Phys-Endocrine/ Bio-Chem

Front 1

proportion of cells in Islets of Langerhans

Back 1

75% beta cells

20% alpha cells

5% delta cells

Front 2

blood flow through cells in Islets of Langerhans

Back 2

beta-->alpha-->delta

Front 3

how do pancreatic hormones get to liver?

Back 3

from pancreatic veins into splenic vein into portal vein

Front 4

how should you measure concentration of insulin in the plasma?

Back 4

- measure C-peptide which is released 1:1

- measuring insulin is inaccurate because 60% removed through first pass metabolism through liver insulinases

Front 5

2 phases of insulin release

Back 5

1. 2-5 mins from readily-reusable pool of preformed insulin in beta cell

2. persists as long as glucose concentration elevated

Front 6

nervous and hormonal stimulus for insulin

Back 6

vagus nerve

incretins- GI hormones

Front 7

effect of exercise on insulin

Back 7

- increases concentration because muscles need glucose

- increase insulin prevents lipolysis and glucose release from liver ---> hypoglycaemia

- resolved by adrenergic release of glucagon

Front 8

four features of signal transduction

Back 8

1. specificity

2. amplification

3. desensitization

4. integration

Front 9

where and from what is epinephrine made?

Back 9

in adrenal medulla

- from tyrosine and phenylalanine

- stored in vesicles in chromaffin cells

Front 10

what are four main types of cell surface receptors and main example?

Back 10

1. G protein: glucagon

2. tyrosine kinase: insulin

3. receptor guanylyl cyclase

4. adhesion receptor/integrin

Front 11

second messenger pathway (typical)

Back 11

1 ligand--> G protein-->adenylyl cyclase-->100 cAMP-->protein kinase A--> phosphorylates 100s proteins

Front 12

half life of insulin

Back 12

6 minutes in plasma

Front 13

what degrades insulin?

Back 13

insulinase in liver and kidney

Front 14

what triggers release of insulin?

Back 14

- increase glucose from GLUT2

- increase a.a. and CCK/gastric inhibiting polypeptides

Front 15

through what transporter does glucose enter muscle and adipose tissue?

Back 15

GLUT4

Front 16

5 effect of insulin

Back 16

1. increase GLUT4 (glucose into muscle/adipose)

2. prevent lipase (prevent f.a. release from adipose)

3. synthesize fatty acid in adipose tissue

4. a.a. uptake in most tissues and protein synth

5. synthesize glycogen in liver and muscle

Front 17

where does glucagon lead to breakdown of glycogen?

Back 17

liver

(not muscle)

Front 18

4 effects of glucagon

Back 18

1. glycogenolysis (in liver)

2. gluconeogenesis

3. lipolysis in adipose tissue (for acetyl-coA and ketone synthesis)

4. a.a. uptake and degradation to make carbon skeletons for gluconeogenesis

Front 19

effects of epinephrine

Back 19

1. prevents release of insulin and uptake of glucose

2. stimulates gluconeogenesis and glycolysis

3. stimulates secretion of glucagon

Front 20

what kind of receptor does epinephrine work on?

Back 20

G-protein

Front 21

epinephrine--> glucose in hepatocyte

Back 21

ATP-->cAMP-->inactive to active PKA--> inactive to active phosphorylase b kinase--> inactive glycogen phosphylase b kinase to active glycogen phosphorylase a kinase --> glycogen to glycogen1-phosphate---------->glucose

Front 22

how does glucose trigger release of insulin?

Back 22

glucose increases ATP in cell--> blocks K+ channel--> depolarizes cell--> Ca+ into cell--> nucleus secretes insulin

Front 23

how does insulin lead to fatty acid synthesis?

Back 23

insulin activates acetyl-coA carboxylase (by dephosphorylating) which converts acetyl-coA into malonyl-coA-----> fatty acid

Front 24

how does insulin increase glucose uptake in cells?

Back 24

insulin bound to receptor signals intracellular glucose receptors to move to cell membrane so more glucose can enter cell

when insulin decreases, glucose receptor goes back into cell and gets recycled

Front 25

how is insulin in cell regulated?

Back 25

- insulin receptor complex goes in cell, insulin broken down by lysosomes and receptors either broken down or recycled back to cell surface when needed

- too much insulin promotes receptor degradation, so less receptors so cell desensitized to insulin

Front 26

what is released during hypoglycaemia and effects

Back 26

cortisol--> gng

glucagon--> gng and glycogenolysis

epinephrine--> glycogenolysis

Front 27

what is considered hypoglycaemia?

Back 27

less than 40 mg/dL blood glucose

Front 28

how does alcohol induced hypoglycaemia work?

Back 28

NAD+ converted to NADH to metabolize alcohol

gluconeogenesis intermediates used to use up so NADH-->NAD+ instead of making glucose

Front 29

diagnosis for diabetes

Back 29

hemoglobin Ac > 6.5%

fasting glucose > 126mg/dl

2-hour glucose/random >200mg/dl

Front 30

features of type 1 diabetic

Back 30

young, normal BMI, polydipsia, polyphagia, ketoacidosis

Front 31

pathophys of type 1 diabetes

Back 31

environmental and dietary habits, viral infection, genetic (HLA Xm 6p21)

Front 32

pathophys of type 2 diabetes

Back 32

insulin resistance in peripheral tissues+ beta cell dysfunction--> hyperglycaemia

Front 33

features of type 2 diabetes

Back 33

middle age, sedentary life, unexplained weight loss/weakness, often asymptomatic

Front 34

macrovascular complications of diabetes

Back 34

- atherosclerosis in aorta/large arteries

- MI

- cerebrovascular disease/stroke

- increase risk of gangrene

Front 35

microvascular complications of diabetes

Back 35

- thickening of BM of capillaries in target organs

- weakened walls--> more leaky capillaries

Front 36

diabetic retinopathy

Back 36

microvascular complication

pre-proliferative: microanurysms, hemorrhage, exudate

proliferative: angiogenesis

- potential retinal detachment

Front 37

diabetic nephropathy

Back 37

i. glomerular lesions- "kimmelstiel-wilson lesions", diffuse mesangial sclerosis

ii. renal vascular lesions- atherosclerosis

Front 38

diabetic neuropathy

Back 38

50% of diabetics, depends on time with diabetes

- hyperglycaemia causes vascular ischemia

i. distal symmetrical sensorimotor- proprioception, fine touch, "stocking/glove"

ii. focal/multifocal asymmetric- carpal tunnel, thoracic, cranial

iii. autonomic neuropathy- pupil, GU, GT, CVS effected

Front 39

diabetic ketoacidosis

Back 39

complication of type 1 diabetes

- decrease insulin-->epinephrine-->glucagon-->hyperglycemia -->osmotic diuresis

- decrease insulin-->increase lipase-->increase fatty acid--> converted into ketones

- ketones+urination compromised: metabolic ketoacidosis

nausea,vomit, respiratory difficulty

Front 40

hyperosmolar diabetes

Back 40

complication of type 2 diabetes

- severe dehydration from osmotic diuresis

- no ketoacidosis because enough insulin to prevent lipolysis

- severe dehydration leads to coma