UTA PATHO COMPREHENSIVE EXAM QUESTIONS AND
ANSWERS GRADED A+
✔✔endocannabinoids - ✔✔- increase appetite, enhance nutrient absorption, stim
lipogenesis, increase white adipose tiss
- inhibit energy expenditure
✔✔angiotensinogen - ✔✔-made by liver & adipocytes
- increased in obesity
- precursor to angiotensin I
- increased levels increase prod of angiotensin II which l/d vasoconstriction, renal
retention of Na and H2O, & release of aldosterone
- increased levels of angiotensin II l/d inflammation, lipogenesis, oxidative stress &
insulin resistance which is associated w/ HTN, atherosclerosis, DM II, & ca
✔✔Ghrelin - ✔✔- prod by gastric mucosa in response to hunger & stim food intake
- causes changes that increase bdy wt & bdy fat
- stim rel of growth hormone, rel of gastric acid, GI motility & insulin secretion
- promotes satiety, vasodilation, & is cardioprotective
- in obsesity levels are lower & there is a blunted response to eating
✔✔glucagon-like peptide - ✔✔- secreted by endocrine cells of intestine
- stim insulin secretion, delays gastric emptying, suppresses appetite & increases
energy use
- levels are decreased in obesity
✔✔Peptide YY - ✔✔- released from endocrine cells of intestine
- inhibits gastric motility & decreases a person's appetite
- levels are decreased in obsesity
✔✔visceral obesity - ✔✔- accumulation of adipose tiss in abdomen & upper bdy
- assoc w/ chronic inflammation, metabolic syndrome, obstructive sleep apnea, DM II,
cardiovascular ds, osteo, fatty liver, & ca
✔✔peripheral obesity - ✔✔- adipose tiss is located on thighs & buttocks causing a pear
shape
- releases less adipokines
✔✔endocrine system & aging - ✔✔- thyroid gland has some atrophy, fibrosis,
inflammation & nodularity
- TSH secretion is slightly increased
- pancreas has a decline in beta cell function which can l/d glucose intolerance & DM
- growth hormone secretion decreases l/d decrease in muscle size & fxn, decreased am
of fat & bone mass, changes in reproductive & cognitive fxn
- elevated levels of PTH are assoc w/ increased mortality
,- decreased vit D levels l/d osteo, ca, autoimmune disorders, DM, cardiovascular ds, &
mental health disorders
- cannot clear glucocorticoids that are produced as well
- less cortisol is used
✔✔anorexia of aging - ✔✔- decrease in appetite or food intake in elderly
- r/s in malnourished state
- r/s from reduced energy requirements, diminished hunger, decreased sense of smell &
taste, decreased saliva secretion, altered GI satiety control
- decreased neuronal activity which increases one's appetite & increased activity from
neurons that suppress appetite; changes l/d decrease food intake
-risk fctrs: functional deficits, medical & psychiatric conditions, loneliness & grief, meds,
polypharm, social isolation, abuse & neglect
- can l/d malnutrition, physical frailty, mitochondrial dysfxn, reduced regen capacity,
increased oxidative stress, imbalanced hormone levels
✔✔islets of langerhans - ✔✔four types of cells:
- alpha cells secrete glucagon
- beta cells secrete gastrin
- delta cells secrete gastrin & somatostatin
- F cells secrete pancreatic polypeptide that stim secretion of gastric acis & inhibits
cholecystokinin secretion
✔✔Insulin secretion - ✔✔- occurs when beta cells are stim by parasymp nervous
system
- elevated glucose levels
- amino acids
- GI hormones such as glucagon, gastrin, secretin, & cholecystokinin
✔✔C-peptide levels - ✔✔Evaluates the amount of insulin being secreted
Help to distinguish between Type 1 and Type 2
✔✔glucose transporters - ✔✔- moves glucose into cell
- GLUT4 is main one & is assoc w/ 21-fold increase in glucose diffusion into cell
✔✔Amylin - ✔✔- hormone secreted by beta cells which helps to regulate glucose
concentration by delaying gastric emptying & supressing glucagon secretion
✔✔Glucagon - ✔✔- responsible for antagonizing insulin & increases bl glucose levels
during times of fasting, exercise, & hypoglycemia
- stim glycogenolysis in liver
- stim by low glucose levels, amino acids such as alanine, glycine, asparagine
- initiates liolysis
✔✔incretin hormones - ✔✔- released by endocrine cells of GI system
, - glucagon-like peptide 1 & glucose dependent insulinotropic polypeptide
- control levels of glucose after a mean by stim glucose dep insulin secretion, inhibiting
glucagon synthesis, slowing gastric emptying, & stim hep glucose secretion
- help to increase intracellular insulin stores
- GLP-1 is a target for DM drug class GLP-1 receptor agonists which help to enhance
fxn of this protein
- dipeptidyl peptidase 4 break down incretins
✔✔DM diagnostic criteria - ✔✔- hgb A1C > 6.5 %
- fasting glucose of > 126 ( no food for 8 hrs)
- 2 hr plasma glucose tolerance test of > 200
- symptoms of DM w/ a random plasma glucose of > 200
✔✔prediabetes lab valuse - ✔✔- hgb A1C 5.7-6.4
- fasting glucose of 100-125
- 2 hr glucose tolerance test of 140-199
✔✔Type 1 DM - ✔✔- usu diagnosed before age 30
- 3 types:
= type 1 A which is autoimmune related
= type 1 B which is idiopathic or nonimmune
= type 3c which is assoc w/ chronic pancreatitis
✔✔type 1 A DM - ✔✔- T cell mediated autoimmune resp destroys beta cells of
pancreas which l/d apoptosis causing a lack of insulin prod. By the time insulin secretion
has decreased enough to cause hyperglycemia , 80-90% of beta cells have been
destroyed
- low levels of insulin l/d increased glucagon secretion which increases glycogenolysis &
gluconeogenesis
- autoimmune destruction of beta cells also l/d decrease in secretion of amylin
- metab of fat, proteins & carbs are altered
- glucose accumulates in blood. glucose exceeds renal threshold & spills into urine
causing osmotic diuresis, polyuria, & polydipsia
- pts have fluctuating glucose levels
- can go into ketosis d/t lack of insulin & have muscle, fat breakdown causing wt loss
- can do into DKA
- must receive insulin b/c they prod it
- hard to reg b/c they are sensitive to insulin
✔✔Type II Diabetes Mellitus - ✔✔- onset is middle age
- more common in native americans, african americans, & family hx of DM
- risk fctrs: age, HTN, physical inactivity, family hx
- pathological defect is insulin resistance
- decrease in # of insulin cell receptors &/or insuff amts of insulin secretion to meet met
needs
- can be treated w/ lifestyle changes and oral meds first
ANSWERS GRADED A+
✔✔endocannabinoids - ✔✔- increase appetite, enhance nutrient absorption, stim
lipogenesis, increase white adipose tiss
- inhibit energy expenditure
✔✔angiotensinogen - ✔✔-made by liver & adipocytes
- increased in obesity
- precursor to angiotensin I
- increased levels increase prod of angiotensin II which l/d vasoconstriction, renal
retention of Na and H2O, & release of aldosterone
- increased levels of angiotensin II l/d inflammation, lipogenesis, oxidative stress &
insulin resistance which is associated w/ HTN, atherosclerosis, DM II, & ca
✔✔Ghrelin - ✔✔- prod by gastric mucosa in response to hunger & stim food intake
- causes changes that increase bdy wt & bdy fat
- stim rel of growth hormone, rel of gastric acid, GI motility & insulin secretion
- promotes satiety, vasodilation, & is cardioprotective
- in obsesity levels are lower & there is a blunted response to eating
✔✔glucagon-like peptide - ✔✔- secreted by endocrine cells of intestine
- stim insulin secretion, delays gastric emptying, suppresses appetite & increases
energy use
- levels are decreased in obesity
✔✔Peptide YY - ✔✔- released from endocrine cells of intestine
- inhibits gastric motility & decreases a person's appetite
- levels are decreased in obsesity
✔✔visceral obesity - ✔✔- accumulation of adipose tiss in abdomen & upper bdy
- assoc w/ chronic inflammation, metabolic syndrome, obstructive sleep apnea, DM II,
cardiovascular ds, osteo, fatty liver, & ca
✔✔peripheral obesity - ✔✔- adipose tiss is located on thighs & buttocks causing a pear
shape
- releases less adipokines
✔✔endocrine system & aging - ✔✔- thyroid gland has some atrophy, fibrosis,
inflammation & nodularity
- TSH secretion is slightly increased
- pancreas has a decline in beta cell function which can l/d glucose intolerance & DM
- growth hormone secretion decreases l/d decrease in muscle size & fxn, decreased am
of fat & bone mass, changes in reproductive & cognitive fxn
- elevated levels of PTH are assoc w/ increased mortality
,- decreased vit D levels l/d osteo, ca, autoimmune disorders, DM, cardiovascular ds, &
mental health disorders
- cannot clear glucocorticoids that are produced as well
- less cortisol is used
✔✔anorexia of aging - ✔✔- decrease in appetite or food intake in elderly
- r/s in malnourished state
- r/s from reduced energy requirements, diminished hunger, decreased sense of smell &
taste, decreased saliva secretion, altered GI satiety control
- decreased neuronal activity which increases one's appetite & increased activity from
neurons that suppress appetite; changes l/d decrease food intake
-risk fctrs: functional deficits, medical & psychiatric conditions, loneliness & grief, meds,
polypharm, social isolation, abuse & neglect
- can l/d malnutrition, physical frailty, mitochondrial dysfxn, reduced regen capacity,
increased oxidative stress, imbalanced hormone levels
✔✔islets of langerhans - ✔✔four types of cells:
- alpha cells secrete glucagon
- beta cells secrete gastrin
- delta cells secrete gastrin & somatostatin
- F cells secrete pancreatic polypeptide that stim secretion of gastric acis & inhibits
cholecystokinin secretion
✔✔Insulin secretion - ✔✔- occurs when beta cells are stim by parasymp nervous
system
- elevated glucose levels
- amino acids
- GI hormones such as glucagon, gastrin, secretin, & cholecystokinin
✔✔C-peptide levels - ✔✔Evaluates the amount of insulin being secreted
Help to distinguish between Type 1 and Type 2
✔✔glucose transporters - ✔✔- moves glucose into cell
- GLUT4 is main one & is assoc w/ 21-fold increase in glucose diffusion into cell
✔✔Amylin - ✔✔- hormone secreted by beta cells which helps to regulate glucose
concentration by delaying gastric emptying & supressing glucagon secretion
✔✔Glucagon - ✔✔- responsible for antagonizing insulin & increases bl glucose levels
during times of fasting, exercise, & hypoglycemia
- stim glycogenolysis in liver
- stim by low glucose levels, amino acids such as alanine, glycine, asparagine
- initiates liolysis
✔✔incretin hormones - ✔✔- released by endocrine cells of GI system
, - glucagon-like peptide 1 & glucose dependent insulinotropic polypeptide
- control levels of glucose after a mean by stim glucose dep insulin secretion, inhibiting
glucagon synthesis, slowing gastric emptying, & stim hep glucose secretion
- help to increase intracellular insulin stores
- GLP-1 is a target for DM drug class GLP-1 receptor agonists which help to enhance
fxn of this protein
- dipeptidyl peptidase 4 break down incretins
✔✔DM diagnostic criteria - ✔✔- hgb A1C > 6.5 %
- fasting glucose of > 126 ( no food for 8 hrs)
- 2 hr plasma glucose tolerance test of > 200
- symptoms of DM w/ a random plasma glucose of > 200
✔✔prediabetes lab valuse - ✔✔- hgb A1C 5.7-6.4
- fasting glucose of 100-125
- 2 hr glucose tolerance test of 140-199
✔✔Type 1 DM - ✔✔- usu diagnosed before age 30
- 3 types:
= type 1 A which is autoimmune related
= type 1 B which is idiopathic or nonimmune
= type 3c which is assoc w/ chronic pancreatitis
✔✔type 1 A DM - ✔✔- T cell mediated autoimmune resp destroys beta cells of
pancreas which l/d apoptosis causing a lack of insulin prod. By the time insulin secretion
has decreased enough to cause hyperglycemia , 80-90% of beta cells have been
destroyed
- low levels of insulin l/d increased glucagon secretion which increases glycogenolysis &
gluconeogenesis
- autoimmune destruction of beta cells also l/d decrease in secretion of amylin
- metab of fat, proteins & carbs are altered
- glucose accumulates in blood. glucose exceeds renal threshold & spills into urine
causing osmotic diuresis, polyuria, & polydipsia
- pts have fluctuating glucose levels
- can go into ketosis d/t lack of insulin & have muscle, fat breakdown causing wt loss
- can do into DKA
- must receive insulin b/c they prod it
- hard to reg b/c they are sensitive to insulin
✔✔Type II Diabetes Mellitus - ✔✔- onset is middle age
- more common in native americans, african americans, & family hx of DM
- risk fctrs: age, HTN, physical inactivity, family hx
- pathological defect is insulin resistance
- decrease in # of insulin cell receptors &/or insuff amts of insulin secretion to meet met
needs
- can be treated w/ lifestyle changes and oral meds first
