Diabetes Patho (Exam 2) Flashcards

1
Q

Diabetes

A

-An epidemic in the united states.

-Over 30 million people. 10% of the populations

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2
Q

What is Diabetes?

A

-A metabolic disorder characterized by HYPERGLYCEMIA that results from defects in insulin secretion, insulin action or both

-It is associated with extensive long term damage when uncontrolled to multiple organ systems

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3
Q

Carbohydrates

A

-Simple sugars and complex chemical units

-Are broken down in the duodenum and proximal jejunum

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4
Q

Carbohydrates in a healthy person

A

-Temporarily spikes glucose then lowers back down to baseline

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5
Q

Diabetes: Liver

A

-Regulating glucose depends on the LIVER.

-Extracts glucose (from the blood)

-Synthesizes it into glycogen (energy storage)

-Glycogenolysis (breakdwon glycogen)

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6
Q

How does the liver help our peripheral tissues?

A

The liver helps out peripheral tissues by extracting glucose from the blood, synthesizes the glucose into glycogen, then breaking down the glycogen for energy (glycogenolysis)

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7
Q

Diabetes: The pancreas

A

-In connection with the liver it controls the body’s fuel supply (glucose/insulin)

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8
Q

2 major functions of the pancrease

A

-Exocrine

-Endocrine

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9
Q

Exocrine functions of the Pancreas

A

-Pancreatic cells secrete directly into ducts (not blood stream) (Digestive enzymes directly into the duct)

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10
Q

Endocrine function of the Pancreas

A

-Cells secrete Insulin directly into blood stream

-What we are focusing on

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11
Q

Pancreas: Islet of Langerhans

A

-Islets are small islands of cell within the pancreases that make up the endocrine function

-Islets of langerhans has both alpha and beta cells

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12
Q

Alpha Cells

A

-Island of Langerhans

-Secrete glucagon in response to low blood sugar

-Glucagon thus stimulates the liver to release stored glucose into the blood

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13
Q

Beta cells

A

-Islet of Langerhans

-Produce insulin, which lowers glucose levels by stimulating the movement of glucose into body tissues

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14
Q

Insulin does what to blood glucose

A

LOWER

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15
Q

Hormones that raise blood glucose levels

A

-Glucagon (Islet)

-Epinephrine (Andrenal Medulla)

-Glucocorticoids (Adrenal cortex)

-Growth hormone (anterior pituitary)

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16
Q

Balancing Act of Hormones

A
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17
Q

Insulin

A

-Beta Cells in the pancreas

-Stimulates uptake, utilization, and storage of glucose

-Stimulates the liver to store glucose (as glycogen)

-Because of the stimulating effects above- insulin decreases plasma concentrations of glucose

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18
Q

Insulin and Lipid Metabolism

A

-Insulin promotes synthesis of fatty acids in the liver. (This occurs once the liver has been saturated with glycogen)

-Insulin inhibits the breakdown of fat in adipose tissue (Can cause a buildup of triglycerides in fat cells)

-On the whole, Insulin has a fat-sparing effect, and drives cells to use carbohydrates instead of fat or energy

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19
Q

What happens when you dont have enough insulin

A

-Cannot breakdown carbohydrate efficiently

-Decreased glucose use by cells

-Rapid build up of glucose in blood = HYPERGLYCEMIA

-Cells have to use alternate sources of energy = fatty acids

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20
Q

What happens when you gont have enough insulin pt.2

A

-Impaired fat metabolism also occurs. (increased lipolysis) (Decrease lipogenesis)

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21
Q

Impaired Fat Metabolism from not having enough insulin causes

A

-Free fatty acids in your blood

-FFA are an alternate energy source for tissues

-Excess FFA is converted to cholesterol and phospholipids

-FFA breaks down to acetyl-CoA (Used by liver or to acetoacetic acid)

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22
Q

Ketone Bodies

A

Occurs when FFA from impaired fat metabolism breaks down into acetyl-CoA…Ketone bodies are created

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23
Q

Complication of Impaired Fat Metabolism: Short term

A

-These increase in serum ketones can cause Ketosis

-Ketosis can cause severe metabolic acidosis—-COMA

-Ketones measured by blood and urine levels

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24
Q

Complications of impaired fat metabolism: Long term

A

-Atherosclerosis because of high serum lipid levels

25
Insulin Deficiency: Protein Metabolsim
-Body is unable to store protein effectively -Increased protein catabolism -Cessation of protein synthesis
26
What does protein metabolism cause?
-Increased protein breakdown---- more amino acids in circulation -Increase use of amino acids as alternative energy source -Protein catabolism = muscle wasting (muscle breaking down)
27
Protein Catabolism: Clinical Picture
-Muscle wasting -Multiple organ dysfunction -Aminoacidemia -Increased urea nitrogen (BUN) (more typically in type 1)
28
Insulin deficit and fluid/electrolyte
1. Increased serum glucose levels 2. Increased plasma oncotic pressure 3. Fluid shifts into intravascular compartment 4. Intracellular dehydration osmotic diuresis
29
Insulin deficit and glycosuria
-Excretion of sugar in the urine -Occurs when hyperglycemia increases beyond what kidneys can reabsorb -Increased acetones in urine
30
3 P's of Insulin Deficencies
Polyphagia - increase hunger (catabolism of fat and protein and cellular starvation) Polydipsia - increase in thirst (Increased serum osmolarity) Polyuria -Increase urination (Osmotic diuresis) (Excreting water) (Loss of electrolyte)
31
Diabetes Mellitus
-Group of metabolic disorders characterized by HYPERGLYCEMIA, resulting from ABSOLUTE or RELATIVE insulin deficiency
32
3 Main types of Diabetes Mellitus
-Type 1 -Type 2 -Gestational
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Blood Glucose Chart
Know Values in screen shot
34
A1C levels
Diabetes: 6.5 or above Pre Diabetes: 5.7 to 6.4 Normal: About 5
35
Fasting Plasma Glucose
Diabetes: 125 or above Pre Diabetes: 100 to 125 Normal: 99 or below
36
Oral Glucose Tolerance Test
Diabetes: 200 or above Pre Diabetes: 140 to 190 Normal: 139 or below
37
Type 1 Diabetes
-Most common pediatric chronic disease -Usually diagnosed around 12 years of age -Can be idiopathic (much less common)
38
Type 1 Diabetes: Autoimmune process
-Genetic predisposition and environmental factors -Slowly progressive disease -T-cell mediated disease that DESTROYS BETA CELLS
39
Type 1 Diabetes =
Complete lack of ENDOGENOUS INSULIN -5-10% of all diabetes cases in the US Insulin dependent diabets (IDDM) Juvenile onset diabetes
40
Type 1 Diabetes: Clinical Manifestations
-Diagnosed around 11-13 years old -Long clinical period of symptoms until the production of insulin goes to almost none. (Results in hyperglycemia and produces symptoms)
41
Type 2 Diabetes
-Genetic-environmental aspect usually responsible -It is INSULIN RESISTANCE and some decreased insulin secretion. (Sub optimal response of insulin sensitive tissues.) (Usually associated with long-term obesity)
42
Type 2 Diabetes Risk Factors
-Age -Obesity -Hypertension -Physical inactivity -Family History
43
Type 2 Diabetes: Clinical Manifestations
-S/S not as evident -Usually vague/non-specfic manifestations of hyperglycemia -Doctors usually test for those at high risk---overweigh, dyslipidemic, hypertensive
44
S/S of Type 2 diabetes
-Usually just vague/non-specific manifestations of hyperglycemia Fatigue Recurrent infections Visual changes Prolonged wound healing
45
Metabolic Complications with TYPE 2 DM
-Impaired insulin secretion---B-cell exhaustion due to overuse -Peripheral insulin resistance -----Increased visceral fat -Increased hepatic glucose production ------ impaired suppression of gluconeogensis within the liver -Altered production of hormones and cytokines by adipose tissue
46
Diabetic Ketoacidosis (DKA)
-More common in type 1 diabetics -Serious complications related to insulin deficiency -Characterized by hyperglycemia, acidosis, and ketonuria
47
Hyperosmolar Hyperglycemic Syndrome (HHNS)
-Type 2 complications -Extremely high hyperglycemia and osmolality, normal pH -Less profound insulin deficiency than DKA but more significant fluid deficiency -Body starts to shut down
48
Hypoglycemia
-Happens in both type of diabetes -Rapid onset -Blood sugar less than 55-60 -Usually related to medications
49
Hypoglycemia S/S
-Pallor -Sweating -Tachy -Palp -Hunger -Restlesness -Anx -Tremors -Convulsion -Coma (Kinda feel like you are dying)
50
Chronic Complications of Diabetes
-Typically associated with poorly controlled diabetes -Insulin resistance/defedcity, chronic hyperglycemia, accumulation of advanced glycation end products, activations of metabolic pathways that cause tissue damage
51
Chronic Complication: Microvascular
Damage to capillaries, retinopathies, nephropatheis, and neuropathies
52
Chronic Complications: Macrovascular
Damage to large vessels, coronary artery, peripheral vascular and cerebral vascular
53
Microvascular Disease
-Frequency and severity of lesions appear to be proportional to duration of the disease -Hypoxia and Ischemia accompany microvascular disease usually in the yes, kidneys, and nerves -Associated with capillary membrane thickening
54
Microangiopathy
Small vessel disease Thickening of the capillary membrane in microvascular disease
55
Diabetic Neuropathy
-Most common complication of diabetes -Related to both metabolic and vascular factors associated with chronic hyperglycemia -Ischemia and demyelination -Loss of pain, temperature and vibration sensations -Can lead to ulcers, infections and result in amputation
56
Diabetic Retinopathy
-Leading Cause of blindness worldwide -Results from relative hypoxemia damage to retinal blood vessels, red blood cell aggregation and hypertension -Small vessels become occluded, causes infarction
57
Diabetic Nephropathy
-Most common cause chronic kidney disease and end stage kidney disease -50% of individuals with diabetes develop diabetic kidney disease -Glomerular basement membrane thicken and becomes sclerosed-thickened and hard, nonfucntional
58
Macrovascular Complications
-More common in type 2 diabetics -Atherosclerosis--thickening, hardening of large arteries: Related CAD, PVD, CVA, Increase infection
59
Diabetes and Infections
-Deadly complication -Diminished warning signs (Neuropathies) -Tissue hypoxia (When skin becomes impaired, healthy cells cannot get there to heal it -Rapid Proliferation of pathogens (Excess serum glucose, which bacteria feed on.) (Decreased circulation of good WBC's) -Fungal, Yeast, UTI, Gangrene