Endo 4 Flashcards

1
Q

What is addison’s disease?

A

Hypofunction of the adrenal cortex:

The cortex will no longer produce cortisol and aldosterone (adrenocortical hormones)

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2
Q

What will be the physiological effects of a lack of cortisol (glucocorticoid hormone)? What will be the associated symptoms?

A

In Addison’s disease, a glucocorticoid hormone deficiency will cause a drop in blood sugar (less lipolysis)
- Lack of energy
- Muscular weakness
- Inability to take stress

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3
Q

What will be the physiological effects of a lack of Aldosterone (mineralocorticoid hormone)? What will be the associated symptoms?

A

There will be an electrolyte imbalance (low Na and high K), low ions, and water will be lost in urine. Plasma volume will decrease as well as as CO

Death by shock after 7 days without mineralocorticoids

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4
Q

What are the possible causes of addison’s disease?

A

Total destruction of the gland because of:
- Autoimmune attack on the adrenal gland
-Tuberculosis

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5
Q

What is Cushing’s disease?

A

Hyperfunction of the adrenal cortex:

Excessive production of glucocorticoids and mineralocorticoids

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6
Q

What are the possible causes of Cushing’s disease?

A

increased circulating levels of ACTH from
- Pituitary tumor
- Adrenal tumor

(characterized by a hyperplasia of one or two of the endocrine sites

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7
Q

What will be the physiological effects of an increase of cortisol (glucocorticoid hormone)? What will be the associated symptoms?

A

Blood glucose and insulin production will increase. This is bc of a decrease in protein synthesis but increase in protein breakdown

-Osteoporosis (loss of protein and Ca in bone)
-Puffiness in face because of fluid retention

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8
Q

What will be the physiological effects of an increase of Aldosterone (mineralocorticoid hormone)? What will be the associated symptoms?

A

Plasma Na will increase from being reabsorbed and can lead to hypertension because of an increase in plsma volume

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9
Q

CASE STUDY: surgery from Cushing disease caused a momentary Addison’s disease

A

Slide 3

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10
Q

What are the endocrine structures of the pancreas?

A

The islets of Langerhans

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11
Q

What percentage of the islets of Langerhans produce which hormones?

A

60%: beta cells that synthesise insulin
25%: alpha cells that synthesise glucagon

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12
Q

Why is insulin more important that glucagon?

A

bc it is the only hormone that can lower blood sugar

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13
Q

Where can glucose be found in the body (and in different tissues)?

A

It is always in the blood, but very little is free in the tissues, it will be transported into cells with insulin and then:
- converted to glycogen in the liver
- Converted to fat and stored in adipose tissue
- Oxidized to produce energy in other various cells

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14
Q

When does insulin deficiency occur?

A

When beta cells are destroyed because of autoimmune disease (causes Diabetes Mellitus)

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15
Q

What happens during insulin deficiency?

door is locked

A

Glucose can’t enter cells, and causes a negative feedback loop to increase breakdown of protein, and get more glucose (keep blood glucose high) with increased gluconeogenesis. The body tries to find new sources of energy with free fatty acids

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16
Q

How is fat used as energy in an insulin deficiency? WHat can this kind of energy usage lead to?

A

There is an increased lipolysis to get access to free fatty acids. However, fat is not effectively used and has incomplete oxidation. This results in an increased circulating acetone and other acids (smelly breath-Ketosis)

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17
Q

What happens if insulin deficiency stays untreated for too long?

A

The build-up in acids lowers the blood pH, a diabetic coma and even death if untreated

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18
Q

What are all the symptoms of Diabetes Mellitus

A

Glucose spilled into urine: GLYCOSUREA
Water follows into urine: POLYUREA
KETOSIS
METABOLIC ACIDOSIS

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19
Q

What is the difference between Type 1 and Type 2 diabetes?

A

Type 1 (insulin dependent): an insulin deficiency because of lack of synthesis or because of a defective insulin release

Type 2 (insulin independent): When insulin levels are normal or abnormally high but are hyporesponsive

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20
Q

Why is there a hyporesponsiveness of insulin in type 2 diabetes?

A

Obesity and overeating cause prolonged high insulin levels which decreases the number of receptors for insulin

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21
Q

What is the treatment for Type 1 diabetes?

A

Administration of insulin. Not too much to not lower blood sugar into a coma inducing state

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22
Q

What is the treatment for type 2 diabetes?

A

A proper diet and exercise to decrease insulin and upregulate the amount of receptors

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23
Q

How is the glucose tolerance test used to asses the presence of diabetes?

A

After an overnight fasting, a patient is given a known amount of glucose. Blood glucose is measured before and after administration (30 mins interval) to see how blood sugar levels react.

If blood sugar returns to normal –> No diabetes
If blood sugar stays high –> low tolerance = diabetes
If blood sugar goes low –> high tolerance = hyperinsulinism

24
Q

What allows control of insulin secretions? (stimulis and receptors/effectors)

A
  • Beta cells respond to the levels of blood sugar
  • Gastrin and vagal impulses from the digestive tract go to the beta cells to induce release of insulin before there even is a change in blood glucose levels
25
Q

What kind of hormone is Glucagon? Where is it synthesized and released from?

A

a peptide hormone
It is synthesized and released from the alpha cells of the pancreas

26
Q

What are the functions of glucagon? (2)

A
  • Raising blood sugar by promoting glycolysis and glucogenesis in the liver
  • increases rate of lipolysis in adipose tissue to increase fatty acid concentration in circulation
27
Q

What is glucagon release controlled by and where is it released from?

A

The concentration of glucose in circulation modifies the activity of pancreatic alpha cells (low blood sugar = more synthesis and release)

28
Q

What is GLP-1? where is it produced?

A

It’s a glucagon-like-peptide, derived from the same precursor as glucagon.
It is produced by an enteroendocrine L cell in the intestine

29
Q

What are the GLP-1 actions? (4)

(muscle and adipose cells, pancreas, digestive tract and brain, heart)

A
  • It increases glucose uptake and oxidation to lower blood sugar
  • It increases insulin secretion in the pancreas
  • It slows down digestion as well as lowering appetite and increasing satiety
  • It can decrease risks of heart disease
30
Q

What are GH and where are they released from?

A

It’s a single chain polypeptide produced by the anterior lobe of the pituitary

31
Q

What is the function of the GH?

A
  • Increase protein synthesis in many tissues
  • Increases the rate of lipolysis to use fatty acids as a source of energy
32
Q

How does the GH increase protein synthesis?

A

It enhances amino acid uptake by cells and increases transcription and translation of mRNA

33
Q

What effect of the GH is NOT mediated by the somatomedins?

A

The increased rate in lipolysis

34
Q

What is the primary role of the somatomedins?

A

They increase protein synthesis and stimulate growth

35
Q

How is the release of GH controlled?

A

(i) GRH (somatoliberin) stimulates the release of GH
(ii) GIH (somatostatin) inhibits the release of GH
–> the presence of somatomedians in the blood has a negative feedback loop effect on the GRH
–> Exercise, sleep, stress and low blood sugar enhance somatostatin effects

36
Q

When, in a day, is there less GH in the circulation? why?

A

During the night because sleep enhanced somatostatins which inhibit GH release

37
Q

Why does exercise impede growth?

A

The energy will be directed towards activity and movement rather than growth

38
Q

What are the effects of a GH deficiency on young people?

A

It leads to a PROPORTIONAL decrease in physical growth (a form of dwarfism)

39
Q

What are the effects of a GH excess on young people?

A

It leads to gigantism

40
Q

What are the effects of a GH excess later in life?

A

A pituitary tumour can cause acromegaly, where many bones (especially cartilaginous regions) get longer and heavier

41
Q

What are the two function of gonads?

A

1-Gametogenesis (the production of reproductive cells aka gamets)
2-Secretion of sex hormones: testosterone (androgen) in males and estrogen and progesterone in female

42
Q

Is the difference in reproductive endocrinology in males and females quantitative or qualitative?

A

Quantitative means both produce the same hormones, but not in the same amount.

43
Q

What is the primary function of estrogen in males?

A

Maintain bone density.

44
Q

How is estrogen produced in males?

A

Produced locally in tissues by converting testosterone into estrogen estradiol with aromatase.

45
Q

What are the consequences of estrogen deficiency in males?

A

1-Leads to increased body fat
2-CAN decrease sexual desire and erectile function

46
Q

How is reprodructive function (general hormones and gamets) controlled?

A

1-GnRH (Gonadotropin releasing hormone) is secreted by the hypothalamus to reach the anterior pituitary gland.
2-This stimulates the release of pituitary gonadotropins (FSH and LH)
3-Both hormones stimulate the development of spermatozoa or ova and secretion of sex steroids.
4-Sex steroids have effect in gonads and other parts of the body.

47
Q

What do gonads produce to control gonadotropin release?

A

Produces inhibin proteins which feed back on the anterior pituitary to block the release of FSH.

48
Q

What is the principal function of testies?

A

1-Spermatogenesis: Production of mature germ cells
2-Steroidogenesis: Production of steroid hormones

49
Q

Guess what?

A

I lovvvve youuu

50
Q

How long is the process or maturation from a spermatogonia to the mature spermatozoon?

A

Approx. 60 days

51
Q

What two cells are critical for maturation of spermatozoa and where are they?

A

1-Leydig cells. They are outside the seminiferous tubes.
2-Sertoli cells. They are within the seminiferous tubes.

52
Q

Do you want o go on a date?

A

Only answer is yes duh.

53
Q

What is the function of leydig cells?

A

In response to LH, they synthesise androgens.

54
Q

What is the function to sertoli cells?

A

In response of FSH, they synthesise ABP (Androgen binding protein) and inhibin.

55
Q

What is spermatogenesis dependent on? What assures the correct conditions?

A

High androgens concentration in the seminiferous tubes.
These concentrations are insured by the presence of ABP.

56
Q

Last thing now

A

You want to marry me?

57
Q

What is the testicular androgen synthesis regulated by? (sexual cells feedback in males)

A

1-Hypothalamic-pituitary-Leydig cell axis: GnRH stimulates LH which stimulates Leydig cells to produce androgen which inhibits GnRH, LH and FSH.
2-Hypothalamic-pituitary-seminiferous-tubules axis: GnRH stimulates FSH which stimulates spermatogenesis and Sertoli cells to produce inhibin. Inhibin inhibits FSH release only.