Exam 2 - Diabetes Pathophysiology

Question 1

diabetes

Answer 1

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

Question 2

what does regulating glucose depend on

Answer 2

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

Question 3

pancreas

Answer 3

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

Question 4

endocrine function

Answer 4

cells secrete insulin directly into the blood stream

Question 5

pancreatic islet

Answer 5

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

Question 6

alpha cells

Answer 6

secrete glucagon in response to low blood sugar

Question 7

glucagon

Answer 7

stimulates the liver to release stored glucose in the blood

Question 8

beta cells

Answer 8

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

Question 9

hormones that raise blood glucose levels

Answer 9

• glucagon
• epinephrine
• glucocorticoids
• growth hormone

Question 10

insulin

Answer 10

• 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

Question 11

insulin and lipid metabolism

Answer 11

• 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

Question 12

what happens when you don’t have enough insulin

Answer 12

• 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)

Question 13

free fatty acids (FFA)

Answer 13

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

Question 14

ketone bodies

Answer 14

substance that are composed of these acid breakdown products

Question 15

short term complications of impaired fat metabolism

Answer 15

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

Question 16

long term complications of impaired fat metabolism

Answer 16

atherosclerosis because of high serum lipid levels

Question 17

insulin deficiency and protein metabolism cause

Answer 17

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

Question 18

protein catabolism

Answer 18

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

Question 19

insulin deficit and fluid/electrolytes

Answer 19

• increased serum glucose levels
• increased plasma oncotic pressure
• fluid shifts into intravascular compartment
• intracellular dehydration

Question 20

insulin deficit and glycosuria

Answer 20

• excretion of sugar in the urine
• occurs when hyperglycemia increases beyond what kidneys can reabsorb
• increased acetones in urine
• essentially pee out glucose

Question 21

polyphagia

Answer 21

• increased hunger
• catabolism of fat and protein and cellular starvation

Question 22

polydipsia

Answer 22

• excessive thirst
• increased serum osmolality

Question 23

polyuria

Answer 23

• excessive urination
• osmotic diuresis
• excreting water
• loss of electrolytes

Question 24

A1C blood levels for diabetes

Answer 24

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

Question 25

fasting plasma glucose levels for diabetes

Answer 25

- normal - 99 or below - pre diabetes - 100 to 125 - diabetes - 126 or above

Question 26

type 1 diabetes

Answer 26

- 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

Question 27

type 1 diabetes - clinical manifestations

Answer 27

- 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

Question 28

type 2 diabetes

Answer 28

- genetic-environmental aspect usually responsible - insulin RESISTANCE and some decreased insulin secretion

Question 29

type 2 diabetes - clinical manifestations

Answer 29

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

Question 30

type 2 diabetes - metabolic complications

Answer 30

- impaired insulin secretion - peripheral insulin resistance - increased hepatic glucose production - altered production of hormones and cytokines by adipose tissue

Question 31

diabetic ketoacidosis (DKA)

Answer 31

- more common in type 1 diabetics - serious complication related to insulin deficiency - characterized by hyperglycemia, acidosis, and ketonuria

Question 32

hyperosmolar hyperglycemic syndrome (HHNS)

Answer 32

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

Question 33

hypoglycemia

Answer 33

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

Question 34

symptoms of hypoglycemia

Answer 34

- pallor - sweating - tachycardia - palpitations - hunger - restlessness - anxiety - temors - convulsion - coma

Question 35

chronic microvascular complication

Answer 35

- damage to capillaries, retinopathies, nephropathies, and neuropathies

Question 36

chronic macrovascular complication

Answer 36

- damage to large vessels, coronary artery, peripheral vascular and cerebral vascular

Question 37

microvascular disease

Answer 37

- 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

Question 38

diabetic neuropathy

Answer 38

- 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

Question 39

diabetic retinopathy

Answer 39

- 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

Question 40

diabetic nephropathy

Answer 40

- 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

Question 41

macrovascular complications

Answer 41

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

Question 42

diabetes and infection

Answer 42

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