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NUR 325 PATHO > Diabetes Patho (Exam 2) > Flashcards

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
Q

Insulin Deficiency: Protein Metabolsim

A

-Body is unable to store protein effectively

-Increased protein catabolism

-Cessation of protein synthesis

26
Q

What does protein metabolism cause?

A

-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
Q

Protein Catabolism: Clinical Picture

A

-Muscle wasting

-Multiple organ dysfunction

-Aminoacidemia

-Increased urea nitrogen (BUN)

(more typically in type 1)

28
Q

Insulin deficit and fluid/electrolyte

A
  1. Increased serum glucose levels
  2. Increased plasma oncotic pressure
  3. Fluid shifts into intravascular compartment
  4. Intracellular dehydration

osmotic diuresis

29
Q

Insulin deficit and glycosuria

A

-Excretion of sugar in the urine

-Occurs when hyperglycemia increases beyond what kidneys can reabsorb

-Increased acetones in urine

30
Q

3 P’s of Insulin Deficencies

A

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
Q

Diabetes Mellitus

A

-Group of metabolic disorders characterized by HYPERGLYCEMIA, resulting from ABSOLUTE or RELATIVE insulin deficiency

32
Q

3 Main types of Diabetes Mellitus

A

-Type 1
-Type 2
-Gestational

33
Q

Blood Glucose Chart

A

Know Values in screen shot

34
Q

A1C levels

A

Diabetes: 6.5 or above

Pre Diabetes: 5.7 to 6.4

Normal: About 5

35
Q

Fasting Plasma Glucose

A

Diabetes: 125 or above

Pre Diabetes: 100 to 125

Normal: 99 or below

36
Q

Oral Glucose Tolerance Test

A

Diabetes: 200 or above

Pre Diabetes: 140 to 190

Normal: 139 or below

37
Q

Type 1 Diabetes

A

-Most common pediatric chronic disease

-Usually diagnosed around 12 years of age

-Can be idiopathic (much less common)

38
Q

Type 1 Diabetes: Autoimmune process

A

-Genetic predisposition and environmental factors

-Slowly progressive disease

-T-cell mediated disease that DESTROYS BETA CELLS

39
Q

Type 1 Diabetes =

A

Complete lack of ENDOGENOUS INSULIN

-5-10% of all diabetes cases in the US

Insulin dependent diabets (IDDM)

Juvenile onset diabetes

40
Q

Type 1 Diabetes: Clinical Manifestations

A

-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
Q

Type 2 Diabetes

A

-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
Q

Type 2 Diabetes Risk Factors

A

-Age
-Obesity
-Hypertension
-Physical inactivity
-Family History

43
Q

Type 2 Diabetes: Clinical Manifestations

A

-S/S not as evident

-Usually vague/non-specfic manifestations of hyperglycemia

-Doctors usually test for those at high risk—overweigh, dyslipidemic, hypertensive

44
Q

S/S of Type 2 diabetes

A

-Usually just vague/non-specific manifestations of hyperglycemia

Fatigue
Recurrent infections
Visual changes
Prolonged wound healing

45
Q

Metabolic Complications with TYPE 2 DM

A

-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
Q

Diabetic Ketoacidosis (DKA)

A

-More common in type 1 diabetics

-Serious complications related to insulin deficiency

-Characterized by hyperglycemia, acidosis, and ketonuria

47
Q

Hyperosmolar Hyperglycemic Syndrome (HHNS)

A

-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
Q

Hypoglycemia

A

-Happens in both type of diabetes

-Rapid onset

-Blood sugar less than 55-60

-Usually related to medications

49
Q

Hypoglycemia S/S

A

-Pallor
-Sweating
-Tachy
-Palp
-Hunger
-Restlesness
-Anx
-Tremors
-Convulsion
-Coma

(Kinda feel like you are dying)

50
Q

Chronic Complications of Diabetes

A

-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
Q

Chronic Complication: Microvascular

A

Damage to capillaries, retinopathies, nephropatheis, and neuropathies

52
Q

Chronic Complications: Macrovascular

A

Damage to large vessels, coronary artery, peripheral vascular and cerebral vascular

53
Q

Microvascular Disease

A

-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
Q

Microangiopathy

A

Small vessel disease

Thickening of the capillary membrane in microvascular disease

55
Q

Diabetic Neuropathy

A

-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
Q

Diabetic Retinopathy

A

-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
Q

Diabetic Nephropathy

A

-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
Q

Macrovascular Complications

A

-More common in type 2 diabetics

-Atherosclerosis–thickening, hardening of large arteries: Related CAD, PVD, CVA, Increase infection

59
Q

Diabetes and Infections

A

-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

NUR 325 PATHO (30 decks)

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