ENDOCRINOLOGY PART 3 Flashcards

1
Q

are small, triangular-shaped glands
located on top of each kidney. They produce hormones such
as cortisol, adrenaline, which play vital roles in regulating
metabolism, electrolyte balance, stress response, and other
essential bodily functions.

A

Adrenal gland

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2
Q

Parts of adrenal gland

A
  1. Adrenal cortex -90%
  2. Adrenal medulla -10%
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4
Q
A
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5
Q

glucocorticoid = cortisol

A

Zona fasciculata

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6
Q

Sex hormones or weak androgens

A

Zona reticularis

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7
Q

Made up of Chromaffin Cells
i. Secretes catecholamines
1. Amine hormones, like
epinephrine, norepinephrine,
dopamine
b. Epinephrine
c. Norepinephrine

A

Adrenal medulla

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8
Q

responsible for electrolyte balance and regulate blood
pressure

A

Aldosterone

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9
Q

Regulate mineral balance

A

Mineralcorticoids - aldosterone

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10
Q

Regulate glucose metabolism

A

glucocorticoids cortisol

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11
Q

Stimulate masculinization

A

androgens

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12
Q

stress hormones, stimulate sympathetic ANS

A

adrenal medulla

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13
Q

principal regulator of electrolyte balance
sodium reabsorption (sodium retention hormone)
○ Main function is to retain sodium

A

mineralcorticoid - aldosterone

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14
Q
A
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15
Q

major determinant of the renal excretion of potassium
regulates blood pressure

A

MINERALOCORTICOID
(aldosterone)

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16
Q
A
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17
Q

synthesis: controlled by the

A

RAAS - RENIN-ANGIOSTENIN-ALDOSTERONE SYSTEM

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18
Q

When sodium is ______, potassium is ____

A

retained - secreted

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19
Q

As to electrolyte balance:
○ It acts on renal tubular epithelium to increase
retention of Na+ and Cl-, and excretion of K+
and H+
○ It promotes the 1:1 exchange of sodium for
potassium or hydrogen ions.

A

MINERALOCORTICOID
(aldosterone)

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20
Q

principal glucocorticoid
only hormone known to inhibit the anterior pituitary
secretion of ACTH by negative feedback

A

GLUCOCORTICOIDS
(cortisol)

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21
Q
A
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22
Q

It is the only hormone that sends negative
feedback to the hypothalamus to stop releasing
CRH, which will also inhibit the secretion of
ACTH

A

GLUCOCORTICOIDS
(cortisol)

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23
Q

enhances glucose production from CHONs, acting as
insulin antagonist

A

GLUCOCORTICOIDS
(cortisol)

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24
Q

Only hypoglycemic agent

A

insulin

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25
Q

stimulates lipolysis and depress immune responses

A

GLUCOCORTICOIDS
(cortisol)

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26
Q

transport protein of cortisol

A

TRANSCORTIN
CORTISOL BINDING GLOBULIN

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27
Q

urinary metabolite:

A

17-hydroxycorticosteroids
17-ketogenic steroids

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28
Q

a.k.a ” weak androgens ”
By-products of cortisol synthesis that are regulated by
ACTH

A

ADRENAL ANDROGEN

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29
Q

precursor of cortisol

A

ACTH

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30
Q

the precursor for your weak androgens

A

CORTISOL

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31
Q

Serve as precursors for the production of more potent
androgens and estrogens in tissues
They circulate bound to

A

adrenal androgens

bound to SHBG - steroid hormone binding globulin

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32
Q

Principal adrenal androgen:

A

DHEA dihydroepiandrosterone

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33
Q

Sulfated form of DHEA:

A

DHEA-S

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34
Q

Precursors of androgens:

A

DHEA AND DHEA-S

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35
Q

Hormones produced from DHEA and DHEA-S:

A

estrogen
testosterone
androstenedione
5-dihydroestosterone

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36
Q

the principal adrenal androgen, is converted
to _____

A

DHEA TO ESTRONE

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37
Q

Principal medullary hormone
produced from norepinephrine and comes only from
the adrenal gland

A

EPINEPHRINE 80%

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38
Q

called the “ fight or flight” hormone (adrenaline)
regulates glucose metabolism (glycogenolysis)

HYPERGLYCEMIC AGENT

A

EPINEPHRINE

hypoglycemic- INSULIN

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39
Q

Best sample collection of epinephrine

A

indwelling catheter

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40
Q

Ratio of norepinephrine to
epinephrine in serum

A

9:1

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41
Q

also produced by the brain
because it is a neurotransmitter.
■ Produced by the CNS and sympathetic
nervous system (SNS)
○ ______ the serum

A

98% norepinephrine

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42
Q

The catecholamines are 50% protein bound.

A

TRUE

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43
Q

highest secretion is found in the brain
acts as a neurotransmitter in both CNS and
sympathetic nervous system (SNS)

A

NOREPINEPHRINE 20%

44
Q

NOREPINEPHRINE
Metabolite in CNS

A

3-methoxy-4-hydroxyphenylglycol

45
Q

major intact catecholamines present in the urine

46
Q

present in highest concentration in the regions of the brain.
mobilize energy stores and prepare the body for
muscular activity and stressful conditions

47
Q

Catecholamines should be rapidly eliminated in the body

48
Q

Major metabolite of medullary metabolies

A

vanillyl mandelic acid

49
Q

Minor metabolites:

A

homivanilic acid

50
Q

Sample for analysis for medullary metabolies

A

24 hour urine

51
Q

This refers to a group of clinical entities that arise from
absent or diminished activity of enzymes involved in
steroidogenesis. The mineralocorticoid, glucocorticoid,
and androgen production pathways can be affected to
varying degrees based on the enzyme affected.

A

congenital adrenal hyperplasia

52
Q

a. Pregnenolone from G region will not turn into
aldosterone, but it can turn into 17a-OH
pregnenolone in the F region
b. 17a-OH pregnenolone in the F region cannot
become cortisol, but it can turn into DHEA in
the R region
c. DHEA in the R region cannot turn into your
androgens
d. Therefore, there will be increased DHEA

53
Q

Pregnenolone and progesterone will not turn
into 17a-OH pregnenolone and 17a-OH
progesterone in the F region
b. Therefore, there would be increase in
aldosterone because there is no formation of
your cortisol and your weak androgens

A

17a-hydroxylase

54
Q

11-Deoxycorticosterone (DOC) will increase

A

11B-HYDROXYLASE

55
Q

Increase progesterone and 17a-OH
progesterone
b. Can continue to form DHEA to form estradiol

A

21B-HYDROXYLASE

56
Q

This is a rare disorder characterized by insufficient
production of adrenal hormones, particularly cortisol and
aldosterone. This deficiency leads to symptoms such as
fatigue, weight loss, low blood pressure, and skin
darkening, often triggered by autoimmune destruction of
the adrenal glands.

A

ADDISON’S DISEASE

57
Q
  1. Aldosterone ↓
  2. Cortisol ↓
  3. Renin ↑
A

PRIMARY ADRENAL INSUFFICIENCY

58
Q

PRIMARY = ORGAN
SECONDARY = PITUITARY
TERTIARY =HYPOTHALAMUS

59
Q

This is a condition characterized by the overproduction of
aldosterone hormone by the adrenal glands, leading to
hypernatremia and hypokalemia. It often results from
adrenal gland tumors or hyperplasia.

A

CONN’s disease -overproduction

hypernatremia
hypokalemia

60
Q
  1. Aldosterone↑
    a. Problem is too much aldosterone
  2. Cortisol (N)
    a. Problem is zona glomerulosa
    b. No problem in zona fasciculata
  3. Renin ↓
    a. Because of high aldosterone levels
A

PRIMARY ALDOSTERONISM

61
Q

aldosterone secretion
in ______ hyperaldosteronism is driven by factors
such as decreased blood flow to the kidneys or activation of the renin-angiotensin- aldosterone system in response to volume depletion or sodium loss.

A

SECONDARY HYPERALDOSTERONISM

62
Q

Problem is in the pituitary gland

Aldosterone ↑
Cortisol (N)
Renin ↑

A

SECONDARY ALDOSTERONISM

63
Q

caused by a
benign tumor of the pituitary gland that leads to
excessive secretion of adrenocorticotropic hormone
(ACTH), which in turn stimulates the adrenal glands to produce too much cortisol.
This is hypersecretion of cortisol (ACTH
independent) due to primary adrenal disease like adenoma
○ features: central obesity, buffalo hump, moon
face, hypertension,hirsutism, purple striae,
easy bruising, muscle weakness

A

CUSHING DISEASE

64
Q

enlargement of estrogen and testosterone levels. It can manifest as a benign swelling or firm mass beneath the nipples
There is a problem in the zona reticularis

Zona reticularis
Estrogen ↑
Testosterone ↓

A

GYNECOMASTIA

65
Q

elevated plasma testosterone in women as a result
of ovarian or adrenal tumor (virilizing adenoma)
excessive hair in women
○ Growth of hair that is not common in women,
like in chest

A

VIRILISM OR HIRSUTISM

66
Q

rare catecholamine-secreting tumors arising
from the chromaffin cells. The name was coined based on
the dusky color of the tumor after staining with chromium

A

PHEOCHROMOCYTOMA

67
Q

●Adrenal medulla
○Increase in catecholamines
●Chromaffin cells
● Catecholamine

A

PHEOCHROMOCYTOMA

68
Q

Fatal malignant condition in children in which cancer
of the nervous system causes excess production of Norepinephrine

A

NUEROBLASTOMA

69
Q

diagnostic test for neuroblastoma

A

24 hour urine
vanillylmandelic acid or homovanillic acid test

70
Q

Blackening and/or bulging of the eyes, problem in the
abdomen, neck, and head
Treated by surgery

A

neuroblastoma

71
Q

Hypertension, hypokalemia, and metabolic
alkalosis

A

hyperaldosteronism

72
Q

Hypertension, anxiety spells, palpitations,
dizziness, and diaphoresis

A

PHEOCHROMOCYTOMA

73
Q

Hypertension, rapid unexplained weight gain,
red/purple stretch marks, and proximal muscle
weakness

A

cushing syndrome

74
Q

Anorexia nervosa, unexplained weight loss, and
skin pigmentation

A

adrenal insufficiency

75
Q

dual-function organ located behind the
stomach in the abdomen. It serves both endocrine functions,
producing hormones like insulin and glucagon to regulate blood
sugar levels, and exocrine functions, secreting digestive enzymes

76
Q

glycogenolysis and gluconeogenesis
○ From alpha cells

77
Q

glycogenesis, glycolysis, lipogenesis
○ From beta cells

78
Q

From delta cells

A

somatostatin

79
Q

causes secretion of HCl, pepsin, pancreatic enzymes by parietal cells;
relaxes iliocecal sphincter

80
Q

a tetradecapeptide with a disulfide bond
first isolated from the hypothalamus: originally
considered a hypothalamic hormone that inhibited
growth hormone secretion

A

SOMATOSTATIN

81
Q

discovered also in the islets of Langerhans and in the GIT

inhibits pituitary (GH and thyrotropin), gastrointestinal
(gastrin, secretin, peptide), and pancreatic (insulin, glucagon) hormones
possesses nonendocrine functions (e.g.,
inhibition of
gastric acid secretion, gastric emptying time and,
pancreatic enzyme release)

A

SOMATOSTATIN

82
Q

first isolated somatostatin peptide

A

Somatostatin - 14

84
Q

with N-terminal extension; a more
potent inhibitor of other islet hormones.

A

somatostatin 28

85
Q

37 amino acid protein

A

islet amyloid polypeptide

86
Q

colocalized and cosecreted with insulin in response to
stimulation with nutrients
inhibits insulin secretion, slow gastric emptying, and
inhibit postprandial glucagon secretion

87
Q

in hyperinsulinemic, pancreatic
cancer, insulin -resistant states, such as
impaired glucose tolerance and early type 2
diabetes (amyloid deposits, fibroid material
derived from IAPP)

A

HIGH LEVEL - TYPE2 DIABETES

88
Q

type 1 diabetes

A

LOW LEVELS OF AMYLIN

89
Q

Hypersecretion of insulin
May be due to tumor, insulinomia
a. Low blood glucose
b. Tumor in beta cells

A

hyperinsulinism

90
Q

Caused by pancreatic cell tumors, which
overproduce gastrin, are called

A

GASTRINOMA
ZOLLINGER ELLISON SYNDROME

91
Q

Hypersecretion of somatostatin by a tumor

Tumor in the delta cells
Low GH

A

somatostatinoma

92
Q

Hypersection of glucagon by a tumor
Presenting with widespread dermatitis, weight loss,
glossitis, and abnormal glucose tolerance associatd
with an islet cell neoplasm of the pancreas on
autopsy specimen

A

GLUCAGONOMA

93
Q

4D SYNDROME OF GLUCAGONOMA

A

diabetes
dermatosis
deep vein thrombosis
depression

94
Q

(due to immune β-cell destruction,
usually leading to absolute insulin deficiency, including
latent autoimmune diabetes of adulthood)

95
Q

Due to a progressive loss of adequate β-cell insulin
secretion frequently on the background of insulin
resistance

A

TYPE 2 PROGRESSIVE

96
Q

Diabetes diagnosed in the second or third trimester of
pregnancy that was not clearly overt diabetes prior to
gestation

A

GESTATIONAL DM

97
Q

known as fibrocytic disease of the pancreas and
mucoviscidosis
an inherited autosomal recessive disorder
characterized by dysfunction of mucous and
exocrine glands throughout the body.

relatively common and occurs in about 1 of 1,600 live births

A

cystic fibrosis

98
Q

manifestations: intestinal obstruction of the
newborn, excessive pulmonary infections in
childhood, or, uncommonly, as pancreatogenous
malabsorption in adults

A

cystic fibrosis

99
Q

causes the small and large ducts and the acini to
dilate and convert into small cysts filled with mucus,
resulting in the prevention of pancreatic secretions
reaching the duodenum or, depending on the age of
the patient, a plug that blocks the lumen of the
bowel, leading to obstruction

A

cystic fibrosis

100
Q

inflammation of the pancreas
ultimately caused by autodigestion of the pancreas as a result of reflux of bile or duodenal contents into the pancreatic duct.
○ Pathologic changes: acute edema; cellular
infiltration, leading to necrosis of the acinar
cells, with hemorrhage as a possible result of
necrotic blood vessels; and intrahepatic and
extrahepatic pancreatic fat necrosis.

A

pancreatitis

101
Q

no permanent damage to the
pancreas

A

acute pancreatitis

102
Q

chronic (irreversible injury), or
relapsing/recurrent

A

chronic pancreatitis

103
Q

4th most frequent form of fatal cancer and causes
about 38,000 deaths each year in the United States
5-year survival rate is about 6% and most patients
die within 1 year of diagnosis
most pancreatic tumors arise as adenocarcinomas
of the ductal epithelium

A

pancreatic carcinoma

105
Q

mineralocorticoid = aldosterone

A

ZONA GLOMERULOSA