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Patho - Exam 3 > Glucose > Flashcards

Glucose Flashcards

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
Q

Type 1 Clinical Manifestations

A 
3 P's
Hyperglycemia symptoms (weight loss, fatigue, blurred vision, paresthesia, dry skin, skin infections, slow wound healing)
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26
Q

Diagnostic Criteria for Type 1

A 
History and physical exam 
Blood glucose levels (fasting, random)
Oral glucose test 
Glycosylated Hemoglobin (HbA1c)
Insulin levels
Positive urine microalbumin
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27
Q

Treatment for Type 1

A

Insulin replacement therapy
Count CHO intake with insulin
Exercise

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28
Q

How is insulin in Type 2?

A

Insulin resistance leads to a reduction in adequate insulin secretion

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29
Q

What is the greatest risk factor for type 2?

A

Obesity

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30
Q

Which type is the most common type in those with diabetes?

A

Type 2

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31
Q

How does reduced insulin secretion occur?

A

Insulin resistance –> beta cell atrophy due to consistently high levels –> reduction in adequate insulin secretion

32
Q

Clinical Manifestations of type 2

A

-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
Q

Diagnostic criteria of Type 2

A

History and physical exam
Blood glucose level
Test for presence of long-term complications (eye exam, heart and kidney function, sensation)

34
Q

What diagnostic criteria differentiates type 1 and type 2?

A

Insulin level

35
Q

What is the first and main treatment of type 2?

A

Weight control through diet and exercise

36
Q

How does exercise influence insulin?

A

Exercise increases insulin sensitivity of cells

37
Q

Treatment for type 2

A

Weight control

Oral glycemic agents

38
Q

What is the goal in type 2 treatment?

A

maintain optimal blood glucose levels

39
Q

Normal range of glucose

A

70-100

40
Q

Normal HbA1c range

A

6.5-7%

41
Q

Prediabetes

A

Impaired fasting plasma glucose or impaired glucose tolerance

42
Q

Hemoglobin A1C
Normal -
Prediabetes -
DM

A

Normal - about 5%
Pre - 5.7-6.4
DM - 6.5 or greater

43
Q

Fasting plasma glucose
Normal -
Prediabetes -
DM

A

Normal - 99 mg/dL or lower
Pre - 100-125 mg/dL
DM - 126 or greater

44
Q

Oral Glucose Tolerance test
Normal -
Prediabetes -
DM

A

Normal - 139 or lower
Pre - 140-199
DM - 200 or greater

45
Q

Acute complications

A

Hypoglcemia
Hyperglycemia (DKA, HHS)
Somogyi effect
Dawn phenomenon

46
Q

Hypoglycemia - level at which clinical manifestation starts

A

45-60 mg/dL

47
Q

Causes of Hypoglycemia

A

Overproduction/overadministration of insulin
Excessive exercise
Infection (body requires more blood sugar)
Inadequate food intake
Several anti-hyperglycemic meds for type 2

48
Q

Clinical manifestations of Hypoglycemia

A 
Pallor
Flushing 
Diaphoresis 
Tremor
Tachycardia
Palpitations 
Blurred vision 
Headache, confusion, poor judgment, anxiety, irritability
49
Q

Complications of Hypoglycemia

A

Seizures, coma, death

50
Q

Treatment for Hypoglycemia

A

IV
Glucose
Orange juice, candy at first, then carbs (more substantial)

51
Q

Two types of hyperglycemia

A

DKA and HHS

52
Q

DKA occurs in which type?

A

Type 1

53
Q

HHS occurs in which type?

A

Type 2

54
Q

Blood sugar level in DKA

A

Greater than 250 mg/dL

55
Q

Patho of DKA

A

No insulin, thus breakdown of fat and ketogenesis, leads to ketoacidosis

56
Q

Clinical manifestations of DKA

A
  • 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
Q

Treatment of DKA

A

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
Q

Clinical manifestations of HHS

A 
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
Q

Is there ketoacidosis in HHS?

A

No ketoacidosis

60
Q

Treatment for HHS

A

Fluid resuscitation to maintain blood volume

Potentially insulin

61
Q

Somogyi effect

A

Rebound hyperglycemia as a result of insulin-induced hypoglycemia

62
Q

In Somogyi, when does hypoglycemia occur?

A

During the night

63
Q

In Somogyi, do you wake up with hypo or hyperglycemia? Why?

A

Rebound hyperglycemia because the body tries to compensate for the hypoglycemia at night by releasing catecholamines, glucagon, cortisol, and growth hormone

64
Q

What is a common mistake patients make to fix somogyi?

A

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
Q

Treatment for Somogyi Effect

A

Decrease bedtime insulin

Oral glycemics

66
Q

Dawn Phenomenon

A

Hormone release leads to steady rise of blood glucose throughout the night

67
Q

With Dawn do you wake up with hypo or hyperglycemia? Why?

A

Hyperglycemia due to early AM release of hormones

68
Q

Treatment for Dawn Phenomenon

A

Limit evening snacks, increase evening inuslin

69
Q

How do you distinguish between Dawn and Somogyi

A

Check blood glucose in the middle of the night for hypoglycemic state

70
Q

Between Dawn and Somogyi, which one experiences hypoglycemia?

A

Somogyi

71
Q

What are the chronic macrovascular complications of DM (typically type 2)?

A

Coronary artery disease
Stroke
PVD

72
Q

Characteristics of macrovascular complications

A

Damage to blood vessels, plaque buildup (atherosclerosis), poor blood flow

73
Q

What are the microvascular complications of DM?

A

Diabetic retinopathy

Diabetic nephropathy

74
Q

Other chronic complications

A 
Diabetic neuropathies 
Slow wound healing
Reduced response 
Increased risk of infection (UTI, Candida, yeast infection)
Dental caries, gingivitis, periodontitis
Cataracts
75
Q

Pregnancy complications in DM

A
  • 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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