Diabetes Flashcards

0
Q

Glucagon

A
  1. Synthesized in the Liver**
  2. Breaks down fats and muscles / not simple carbs
  3. Helps maintain steady blood glucose when you have used all simple carbohydrates
    - GLUCAGON IS FOR WHEN GLUCOSE IS GONE
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1
Q

Risk Factors after Liver Biopsy

A
  1. Assess the lungs for: ** PRIORITIZE THE LUNG COLLAPSE
    - NOTHING - collapsed lung - silent lung
  2. Bleeding
    - Clotting factors come from the liver so check for bleeding if there are liver issues
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2
Q

Diabetes Type 1

A
  1. Juvenile-onset diabetes
  2. Results from autoimmune process that destroys beta cells of the pancreas
  3. Leads to loss of insulin production
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3
Q

Diabetes Type II

-Pathophysiology

A
  1. Adult-onset diabetes

2. Insulin Resistance

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4
Q

Diabetes Type II

-Risk factors

A
  1. Age
  2. Obesity
  3. Family Hx
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5
Q

Diabetes Type II

-Process

A
  1. Increases insulin secretion to compensate for peripheral tissue resistance until system fails
  2. If pancreas “burns out” then the type II diabetic will need insulin replacement just like a Type I diabetic
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6
Q

Diabetes

-Definition

A
  1. Starvation in the midst of plenty
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7
Q

Hyperglycemia

-S/S

A
  1. Weight loss
  2. Polyphagia (excessive appetite)
  3. Elevated blood glucose
  4. Increase infections
  5. Polydypsia
  6. Polyuria
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8
Q

Normal Fasting Plasma Glucose

A
  1. < 126 mg/dL
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9
Q

Normal Random plasma Glucose

A
  1. <200 mg/dL
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10
Q

Normal 2 hr Post-Glucose Tolerance test

A
  1. Plasma glucose < 200 mg/dL
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11
Q

HBA1C

A
  1. Refers to the permanent attachment of glucose to hbg molecules and reflects the average plasma glucose exposure over the LIVE OF THE RBC
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12
Q

Process of Inulin Production

A
  1. Islets of langerhan (Beta cells) in the pancreas produce insulin in response to blood glucose levels.
    - Insulin is the bus that drives glucose into the cell
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13
Q

Type 1 Diabetes

-Pathologic process

A
  1. Autoimmune disease that causes immune system to attack beta cells in the pancreas.
    - Pt then loses insulin production capabilities
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14
Q

Type 2 Diabetes

-Pathologic process

A
  1. Insulin resistance
  2. Beta cells and islets of langerhans are capable of producing insulin
  3. Cells that are receiving the insulin are resistant
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15
Q

Type 2 Diabetes

-What happens over time

A
  1. Blood glucose increases because insulin cannot move it into the cell.
  2. The pancreas then goes into overdrive and produces large amounts of insulin
  3. After years, the pancreas and beta cells cannot compensate and insulin levels drop. Blood glucose levels then go well above normal
16
Q

Type 1 Diabetes Complications

-Diabetic Ketoacidosis (DKA) Causes

A
  1. Caused by increase glucose demand from a stressor (infection)
    or
  2. Pt stops taking insulin administration
17
Q

Type 1 Diabetes Complications

-Diabetic Ketoacidosis (DKA) Manifestations

A
  1. Blood Glucose becomes VERY high
  2. Cells shift to using proteins and lipids for energy because there is not enough insulin moving glucose into the cell
  3. Breakdown of proteins and lipids causes Kitone bodies
18
Q

Insulin

-Na/K pump

A
  1. Insulin is the regular of the sodium/potassium pump. If insulin is not present there is hypokalemia inside of the cell.
  2. When insulin is restored, the serum potassium can drop very quickly to compensate for the intercellular hypokalemia
19
Q

Diabetes

-Long-term Effects

A
  1. Due to hyperglycemia in the cell which causes damage to the endothelial and atherosclerosis
20
Q

Glycolysis

A
  1. = ATP

2. Storage as: Glycogen (glycogenesis), fat and protein

21
Q

Hyperglycemia

-S/S

A
  1. Weight loss
  2. Polyphagia (excessive appetite)
  3. Elevated Blood glucose
  4. Increased infections
  5. Polydypsia
  6. Polyuria
22
Q

Hyperglycemia

-Diagnostics

A
  1. Fasting plasma glucose greater than 126 mg/dL
  2. Random plasma glucose greater than 200 mg/dL
    - w/ polyuria & polydipsia
  3. 2 hour post glucose tolerance test with BG level greater than 200mg/dL
23
Q

Hyperglycemic Treatment

-For High Blood Sugar?

A
  1. Reduce pt’s sugar intake

2. Metformin (decreases hepatic gluconeogenesis

24
Q

Hyperglycemic Treatment

-For increasing Insulin Secretion

A
  1. Sulfonylyreas (glypizyde)
25
Q

Hyperglycemic Treatment

-For decreasing insulin Resistance

A
  1. Thiazolidinediones

- Ex. Actos or avandia

26
Q

Hypoglycemia

-Adrenergic S/S

A
  1. Diaphoresis
  2. Weakness
  3. Hunger
  4. Headache
  5. Anxiety
27
Q

Hypoglycemia

-Neuroglucopenic S/S

A
  1. Confusion
  2. Slurred speech
  3. Coma & Seizure
28
Q

Hypoglycemia

-Causes

A
  1. Excess insulin due to excessive diabetes treatment
  2. Decreased glucagon
  3. Decreased cortisol (adrenal insufficiency)
  4. Decreased Growth Hormone
  5. Liver failure of glycogen storage disease
29
Q

Somogyi Effect

A
  1. Combination of hypoglycemia followed by rebound hyperglycemia
30
Q

Dawn Phenomenon

A
  1. Early morning rise in blood glucose concentration w/ no hypoglycemia during the night
31
Q

Diabetic Retinopathy

A
  1. Leading cause of blindness worldwide and in adults less than 60 years of age in the US
  2. Seems to develop more rapidly in individuals with type 2 diabetes
32
Q

Diabetic Nephropathy

A
  1. Most common cause of end-stage kidney disease

2. 1st manifestation of kidney dysfunction is microalbuminuria

33
Q

Diabetic Neuropathy

A
  1. Most common cause of neuropathy in western world
    &
  2. Most common complication of diabetes