Endocrine 1: Pancrease

Front 1

3 Characteristics of the endocrine system

Back 1

1. ductless
2. Hormones secreted > interstitial space > into the blood
3. No anatomic connections among endocrine organs

Front 2

2 roles of homeostasis of the endocrine system

Back 2

1. Coordinates and integrates cellular activity
2. Inter-relationship of chemical messengers

Front 3

What is the role of target organs in the endocrine system

Back 3

- hormones bind to receptors on cells of target organs
- biologic response results

Front 4

3 structures that make-up hormones of the endocrine system

Back 4

1. Proteins (peptides)
2. Steroids
3. Amino acid derivatives (amines)

Front 5

make-up of protein (peptide) hormones & ex. of peptide hormones

Back 5

- most hormones
- contain CHO & so are glycoproteins
- synthesized on endoplasmic reticulum of endocrine cells then transferred to Golgi apparatus for packaging into secretory vesicles
- Ex. Insulin, ACTH, Glucagon, TSH

Front 6

Make-up of Steroid hormones & ex.

Back 6

- derived from Cholesterol
- usually not stored
- Ex. Cortisol, Aldosterone

Front 7

Make-up of Amino acid derivative hormones (amines) & ex

Back 7

- synthesized from amino acid tyrosine
- include catecholamines
- Ex. Catecholamines, Thyroid hormones
- thyroxine & epi have similar cardiac effects as catecholamines

Front 8

Neurotransmitters

Back 8

released by axons into synapse (ANS)

Front 9

Endocrine (telecrine)

Back 9

released into circulation then travels to target via the blood

Front 10

Neuroedocrine

Back 10

secreted by neurons into circulation influencing cellular fxn at another location

Front 11

Paracrine

Back 11

hormone is released from 1 cell & produces effect on a neighboring cell of a different type often in the same organ via interstitial space

Front 12

Autocrine

Back 12

hormone produces effect on the same cell that released it

Front 13

Cytokines

Back 13

peptides secreted by cells into the ECF which can fxn as autocrines, paracrines, or endocrine hormones.... i.e. interlukens

Front 14

describe how Peptides & Catecholamines are transported

Back 14

water soluble hormones dissolved in plasma & transported to traget tissue via the interstitial space

Front 15

describe how Steroids & Thyroid hormones are transported

Back 15

plasma protein bound such that less than 10% of hormone is free in solution; reservoir

Front 16

Metabolic Clearance rate

Back 16

rate of disappearance of hormone from the plasma/concentration of hormone per mL plasma

Front 17

4 ways clearance of hormones occurs

Back 17

1. metabolic destruction by tissues
2. binding with tissues
3. excretion into bile by the liver
4. excretion into the urine by the kidneys

Front 18

3 receptor locations

Back 18

1. cell membrane surface
2. cytoplasm
3. cell nucleus

Front 19

hormones where the target receptor is on the cell membrane surface

Back 19

1. Proteins
2. Peptides
3. catecholamines

Front 20

hormone where the target receptor is on the cytoplasm

Back 20

Steroid

Front 21

hormones where the target receptor is on the cell nucleus

Back 21

1. thyroid hormone receptor
2. chromosomes assoc.

Front 22

the ultimate fxn of the endocrine and neuroendocrine system

Back 22

adapt to changing environments and maintaining homeostasis

Front 23

(ex of) Negative feedback in the endocrine system

Back 23

Tropic hormone (TSH) stimulates the release of another hormone (thyroid hormone) > negative feedback on the anterior pituitary > inhibition of further release of TSH

Front 24

(ex of) Positive feedback

Back 24

Lutenizing hormone from stimulation of estrogen on anterior pituitary > lutenizing hormone act on ovaries to stimulate increased secretion of estrogen > increased LH and when appropriate levels are achieved negative feedback takes place

Front 25

what is Neuro-control of hormones

Back 25

it relates to the neuro & endocrine system and neuro-transmitters are mediators of neuro-control

Front 26

Role of Pancrease

Back 26

- central role in digestion and in metabolism, utilization, & storage of energy substrates

Front 27

2 major tissue types in the pancrease

Back 27

1. Acini (lobules)
2. Islets of Langerhans

Front 28

describe Acini (lobules) tissue type of pancrease

Back 28

divided by connective tissue & connected to a duct (exocrine) > pancrease duct > duodenum
- ex. amilase secretion into duodenum

Front 29

describe the Islets of Langerhans of the pancrease

Back 29

- cluster of endocrine cells
- 0.3mm diameter arranged around capillary (highly vascularized)
- embedded within Acini
- b/c islet cells are very vascular it makes it easy for hormones that get secreted by islet cells to go into interstitial space & into the circulation

Front 30

resting muscle membrane only slightly permeable to glucose in absence of insulin except: (3 ways)

Back 30

1. moderate-heavy exercise causes contraction which makes fivers more permeable to glucose
2. following a meal with blood glucose levels high and lrg amounts of insuling secreted there is rapid transport of glucose and preferential use of glucose by the muscle fibers so increases the rate of glucose transport by 15 times
3. glucose is then stored in the liver as glycogen and when bld sugar drops between meals the liver glycogen gets put back into glucose

Front 31

4 things follow glucose ingestion that are the effects of insulin on CHO metabolism

Back 31

1. insulin secreted inactivates liver phosphorylase
2. insulin enhances glucose uptake from blood and liver by increasing glucokinase activity
3. insulin increase activity of enzymes leading to glycogen synthesis: inhibit glycogenolosis
4. net result; glycogen can increase to a total of 5-6% of the liver mass or 100g of stored glycogen

Front 32

5 effects on decreased blood glucose

Back 32

1. decrease insulin secretion by beta cells with low bld gluc
2. glycogen synthesis stops
3. glycogen is spit into glucose with activation of phosphorylase=glycogenolosis
4. glucose phospates now activated by lack of insulin removing the phosphate radical from glucose
5. glucose diffuses back into the blood

Front 33

major fxn of insulin and it's secondary fxn

Back 33

increases the rate of glucose transport into the resting muscle cell by 15 times
Secondary fxn: promotes uptake, storage, and use of glucose by the liver

Front 34

Primary target of insulin

Back 34

skeletal muscle

Front 35

where is insulin synthesized?

Back 35

beta cells

Front 36

what happens with inhibition of gluconeogenesis?

Back 36

1. decreased amt & activity of liver enzymes
2. decreased release of amino acids from muscle and other tissues

Front 37

what is the only substrate the brain can used for energy

Back 37

glucose
brain cells can use glucose w/o insulin being present

Front 38

4 CNS symptoms that develop when glucose levels drop below 50mg/100mL

Back 38

1. Irritability
2. Syncope
3. Seizures
4. Coma

Front 39

list the steps how excess glucose becomes fat

Back 39

1. excess glucose
2. Pyruvate
3. acetyl CoA
4. fatty acids
5. triglycerides
6. LDL
7. adipose tissue

Front 40

what is the end product of fatty acid oxydation in the body if there isn't insulin

Back 40

Aceto-acetic acid
some aceto-acetic acid converts to beta hydroxy-butaric acid and acitone = ketone bodies, causing ketosis and acidosis

Front 41

5 effects of insulin on protein metabolism

Back 41

1. promotion of protein synthesis and storage
2. Lack of insulin results in protein depletion & increased amino acids in the blood
3. Catabolism of protein results in increased urea excretion (from muscle brk down)
4. protein wasting contributes to muscle weakness and organ dysfxn in DM
5. insulin fxns synergistically with GH to promote growth

Front 42

What is the rate limiting step for glucose metabolism w/ beta cell

Back 42

Phosphorilation

Front 43

Major mechanism for glucose sensing and change in amt of insulin secreted

Back 43

conversion of glucose to glucose-6-phosphate

Front 44

factors that increase insulin secretion

Back 44

1. increased blood glucose
2. increased blood free fatty acids
3. increased blood amino acids
4. GI hormones (gastrin, secretin, gastric inhib peptide etc)
5. glucagon, GH, cortisol
6. parasympathetic stimulaion: Ach
7. B-adrenergic stimulation
8. insulin resistance (obesity)
9. sulfonylurea drugs (glyburide, tolbutamide)

Front 45

factors that decrease insulin secretion

Back 45

1. decreased blood glucose
2. fasting
3. somatostatin
4. alpha-adrenergic activity
5. Leptin

Front 46

how long does it take inulin secretion to decrease when glucose levels fall

Back 46

3-5min

Front 47

What is Glucagon?
What secretes it?
What is its role?
What is its target organ?
What is it inhibited by?

Back 47

1. Glucagon is a polypeptide hormone
2. Secreted by the Alpha cells of the pancrease
3. It increases blood glucose concentrations; Brks glycogen down into glucose; opposes insulin; makes glucose from non-CHO sources (amino acids and fats)
4. Glucagon's target organ is the liver
5. inhibited by hyperglycemia

Front 48

What is Somatostatin and what does it do?
What secretes it?
What stimulates its secretion?
What is its role?

Back 48

1. Polypeptide that causes decreased secretion of insulin and glucagon, decreases GI motility, and decreases secretion and absorption in the GI tract
2. It is secreted by the Beta Cells of the illetes
3. Secretion is stimulated by increased blood glucose, amino acids, fatty acids, and GI hormones
4. It's role: increase the length of time food is in GI tract and prevent rapid exhaustion of food nutrients
(chemically identical to GH inhibitory hormone)

Front 49

What inhibits the secretion of Somatostatin

Back 49

1. decreased secretion of insulin and glucagon
2. decreased GI motility
3. decreased secretion and absorption in GI tract

Front 50

3 organs where glucose is the only nutrient normally used

Back 50

1. Brain
2. Retina
3. Germinal epithelium of the gonads

Front 51

What is Type 1 DM?

Back 51

Syndrome of impaired metabolism of CHO, fats, and protein.
Impaired entry of glucose into cells causing increased levels in the blood d/t no insulin and beta cell destruction

Front 52

Signs and Symptoms of Type 1 DM

Back 52

1. increased BS
2. increased fat utilization
3. protein depletion
4. polydipsia, polyuria, and polyphagia

Front 53

Describe what happens in the dehydrated type 1 DM

Back 53

1. increased plasma osmolarity
2. increased glucose in urine
3. increased water and NA loss
- cellular starvation stimulates hunger, stimulating compensatory response to increased release and avail. of fuel substrates (fat and protein)

Front 54

What is the threshold for glucose to spill into urine

Back 54

plasma levels of greater than or equal to 180mg/dL glucose

Front 55

What is the sequellae of chronically high BS levels in Type 1 DM?

Back 55

1. bld vessel abnormalities
2. increased risk for MI, CVA, ESRD, retinopathy, & PVD
3. Neuropathy: peripheral & autonomic
4. increased fat utilization: metabolic acidosis
5. tissue/muscle wasting

Front 56

Patho of Type 2 DM

Back 56

- insulin resistance secondary to abnormal signaling linking receptor activation with cellular effects
- compensatory increased insulin secretion
- metabolic syndrom (syndrome X)
- inadequate response of beta cells to glucose levels result in decreased mass of beta cells
- decreased response of peripheral tissue to insulin
- cannot increase insulin production after meals

Front 57

Type 2 DM may be d/t:

Back 57

1. problem with glucose transport
2. abnormal insulin synthesis
3. abnormal insulin processing
4. abnormal insulin storage
5. abnormal insulin secretion

Front 58

Hgb A1C

Back 58

the Hgb at which glucose is bound
- most accurate measure of long term control and effectiveness of tx
-avg blood sugar over 2-3months b/c lifespan of RBC = 120 days.
Non-DM < 6%
goal of therapy < 7.5%

Front 59

Signs and symptom of DKA
Goal in BS correction

Back 59

1. dyspnea
2. hyperventilation
3. n/v
4. abdominal pain
5. change in sensorium
- Goal to drop BS = decrease by 75-100mg/dL/hr or 10% per hr
- 10 units insulin/hr or 0.1units/kg/hr

Front 60

Hyperosmolar NonKetotic Syndrome

Back 60

Osmotic diuresis d/t increased blood sugar causing dehydration and hyperosmolar situation

Front 61

What is the diabetic complication associated with the highest mortality

Back 61

Nephropathy

Front 62

d/t to diabetic neuropathies you may see what pathophysiologic abnormalities

Back 62

1. resting tachycardia
2. low BP or labile BP
3. decreased or absent beat to beat variability
4. may not respond normally to atropine
5. HTN
6. neurogenic bladder
7. absence of sweating
8. gastroporesis (20-30%)

Front 63

What are some vascular anomalies associated with DM

Back 63

1. CAD
2. Cerebral vascular dx
3. PVD
4. Retinopathy
5. Neuropathy
6. Stiff joint syndrome (30-40%)