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dmd 5248 > Pancreas/Adrenal Hormones and Endocrine Pathology > Flashcards

Pancreas/Adrenal Hormones and Endocrine Pathology Flashcards

1
Q

What are the subdivisions of the adrenal glands

A

cortex and medulla

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2
Q

what are the functions of the adrenal cortex

A 
store lipids (cholesterol and fatty acids)
maufacture steroid hormones (corticosteroids)
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3
Q

what are the functions of the adrenal medulla

A

production of epinephrine and norepineprhine

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4
Q

what are the divisions of the adrenal cortex, and what do they produce

A 
zona glomerulosa (mineralocorticoids-aldosterone)
zona fasciculata (glucocorticoids-cortisol)
zona reticularis (androgens)
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5
Q

what is the function of aldosterone, and what causes it secretion

A

stimulates conservation of sodium and elimination of potassium.
it is stimulated by low Na in blood (or high K), low blood volume, and low bp

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6
Q

what are the actions of glucocorticoids

A

they accelerate glucose

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7
Q

what are the hormones of the adrenal medulla

A

epinephrine and norepinephrine

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8
Q

what are the actions of epinephrine and norepinephrine

A

mobilization of muscular glycogen and breakdown of glucose for ATP
fats are broken down into fatty acids - ATP production
glycogen breakdown in liver
increased heart rate and contractility

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9
Q

What are the characteristics of the exocrine pancreas

A

clusters of pancreatic acini and ducts that take up almost all of the pancreas and secrete alkaline into the digestive tract

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10
Q

What are the characteristics of the endocrine pancreas

A

cell clusters called pancreatic islets (islets of langerhans) with alpha, beta, delta, and F cells

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11
Q

What are the 4 types of cells in pancreatic islets, and what are their secretions

A

alpha cells - glucagon
beta cells - insulin
delta cells - hormone similar to GH-IH
F cells - pancreatic polypeptide

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12
Q

what does GH do in children and adults

A

children - muscle and skeletal development

adults - maintain blood glucose, mobilizes lipid reserves

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13
Q

what is the general adaptation syndrome (GAS)

A

the hormonal stress response

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14
Q

what are the phases of the general adaptation syndrome

A

alarm phase
resistance phase
exhaustion phase

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15
Q

what are the characteristics of the alarm phase of GAS

A

increased catacholamines from the adrenal medulla due to stress =

  • increased mental alertness
  • increased energy use by cells
  • mobilization of glycogen and lipid reserves
  • changes in circulation
  • sweating
  • increased heart rate
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16
Q

what are the characteristics of the resistance phase of GAS

A

increase in GH, glucagon, cortisol, aldosterone, renin due to stress

  • mobilization of remaining lipids and protein (break down of tissues)
  • elevation of blood glucose
  • conservation of Na and water
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17
Q

What are the charateristics of the exhaustion phase of GAS

A
  • lipid reserves exhausted
  • damage to organs
  • inability to produce glucoccorticoids
  • failure to balance electrolytes
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18
Q

what are the three classifications of endocrine pathologies

A

primary, secondary, and tertiary problems

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19
Q

what are primary, secondary, and tertiary problems of the endocrine system

A 
primary = issue is with the final gland
secondary = issue is with the pituitary gland
tertiary = issue is with the hypothalamus
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20
Q

how does ADH work

A

it places aquaporins into the collecting duct = water reabsorption

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21
Q

how is hypersecretion of ADH diagnosed

A

normal adrenal and tyroid function, water retention, hyponatremia (low Na), and hypoosmolarity

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22
Q

what causes ADH hypersecretion

A

ectopic production of ADH
surgery (stress)
drugs
cranial abnormalities

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23
Q

how is ADH hypersecretion treated

A

water restriction, removal of ADH producing tumor, ADH receptor blockers

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24
Q

What is hyposecretion of ADH called

A

diabetes insipidus (polyuria, and polydipsia - thirst) dilute urine, dehydration

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25
Q

what are the three types of diabetes insipidus

A

neurogenic - insufficient ADH
nephrogenic - insufficient ADH response
Psychogenic - drinking too much water

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26
Q

how do you clinically differentiate between the three types of diabetes insipidus

A
  1. restrict water if urine osmolarity increases = PSYCHOGENIC
  2. if it doesnt increase give them ADH
  3. If urine osmolarity increases = NEUROGENIC
  4. if it doesn’t increase = Nephrogenic
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27
Q

what are the treatments for the different types of diabetes insipidus

A 
neurogenic = supplement ADH
nephrogenic = drink a lot and eat NaCl
psychogenic = water restriction
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28
Q

what causes oxytocin release

A

cervix stretching, breast stimulation, baby crying, stress

29
Q

what is the problem with low oxytocin, and high oxytocin

A

hyposecretion = lack of milk, long labor, lack of compassion/bonding
hypersecretion - galactorrhea

30
Q

what happens to the anterior pituitary hormones when the hypothalamus isn’t working

A

all pituitary hormones decrease, except prolactin, which increases because PIF (inhibits prolactin) isn’t secreted

31
Q

if you have low levels of anterior pituitary hormones how do you determine if that is due to hypothalamic or anterior pituitary issues

A
  1. take a blood sample of hormones
  2. give them some hypothalamic releasing factor
  3. take another blood sample
  4. if the hypothalamic releasing factor increased the hormone levels then it is a hypothalamus problem, if it didn’t then its a pituitary problem
32
Q

what is pan hypopituitarism, and what causes it

A

when all of the anterior pituitary hormones are deficient, it it caused by non specific damage to the pituitary

33
Q

what are the two causes of hypopituitarism

A 
pituitary infarction (hemorrage in the brain)
empty sella syndrome
34
Q

what are the 4 causes of hyperpituitarism

A

benign pituitary adenoma
destruction of an end organ
hypothalamic disorder
carcinoma

35
Q

what is the most common hormone to be hyper expressed by the pituitary gladn

A

PRL

36
Q

what effect does a pituitary tumor have on the visual field

A

as the tumor grows it increases the blind spot in each eye

37
Q

what are the initial symptoms of a hyperpituitarism caused by a tumor

A

visual defect
headache
occulomotor palsies

38
Q

What stimulates, and inhibits prolactin release from the ant. pit.

A

stimulated by
- TRH and Oxytocin (from hypothalamus)
- stress, high estrogen, ovulation, suckling
Inhibited by
- somatostatin and dopamine (PRL causes this - feedback)
- estrogen and progesterone (pregnancy)

39
Q

what are the actions of PRL

A

proliferation of mammary tissue
sythesis milk proteins
calcium mobilization
stimulates immune system

40
Q

what are the effects of hypersecretion of PRL

A 
females
- amenorrhea
- galactorrhea
- hirsutism
- osteopenia
males
- hypogonadism
- impaired libido
- infertility
- gynecomastia
- galactorrhea
41
Q

what is the main treatment for PRL hypersecretion

A

dopamine agonists

42
Q

what is the problem with low PRL

A

poor milk production

decreased immune function

43
Q

What stimulates and inhibits the secretion of GH

A 
stimulated by
- GHRH
- Ghrelin (from stomach)
- estrogen and testosterone
inhibited by
- somatostatin (- feedback of GH on hypothalamus)
- IGF (somatomedins)
44
Q

what are the actions of GH

A 
stimulate IGF production
growth of long bones (with IGF)
increase protein AA incorporation (with IGF)
inhibit protein breakdown (with IGF)
increase lipolysis (with IGF)
inhibits hepatic glucose uptake
stimulates the immune system
45
Q

hypersecretion of GH =

A

gigantism

acromegaly

46
Q

how is hypersecretion of GH treated

A

somatostatin analogs

47
Q

What stimulates and inhibits the release of TSH

A 
stimulated by 
- TRH
- Cold
Inhibited by
- T3
- Dopamine
- Somatostatin
- stress
48
Q

what are the actions of T3

A

regulates the basal metabolic activity of most cells

increase mRNA synthesis

49
Q

What is the difference between congenital cretinism and developmental cretinism

A

congenital cretinism is when a pregnant mother and the fetus both have hypothyroidism. developmental cretinism is when only the fetus has hypothyroidism (less severe, can be treated with thyroid supplements)

50
Q

What is hashimoto thyroiditis

A

autoimmune destruction of thyroid gland, most common cause of hypothyroidism

51
Q

what is dequervain thyroiditis

A

enlaged sore thyroid following a URI

52
Q

What is silent thyroiditis

A

alternating hypothyroiditis and hyper thyroiditis occuring in middle age, or postpartum women

53
Q

What is Reidel thyroiditis

A

rare hypothyroidtis with a large mass that compresses the trachea

54
Q

what is graves disease

A

an autoimmune hyperthyroidism where anti TSH-receptors bind, and ACTIVATE TSH receptors, causing high levels of T3 and T4
(SCALLOPED COLLOID)

55
Q

When do patients get goiters

A

too much TSH, can be normal, high, or low levels of T3 and T4

56
Q

which goiter is more likely a tumor diffuse or nodular

A

nodular

57
Q

what is the difference between cushing disease and cushing syndrome

A

cushing disease is elevated ACTH production due to a pituitary tumor which causes elevated cortisol. cushing syndrome is elevated cortisol caused by an adrenal tumor or taking too much cortisol

58
Q

how does MCH relate to ACTH

A

when ACTH is synthesized, it is broken off of POMC. one peice becomes ACTH the other becomes MCH

59
Q

what does high MCH cause

A

hyperpigmentation

60
Q

What does elevated cortisol cause

A 
insulin resistance
weight gain
increased blood glucose
muscle wasting
osteoporosis
decreased immunity
sensitivity to catecholectamines
61
Q

how do you differentiate between causes of high cortisol levels

A 
dexamethasone test (synthetic cortisol)
if low does decreases ACTH and cortisol it is chronic stress causing it. 
if it takes a high does to decrease ACTH and cortisol it is a pituitary tumor
if nothing decreases ACTH and cortisol it is caused by ectopic ACTH
62
Q

what happens with catecholectamine hypersecretion

A

it is caused by adrenal medulla hyperfunction (tumors of the chromaffin cells) and it causes elevated HR, elevated BP, diaphoresis, weight loss, hyperglycemia

63
Q

What is addison disease

A

primary adrenal insufficiency, too little cortisol and mineralocorticoids. typically caused by autoimmunity

64
Q

what are the symptoms of addison disease

A

slow onset
weakness
hypotension
skin hyperpigmentation

65
Q

What is MEN

A

multiple endocrine neoplasia

66
Q

What is MEN 1 vs. MEN 2

A

MEN 1 is when most of the neoplasia is outside of the thyroid (parathyroid, pancreas, and pituitary)
MEN 2 is when most of the neoplasia is found in the thyroid

67
Q

What is the main difference between MEN 2a and MEN 2b

A

MEN 2b includes marfan characteristics

68
Q

What determines which part of the body with store fat

A

the areas with lipoprotein lipase LPL will gain the most fat

dmd 5248 (12 decks)

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