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NUR325 > Exam 2 - Diabetes Pathophysiology > Flashcards

Exam 2 - Diabetes Pathophysiology Flashcards

1
Q

diabetes

A

metabolic disorder characterized by hyperglycemia that results from defects in insulin secretion and/or insulin action

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2
Q

what does regulating glucose depend on

A
  • the liver
  • it extracts glucose
  • synthesizes it into glycogen (energy storage)
  • glycogenolysis (breakdown glycogen)
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3
Q

pancreas

A
  • in connection with the liver it controls the body’s fuel supply of glucose/insulin
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4
Q

endocrine function

A

cells secrete insulin directly into the blood stream

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5
Q

pancreatic islet

A
  • small islands of cells within the pancreas that make up the endocrine function
  • alpha cells
  • beta cells
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6
Q

alpha cells

A

secrete glucagon in response to low blood sugar

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7
Q

glucagon

A

stimulates the liver to release stored glucose in the blood

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8
Q

beta cells

A

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

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9
Q

hormones that raise blood glucose levels

A
  • glucagon
  • epinephrine
  • glucocorticoids
  • growth hormone
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10
Q

insulin

A
  • hormone secreted by the pancreas (beta cells)
  • stimulates uptake, utilization, and storage of glucose
  • stimulates the liver to store glucose
  • decreases plasma concentrations of glucose
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11
Q

insulin and lipid metabolism

A
  • insulin promotes synthesis of fatty acids in the liver
  • insulin inhibits the breakdown of fat in adipose tissue
  • insulin drives cells to use carbohydrates instead of fat for energy
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12
Q

what happens when you don’t have enough insulin

A
  • cannot breakdown carbohydrates efficiently
  • decreased glucose use by cells
  • hyperglycemia
  • cells have to use alternate sources of energy = fatty acids
  • impaired fat metabolism
  • increased lipolysis (fat breakdown)
  • decreased lipogenesis (formation of fat)
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13
Q

free fatty acids (FFA)

A
  • alternate energy source for tissues
  • excess is converted to cholesterol and phospholipids
  • breaks down to acetyl-CoA
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14
Q

ketone bodies

A

substance that are composed of these acid breakdown products

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15
Q

short term complications of impaired fat metabolism

A
  • increased serum ketones
  • ketosis
  • measured by blood and urine levels of ketones
  • ketosis can cause severe metabolic acidosis (coma)
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16
Q

long term complications of impaired fat metabolism

A

atherosclerosis because of high serum lipid levels

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17
Q

insulin deficiency and protein metabolism cause

A
  • body unable to store protein effectively
  • increased protein catabolism (muscle wasting)
  • cessation of protein synthesis
18
Q

protein catabolism

A
  • muscle wasting
  • multiple organ dysfunction
  • aminoacidemia
  • increased urea nitrogen (BUN)
    -more typical in type 1 diabetic
19
Q

insulin deficit and fluid/electrolytes

A
  • increased serum glucose levels
  • increased plasma oncotic pressure
  • fluid shifts into intravascular compartment
  • intracellular dehydration
20
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
  • essentially pee out glucose
21
Q

polyphagia

A
  • increased hunger
  • catabolism of fat and protein and cellular starvation
22
Q

polydipsia

A
  • excessive thirst
  • increased serum osmolality
23
Q

polyuria

A
  • excessive urination
  • osmotic diuresis
  • excreting water
  • loss of electrolytes
24
Q

A1C blood levels for diabetes

A
  • normal - about 5
  • pre diabetes - 5.7 to 6.4
  • diabetes - 6.5 or above
25
Q

fasting plasma glucose levels for diabetes

A
  • normal - 99 or below
  • pre diabetes - 100 to 125
  • diabetes - 126 or above
26
Q

type 1 diabetes

A
  • most common pediatric chronic disease
  • can be idiopathic
  • usually an autoimmune process
  • genetic predisposition and environmental factors
  • slow progressive disease
  • t-cell mediated disease that destroy beta cells
  • complete lack of ENDOGENOUS INSULIN
27
Q

type 1 diabetes - clinical manifestations

A
  • long pre-clinical period of symptoms until the production of insulin goes to almost none
  • results in hyperglycemia and produces symptoms
  • same diagnostic criteria as type 2
28
Q

type 2 diabetes

A
  • genetic-environmental aspect usually responsible
  • insulin RESISTANCE and some decreased insulin secretion
29
Q

type 2 diabetes - clinical manifestations

A
  • symptoms not as evident
  • usually just vague/non-specific manifestations of hyperglycemia
  • fatigue, recurrent infections, visual changes, prolonged wound healing
30
Q

type 2 diabetes - metabolic complications

A
  • impaired insulin secretion
  • peripheral insulin resistance
  • increased hepatic glucose production
  • altered production of hormones and cytokines by adipose tissue
31
Q

diabetic ketoacidosis (DKA)

A
  • more common in type 1 diabetics
  • serious complication related to insulin deficiency
  • characterized by hyperglycemia, acidosis, and ketonuria
32
Q

hyperosmolar hyperglycemic syndrome (HHNS)

A
  • type 2 complication
  • extremely high hyperglycemia and osmolality, normal pH
  • less profound insulin deficiency than DKA by more significant fluid deficiency
33
Q

hypoglycemia

A
  • happens in both types of diabetes
  • rapid onset
  • blood sugar less than 55-60
  • usually related to medications
34
Q

symptoms of hypoglycemia

A
  • pallor
  • sweating
  • tachycardia
  • palpitations
  • hunger
  • restlessness
  • anxiety
  • temors
  • convulsion
  • coma
35
Q

chronic microvascular complication

A
  • damage to capillaries, retinopathies, nephropathies, and neuropathies
36
Q

chronic macrovascular complication

A
  • damage to large vessels, coronary artery, peripheral vascular and cerebral vascular
37
Q

microvascular disease

A
  • frequency and severity of lesions appear to be proportional to duration of disease
  • hypoxia and ischemia accompany usually in the eyes, kidneys, and nerves
  • capillary membrane thickening
38
Q

diabetic neuropathy

A
  • most common complication of disease
  • related to both metabolic and vascular factors associated with chronic hyperglycemia
  • loss of pain, temperature, and vibration sensations
  • can lead to ulcers, infection, and result in amputation
39
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
40
Q

diabetic nephropathy

A
  • most common cause for chronic kidney disease and end stage kidney disease
  • 50% of individuals with diabetes develop diabetic kidney disease
  • glomerular basement membrane thickens and becomes sclerosed, nonfunctional
41
Q

macrovascular complications

A
  • atherosclerosis: thickening, hardening of large arteries
  • coronary artery disease, peripheral vascular disease, cerebrovascular accidents (stroke), increased risk of infection
42
Q

diabetes and infection

A
  • diminished warning signs
  • tissue hypoxia
  • rapid proliferation of pathogens
  • fungal/yeast/UTI/gangrene

NUR325 (8 decks)

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