues

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95
Q

Additional Clinical Manifestations: T2DM

Prolonged healing: what would impede release of O2 into tissues?

A

Glycosolated hgb in RBCS impedes release of O2 to tissues

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96
Q

Additional Clinical Manifestations: T2DM:

Why would visual changes occur?

A

Increased glucose damages the small vessels in the eye, leading to vision changes.

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97
Q

Additional Clinical Manifestations: T2DM:

What leads to weight gain?

A

Increased weight or obesity predispose an individual to type 2 diabetes.

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98
Q

Chronic complications of DM:

What parts of the body does DM effect?

A

Retina, kidney, RBCs, nerves, & blood vessels cells

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99
Q

Chronic complications of DM:

Part of the body that DM effects, (Retina, kidney, RBCs, nerves, & blood vessels cells) why do effects occur?

A

Glucose in increased amounts in these cells that do not require insulin

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100
Q

Chronic complications of DM

What does glucose do to (Retina, kidney, RBCs, nerves, & blood vessels cells)?

What is glucose converted to?

A

Glucose readily diffuses in excess into these cells & is converted to sorbitol (an alcohol) which is osmotically active (pulls in H2O)

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101
Q

Chronic complications of DM

When glucose readily diffuses in excess into (Retina, kidney, RBCs, nerves, & blood vessels) cells, what does it do to the cells?

A

Alters cell function by direct effect & effect of excess intracellular H2O

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102
Q

Chronic complications of DM:

What accumulates in toxic levels? What does it contribute to?

A

More sorbitol & lower levels of glutathione accumulate to toxic levels

Contribute to chronic tissue damage

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103
Q

Chronic complications of DM:

How does hyperglycemia effect other cells?

A

Hyperglycemia leads to attachment of glucose to proteins, lipids, & nucleic acids (glycation)

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104
Q

Chronic complications of DM:

What does glycation lead to?

A

leads to advanced glycation end products (AGEs)

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105
Q

Chronic complications of DM

What do AGEs cause?

A

Interfere with many crucial cellular processes

Microvascular damage:

MACROVASCULAR damage:

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106
Q

Chronic complications of DM

Microvascular damage:

A

capillaries, retinopathies, nephropathies, neuropathies

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107
Q

Chronic complications of DM

MACROVASCULAR damage:

A

MACROVASCULAR damage: larger vessels, CAD, PVD, Cerebral VD

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108
Q

Chronic complications of DM:

When sugar bombards basement membrane of small BVs, capillaries

A

When sugar bombards basement membrane of small BVs, capillaries it leads to structural defects – leakier, thicker

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109
Q

Chronic complications of DM:

What would happen to oxygen delivery, why? What happens to oxygen in the tissues?

A
  • Decreased O2 delivery due to glycosylated hgb (HgbA1c) – increases its affinity for O2 which leads to less released to tissues
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110
Q

Chronic complications of DM:

What is not catalyzed due to a build up of glucose? What does this lead to?

A
  • Fibrin not catalyzed with attached glucose, –> builds up & blocks vessels.
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111
Q

Chronic complications of DM:

Fibrin not catalyzed with attached glucose, –> builds up & blocks vessels.

What happens to platelets?

A

↑’d platelet aggregation, initiation of clotting process

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112
Q

Chronic complications of DM:

What does DM cause in the intima of blood vessels?

A
  • Collagen – attached glucose makes intima of BVs “sticky” – lipoproteins collect
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113
Q

Chronic complications of DM:

What happens with Fat-protein (cholesterol and TGs) when glucose is attached?

A

Fat-protein (cholesterol & TGs) – when glucose attached, abnormally deposited in bv walls

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114
Q

Chronic complications of DM:

What happens with TGs?

A

Increased production of TGs by liver & low HDL

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115
Q

Chronic complications of DM:

How would atherosclerosis occur?

A

Bad cholesterol is loaded down with glucose & is abnormally deposited –> atherosclerosis

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116
Q

Degenerative Changes Related to Diabetes include:

A

Microangiopathy

Macroangiopathy

Neuropathy

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117
Q

Degenerative Changes Related to Diabetes: Microangiopathy

Have effects on what?

A

Effects on Small Blood Vessels

Effects on Eyes

118
Q

Degenerative Changes Related to Diabetes: Microangiopathy:

What effect does it have on small blood vessels

A

Thickening and hardening of capillary basement membrane

Tissue necrosis

119
Q

Degenerative Changes Related to Diabetes: Microangiopathy:

What effect does it have on the eyes?

A

Retinopathy:

Cataracts:

Nonproliferative phase

Proliferative phase

120
Q

Degenerative Changes Related to Diabetes: Microangiopathy: Effect on the Eyes:

Retinopathy

A

leading cause of blindness

121
Q

Degenerative Changes Related to Diabetes: Microangiopathy: Effect on the Eyes:

Cataracts

A

Cataracts: clouding of the lens

122
Q

Degenerative Changes Related to Diabetes: Microangiopathy: Effect on the Eyes:

Nonproliferative phase: What happens to retinal capillaries?

A

retinal capillaries become more permeable

123
Q

Degenerative Changes Related to Diabetes: Microangiopathy: Effect on the Eyes:

Nonproliferative phase: What happens to veins?

A

veins dilate & twisted “sausage string”

124
Q

Degenerative Changes Related to Diabetes: Microangiopathy: Effect on the Eyes:

Nonproliferative phase: What happens to retinal vessels?

A

Retinal vessels start to change shape

125
Q

Degenerative Changes Related to Diabetes: Microangiopathy: Effect on the Eyes:

Nonproliferative phase: When retinal vessels start to change shape, what happens?

A

retinal ischemia –> infarcts

126
Q

Degenerative Changes Related to Diabetes: Microangiopathy: Effect on the Eyes:

Proliferative phase: What occurs?

A

neovascularization – new BVs form pulls on vitreous humor, causes detachment, scaring

127
Q

Degenerative Changes Related to Diabetes: Microangiopathy: Effect on the Eyes:

Proliferative phase: neovascularization

A

neovascularization – new BVs form pulls on vitreous humor, causes detachment, scaring

128
Q

Diabetes effect on kidneys:

A

Diabetic nephropathy: damages glomeruli

Glomerulosclerosis

Glomerular perfusion pressure changes

Chronic renal failure

129
Q

Degenerative Changes Related to Diabetes: Macroangiopathy

How does this occur?

A

Oxidative stress damages blood vessels, promoting atherosclerosis

130
Q

Degenerative Changes Related to Diabetes: Macroangiopathy

Oxidative stress damages blood vessels, promoting atherosclerosis and can cause:

A

Myocardial infarction (heart attack),

arrhythmias

Cerebrovascular accident (stroke)

Peripheral vascular disease (arterial obstruction, ischemia)

Leg and foot ulcers

Intermittent claudication (pain in feet and legs with exercise)

Delayed healing, infections, and gangrene

Amputation of the leg

DM & htn co-exist

Higher incidence of HF

131
Q

Degenerative Changes Related to Diabetes: Macroangiopathy

Oxidative stress damages blood vessels, promoting atherosclerosis and can cause
Cerebrovascular accident (stroke)

How?

A

Atherosclerosis of cerebral vessels from insulin resistance & hyperglycemia

132
Q

Degenerative Changes Related to Diabetes: Macroangiopathy

Why would there be higher incidences of HF?

A

Increased amts of collagen in vessel wall, ventricular hypertrophy, reduced compliance during diastole

133
Q

Degenerative Changes Related to Diabetes: Neuropathy

What are the two types of neuropathy that occur?

A

Peripheral Neuropathy

Autonomic Neuropathy

134
Q

Degenerative Changes Related to Diabetes: Neuropathy

Peripheral Neuropathy

A

peripheral nerves are damaged

135
Q

Degenerative Changes Related to Diabetes: Neuropathy

Peripheral Neuropathy- what cells are damaged?

A

Vessel ischemia & and sorbital damage to Schwann cells

136
Q

Degenerative Changes Related to Diabetes: Neuropathy

What are the effects of Peripheral Neuropathy?

A

Impaired sensation
Burning pain in legs and feet
Pain perception reduced
Numbness, tingling, weakness

137
Q

Degenerative Changes Related to Diabetes: Neuropathy

Autonomic Neuropathy

A

nerves that manage everyday functions, such as sweating and digestion, are damaged.

138
Q

Degenerative Changes Related to Diabetes: Neuropathy

Autonomic Neuropathy: What is impaired, what does it lead to?

A

Impaired vasomotor function – postural hypotension

139
Q

Degenerative Changes Related to Diabetes: Neuropathy

Autonomic Neuropathy: What are the effects of it?

A

Bladder incontinence or retention, infection - paralytic bladder

Impotence

Diarrhea

Gastroparesis (delayed gastric emptying),

gastric atony

Orthostatic hypotension

140
Q

Diagnostics tests for DM:

A

Self-Monitoring of Blood Glucose (SMBG)

Fasting Plasma Glucose (FPG)

Random Plasma Glucose

HgbA1c*

Oral glucose tolerance test (OGTT)

141
Q

Diagnostics: Self-Monitoring of Blood Glucose (SMBG)

For T1DM, when should it be done?

A

T1DM more often, before meals, HS, & prn

142
Q

Diagnostics: Self-Monitoring of Blood Glucose (SMBG)

When in the hospital, when should be done?

A

Before meals & HS when on insulin in hospital

143
Q

Diagnostics: Fasting Plasma Glucose (FPG)
What is the value for diabetics?

A

126 mg/dl or higher when fasting

144
Q

Diagnostics: Self-Monitoring of Blood Glucose (SMBG)

What are the target values before meals?

A

Target values 80-130 mg/dl before meals

145
Q

Diagnostics: Self-Monitoring of Blood Glucose (SMBG)

What are the target values after meals?

A

< 180mg/dl 1-2 hrs after meal

146
Q

Diagnostics: Fasting Plasma Glucose (FPG)
What is the norm value?

A

Normal < 100 mg/dL

147
Q

Diagnostics: Fasting Plasma Glucose (FPG)

What is the values for diabetics

A

Diabetes 126 mg/dl or higher when fasting

148
Q

Diagnostics: Random Plasma Glucose
Values?

A

DM > or equal to 200

149
Q

Diagnostics: HgbA1c*

A

Glucose interacts with Hgb in RBCs, forms glycosylated derivatives

150
Q

Diagnostics: HgbA1c*

What is it control over?

A

Control over 2-3 months

151
Q

Diagnostics: HgbA1c*

What is DM values?

A

DM≥ 6.5% (DM good control < 6.5%)

152
Q

Diagnostics: HgbA1c*

What are normal values?

A

Normal < 5.7%

153
Q

Diagnostics: HgbA1c*

What are prediabetic values?

A

Prediabetes 5.7% to 6.4% (increased risk)

154
Q

Diagnostics: Oral glucose tolerance test (OGTT)
What is it used for?

A

Used to confirm DM when others not definitive

155
Q

Oral glucose tolerance test (OGTT)

What are normal, PreDM and DM values?

When is it assessed?

A

Normal < 140
PreDM 140-199 mg/dl
DM ≥ 200

2h post-glucose liquid

156
Q

DM: Lifestyle Modifications

Who is it used for? When?

A

Used for all, regardless of drug therapy

Continued w/ drug TX

May be initial for T2DM

157
Q

DM: Lifestyle Modifications include:

A

Weight control

Diet

Physical activity

158
Q

Lifestyle Modifications:

Why is exercise recommended?

A

Exercise lowers blood glucose levels and boosts sensitivity to insulin,

159
Q

Lifestyle Modifications:

How much exercise is recommended?

A

≥ 150 minutes of moderate-intensity aerobic activity weekly

160
Q

Lifestyle Modifications:

What can strenuous exercise lead to?

A

Strenuous exercise ~ hypoglycemia

161
Q

Who is most at risk of DKA? Type 1 or Type 2?

A

Individuals with Type 1 diabetes

Newly diagnosed, young

162
Q

Who is at more risk of developing Hyperglycemic nonketotic syndromes?

A

Older patients with Type 2 diabetes

163
Q

What are the symptoms of Diabetic ketoacidosis? How quick is onset?

A

Kussmaul respirations

Fruity or acetone odor of breath

Abdominal pain,

polyuria,

polydipsia,

dehydration

Rapid onset

164
Q

What lab results would indicate Diabetic Ketoacidosis?

A

Glucose levels > 250 mg/dl

Reduction in bicarb concentration
HCO3 < 15

pH < 7.35

165
Q

What lab results would indicate Hyperglycemic Non-ketotic Syndromes?

A

Glucose levels > 600

Lack of ketosis / Ketones are absent

Serum osmolarity > 320

166
Q

What are symptoms of Hyperglycemic Non-ketotic Syndrome? How fast is onset?

A

Altered mental status,

dehydration

Gradual onset

167
Q

Hypoglycemia: What is a glucose level for this?

A

Blood glucose <55-60 mg/dL

168
Q

Hypoglycemia: Who is at most risk?

A

?????

169
Q

Hypoglycemia: Which cardiac drug puts diabetic most at risk?

A

Beta Blockers

because inhibits the sympathetic nervous system; beta blockers also used to mask the tachcardia.

170
Q

Hypoglycemia: if patient is cold and clammy, what do they need?

A

Cold and clammy: need some candy

171
Q

Hypoglycemia: What are Adrenergic/sympathetic effects:

A

anxiety, sweating, vasoconstriction (pale, cool skin), tachycardia

172
Q

Hypoglycemia:

What is Rapid treatment for conscious patients?

A

Fast acting oral-sugar

173
Q

Hypoglycemia:

What is Rapid treatment for unconscious or severe hypoglycemia patients?

A

No gag reflex present –> NPO

1st line: IV glucose (50% Dextrose/D50)

Alternative: glucagon (for home use)

174
Q

Hypoglycemia: Symptoms?

A

Tremors, tachycardia
Irritability
Restless
Excessive hunger
Diaphoresis

175
Q

In DKA, what is altered due to insulin deficiency?

A

Altered fat metabolism

Altered glucose metabolism

176
Q

DKA: Altered fat metabolism

A

Insulin deficiency leads to the liver breaking down fats into glycerol and FFAs.

FFAs causes build up of ketones which leads to ketosis

Buildup of ketoacids —> acidosis –> ketoacidosis

177
Q

DKA: Altered fat metabolism

What are the symptoms of this?

A

Hyperventilate, fruity smell to urine & breath or acetone.

Appear drunk

178
Q

DKA: Altered glucose metabolism

A

Insulin def —> increased glucose production & decrease glucose utilization

Glycerol converted to glucose

More glucose being made than used –> hyperglycemia —> exceeds capacity of renal tubules

Osmotic diuresis –> loss of large volumes of water

Dehydration –> hemoconcentration

179
Q

Diabetic Ketoacidosis (DKA) Pathophysiology:

Glucagon release: What does it cause?

A

Hyperglycemia (BG > 250)

Glycosuria (osmotic diuresis)

180
Q

Diabetic Ketoacidosis (DKA) Pathophysiology:

Glucagon release: What process occurs? WHy?

A

Gluconeogenesis is caused by epinephrine, cortisol, and glucagon

181
Q

Diabetic Ketoacidosis (DKA) Pathophysiology:

Glucagon release: How else is blood glucose increased?

A

Increased blood glucose from hepatic breakdown and decreased peripheral utilization

182
Q

Diabetic Ketoacidosis (DKA) Pathophysiology:

Glucagon release: What are symptoms?

A

Polyuria,

Polydipsia

N/V

Tachycardia,

hypotension

↑’d BUN, high serum osmolality

183
Q

Diabetic Ketoacidosis (DKA) Pathophysiology:

Glucagon release: symptoms

What does Polyuria, Polydipsia cause?

A

osmotic diuresis, dehydration

184
Q

Diabetic Ketoacidosis (DKA) Pathophysiology:

Glucagon release: symptoms

What is N/V caused by?

A

electrolyte imbalance & acidosis

185
Q

Diabetic Ketoacidosis (DKA) Pathophysiology:

Glucagon release: symptoms
What are the electrolyte imbalance & acidosis levels?

A

Low Na+

K+ high or low- depends on dehydration & acidosis
–But there’s total body depletion of K+

186
Q

Diabetic Ketoacidosis (DKA) Pathophysiology:

Glucagon release: Symptoms

What does tachycardia and hypotension cause?

A

Confusion, seizures

187
Q

What are causes of DKA?

A

Undetected diabetes mellitus

Increased insulin requirement
-stress, illness, medications (steroids, hydrochlorothiazide)
- body releases glucagon, cortisol, and catecholamines due to additional stress

Skipping meals

Non-compliance with treatment regimen

188
Q

What is patient education required for DKA?

A

-When sick, monitor blood glucose and ketone levels in urine

-Notify if have decreased appetite, decreased fluid intake and increased urination

-Keep hydrated every hour

189
Q

Diabetic Ketoacidosis (DKA) Pathophysiology: Fat breakdown

What is formed?

A

Ketone formation

190
Q

Diabetic Ketoacidosis (DKA) Pathophysiology:

Ketone formation leads to what?

A

Ketonuria

Ketoacidosis

191
Q

Diabetic Ketoacidosis (DKA) Pathophysiology:

What is ketoacidosis?

A

Breakdown of ketones

192
Q

Diabetic Ketoacidosis (DKA) Pathophysiology:

What are effects of Ketoacidosis (breakdown of ketones)?

A

“Fruity breath”

Acidosis: pH < 7.35, HCO3 < 15

193
Q

Diabetic Ketoacidosis (DKA) Pathophysiology:

What creates “fruity breath”

A

Acetone is one of the ketones that is present in excess.

It is exhaled, giving the breath a fruity odor.

194
Q

Diabetic Ketoacidosis (DKA) Pathophysiology:

Ketone formation creates a build up of what?

A

Buildup of metabolic acids from incomplete metabolism of fats/lipids

195
Q

Diabetic Ketoacidosis (DKA) Pathophysiology:

What is a symptom of Ketone formation? (Having to do with breathing?)

What are other symptoms of fat breakdown?

A

Deep respirations (Kussmaul Breathing)

Abdominal pain

196
Q

Skipped slide 31

A
197
Q

Hyperosmolar Hyperglycemic Non-Ketotic Syndrome (HHNKS): What is it a complication of?

A

Complication of T2DM

198
Q

Hyperosmolar Hyperglycemic Non-Ketotic Syndrome (HHNKS): What kind of people experience this?

A

Occurs in diabetic people who make enough insulin to prevent DKA, but not enough insulin to prevent severe hyperglycemia, osmotic diuresis, and extracellular fluid depletion.

Occurs mostly in elderly with comorbidities

199
Q

Hyperosmolar Hyperglycemic Non-Ketotic Syndrome (HHNKS): How common is it compared to DKA?

A

Less common than DKA

200
Q

Hyperosmolar Hyperglycemic Non-Ketotic Syndrome (HHNKS):

What is prevented, why?

A

Lesser degree of insulin deficiency, so lipolysis & ketone production prevented

201
Q

Hyperosmolar Hyperglycemic Non-Ketotic Syndrome (HHNKS):

Hyperglycemia is profound, what does it lead to?

A

Hyperglycemia more profound (600-1000mg/dl) –> more polyuria & fluid deficiency

202
Q

Hyperosmolar Hyperglycemic Non-Ketotic Syndrome (HHNKS):

What is more severe in HHNKs than DKAs?

A

Dehydration is more severe in HHS compared to DKA

203
Q

Hyperosmolar Hyperglycemic Non-Ketotic Syndrome (HHNKS):

What are causes?

A

Causes: infection, meds, comorbidities, TPN

204
Q

Hyperosmolar Hyperglycemic Non-Ketotic Syndrome (HHNKS):

What are clinical features?

A

Clinical features: high serum glucose & osmolarity without metabolic acidosis, neuro changes, profound dehydration, K+ alterations (high or normal initially then low)

205
Q

Insulin Products High Alert:

A

Insulin Lispro

Regular Insulin

NPH Insulin

Insulin Glargine

206
Q

What is the brand name of Insulin Lispro?

A

Humalog

207
Q

What is the brand name of Regular Insulin?

A

Humulin R

208
Q

What kind of insulin is Insulin lispro?

A

Short-Duration, Rapid-Acting Insulin

209
Q

What is Insulin lispro similar to?

A

Analog of human insulin

210
Q

How is onset of Insulin lispro? How long is duration?

A

Rapid onset (15 to 30 minutes)

Short duration (persists 3 to 5 hours)

Very rapid onset and short duration

211
Q

How does Insulin lispro compare to regular insulin?

A

Acts faster than regular insulin but shorter duration of action

212
Q

When is Insulin Lispro administered ?

A

Administered 15 minutes immediately before eating

213
Q

How Insulin Lispro given? (SubQ, IM?)

A

SubQ or insulin pump

214
Q

What must Insulin Lispro be used in conjunction with?

A

Must be used in conjunction with intermediate or long acting for glycemic control btwn meals

215
Q

What is a Short-Duration, Slower-Acting Insulin?

A

Regular insulin [Humulin R]

216
Q

When do effects of Regular Insulin start?

A

Effects begin in 30 to 60 minutes

217
Q

When is Regular Insulin administered?

A

Generally adm 30-60 min before meals

218
Q

When is the peak for Regular Insulin?

A

Peak in 1 to 5 hours

219
Q

What is the duration for Regular Insulin?

What kind of solution is it?

A

Duration up to 10 hours

Clear solution

220
Q

What type of regular insulin is available?

How is it given?

What kind of patients is it for?

A

Only type that’s available in U-500 strength

More concentrated – never give IV, given via U-500 insulin syringe

Used for patients that take >200 units/day

221
Q

What is a Intermediate-Duration Insulin?

A

​NPH insulin [Humulin N, Novolin N]

222
Q

Intermediate-Duration Insulin: ​NPH insulin

How often is it given? What type of injection is given?

A

Injected 2 or 3x daily to provide glycemic control between meals and HS

Administered by subQ injection only

223
Q

Intermediate-Duration Insulin: ​NPH insulin

When can it NOT be administered? Why?

A

Delayed onset, so cannot be administered at mealtime to control postprandial hyperglycemia

224
Q

Which is the only insulin suitable for mixing with short acting insulins?

A

Only one suitable for mixing with short-acting insulins is NPH.

225
Q

Intermediate-Duration Insulin: NPH insulin

What is possible due to foreign proteins?

A

Allergic reactions are possible due to foreign proteins

226
Q

Intermediate-Duration Insulin: NPH insulin

What must be done with cloudy suspensions?

A

Cloudy suspensions that must be agitated before administration

227
Q

What is an example of Long-Duration Insulin?

What kind of insulin is it?

A

Insulin glargine [Lantus]

Modified human insulin

228
Q

Long-Duration Insulin: Insulin glargine [Lantus]

How long is duration of action?

A

Prolonged duration of action (up to 24 hours)

229
Q

Long-Duration Insulin: Insulin glargine [Lantus]

When can it be done?

A

Can be done anytime of day, but mostly at night

230
Q

Long-Duration Insulin: Insulin glargine [Lantus]

What does it mimic?

A

Mimics basal insulin secretion of the pancreas in individuals without diabetes.

231
Q

Long-Duration Insulin: Insulin glargine [Lantus]

How does it compare to NPH insulin?

A

Reduces fasting blood glucose levels more efficiently and with less nocturnal hypoglycemic events compared with (NPH)

232
Q

Long-Duration Insulin: Insulin glargine [Lantus]

What is the max starting dose?

A

The maximum starting dosage of Lantus is 10 units per day

233
Q

Insulin specs:

Pharmacokinetic differences

A

Sliding scale
Scheduled fixed-doses
QHS

234
Q

Insulin specs:
Appearance

A

Clear, colorless
Except NPH ~ hazy

235
Q

Insulin specs:

Storage

A

Refrigerator, room temp, never frozen

Discard after 30d

236
Q

Insulin specs:

What insulin can be given IV?

A

Rapid & short insulin only

237
Q

Insulin specs:

Where is insulin given subQ?

A

Upper arm, thigh, abdomen

238
Q

Insulin specs:

Injecting insulin into the same area repeatedly can cause what?

A

Injecting insulin into the same area repeatedly can cause Lipodystrophy

239
Q

Insulin specs:

What are adverse effects of insulin?

A

Electrolyte imbalances ~ ↓ K

Hypoglycemia: Blood glucose below 55-60 mg/dL

240
Q

Insulin specs:

What is considered hypoglycemic?

A

Blood glucose below 55-60 mg/dL

241
Q

Insulin specs:

What are drug interactions of insulins?

A

Hypoglycemic agents

Hyperglycemic agents

Bblockers

242
Q

Insulin specs:
Drug interactions of insulin + hypoglycemic agents

What are examples of hypoglycemic agents?

A

Sulfonylureas , alcohol

243
Q

Insulin specs:
Drug interactions of insulin + hyperglycemic agents

What are examples of hyperglycemic agents?

A

GCs, sympathomimetics, thiazides

244
Q

Insulin specs:
Drug interactions of insulin + beta blockers

What are examples of hyperglycemic agents?

A

GCs, sympathomimetics, thiazides

245
Q

Insulin specs:
Drug interactions of insulin + beta blockers

A

Delay awareness of hypoglycemia
Mask signs

246
Q

Oral drugs & Non-insulin Injectables – sites of action

Which drugs stimulate insulin secretion in pancreas?

A

Sulfonyureas

DPP-4 Inhibitors

GLP-1 receptor agonists

247
Q

Oral drugs & Non-insulin Injectables – sites of action

Which drugs suppress glucagon secretion in pancreas?

A

Amylin

GLP-1 receptor agonists

DPP-4 inhibitors

248
Q

Oral drugs & Non-insulin Injectables – sites of action

Which drugs cause appetite control in brain?

A

Amylin

GLP-1 receptor agonists

249
Q

Oral drugs & Non-insulin Injectables – sites of action

Which drugs cause increased incretin effect in gut?

A

Amylin

GLP-1 receptor agonists

DPP4 inhibitors

250
Q

Oral drugs & Non-insulin Injectables – sites of action

Which drugs cause decreased hepatic glucose products in liver?

A

Metformin

251
Q

Oral drugs & Non-insulin Injectables – sites of action

Which drugs cause decreased glucose reabsorption in kidneys?

A

SGLT-2 inhibitors

252
Q

Oral drugs & Non-insulin Injectables – sites of action

Which drugs cause increased glucose uptake in muscles?

A

Metformin

253
Q

Oral drugs & Non-insulin Injectables – sites of action:

Which drugs cause increased glucose uptake in fat storing cells?

A

Metformin

254
Q

Oral antidiabetic agents & Non-insulin Injectables:

What are the groups of meds?

A
  1. Biguanides (Metformin [Glucophage])
  2. Sulfonylureas
  3. SGLT-2 Inhibitors
  4. DPP4-inhibitor
  5. NON-INSULIN INJECTABLE AGENTS
255
Q

Oral antidiabetic agents & Non-insulin Injectables:

Biguanides
Is also called?

A

(Metformin [Glucophage])

256
Q

What is used for initial tx of T2DM? What is the drug of choice?

A

Biguanides (Metformin)

257
Q

Oral antidiabetic agents & Non-insulin Injectables:

What does Biguanides (Metformin) do?

A

Inhibits glucose production by the liver

258
Q

Oral antidiabetic agents & Non-insulin Injectables:

What does Biguanides (Metformin) do to already existing glucose? How?

A

↑ glucose uptake by muscle and adipose tissue by sensitizing insulin receptors

259
Q

Oral antidiabetic agents & Non-insulin Injectables:

What does Biguanides (Metformin) NOT do?

A

Does not stimulate insulin release from pancreas

260
Q

Oral antidiabetic agents & Non-insulin Injectables:

How is Biguanides (Metformin) excreted?

A

Excreted unchanged by the kidneys (caution in RF)

261
Q

Oral antidiabetic agents & Non-insulin Injectables:

Who should Biguanides (Metformin) be used cautiously in?

A

Excreted unchanged by the kidneys (caution in RF)

262
Q

Oral antidiabetic agents & Non-insulin Injectables:

Biguanides (Metformin [Glucophage])

What are adverse reactions to this med?

A

N/v/d,

↓ appetite & absorption of folate, vit B12,

lactic acidosis (not good for renal pts)

263
Q

Oral antidiabetic agents & Non-insulin Injectables:

Biguanides (Metformin [Glucophage])

I dont’ understand slide

Symptoms of lactic acidosis?

A

Pt ed lactic acidosis sx: hyperventilation, myalgia, malaise

264
Q

Oral antidiabetic agents & Non-insulin Injectables:

What are drug interactions of Biguanides (Metformin [Glucophage])?

A

Etoh (inhibit lactic acid breakdown)
IV Contrast media

265
Q

Oral antidiabetic agents & Non-insulin Injectables:

Drug interactions of Biguanides (Metformin [Glucophage]):

What does IV contrast media do?

What to do if you need contrast?

A

Risk of RF

D/c a day or two before scan & resume 48 hrs after procedure

266
Q

Oral antidiabetic agents & Non-insulin Injectables:

Sulfonylureas include what?

A

(Glimepiride, Glipizide, Glyburide)

267
Q

Oral antidiabetic agents & Non-insulin Injectables:

Sulfonylureas- 1st and 2nd gen are special why?

A

1st & 2nd gen (more potent, lower doses)

268
Q

Oral antidiabetic agents & Non-insulin Injectables:

Sulfonylureas- What do they promote?

A

Promote insulin secretion by pancreas & increase tissue response to insulin

269
Q

Oral antidiabetic agents & Non-insulin Injectables

How do Sulfonylureas (Glimepiride, Glipizide, Glyburide) act?

A

Sulfonylureas close ATP-sensitive (K++ ) channels in pancreatic beta cells, causing the cells to depolarize and open voltage-gated (Ca+ ) channels. The influx of calcium ions triggers the release of insulin.

270
Q

Oral antidiabetic agents & Non-insulin Injectables:

What is an adverse reaction to Sulfonylureas (Glimepiride, Glipizide, Glyburide)?

A

ADRs: Hypoglycemia

271
Q

Oral antidiabetic agents & Non-insulin Injectables:

SGLT-2 Inhibitors include what?

A

SGLT-2 Inhibitors Sodium-Glucose Co-Transporter2 Inhibitors (Canagliflozin, Dapagliflozin)

272
Q

Oral antidiabetic agents & Non-insulin Injectables:

SGLT-2 Inhibitors Sodium-Glucose Co-Transporter2 Inhibitors (Canagliflozin, Dapagliflozin)- WHat do they do?

A

Block reabsorption of filtered glucose in the kidney via the SGLT2 receptor –> glucosuria

273
Q

Oral antidiabetic agents & Non-insulin Injectables:

SGLT-2 Inhibitors- What kind of effects do they have?

A

Cardiac effects:

reduction in intracellular calcium & mitochondria-induced cellular damage that cause cardiac remodeling

274
Q

Oral antidiabetic agents & Non-insulin Injectables:

SGLT-2 Inhibitors-What are the adverse reactions?

A

Genital fungal infections,

UTI,

increased urination

275
Q

Oral antidiabetic agents & Non-insulin Injectables:

DPP4-inhibitor include what?

A

(Sitagliptin [januvia])

276
Q

Oral antidiabetic agents & Non-insulin Injectables:

DPP4-inhibitor

What do these drugs do?

A

Enhancing the actions of incretin hormones

Suppress postprandial release of glucagon

277
Q

Oral antidiabetic agents & Non-insulin Injectables:

What does incretins do

A

Incretins stimulate glucose-dependent insulin release

278
Q

Oral antidiabetic agents & Non-insulin Injectables:

NON-INSULIN INJECTABLE AGENTS include what?

A

NON-INSULIN INJECTABLE AGENTS:

Glucagon-like Peptide GLP-1 receptor agonists (Exenatide [Byetta],

Liraglutide [Victoza],

Semaglutide [Ozempic, Wegovy])

Pramlintide

278
Q

Oral antidiabetic agents & Non-insulin Injectables:

DPP4-inhibitor (Sitagliptin [januvia])

mode of action?

A

MOA: inhibits DPP-4, an enzyme that inactivates incretin

278
Q

Oral antidiabetic agents & Non-insulin Injectables:

DPP4-inhibitor (Sitagliptin [januvia])

Adverse Reactions?

A

ADRs: pancreatitis

278
Q

Oral antidiabetic agents & Non-insulin Injectables:

NON-INSULIN INJECTABLE AGENTS are what exactly?

A

Incretin mimetics/GLP-1 Receptor Agonists

278
Q

Oral antidiabetic agents & Non-insulin Injectables:

What does GLP-1 do?

A

GLP-1 is secreted from the gut after meal, increasing the insulin secretion from the β-cells

278
Q

Oral antidiabetic agents & Non-insulin Injectables:

What are the effects of what GLP-1 does?

A

Slows gastric emptying, stimulate release of glucose-dependent insulin, inhibit postprandial release of glucagon, and suppress appetite

279
Q

Oral antidiabetic agents & Non-insulin Injectables:

NON-INSULIN INJECTABLE AGENTS Glucagon-like Peptide GLP-1 receptor agonists (Exenatide [Byetta], Liraglutide [Victoza], Semaglutide [Ozempic, Wegovy])

ADRs: ?

A

ADRs: GI effects (n/v/d), including pancreatitis

279
Q

NON-INSULIN INJECTABLE AGENTS:

What does Pramlintide do?

A

Hormone co-released with insulin from pancreas

Delays gastric emptying and suppresses glucagon release

Reduce appetite

280
Q

NON-INSULIN INJECTABLE AGENTS Glucagon-like Peptide GLP-1 receptor agonists (Exenatide [Byetta], Liraglutide [Victoza], Semaglutide [Ozempic, Wegovy])

What are adverse reactions of pramlintide? why?

A

hypoglycemia with insulin use since it’s specifically indicated for use in combo with mealtime insulin

280
Q

NON-INSULIN INJECTABLE AGENTS Glucagon-like Peptide GLP-1 receptor agonists (Exenatide [Byetta], Liraglutide [Victoza], Semaglutide [Ozempic, Wegovy])

What is Pramlitide a mimetic of?

A

Amylin Mimetic

281
Q

Glucagon:

What is the mode of action?

A

Stimulates liver production of glucose from glycogen stores (glycogenolysis)

282
Q

Glucagon:

How is the response to glucagon when it is administered?

A

Response to agent is delayed

283
Q

What is glucagon an alternative to?

A

ALT to IV glucose

284
Q

How is glucagon administered?

A

Home use, given subQ

285
Q

Who can’t glucagon be given to why?

A

Hypoglycemia from starvation b/c it promotes glycogen breakdown
Pts who are starved have little or not glycogen stores left

PATHO/PHARM II (27 decks)

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