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Pathophysiology > Test 6 > Flashcards

Test 6 Flashcards

1
Q

What are four hormones that can effect Blood Glucose Levels?

A

Cortisol, Glucagon, Epinephrine and the Growth Hormone

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2
Q

Which hormones inhibit the release of Insulin?

A

Cortisol, Glucagon, Epinephrine and the Growth Hormone

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3
Q

Most important of the Glucocorticoid Hormones from the Adrenal Cortex and it has to be present for other three Hormones to work

A

Cortisol

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4
Q

Hormone secreted by the Islets of Langerhans that releases Glucose from stored Glycogen

A

Glucagon

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5
Q

Helps to maintain blood Glucose levels during Stress by inhibiting Insulin release

A

Epinephrine

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6
Q

Antagonizes the effects of Insulin by decreasing Glucose uptake and usage by the cells

A

Growth Hormone

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7
Q

These Counter-Regulatory Hormones bind to specific receptors on cells and they stimulate the enzymes in a pathway to take stored Glycogen and turn it into _________

A

Glucose

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8
Q

What produces insulin?

A

The Beta Cells in the Islets of Langerhans of the Pancreas

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9
Q

Insulin release is regulated by _____________.

A

Blood glucose levels

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10
Q

As Blood Glucose Levels rise (Increases), insulin secretion _________.

A

Increases

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11
Q

As Blood Glucose Levels decrease, insulin secretion __________

A

Decreases

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12
Q

The Only Hormone Known to Have a Direct Effect on Lowering Blood Glucose Levels is __________

A

Insulin

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13
Q

Insulin is released within minutes of consuming a meal and serum Insulin reach a peak approximately __-__ minutes

A

3-5

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14
Q

True or False

Insulin is required to move Glucose into the cells

A

True

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15
Q

Insulin binds to a Receptor on a cell and causes what two things to occur:

A
  1. Proteins that are located in the cytoplasm of the cell are inserted into the cell membrane
    * These proteins are what glucose binds to

2.Glucose moves into the cell by Facilitated Diffusion; does not require Energy
When Glucose binds to the proteins, it undergoes a confirmation change and shuttles Glucose in

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16
Q

As long as the concentration of Glucose is high outside the cell and protein carriers are there, you will see movement of Glucose ____________.

A

Going into the cell

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17
Q

What is the the reason Glucose isn’t always entering the cell?

A

Because the protein carriers are not always present

*You need Insulin to bind to the Receptor

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18
Q

_________ get inserted into the cell membrane and

________ binds to the protein carrier and is shuttled into the cell

A

Protein carriers; Glucose

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19
Q

What are the functions on insulin?

A
  1. Movement of Glucose into a Cell
  2. controls the production of enzymes responsible for Cellular Metabolism
  3. stimulates all the enzymes necessary for Glucose to get converted to Glycogen
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20
Q

What cells store the greatest amounts of glycogen?

A

Liver and Muscle Cells

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21
Q

Needed to produce the Enzymes required for the conversion of Glucose down Metabolic Pathways. __________

A

Insulin

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22
Q

How is glucose converted to adipose tissue?

A

Glucose to Glycerol and Fatty Acids to Storage of Triglycerides in Adipose Tissue

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23
Q

Do Epithelial cells of the Gut require/ don’t require Insulin for Glucose Uptake

A

DO NOT REQUIRE

*Absorbs Glucose from the Small Intestine and then Glucose enters the blood stream

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24
Q

Do the neurons of the brain require Insulin for Glucose uptake?

A

DO NOT REQUIRE

Glucose can automatically enter a neuron via Facilitated Diffusion; Not Insulin Dependent

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25
Q

What is the the primary fuel for the Brain and the Nervous System?

A

Glucose

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26
Q

The fact that the Brain is limited to storing only Glucose for a few minutes, it requires a Continuous supply of ________.

A

Glucose

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27
Q

Chronic disorder of carbohydrate metabolism resulting from insufficient production of Insulin or from inadequate utilization of this hormone by the body’s target cells. _________

A

Diabetes Mellitus (Hyperglycemia)

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28
Q

What can result in Hyperglycemia

A

Insulin Deficit

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29
Q

Type 1 Diabetes is also referred to as:

A

Insulin Dependent Diabetes Mellitus (IDDM)

Child Onset / Juvenile Diabetes

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30
Q

What type of Diabetes is the most serious form?

A

Type 1 Diabetes

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31
Q

What type of Diabetes accounts for 10% of all Diabetics?

A

Type 1 Diabetes

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32
Q

Diagnosis is rare during the first 9 months of life and peaks at what age?

A

12 years old

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33
Q

Type 1 diabetes develops most commonly in what age group?

A

The Young

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34
Q

What is the range in which children are diagnosed with Type 1 diabetes?

A

1 in 400 – 500

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35
Q

Type 2 diabetes is also referred to as:

A

Non-Insulin Dependent Diabetes Mellitus (NIDDM)

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36
Q

What type of diabetes is the most common and mildest form?

A

Type 2

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37
Q

Incidence estimated at about 9% of the population (18 million) greater than ____ years of age

A

20 years of age

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38
Q

Type 2 diabetes effects people primarily after age ____.

A

40

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39
Q

Approximately half the cases are found in individuals greater than ____ years of age

A

55

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40
Q

What type of diabetes is becoming more common in obese adolescents and children?

A

Type 2

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41
Q

What are the common factors resulting in the initial stage of diabetes?

A
  1. Insulin deficit results in decreased transportation and use of Glucose in many cells of the body
  2. Hyperglycemia: Increase in Blood Glucose Levels
  3. Glucosuria: Excess Glucose in the Urine
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42
Q

Three “Ps” are the three most common signs and symptoms. What are they?

A
  1. Polyuria: Excessive urination
  2. Polydipsia: Excessive Thirst
  3. Polyphagia: Increase in Appetite
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43
Q

Glucose acts as a _______ and causes large amount of urine to be excreted with loss of fluid and electrolytes (sodium) from the body tissues.

A

Diuretic

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44
Q

What results in fluid loss through the Urine?

A

Dehydration

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45
Q

A great loss of water occurs with __________.

A

Glucose

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46
Q

What occurs with Polydipsia?

A

Dehydration causes excess thirst

By drinking large amounts of water, the person compensates for the fluid loss

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47
Q

Result of lack of nutrients entering the cells stimulates appetite

A

Polyphagia: Increase in Appetite

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48
Q

Progressive Effects are seen more with what type of diabetes?

A

Type 1

*Occurs when Insulin Deficit is severe or prolonged

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49
Q

A decrease in Glucose is also seen with people on _________

A

Sarvation diets

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50
Q

Lack of Glucose in body cells results in what?

A

Catabolism of Proteins
Catabolism of Fats
Causes excessive amounts of Fatty Acids and their metabolic wastes: Ketones or Ketoacids

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51
Q

Name for Excessive Ketones in the blood

A

Ketoacidosis

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52
Q

Ketoacids bind with the ____________ in the blood

A

Bicarbonate Buffer

*Leading to decreased Serum Bicarbonate

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53
Q

What is the end result of decreased Serum Bicarbonate?

A

Decrease in the pH of body fluids

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54
Q

As Dehydration occurs, GFR ___________

Excretion of Ketoacids _____________

A

Decreases; Decreases

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55
Q

Decrease in GFR and Excretion of Ketoacids results in what?

A

Decompensated Metabolic Acidosis: Diabetic Ketoacidosis or Diabetic Coma
Life threatening

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56
Q

Type 1 Diabetes is sub-dived into what two types?

A
  1. Autoimmune Disease (represents 95% of Type 1 Diabetes)

2. Idiopathic

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57
Q

Islet Cell Antibodies against the Beta Cells of the Pancreas can be detected in the blood of newly diagnosed patients with Type 1

A

Autoimmune Disease

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58
Q

Islet Cell antibodies may also exist for years before the onset of ____________

A

Hyperglycemia

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59
Q

Pathogenesis:

Islets of Langerhans show a depletion of Beta cells in what type of diabetes?

A

Type 1

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60
Q

Cells are replaced by _________

A

Fibrous Tissue

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61
Q

Suggestive of an Autoimmune Reaction which may be triggered by an environmental agent (Viral Infection) that results in an Immune Response and ____________.

A

Antibody Production

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62
Q

Common Theory for Type 1 Diabetes is:

A

Genetic-Environmental Interaction

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63
Q

Environmental Factors for Type 1 Diabetes include:

A

Sudden onset of Type 1 Diabetes may be related to a Viral Infection
Seasonal occurrences of Type 1: More new cases documented during fall and winter in the northern hemisphere
Seasonal occurrences may be suggestive of “Mini-Epidemics” consistent with Viral Infections

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64
Q

Mechanisms of Type 1 Diabetes includes:

A

Loss of Beta Cells resulting in an absolute Insulin deficit

Glucose uptake and metabolism are compromised

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65
Q

Disease results from _________________

A

A genetic susceptibility

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66
Q

What percentage of first degree relatives develop impaired Glucose Intolerance or Type 2 Diabetes

A

15-25%

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67
Q

Beta cells are essentially __________.

A

undamaged

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68
Q

Beta cells are capable of producing _________ but secretion in response to stimulation by Glucose may be Delayed

A

Glucose

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69
Q

Key Defects of Type 2 Diabetes include:

A

Insulin Resistance
Involves the inability of the uptake and utilization of Glucose in various target tissues such as Muscle and the Liver

Insulin resistance is based on slower cycling of the Glucose Carrier Proteins to the cell membrane surface

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70
Q

The Majority of Type 2 Diabetics are __________

A

Over weight

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71
Q

Individuals with __________ are at a greater risk for development of Type 2

A

Upper Body Obesity

*Increased abdominal girth

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72
Q

Obese individuals have an _______ resistance to Insulin

A

Increase

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73
Q

Obese individuals also have an

A

impaired suppression of Glucose from their Liver

Increased release of Glucose by the Liver

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74
Q

Mechanisms of Type 2 include:

A

Impaired Insulin Release from the Pancreas
Insulin Resistance
Increased Glucose Production from the Liver

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75
Q

Sings and symptoms of TYPE 2 diabetes include:

A

Glycosuria

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76
Q

TRUE OR FALSE

If Glucose is 100 mg/dl in the plasma, then it will also be 100mg/dl in Bowman’s Capsule space

A

TRUE

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77
Q

Glucose is reabsorbed by the _________

A

PCT by active transport via a protein pump

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78
Q

Normal Blood Glucose Levels (fasting) are:

A

70 - 110 mg/dl

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79
Q

Renal Threshold Levels are:

A

180/200 mg/dl

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80
Q

True or False

Once we saturate these protein pumps, we can’t move Glucose any faster into the blood stream

A

TRUE

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81
Q

Any excess Glucose will spill into the urine resulting in __________.

A

Glycosuria

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82
Q

Signs and symptoms of Diabetes include:

A
  1. Polyuria
  2. Polydipsia
  3. Polyphagia
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83
Q

Metabolic changes result in poor use of food products, contributing to ________ and ____________.

A

Lethargy and Fatigue

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84
Q

Weight Loss is a symptom of what type of diabetes?

A 
Type 1  (Since there is no Insulin available, the body is burning both fats and proteins for energy)
Also occurs because of fluid loss in osmotic Diuresis
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85
Q

Obesity is a symptom of what type of diabetes?

A

Type 2

*Not all Diabetics are obese, or not all obese individuals are Diabetics

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86
Q

Increase abdominal girth is a symptom of what type of diabetes?

A

TYPE 2

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87
Q

Major sign of Diabetes is ________

A

Glycosuria

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88
Q

Presence of Ketones (Ketone Bodies) in urine is another sign of Diabetes mellitus

A

Ketonuria

*Result of Fat catabolism

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89
Q

Diagnostic test for Diabetes include:

A

Urinalysis
Fasting Blood Glucose (Sugar) - FBS
Glucose Tolerance Test (GTT)
Glycosylated Hemoglobin (HbA1C or A1C) *A1C is the preferred term

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90
Q

Normal values for FBS are:

A

70 - 110 mg/dl

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91
Q

A diagnosis of Diabetes is made if the FBS (plasma) level is ___________________

A

Is greater than 126 mg/dl for two consecutive tests

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92
Q

2 Hour post-load for FBS should be:

A

Should be less than 140 mg/dl

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93
Q

Glucose Tolerance Test (GTT):

Within 3 hours, patient should be ______________________

A

Back to the baseline of Glucose

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94
Q

For the Glucose Tolerance Test (GTT) a Diabetic patient would:

A

May begin with an elevated FBS
Glucose levels increase after drinking glucose
May be equal or Greater than 200 mg/dl
They are not utilizing the Glucose they drank

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95
Q

When Hemoglobin is released from the Bone Marrow it normally ___________

A

Does not contain Glucose

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96
Q

The Glycosylated Hemoglobin Concentration (HbA1C or A1C) Represents what?

A

The average blood Glucose level over the past Several Weeks (2 – 3 months)

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97
Q

The goal for the average blood Glucose level is:

A

Less than 7.0%

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98
Q

Normal Glycemic Levels are:

A

Less than 6.0%

*Beneficial in diagnosing a Non-compliant patient

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99
Q

Three major acute complications exist for Diabetes:

A
  1. Hypoglycemia / Low Blood Sugar / Insulin Reaction (Shock)
  2. Diabetic Ketoacidosis (DKA)
  3. Hyperosmolar Hyperglycemic Nonketotic Coma
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100
Q

Hypoglycemia / Low Blood Sugar / Insulin Reaction (Shock) results from what?

A

An Inadequate level of circulating Glucose

KNOW *Adults: 45 - 60 mg/dl

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101
Q

Hypoglycemia / Low Blood Sugar / Insulin Reaction (Shock) usually occurs suddenly in __________

A

Type 1

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102
Q

Inadequate level of circulating Glucose results of:

A

Strenuous exercise
An error in Insulin Dosage
Vomiting
Skipping a meal after taking Insulin

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103
Q

Lack of glucose affects the Nervous system by:

A

Neurons can’t use Fats or Proteins as an Energy Source

Clinical manifestations relate to Low blood Glucose levels

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104
Q

Examples of Impaired Neurologic Function of Diabetes

A

Poor concentration
Slurred speech
Lack of coordination
Staggering gait

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105
Q

Stimulation of the Sympathetic Nervous System include:

A

Increased pulse
Pale, moist skin
Anxiety
Tremors

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106
Q

Hypoglycemia can affect the brain by:

A

Cause Brain damage if not treated promptly

Patient can become unconscious, experience seizures and death can occur

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107
Q

Treatment for an Insulin Reaction / Hypoglycemia include:

A

Immediate administration of a concentrated Carbohydrate: Sweetened fruit juice or candy
If patient is unconscious: Administration of Glucose or Glucagon Intravenously
Administration of Epinephrine also raises blood sugar levels

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108
Q

A Diabetic Patient Going into a Coma Could be due to Either an __________ or ____________ in Blood Glucose Levels

A

Increase or Decrease

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109
Q

Necessary to administer Glucose to prevent _____________

A

Neuronal Death

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110
Q

If a coma is due to increase in blood sugar what will be done?

A

Glucose given will only raise blood sugar slightly

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111
Q

Specific to Type 1 Diabetes

A

Diabetic Ketoacidosis (DKA)

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112
Q

Often preceded by physical or emotional Stress and develops over a few days
*Infection, pregnancy, or extreme anxiety

A

Diabetic Ketoacidosis (DKA)

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113
Q

Stress results in the release of _________ and predisposes one to the development of DKA

A

Cortisol

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114
Q

Lipid metabolism results in the accumulation of___________ in the blood

A

Ketone Bodies

*Can produce nausea and vomiting

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115
Q

Fruity, acetone smell characteristic odor that is often detected on the Breath of a diabetic patient.

A

Ketone Bodies

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116
Q

What is the pH of plasma:

A

Less than 7.3

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117
Q

Signs & Symptoms of Dehydration

A 
Dehydration
Thirst
Decreased skin turgor
Skin with decreased turgor remains elevated and returns slowly to its normal position.
Dry oral mucosa
Warm, dry skin
Rapid, weak pulse
Low Blood Pressure
Oliguria
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118
Q

Signs & Symptoms: Ketoacidosis (DKA)

A

Deep, rapid respirations (Kussmaul’s Respirations) with Acetone Breath
Lethargy & decreased responsiveness

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119
Q

What happens if Diabetic Ketoacidosis (DKA) remains untreated?

A

CNS Depression develops and results in a Coma
Caused by the combined effects of Ketoacidosis and Dehydration
Toxic effects of Ketone Bodies on the Brain
Develops in extreme elevation of blood Glucose level

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120
Q

Develops in extreme elevation of blood Glucose level

A

Blood Glucose levels above 250 mg/dl

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121
Q

May develop a Coma with blood sugars of 400 - 800 mg/dl

A

Type 1

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122
Q

Treatment of Diabetic Ketoacidosis (DKA) would be:

A

Administer Insulin as well as replacement of Fluid and Electrolytes
Bicarbonate administration is essential to reverse Acidosis
Resolve the initial cause

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123
Q

Hyperosmolar Hyperglycemic Nonketotic Coma Develops more frequently in _________.

A

Type 2 Diabetes

*Blood Sugar levels of 800 - 1500 mg/dl

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124
Q

Dehydration is more severe due to ___________________

A

Extremely high blood sugar levels

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125
Q

Often associated with an infection or carbohydrate overload

A

Hyperosmolar Hyperglycemic Nonketotic Coma

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126
Q

Results in a decrease perfusion to the Brain and results in a Coma

A

Hypovolemia

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127
Q

Hyperglycemia and dehydration develop because of ________________

A

The relative Insulin deficit, but sufficient

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128
Q

What is able to prevent Ketoacidosis

A

Insulin

*Patient’s will display S&S for Dehydration, but will not experience S&S of Ketoacidosis

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129
Q

Hyperosmolar Hyperglycemic Nonketotic Coma will experience _____________

A

Lethargy and Decreasing Responsiveness

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130
Q

Type 2 Diabetics have Insulin, but they have _________________

A

A decrease effect of Insulin

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131
Q

Chronic Complications occur when?

A

When blood Glucose levels are poorly controlled and result in Hyperglycemia

132
Q

What is the most clearly established risk factor associated with the complications.

A

Hyperglycemia

133
Q

Degenerative changes occur in the ________________.

A

Insulin-Independent Body Tissues

134
Q

Tissues that __________ require Insulin for Glucose Uptake

A

DO NOT

135
Q

What is the rationale for chronic complications:

A

Intracellular Glucose levels In these tissues approach or equal blood Glucose levels

136
Q

What happens in Microangiopathy (Small Vessel Damage)

A

In small vessels, altered Carbohydrate metabolism causes faulty deposition of the Basement Membrane material
Basement membrane becomes thick and hard
Causes obstructions
Weakens the blood vessels and interferes with normal capillary permeability
Obstruction: Results in reduced blood flow
Rupture of capillaries and small blood vessels

137
Q

What is the end result of Microangiopathy (Small Vessel Damage)?

A

Results in Tissue Necrosis, Loss of Function and Prolonged Healing!!!

138
Q

Hypertension usually accompanies _________ Diabetics, especially with the obese

A

Type 2

139
Q

Weakens the blood vessels which leads to Aneurysm formation and eventually they may rupture within the Retina

A

Diabetic Retinopathy

*Some degree of Blindness

140
Q

Examples of Microangiopathy are:

A

Diabetic Retinopathy

Diabetic Nephropathy

141
Q

Initially, filtration is increased, period of proteinuria, and in the later stages GFR progressively _____________

A

Declines (Decreases)

142
Q

In Diabetic Nephropathy Glomerular vessels (Glomeruli) are also subject to _______________.

A

Basement Membrane Damage

143
Q

With Diabetic Nephropathy what happens as complications:

A

Nephron function is progressively lost resulting in Chronic Renal Failure!!!

144
Q

What is the leading cause of End-Stage Renal Disease?

A 
Diabetic Nephropathy (Chronic Renal Failure)
*Responsible for 40% of patients in End-Stage Renal Failure
145
Q

Macroangiopathy (Large Vessel Damage) results in _______________

A

Atherosclerosis (Developed prematurely)

146
Q

Hyperlipidemia could also result in _____________

A

Atherosclerosis

147
Q

Lipids are removed from Adipose Tissues and are delivered by the _______________.

A

Vascular System

*Higher incidence of MI and CVA

148
Q

Major cause of death in Diabetes is _____________

A

Myocardial Infarction

149
Q

Atherosclerosis results in ___________

A

Myocardial Infarction

150
Q

Examples of Macroangiopathy (Large Vessel Damage) would be:

A

Atherosclerosis
Peripheral Vascular Disease (Impairment of Wound Healing)
Peripheral Neuropathy

151
Q

Minor wounds, which normally should heal quickly, can pose a serious threat that result ___________________

A

A Reduction of blood flow
Poor oxygen deliver which can result in the growth of anaerobic microbes
Development of Neuropathic Ulcers
Risk of Gangrene

152
Q

Prolonged Healing is noted in ______________ AND ____________.

A

Microangiopathy and Mracoanigiopathy

153
Q

Degenerative changes occur in ___________ and _________

A

both unmyelinated and myelinated axons

154
Q

Examples of Peripheral Neuropathy would be:

A

a. Numbness
b. Tingling sensations
c. Pain
d. GI motility
Delayed gastric emptying leads to bouts of diarrhea, especially at night and constipation
Result of a Degeneration of the Autonomic Nervous System
e. Bladder Dysfunction
Bladder paralysis with urinary retention
Increases incidence of UTIs
f. Impotence in males
g. Abnormal reflexes
Absence of ankle and knee jerk reflexes

155
Q

Chronic Complications of diabetes would include:

A 
Microangiopathy (Small Vessel Damage) 
Macroangiopathy (Large Vessel Damage) 
Peripheral Neuropathy 
 Susceptibility to Infection
Cataracts
Glaucoma
156
Q

Infections in the feet and legs persist and are slow to heal resulting in __________and _________

A

Gangrene and Amputation

157
Q

Prevents Diabetics from detecting pain of their feet and unable to adjust their gait to avoid placing pressure which is potentially causing trauma and necrosis

A

Neuropathy

158
Q

Degenerative process related to the abnormal metabolism of Glucose

A

Cataracts

159
Q

Cataracts results in the accumulation of ___________

A

Sorbitol

160
Q

Increased pressure in the Eye

Increased incidence in Diabetes

A

Glaucoma

161
Q

What is the treatment goal for diabetes?

A

Maintain normal blood glucose levels in order to prevent or delay the Chronic Diabetes Complications

162
Q

Treatment for Diabetes includes:

A 
Diet
Exercise (Decreases the need for Insulin)
Oral Medications
Insulin Therapy
Transplantation
163
Q

Exercise is a concern for Concern with Insulin-Dependent Diabetics because:

A

Increased risk of Hypoglycemia

164
Q

True or False Type 2 Diabetes (only): :

Many Type 2 patients would then be able to control their diabetes with a combination of weight loss and exercise

A

TRUE

165
Q

True or False Type 2 Diabetes (only): :

Over time, Insulin resistance may actually improve if the patient loses weight

A

TRUE

166
Q

Oral Hypoglycemic drugs may be used with Type ______

A

Type 2 diabetics
*increase in the release of Insulin from the Beta cells
One would have to have healthy Beta cells and functional Insulin to benefit from these drugs

167
Q

Which drug reduces Insulin Resistance?

A

Glucophage (metformin)

168
Q

Which drug increases tissue sensitivity to Insulin?

A

Avandia (rosiglitazone)

169
Q

Treatment always required for Type 1 for the remainder of their lives is __________

A

Insulin Therapy

170
Q

Insulin must be administered by __________________

A

by Injections (subcutaneous) because the protein is destroyed in the GI tract

171
Q

Newer forms of Insulin Therapy include:

A

Multiple daily Insulin injections

Use of an Insulin Pump which provides continues infusion

172
Q

The inhaled insulin is called __________

A

Afrezza
Taken before meals
Absorbe more quickly via cells from the Lungs
Rapid Peak
Peaks in the blood in 15 – 20 minutes (Injected Insulin taken before a meal typically peaks in 1 hour)
Also cleared more rapidly from

173
Q

Pancreas Transplants have been performed since _____________

A

1966

174
Q

Prognosis for Diabetes is ___________

A

Variable

175
Q

Most common form of Hyperthyroidism would be __________

A

Graves’ Disease

*increased levels of T3 and T4

176
Q

Grave’s Disease Occurs more frequently in women over _______

A

30 years old

177
Q

Grave’s Disease is what kind of disorder?

A

Autoimmune Disorder

178
Q

Clinical Manifestations of Grave’s Disease would be:

A

Toxic goiter: Hyperactivity & enlargement of the Thyroid Gland
Weight loss despite increased appetite
Heat intolerance, Excessive Sweating
Tremors, Nervousness, & Palpitations
Exophthalmos: Abnormal protrusion of the eyes

179
Q

Form of severe Hypothyroidism would be ___________

A

Hashimoto’s Disease

180
Q

What type of disorder would Hashimoto be:

A

Destructive, Chronic Autoimmune Disorder

181
Q

Clinical Manifestations of Hashimato would be:

A

Inflammation of Thyroid Gland; Immune Mediated
Initially, presents with an enlarged Thyroid Gland (goiter) and is infiltrated with Lymphocytes
Eventually, Fibrosis may reduce the size of the Thyroid Gland
SYMPTOMS: Energy Loss, Fatigue, Forgetfulness, Sensitive to Cold, Weight Gain with Anorexia, Bradycardia, and Enlarged Heart

182
Q

What is Cushing’s Syndrome caused by?

A

Hypersecretion of ACTH from Pituitary Adenomas and excessive amount of Glucocorticoids (cortisol)

183
Q

Clinical Manifestations of Cushing’s Syndrome would be:

A 
Moon Face, Buffalo Hump, Obese Trunk, Muscle Wasting in Extremities and Osteoporosis 
Bruising and Striae of Skin
Hypertension, Glucose Intolerance
Fatigue, Weakness, Delayed Healing
High Risk of Infections
Poor Stress Response
184
Q

Adrenal Insufficiency with deficiency of Adrenocortical secretions: Glucorticoids, Mineralocorticoids and Androgens

A

Addison’s Disease

185
Q

70% of Addison’s Disease cases associated with an _______________

A

Autoimmune Disorder (Adrenalitis)

186
Q

What can also cause Addison’s Disease:

A

Infections (TB and Fungal)

Immunosuppression and AIDS

187
Q

Clinical Manifestations of Addison’s Disease would be:

A

High risk of Infection
Poor Stress Response
Weight Loss, Fatigue
Anorexia, Nausea, Diarrhea
Hypotension
Syncope (Fainting or loss of consciousness)
Hyperpigmentation (skin, nails and of the mucous membranes, especially of the mouth)

188
Q

CSF Examination is commonly obtained by:

A

A Lumbar Puncture

Between L3 and L4 or L4 and L5

189
Q

A clear colorless fluid that fills the ventricles within the Brain and the Subarachnoid Spaces around the Brain and Spinal Cord

A

CSF

190
Q

CSF is made up of _________

A

99% Water

Glucose,proteins, urea, salts

191
Q

CSF can be examined for _________

A

Gross appearance, pressure, glucose and protein content

192
Q

The number and types of blood cells present and the presence of bacteria, viruses, and fungi can be determined by ________

A

A culture

193
Q

May be attached to a syringe to measure the pressure

A

Monometer

*Noted in patients with Increased Intracranial (ICP)

194
Q

A closed, non-expandable vault which contains the Brain, Blood and CSF

A

Skull

195
Q

Any increase in blood, inflammatory exudate or a mass, such as a tumor causes an __________________

A

Increase in pressure within the Brain

196
Q

Increased ICP is associated with

A 
Brain Hemorrhage
Trauma
Cerebral Edema
Infection
Tumors
Accumulation of Excessive Amounts of CSF
197
Q

Clinical Manifestations of ICP:

A 
Decreased level of consciousness
Headache
Vomiting
Changes in Vital Signs:  
Increase blood pressure
Decrease heart rate
Signs Affecting Vision
Papilledema
Pupils, are fixed and dilated
198
Q

Noninvasive X-ray technique that is more sensitive than the conventional X-ray

A

Computed Tomography (CT Scan)

199
Q

Imaging procedure relies on Magnets and computers to produce images
An individual is surrounded by a magnetic field which causes hydrogen atoms to line up in a certain fashion

A

Magnetic Resonance Imaging (MRI)

  • Ionizing Radiation is not required
  • Radio waves provide the energy source
200
Q

Process of recording the Electric currents developed in the brain by placing electrodes on the skull

A

Electroencephalogram (EEG)

201
Q

Abnormal patterns in an EEG may result in:

A

Seizure disorders, tumors or injuries

202
Q

In regards to seizures its also referred to as ____________

A

Convulsions

203
Q

What causes seizures?

A

Excessive discharge of Neurons in the brain

204
Q

Seizures may be precipitated by:

A

Inflammation
Hypoxia
Bleeding
*Seizure may be manifested by involuntary repetitive movements or abnormal sensations

205
Q

Primary Malignant tumor of the Brain is called _________

A

Glioma

206
Q

In the adult, the Neuroglial Cells of the CNS provide for what three things?

A

Repair, support and protection of the Neurons

207
Q

The Supporting cells and not the Neurons are called?

A

Neuroglial Cells

208
Q

Glioma tumor is classified according to what?

A

their cell of Origin and the Location of the tumor

209
Q

True or False

Primary Malignant Tumors very rarely metastasize outside the CNS

A

TRUE

210
Q

Quite common and they usually metastasize from Breast or Lung Tumors

A

Secondary Brain Tumors

211
Q

CNS progressive Demyelinated disorder

Involves neurons of the Brain, Spinal Cord and Cranial Nerves

A

Multiple Sclerosis (MS)

212
Q

What part of the Nervous system is involved with MS?

A

CNS (Peripheral Nervous System is not involved)

213
Q

Chronic disease characterized by episodes of exacerbation and remission of neurologic symptoms over many years in several different locations of the CNS

A

Multiple Sclerosis (MS)

214
Q

Approximately 85% of cases demonstrate this form of MS?

A

Relapsing-remitting MS (RRMS)

*NO apparent progression of disease

215
Q

After 10 to 20 years, the course of RRMS shifts to _____________

A

A progressive Type

216
Q

Statistics of Multiple Sclerosis:

Who is affected more?

A

Women are affected twice as often as men between age 20-40

217
Q

What age is the peak of MS

A

30 years old

218
Q

What race is more prone to MS?

A

Occurs in all races, but it is chiefly a disorder of Caucasians

219
Q

What is the Etiology of MS?

A

Idiopathic

220
Q

What is the Epidemiology of MS

A

Interaction between a Viral illness in the teen years and a genetic predisposition

221
Q

Where is MS the most prevalent?

A

Areas far from the equator and thus in the colder northern latitudes
*More common in the Great Lakes, northern Atlantic states and Pacific Northwest than in the southern parts of the US

222
Q

True or False

MS disease is uncommon in the tropics

A

TRUE

223
Q

What Vitamin appears to have an good impact on MS?

A

Vitamin D

*Vitamin D supplementation with therapy

224
Q

What is a predisposing factor to get MS and worsen it?

A

Smoking

*Maybe involves Bronchial Mucosal Immunity

225
Q

First degree relatives of an affected person have a _____________

A

15 times higher risk of developing the disease than the general population

226
Q

Pathophysiology of Multiple Sclerosis

A

Involves the Demyelination of Nerve Fibers in the white matter of the Brain, Spinal Cord and Optic Nerves
*Characterized by the destruction of the Myelin Sheath

227
Q

In the CNS, Myelin is produced by ________________

A

Oligodendrocytes

228
Q

The lesions of MS consist of _______________

A

hard, sharp-edged demyelinated patches throughout the white matter of the CNS

229
Q

The lesions OF MS are referred to as ___________

A

Plaque

230
Q

In active plaque what is happening:

A

Myelin breakdown is ongoing
Lesions contain only a small amount of Myelin proteins and increased amounts of Proteolytic Enzymes, Macrophages, Lymphocytes and Plasma Cells

231
Q

In older lesions what is happening:

A

Oligodendrocytes are decreased in number or absent

232
Q

Multiple Sclerosis is considered an ______________

A

Autoimmune Disorder

233
Q

The lesions of MS are thought to be a result of an ____________________

A

Immune-Mediated Inflammatory response that occurs in susceptible individuals

234
Q

TRUE OR FALSE:

Demyelination process is marked by Lymphocyte invasion into the CNS

A

TRUE

235
Q

What two things contribute the damage to the Oligodendrocytes?

A

Killer T Cells and Macrophages

236
Q

IgG secreted by ______________

A

Plasma Cells (Found in CFS)

237
Q

With Immunoelectrophoresis, it is shown that the IgG in the CNS is composed of ________________

A

oligoclonal bands

238
Q

What is useful in the Diagnosis of MS

A

CSF Oligoclonal IgG

239
Q

In time, neural degeneration becomes _______________

A

Irreversible

* Function is lost permanently

240
Q

The clinical presentation depends on:

A

Location, extent and pattern of the development of the Plaques

241
Q

Signs and Symptoms include:

A 
Optic Neuritis
Diplopia:  Double vision
Scotoma:  A spot in the visual field
Fatigue
Paresthesias
Nystagmus
242
Q

About _______ of patients presenting with Optic Neuritis are eventually diagnosed with MS

A

50%

243
Q

Loss of sensation of touch accompanied by tingling or burning sensation on the face or extremities
Symptoms may range from annoying to severe

A

Paresthesias

244
Q

One of the most common problems

Seen in about 70% of patients with MS is ____________

A

Fatigue

245
Q

Motor Signs and Symptoms of Multiple Sclerosis include:

A 
Muscular Weakness
Unsteady Gait
Hyperreflexia is detectable 
Paraplegia or Quadriplegia 
Dysphagia
Speech Problems
246
Q

Initially weakness of the legs often occurs

Related to Plaques on the Corticospinal Tract

A

Muscular Weakness

247
Q

Loss of balance and poor coordination

A

Unsteady Gait

248
Q

Occurs occasionally as MS plaque and associated edema block transmission in the Spinal Cord

A

Paraplegia or Quadriplegia

249
Q

Person may experience increased urinary frequency and urgency
Difficulty in urinating

A

Urinary Incontinence

250
Q

Rare, but constipation is common with severe disease

A

Bowel Incontinence

251
Q

Poor articulation
Clumsiness in the uttering of words
Speech may be difficult to understand

A

Dysarthria

252
Q

MS may be a challenge to diagnose because:

A

S&S are so variable and sporadic

253
Q

Diagnostic Test for MS include:

A

History & Physical
MRI
CT Scans
Evoked Response Studies

254
Q

The MRI Diagnostic Test imaging procedure of choice for either:

A

Confirming the diagnosis of MS

Monitoring the disease progression in the CNS

255
Q

May be useful if MRI is unavailable or MRI findings are ________________

A

nondiagnostic

256
Q

Most patients become physically incapacitated over a period of ____________.

A

20-30 years

257
Q

Complications of MS include:

A 
Paralysis
Respiratory Infection:  
Because of impaired Ventilation
Cystitis / Kidney Infection
Death
258
Q

Treatment for MS includes:

A

Palliative
No specific treatment
Interferon beta-1b – (Betaseron)
Physical Therapy

259
Q

The number of exacerbations of MS may be reduced by

A

Avoiding excessive fatigue, stress, injury, or infection

260
Q

Mainstay for acute relapses of MS is _______________

A

Corticosteroids

261
Q

What is the prognosis of MS

A

Unpredictable course

262
Q

Approximately, 1/3 of the patients with MS, suffer from significant physical disability within __________________

A

20-25 years of the onset

263
Q

A slowly degenerative CNS disorder is called ________________

A

Parkinson’s Disease

264
Q

What are the statistics of Parkinson’s Disease?

A

Approximately 500,000 - 1.5 million people in the US

265
Q

What age does Parkinson’s Disease typically begin?

A

After Age 60

266
Q

What is the course of Parkinson’s Disease

A

10-20 years

267
Q

Basal Nuclei are important in:

A

Starting, stopping and monitoring the intensity of movements executed by the Cerebral Cortex

268
Q

Pathophysiology of Parkinson’s Disease results from _______________.

A

Degeneration of the dopamine-releasing neurons of the Substantia Nigra

269
Q

Two darkly pigmented, brain stem nuclei that are located in the Midbrain

A

Substantia nigra

270
Q

Substantia Nirgra send their axons up to the Basal Ganglia (Corpus Striatum) and release the inhibitory neurotransmitter ________________

A

Dopamine

271
Q

The Basal Ganglia produce an excess of signals that effect __________________

A

Voluntary muscles in several areas of the body

272
Q

Inhibits the excitatory effects of the Acetylcholine produced by other Neurons in the Basal Ganglia

A

Dopamine

273
Q

What is the Etiology of Parkinson’s Disease?

A

Unknown

274
Q

A secondary form of Parkinson’s Disease is called?

A

Parkinsonism

*Occurs with Poisoning / Toxins

275
Q

Etiology: Secondary Parkinson’s Disease

A

Post Encephalitis
Rare
Associated with Viral Encephalopathy
Trauma or Vascular Disease

276
Q

What is the most common cause of the Secondary form of PD?

A

Drug induced Parkinson’s Disease (reversible)

*Side effect of Major Tranquilizers

277
Q

Signs and Symptoms of Parkinson’s Disease include:

A 
Resting Tremor
Pill Rolling Tremor
Nodding Movement of the Head
Muscle Rigidity
Bradykinesia
Akinesia
Shuffling Gait
Postural Changes
Mask-like Facial Expression
278
Q

Typically enhanced by emotional stress

A

Resting Tremor

279
Q

Complete or partial loss of muscle movement would be called ___________.

A

Akinesia

280
Q

Basal Ganglia also influence the _______.

A

ANS

281
Q

Signs and Symptoms: Autonomic Nervous System (ANS)

A 
Excessive Production Saliva
Excessive Sebaceous Gland Secretion
Constipation
Urinary retention
Orthostatic Hypotension
282
Q

Diagnostic Test for PD include:

A

H&P
Urinalysis
EEG

283
Q

Decreased levels of Dopamine would be seen on what Diagnostic Test:

A

Urinalysis

284
Q

Complications of PD:

A 
Debilitating disease
Dementia
Progressive Dementia may be associated with the advance stages of the disease
Occurs in about 20% of the patients
Involves the Cortical Neurons 
 Pneumonia
Leading cause of death
285
Q

The leading cause of Death would be:

A

Pneumonia

286
Q

The treatment for PD would be:

A

NO CURE

287
Q

Nonpharmacologic Treatment of PD include:

A

Physical therapy helps the patient to maximize his or her mobility
Daily exercise
Heat and massage help to relieve muscle cramps
Adequate Nutrition

288
Q

Pharmacologic Treatment Include:

A

Levadopa (l-dopa)

Selegiline (Eldepryl)

289
Q

Surgical procedure used to relieve some of the S&S

A

Deep Brain Stimulation (DBS)

*Use MRI/CT scanning to map out the precise area of the brain

290
Q

What is the most common targeted in Deep Brain Stimulation?

A

Subthalamic nucleus

291
Q

Electrodes are surgically planted in one of the three targeted Brain regions which are:

A
  1. Subthalamic nucleus (most common target)
  2. Globus pallidus (Basal Nuclei/Ganglia)
  3. Thalamus (primarily used to treat tremor)
292
Q

Proposed treatment of the Vaccine is to slow or stop PD

A

Parkinson’s Vaccine - PD01A

293
Q

What is the prognosis of PD:

A

Chronic, progressive disorder

Not fatal, but it will shorten life expectancy significantly

294
Q

Progressive loss of intellectual function to the point where it interferes with work, relationships and personal hygiene

A

Alzheimer’s Disease (AD)

295
Q

Accounts for over 50% of all cases of Dementia. _______________

A

Alzheimer’s Disease (AD)

296
Q

What age does Alzheimer’s Disease affect?

A

Older people greater than 65 years of age

*Occurs in 25% of people older than 85 years of age

297
Q

Effects approximately _____-______ million Americans

A

4.5 – 5.4

298
Q

Which gender does Alzheimer’s Disease affect primarily?

A

WOMEN

299
Q

What is the pathophysiology of AD?

A

Characterized by atrophy of the Cortical parts of the Frontal and Temporal parts of the Brain

300
Q

What are the microscopic Features of AD?

A

Widening of the Sulci and slender Gyri

Atrophy leads to dilated Ventricles

301
Q

Neurochemical Features of Alzheimer’s would be:

A

A decrease in the level of Choline Acetyltransferase activity in the Cerebral Cortex and the Hippocampus

302
Q

Enzyme required for the synthesis of Acetylcholine, a Neurotransmitter which is associated with Memory

A

Choline Acetyltransferase

303
Q

Are abnormal proteins that are produced by the same Neurons that produce Acetylcholine
Neurotransmitter for Short Term Memory

A

Beta Amyloid Proteins

304
Q

Resistant to chemical or enzymatic breakdown and thus are persistent and remain long after the Neurons die

A

Neurofibrillary Tangles

305
Q

Microscopic exam of the areas of degeneration reveal Plaquelike material

A

Neuritic (Senile) Plaques

306
Q

Senile Dementia is onset _________

A

After 65

307
Q

Etiology: Genetic Factors of AD

A

Early-Onset / Pre-senile

Develops between ages 30 – 60 years

308
Q

Presenilin-1 (PS1) Gene on Chromosome #____

A

14

309
Q

Presenilin-2 (PS2) on Chromosome #_____

A

1

310
Q

AD is inherited as _____________

A

An Autosomal Dominant

311
Q

Amyloid Precursor Protein (APP) Gene) on Chromosome #___

A

21

312
Q

One form of Late-Onset is associated with a mutation on Chromosome #___

A

19

313
Q

Signs and Symptoms: First Stage

A

May last 2 – 4 years
Involves Short Term Memory Loss
Initially the symptoms are insidious
Patient is unaware of the onset of the disease and often attributed to forgetfulness
Individual will become progressively more forget-full, particularly in relationship to recent events

314
Q

Signs and Symptoms: Second (Confusional) Stage

A

May last several years
Long Term Memory Loss occurs as the disease progresses
Marked by impairment of cognitive functioning
Person becomes disorientated and confused

315
Q

Signs and Symptoms: Second (Confusional) Stage (continued)

A

Ability to concentrate declines
Lose ability to problem solve or perform mathematical calculations
Judgment gradually deteriorates
Language Impairment
Difficulty in remembering or retrieving words
Managing activities of daily living becomes a challenge
Mental Status
Depression occurs when a person is aware of their deficits
Irritability
Agitation and hostility
Prone to mood swings

316
Q

Signs and Symptoms: Terminal Stage

A

Lasts 1 – 2 years, although in some patients it has persisted for up to 10 years
Person becomes incontinent and unable to recognize family or friends
Usually institutionalized at this point

317
Q

Diagnostic Tests for AD are:

A

History& Physical
CT Scan or MRI
Autopsy

318
Q

Treatment for AD:

A

No specific treatment and to date no Cure has been identified
Medications

319
Q

What is the prognosis of AD:

A

Survival ranges up to 20 Years, with an average of 7 years

320
Q

Treatment Modalities for Type 2 diabetes include:

A

Adequate diet specific to the patients needs, Insulin therapy (eventually), Exercise, Liver transplant, Oral hypoglycemic drugs (when diet and exercise are INadequate), glucophage (which lowers insulin resistance), and Avandia (which raises the tissues sensitivity to insulin).

321
Q

Which of the following conditions is caused by long-term exposure to high levels of cortisol?

A

Crushing’s Disease

322
Q

A fasting blood glucose test level of _________________ indicates diabetes

A

126 mg/dl or higher on two separate tests

323
Q

Early-Onset / Pre-senile of Alzheimer’s develops in what age?

A

30-60

324
Q

Neurotransmitter for Short Term Memory

A

Beta Amyloid Proteins

325
Q

What are the signs of Addison’s Disease

A

Fatigue
Weight Loss
Hypotenstion
Hyperpigmentation

Pathophysiology (7 decks)

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