Pathophysiology Ch. 31 - 33 Endocrine

Front 1

The endocrine glands are:

Back 1

the pituitary gland (hypophysis), the two adrenal glands, the thyroid gland, the four parathyroid glands, the endocrine portion of the pancreas, the gonads, the pineal gland, and the thymus.

Front 2

Endocrine hormones circulate in the blood stream as:

Back 2

either free or bound molecules.

Front 3

Describe the type, duration, and effectiveness of free and bound Endocrine hormones:

Back 3

Free hormones are:
water soluble proteins or peptides, have a shorter half-life, and have a direct impact.

Bound hormones are:
Steroid & Thyroid hormones which are transported by carriers made by the liver, have a longer half-life, and have an indirect impact.

Front 4

Hormone half-life is positively correlated with:

Back 4

the % of protein binding.

Front 5

Hormone receptors are located:
and their function is to:

Back 5

either on the surface or inside the target cell;
their function is to RECOGNIZE specific hormones and TRANSLATE the hormonal signal into a cellular response.

Front 6

What is up-regulation?
What is down-regulation?

Back 6

Up-regulation occurs when receptor synthesis INCREASES in response to DECREASED levels of hormone.
Down-regulation occurs when receptor synthesis DECREASES in response to EXCESSIVE levels of hormone.

Front 7

What common chemical state affects hormone-receptor binding?

Back 7

pH of body fluids; eg.. ketoacidosis reduces insulin binding.

Front 8

The hypothalamus and the pituitary are together known as the:

Back 8

hypophysis.

Front 9

The levels of many hormones are regulated by this type of mechanism:

Back 9

Negative feedback mechanism.

Front 10

Describe the negative feedback mechanism:

Back 10

Hypothalmus “reads” the incoming levels, Sends message to the pituitary where the hormone is stopped or increased.
Occurs rapidly and within a few seconds a small adjustment is being made.

Front 11

Describe the neg. feedback loop for TSH:

Back 11

The Hypothalamus detects levels of thyroid hormone. If low, the Hypothalamus stimulates the pituitary to release TSH which stimulate the Thyroid to release thyroid hormone. If high, it doesn't.

Front 12

Describe the Hypothalamus-Pituitary axis feedback:

Back 12

CNS stim acts on the Hypothalamus, which releases Stimulating hormones.
The stimulating hormones act on the Pituitary, which releases Tropic hormones.
The Tropic hormones act on the Target gland, which releases the hormone. The hormone acts on the target tissue.

Front 13

The _______________systems work together to regulate metabolism.
________________ controls Epinephrine & NE

Back 13

Endocrine and nervous.
Hypothalamus

Front 14

When checking for a hormonal abnormality, always check for the specific hormone but also check for:

Back 14

secondary causes of hypothalamus and pituitary gland problems:
Adenomas are benign tumors that can compress the pituitary gland
Pheochromacytoma of the adrenal glands (adrenaline surge)

Front 15

Rate or timing of secretion:

Back 15

Cyclic patterns such as estrogen
Constant levels such as thyroxine
Intermittently based on demands such as insulin and glucagon
Diurnal pattern –ACTH and cortisol
Highest in the morning and lowest at night

Front 16

Where is insulin not needed for glucose transport?

Back 16

Brain cells don't need insulin for transport, Intestinal cells don't need it for absorptions, muscle cells can utilize glucose without a proportionate amounts of insulin.

Front 17

Describe the importance of glucose for Brain and nervous tissue.

Back 17

They rely almost exclusively on glucose for energy. The brain cannot make or store more than a few minutes worth of glucose, so a constant supply from the circulation is necessary.

Front 18

In those without DM, blood glucose levels are tightly regulated between:

Back 18

80 and 90mg/dL

Front 19

How much glucose from each meal is stored? Where?

Back 19

2/3 of all glucose is removed from the blood and stored as glycogen in the liver and skeletal muscle, the rest is used immediately.

Front 20

Glucose that is not needed for energy, what happens?

Back 20

When the liver & skeletal muscle is saturated, all additional glucose will be converted to fatty acids and stored as triglycerides in the adipose tissue cells.

Front 21

How is blood sugar regulated between meals?

Back 21

The pancreas releases glucagon, which stimulates the liver to release glucose from glycogen (Glycogenolysis).

Front 22

Glycogenolysis:

Back 22

converting stored glycogen into glucose

Front 23

Gluconeogenesis:

Back 23

converting amino acids, glycerol and lactic acid into glucose

Front 24

Glycogenesis:

Back 24

In conjunction with the hormone insulin, the liver responds to high levels of blood glucose by converting glucose to glycogen.

Front 25

Almost all body cells, with the exception of these, can use fatty acids interchangeably with glucose for energy.

Back 25

Brain, Nervous tissue, and RBCs.
Fatty acids cannot be converted to the glucose needed by the brain for energy.

Front 26

Insulin is released by:

Back 26

the Beta-cells of the Islet of Langerhans.

Front 27

What are all the things that Insulin does:

Back 27

Promotes glucose uptake into the cells
Promotes glycogenesis
Promotes protein synthesis
Promotes triglyceride synthesis by liver
Prevents glycogenolysis and Lipolysis
Prevents gluconeogenesis

Front 28

The beta cells cleave proinsulin into:

Back 28

active insulin and biologically inactive C-Peptide (connecting peptide).

Front 29

C-Peptide can be measured clinically to study Beta-cell function. Why is this significant for those w/ Type 2 DM?

Back 29

Those with Type 2 DM with very little or no remaining beta-cell function will have very low or non-existant serum C-Peptide levels.

Front 30

Glucagon is released by:

Back 30

the alpha-cells of the Islet of Langerhans.

Front 31

What does Glucagon do?

Back 31

Helps maintain steady blood glucose levels between meals and during fasting; acts directly on the liver to initiate Glycogenolysis within minutes. Also stimulates increase of amino acids into liver and initiates Gluconeogenesis, so that BG levels are maintained over time, since liver glucose levels are limited.

Front 32

Describe pathogenesis of Type 1 DM:

Back 32

Insulin deficit does not allow glucose to be transported into cell (mitochondria)
Serum glucose levels rise (hyperglycemia)
Excess glucose spills into the urine (glycosuria) as the level of glucose in the filtrate exceeds the capacity of the renal tubular transport limits to reabsorb it
Glucose in the urine exerts osmotic pressure in the filtrate & large volumes of urine are excreted (polyuria), leading to hypotension.
Fluids and electrolytes (Na and K) from the body are lost in the excess urine
Fluids loss from urine and high glucose levels draw water from the cells, resulting in cell dehydration
Causes increased thirst response (polydipsia)
Lack of nutrients and glucose entering the cell stimulates appetite (polyphagia)

Front 33

Pathogenesis of DKA:

Back 33

Insulin deficit does not allow glucose to enter the cell
Increased glucagon release
Lack of glucose in the cells results in rapid catabolism of fats and proteins for immediate energy
Leads to excessive fatty acids and their metabolites (ketones or amino acids) in the blood
Liver is limited by the amount of ketones it is able to process in a certain period of time, the excess is returned to the circulation (ketoacidosis)
Ketones bind with bicarb and lead to a decrease in pH (acidosis)
Ketoacids are excreted in urine
Dehydration develops from polyuria
GFR is decreased, limits excretion of ketoacids
Dehydration – increased thirst, skin turgor poor, tachycardia, hypotension
Hyperosmolarity of extracellular fluids from hyperglycemia leads to a shift in potassium from the intracellular to the extracellular compartments
Electrolyte imbalances – Low serum Na and High K
Kussmaul’s respirations (rapid and deep)
Sweet breath (acetone)
Lethargy, weakness, abdominal cramps, n/v
May lead to death, coma from decompensated metabolic acidosis