Pancreas Physio Final Exam Spring 2011

Front 1

T or F: Pancreas is solely an endocrine organ.

Back 1

False, it is both endocrine and exocrine.

Front 2

What makes up most of the Langerhans cells of the pancreas?

Back 2

Beta Cells (60%)

Front 3

What are the four types of cells that constitute of the endocrine portion of the pancreas?

Back 3

Alpha, Beta, Delta, and F cells

Front 4

What is the secretion of the alpha cells?

Back 4

glucagon

Front 5

What is the secretion of the beta cells?

Back 5

insulin

Front 6

What is the secretion of the delta cells?

Back 6

somatostatin (GHRIH)

Front 7

What is the secretion of the F cells?

Back 7

pancreatic polypeptide (stimulate gastric chief cells & inhibits bile, pancreatic secretion, and intestinal mobility)

Front 8

What is the second most prominent type of Islets of Langerhans cells?

Back 8

alpha cells (25%)

Front 9

T or F: Glucagon secretion mobilizes glucose, fatty acids, and amino acids

Back 9

True

Front 10

T or F: Glucagon function is consider ANABOLIC

Back 10

False, it is CATABOLIC

Front 11

T or F: Insulin function is consider ANABOLIC

Back 11

True

Front 12

Secretion of Insulin (INCREASES/ DECREASES) storage of glucose, fatty acids, and amino acids?

Back 12

INCREASE

Front 13

Where is somatostatin (GHRIH) hormone mostly found in?

Back 13

Hypothalamus and Pancreas

Front 14

Is glucagon, somatostatin and pancreatic polypeptide ONLY secreted by the cells of the pancreas?

Back 14

NO, they are also secreted by cells in the mucosa of the gastrointestinal tract.

Front 15

T or F: Insulin is a steroidal type of hormone.

Back 15

False; it is a polypeptide hormone

Front 16

Describe the structure of Insulin:

Back 16

Polypeptide composed of the A and B chains connected by DISULFIDE bonds.

Front 17

T or F: Insulin is synthesized in its complete active form.

Back 17

False, it is synthesized as a preprohormone which gets activated upon its cleavage. (prepro- -> pro:proinsulin -> insulin)

Front 18

Deficiency in Insulin causes what in 5% of the population?

Back 18

Diabetes Mellitus

Front 19

T or F: The most sever Diabetes Mellitus is Type II.

Back 19

False, it is Type I

Front 20

What can cause diabetes mellitus type I?

Back 20

loss of insulin due to the structure of the Beta cells in the pancreas.

Front 21

T or F: Diabetes Mellitus Type I is insulin DEPENDENT.

Back 21

True

Front 22

Around what age it is normal to get Diabetes Mellitus Type II?

Back 22

Around and after 40 y.o.a.

Front 23

tT or F: Diabetes Mellitus Type II is primarily (first) controlled with Hypoglycemic DRUGS.

Back 23

False, you first try to correct the diet and increase exercise.

Front 24

In which type of people is Diabetes Mellitus most often common?

Back 24

Overweight, 40 years of age

Front 25

T or F: Type I can lead to KETOSIS in acute cases.

Back 25

True

Front 26

During Type II Diabetes Mellitus does insulin ELEVATED leves cause (INCREASE/ DECREASE) in the sensitivity to insulin?

Back 26

DECREASE

Front 27

How much is genetics involved in Type I vs Type II Diabetes Mellitus?

Back 27

Type I not so much
Type II strong genetic link

Front 28

What are some extracellular characteristics found in Diabetes Mellitus?

Back 28

Hyperglycemia (sugar in blood raised)
Glycosurea (glucose in urea)
Polyurea (larger water flow of urine)
Ketosis (protein catabolism)
Polydipsia (drinking)
Polyphagia (hunger & weight loss increase)
Reduced Growith (protein catabolism)

Front 29

During Hyperglycemia, is protein CATABOLISM (INCREASED/ DECREASED)?

Back 29

INCREASED; so that aa can be used in the glucoNEOgenic pathway

Front 30

What are some things that can increase the uptake of glucose to reduce hyperglycemia?

Back 30

Exercise
Hormones

Front 31

T or F: Gestetional diabetes is NOT a health risk because it is transient.

Back 31

False, it is a health risk for one and for the fetus

Front 32

What are the normal Plasma Glucose Levels?

Back 32

90mg%

Front 33

Can hyperglycemia affect the capacity of the kidney?

Back 33

Yes (glycosurea)

Front 34

What is the composition of URINE during hyperglycemic states?

Back 34

SUGARY (glucose execreted in large amounts)

Front 35

T or F: Glycosurea is when the capacity of the kidney to reabsorb is EXCEEDED

Back 35

True

Front 36

What is Polyurea and its cause?

Back 36

Larger urine flow due to glucose draws in water.

Front 37

Explain KETOSIS:

Back 37

Due to LOW intracellular glucose levels (since no insulin) protein and fat CATABOLISM are INCREASED -> KETONE BODIES -> acidosis (prolong- death or coma)

Front 38

How is insulin secretion stimulated?

Back 38

By the intracellular transport diffusion of glucose activating Beta cells through membrane depolarization and Ca2+.

Front 39

T or F: Insulin decreases the number of glucose transporters in the cell membrane

Back 39

False, it is increased to increase the rate of facilitated transport of glucose into a cell.

Front 40

What is the role of GlucoKinase in the liver?

Back 40

Glucose ----> Glucose-6-Phosphate

Front 41

What is the MAIN and MAJOR control of insulin release?

Back 41

GLUCOSE

Front 42

What are the two phases that the effect of glucose has?

Back 42

1st phase: rapid peak of insulin (within 5 min) ***Due to Release of exiting stores
2nd phase: Due to synthesis of insulin

Front 43

What is most effective in promoting insulin release from beta cells, is it INTRAVENOUS glucose or ORAL glucose?

Back 43

ORAL glucose

Front 44

Prolonged stimulation of beta cells by glucose can lead to a condition of the pancreatic cells known as?

Back 44

Hypertrophy of beta cells (burn out) so DECREASE of insulin release.

Front 45

Other factors affecting the release of insulin?

Back 45

Amino acids
Beta-Keto acids
Growth Hormone
Glucocorticoids

Front 46

What are some examples of incretins?

Back 46

Glucagon-like peptide (GLP-1)
Glucose-dependent insulinotropic peptide (GIP)

Front 47

GLP-1 (incretin) comes from which type of cells of the GUT?

Back 47

L cells

Front 48

GIP (incretine) comes from which type of cells of the GUT?

Back 48

K cells

Front 49

What is the role of incretins in the GUT?

Back 49

Further stimulate the release of insulin.

Front 50

What is the main function of Glucagon peptide hormone?

Back 50

RAISE blood glucose levels.

Front 51

What is the main organ functioning to increase glucose levels during low levels?

Back 51

LIVER

Front 52

What are 4 ways you can increase glucose levels in the blood?

Back 52

Glycogenolytic (glycogen -> glucose)
Gluconeogenic (aa -> glucose)
Lipolytic (fatty acids -> ENERGY)
* can lead to Ketogenic

Front 53

As glucose and insulin go up, glucagon goes (UP/DOWN)

Back 53

DOWN

Front 54

T or F: Somatostatin has a positive effect on insulin and glucagon release.

Back 54

False, has a NEGATIVE effect as it INHIBITS both.