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Patho - Exam 3 > Glucose > Flashcards

Glucose Flashcards

(75 cards)

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1
Q

Pancreatic acini

A

Secretes digestive juices from the pancreas into the dudodenum

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2
Q

Islet of Langerhans

A

Responsible for secreting hormones that affect blood sugar levels

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3
Q

Alpha cells

A

Secrete glucagon

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4
Q

Beta cells

A

Secrete insulin

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5
Q

Delta cells

A

Secrete somatostatin

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6
Q

Somatostatin

A

Inhibit release of insulin and glucagon and decreases release of pituitary gland hormones

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7
Q

What slows down GI activity after ingesting food?

A

Somatostatin

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8
Q

What is required by the cells for the uptake of glucose?

A

Insulin

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9
Q

Functions of Inuslin

A
  • -Binds to receptors to trigger series of events that transport glucose into the cell
  • Promotes protein synthesis and formation
  • Lipid storage
  • Facilitates transport of potassium, phosphate, and magnesium into the cells
  • Increases glycogen synthesis, decreases gluconeogenesis
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10
Q

Function of Glucagon

A

Promotes glycogen breakdown
Increases gluconeogenesis
(Increases blood sugar)

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11
Q

When is Glucagon secreted?

A

Between meals when there is no take (b/c blood sugar is getting lower) to prevent hypoglycemic state

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12
Q

Insulin secretion increases when there is an increase in…

A

Blood glucose, amino acids, glucagon, gastrin

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13
Q

Insulin secretion decreases when there is…

A

Low blood glucose, high insulin levels

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14
Q

Insulin works on positive or negative feedback?

A

Negative

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15
Q

Catecholamines

A

Help maintain blood glucose levels during periods of stress

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16
Q

Two types of catecholamines

A

Epinephrine and norepinephrine

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17
Q

Growth Hormone

A

Increases protein synthesis in all cells of the body, mobilizes fatty acids from adipose tissue, and antagonizes effects of insulin

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18
Q

Glucocorticoids

A

Stimulate gluconeogenesis by the liver

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19
Q

DM

A

Inability to regulate glucose leading to the inadequate metabolism of macronutrients

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20
Q

How much insulin is there in Type 1?

A

None

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21
Q

How does Type 1 occur?

A

Usually occurs due to cell-mediated immunodestruction of beta cells in the pancreas (manifests after 90% of beta cells are destroyed)

Type IV hypersensitivity reaction

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22
Q

Type 1a

A

Immune mediated DM

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23
Q

Type 1b

A

Idiopahic diabetes (no evidence of autoimmune destruction of beta cells)

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24
Q

Type 1 leads to (2)

A

Hyperglycemia and Hyperketonemia

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25
Type 1 Clinical Manifestations
``` 3 P's Hyperglycemia symptoms (weight loss, fatigue, blurred vision, paresthesia, dry skin, skin infections, slow wound healing) ```
26
Diagnostic Criteria for Type 1
``` History and physical exam Blood glucose levels (fasting, random) Oral glucose test Glycosylated Hemoglobin (HbA1c) Insulin levels Positive urine microalbumin ```
27
Treatment for Type 1
Insulin replacement therapy Count CHO intake with insulin Exercise
28
How is insulin in Type 2?
Insulin resistance leads to a reduction in adequate insulin secretion
29
What is the greatest risk factor for type 2?
Obesity
30
Which type is the most common type in those with diabetes?
Type 2
31
How does reduced insulin secretion occur?
Insulin resistance --> beta cell atrophy due to consistently high levels --> reduction in adequate insulin secretion
32
Clinical Manifestations of type 2
-Often asymptomatic and vague in comparison to type 1 -BUT chronic damage can occur throughout the body Neuropathy (damage of nerves) Recurrent infections Coronary artery disease PVD Diabetic retinopathy (visual changes) Nephropathy (kidneys) Fatigue
33
Diagnostic criteria of Type 2
History and physical exam Blood glucose level Test for presence of long-term complications (eye exam, heart and kidney function, sensation)
34
What diagnostic criteria differentiates type 1 and type 2?
Insulin level
35
What is the first and main treatment of type 2?
Weight control through diet and exercise
36
How does exercise influence insulin?
Exercise increases insulin sensitivity of cells
37
Treatment for type 2
Weight control | Oral glycemic agents
38
What is the goal in type 2 treatment?
maintain optimal blood glucose levels
39
Normal range of glucose
70-100
40
Normal HbA1c range
6.5-7%
41
Prediabetes
Impaired fasting plasma glucose or impaired glucose tolerance
42
Hemoglobin A1C Normal - Prediabetes - DM
Normal - about 5% Pre - 5.7-6.4 DM - 6.5 or greater
43
Fasting plasma glucose Normal - Prediabetes - DM
Normal - 99 mg/dL or lower Pre - 100-125 mg/dL DM - 126 or greater
44
Oral Glucose Tolerance test Normal - Prediabetes - DM
Normal - 139 or lower Pre - 140-199 DM - 200 or greater
45
Acute complications
Hypoglcemia Hyperglycemia (DKA, HHS) Somogyi effect Dawn phenomenon
46
Hypoglycemia - level at which clinical manifestation starts
45-60 mg/dL
47
Causes of Hypoglycemia
Overproduction/overadministration of insulin Excessive exercise Infection (body requires more blood sugar) Inadequate food intake Several anti-hyperglycemic meds for type 2
48
Clinical manifestations of Hypoglycemia
``` Pallor Flushing Diaphoresis Tremor Tachycardia Palpitations Blurred vision Headache, confusion, poor judgment, anxiety, irritability ```
49
Complications of Hypoglycemia
Seizures, coma, death
50
Treatment for Hypoglycemia
IV Glucose Orange juice, candy at first, then carbs (more substantial)
51
Two types of hyperglycemia
DKA and HHS
52
DKA occurs in which type?
Type 1
53
HHS occurs in which type?
Type 2
54
Blood sugar level in DKA
Greater than 250 mg/dL
55
Patho of DKA
No insulin, thus breakdown of fat and ketogenesis, leads to ketoacidosis
56
Clinical manifestations of DKA
- Kussmaul's respiration (rapid, deep breathing, compensation for acidosis) - Fruity breath (acetone in body blown off with breath) - Tachycardia to compensate for low BP - Altered level of consciousness - Nausea, vomiting, abdominal pain - Polyuria - Dehydration
57
Treatment of DKA
Insulin ! Check potassium to avoid hypokalemia Manage acidosis (administer bicarbonate) May not need a lot of fluids because blood sugar is not as high like in HHS
58
Clinical manifestations of HHS
``` Severe hyperglycemia Low blood volume secondary to severe dehydration -CNS manifestations -Dry, warm skin -Dry rough oral mucosa -Decreased BP -Tachycardia -Decreased O2 and glucose to the brain leads to lethargy, weakness, confusion Increased plasma osmolarity ```
59
Is there ketoacidosis in HHS?
No ketoacidosis
60
Treatment for HHS
Fluid resuscitation to maintain blood volume | Potentially insulin
61
Somogyi effect
Rebound hyperglycemia as a result of insulin-induced hypoglycemia
62
In Somogyi, when does hypoglycemia occur?
During the night
63
In Somogyi, do you wake up with hypo or hyperglycemia? Why?
Rebound hyperglycemia because the body tries to compensate for the hypoglycemia at night by releasing catecholamines, glucagon, cortisol, and growth hormone
64
What is a common mistake patients make to fix somogyi?
Over-administration of evening insulin - people think they need to administer more insulin before sleep to prevent hyperglycemia in the morning -But actually they are exacerbating the situation
65
Treatment for Somogyi Effect
Decrease bedtime insulin | Oral glycemics
66
Dawn Phenomenon
Hormone release leads to steady rise of blood glucose throughout the night
67
With Dawn do you wake up with hypo or hyperglycemia? Why?
Hyperglycemia due to early AM release of hormones
68
Treatment for Dawn Phenomenon
Limit evening snacks, increase evening inuslin
69
How do you distinguish between Dawn and Somogyi
Check blood glucose in the middle of the night for hypoglycemic state
70
Between Dawn and Somogyi, which one experiences hypoglycemia?
Somogyi
71
What are the chronic macrovascular complications of DM (typically type 2)?
Coronary artery disease Stroke PVD
72
Characteristics of macrovascular complications
Damage to blood vessels, plaque buildup (atherosclerosis), poor blood flow
73
What are the microvascular complications of DM?
Diabetic retinopathy | Diabetic nephropathy
74
Other chronic complications
``` Diabetic neuropathies Slow wound healing Reduced response Increased risk of infection (UTI, Candida, yeast infection) Dental caries, gingivitis, periodontitis Cataracts ```
75
Pregnancy complications in DM
- Blood sugar can damage vasculature of placenta - Increased incidence of spontaneous abortions - Infants increase size and weight for date, may experience rebound hypoglycemia in first hours postnatal

Patho - Exam 3 (4 decks)

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