Diabetes Mellitus

Question 1

glycogen

Answer 1

stored glucose

Question 2

glycogenesis

Answer 2

formation of glycogen

Question 3

glycolysis

Answer 3

breakdown of glucose by enzymes

Question 4

gluconeogenesis

Answer 4

reverse of glycolysis (formation of glucose)

Question 5

glucose metabolism

Answer 5

glycogen, glycogenolysis, gluconeogenesis

Question 6

fat metabolism

Answer 6

lipolysis, metabolic acidosis, ketoacidosis

Question 7

lipolysis

Answer 7

breaking down of triglycerides to fat

Question 8

glycogenolysis

Answer 8

breaking down stored glucose from glycogen

Question 9

protein metabolism

Answer 9

proteins broken down to amino acids

Question 10

insulin

Answer 10

lowers blood glucose levels
-causes glucose uptake by target cells
-stores glucose as glycogen or fat

Question 11

glucose-regulating hormones

Answer 11

insulin, somatostatin, amylin, gut-derived hormones
-glucagon, epinephrine, GH, glucocorticoid

Question 12

alpha cells in pancreatic langerhans

Answer 12

secrete glucagon

Question 13

beta cells in pancreatic langerhans

Answer 13

create insulin

Question 14

delta cells in pancreatic langerhans

Answer 14

secrete statin

Question 15

glucagon with glucose, fat, protein metabolism

Answer 15

glucose:
-glycogen breakdown
-increase gluconeogenesis
fat:
-adipose lipase makes fatty acids usable for energy
proteins:
-increased amino acid uptake by the liver
-amino acids>gluconeogenesis>glucose

Question 16

insulin with glucose, fat, protein metabolism

Answer 16

glucose:
-increase transport to muscle, fat tissue
-glycogen synthesis
-decreases gluconeogenesis
fat:
-triglyceride synthesis by the liver
-increased fatty acids into adipose cells
-converts fatty acids to triglycerides
-stores fat by stopping triglyceride breakdown
proteins:
-amino acids go into cells (AT)
-increase protein synthesis
-decreases protein breakdown

Question 17

insulin-dependent glucose transporter (GLUT-4)

Answer 17

insulin binds to insulin receptors>intracellular signal>GLUT-4 receptor comes to cell membrane>glucose is transported

Question 18

classifications of diabetes mellitus

Answer 18

prediabetes
type 1
type 1
gestational
DM from other causes

Question 19

prediabetes (type 2)

Answer 19

blood glucose is elevated but not enough for a diagnosis
-IFG 100-125 mg/dL
-IGT 140-199 mg/dL (2 hour test)
treated with lifestyle modifications

Question 20

diabetes mellitus type 1

Answer 20

total lack of insulin-beta cells destroyed
-glucose won’t enter muscle or fat tissue
-autoimmune
-decreased glucose uptake
-hyperglycemia
treated with insulin injections, diagnosed usually in childhood

Question 21

diabetes mellitus type 2

Answer 21

dysfunctional beta cells-impaired insulin
-defective insulin receptors
-insulin destruction before effective
-beta cell exhaustion/dysfunction from hypertrophy (become atrophic)
-genetic component and obesity/inactivity
-hyperglycemia
-increased glucose output by liver
treated with diet/exercise, medication

Question 22

type 1 and 2 manifestations

Answer 22

3 Ps:
-polyuria from osmotic diuresis (excessive H20 loss)
-polydipsia from dehydration
-polyphagia from hunger (fat, protein broken down for energy)
fatigue, paresthesia (tingling), infections

Question 23

type 1 manifestations

Answer 23

nausea, severe vomiting, abdominal pains and cramping

Question 24

type 2 manifestations

Answer 24

muscle wasting, blurred vision, hand and foot numbness/tingling, dry skin, slow healing of skin damage

Question 25

diagnostic testing

Answer 25

HbA1c >/= 6.5%
FPG >/= 126 mg/dL
2 hour PG >/= 200 mg/dL
random glucose >/= 200 mg/dL (hyperglycemia)

Question 26

type 1 vs type 2 onset

Answer 26

type 1:
-childhood, younger age
-abrupt symptoms
-recent weight loss
-uncommon family history
-autoimmune
-early or late islet problems
-almost no beta cells
-almost no insulin
-insulin required
type 2:
-usually adulthood
-gradual symptoms/asymptomatic
-obesity
-common family history
-late islet problems
-slightly reduced beta cells
-elevated/normal insulin
-insulin not needed AT FIRST
-can be improved

Question 27

metabolic syndrome

Answer 27

preventable X factors: abdominal obesity, hyperglycemia, hypertension, lipid intake
-hypertrophy+hyperpigmentation in skin
-muscle dysfunction
-atherosclerosis

Question 28

gestational DM

Answer 28

abnormal glucose regulation during 2nd-3rd trimester of pregnancy
-mom at risk for diabetes postpartum
causes fetal abnormalities:
-macrosomia (large bodies)
-hypoglycemia (<45 mg/dL)
-hypocalcemia
-polycythemia
-hyperbilirubinemia

Question 29

acute complications of DM

Answer 29

ketoacidosis, hyperosmolar hyperglycemic state, hypoglycemia
-life threatening

Question 30

diabetic ketoacidosis

Answer 30

primarily type 1:
-increased lipolysis, ketones
-from an absence of insulin
-hyperglycemia (>250 mg/dL)
-low bicarbonate
-low arterial pH
-+urine, serum ketones
in type 2:
-from severe stress: stroke, sepsis, myocardial infarction
low arterial pCO2
-acidosis-induced hyperkalemia
-hyperventilation

Question 31

diabetic ketoacidosis process

Answer 31

low insulin, high glucagon
-glucagon causes gluconeogenesis, ketogenesis by the liver
-high blood glucose levels from excess
-free fatty acids in adipose tissue produces ketones
fruity breath-big sign

Question 32

hyperosmolar hyperglycemic state (HHS)

Answer 32

insulin deficiencies reduce glucose use but cause hyperglucagonemia and glycogenolysis
-glycosuira causes dehydration
-blood glucose>600 mg/dL
-hyperosmolarity>310
-no ketoacidosis
mostly in type 2

Question 33

hypoglycemia manifestations

Answer 33

altered CNS function
-headaches, lethargy, altered behavior, coma, seizures
ANS activation
-hunger, anxiety, tachycardia, sweating, constricted skin vessels (clammy skin)

Question 34

hypoglycemia treatment

Answer 34

15-15 rule
-repeat if blood glucose<70 mg/dL
glucagon IM, 50% dextrose IV, oxygen