ENDOCRINOLOGY PART 3 Flashcards
(104 cards)
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
2
Q
Parts of adrenal gland
A
- Adrenal cortex -90%
- Adrenal medulla -10%
4
Q
A
5
Q
glucocorticoid = cortisol
A
Zona fasciculata
6
Q
Sex hormones or weak androgens
A
Zona reticularis
7
Q
Made up of Chromaffin Cells
i. Secretes catecholamines
1. Amine hormones, like
epinephrine, norepinephrine,
dopamine
b. Epinephrine
c. Norepinephrine
A
Adrenal medulla
8
Q
responsible for electrolyte balance and regulate blood
pressure
A
Aldosterone
9
Q
Regulate mineral balance
A
Mineralcorticoids - aldosterone
10
Q
Regulate glucose metabolism
A
glucocorticoids cortisol
11
Q
Stimulate masculinization
A
androgens
12
Q
stress hormones, stimulate sympathetic ANS
A
adrenal medulla
13
Q
principal regulator of electrolyte balance
sodium reabsorption (sodium retention hormone)
○ Main function is to retain sodium
A
mineralcorticoid - aldosterone
14
Q
A
15
Q
major determinant of the renal excretion of potassium
regulates blood pressure
A
MINERALOCORTICOID
(aldosterone)
16
Q
A
17
Q
synthesis: controlled by the
A
RAAS - RENIN-ANGIOSTENIN-ALDOSTERONE SYSTEM
18
Q
When sodium is ______, potassium is ____
A
retained - secreted
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)
20
Q
principal glucocorticoid
only hormone known to inhibit the anterior pituitary
secretion of ACTH by negative feedback
A
GLUCOCORTICOIDS
(cortisol)
21
Q
A
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)
23
Q
enhances glucose production from CHONs, acting as
insulin antagonist
A
GLUCOCORTICOIDS
(cortisol)
24
Q
Only hypoglycemic agent
A
insulin
25
Q
stimulates lipolysis and depress immune responses
A
GLUCOCORTICOIDS
(cortisol)
26
transport protein of cortisol
TRANSCORTIN
CORTISOL BINDING GLOBULIN
27
urinary metabolite:
17-hydroxycorticosteroids
17-ketogenic steroids
28
a.k.a ” weak androgens ”
By-products of cortisol synthesis that are regulated by
ACTH
ADRENAL ANDROGEN
29
precursor of cortisol
ACTH
30
the precursor for your weak androgens
CORTISOL
31
Serve as precursors for the production of more potent
androgens and estrogens in tissues
They circulate bound to
adrenal androgens
bound to SHBG - steroid hormone binding globulin
32
Principal adrenal androgen:
DHEA dihydroepiandrosterone
33
Sulfated form of DHEA:
DHEA-S
34
Precursors of androgens:
DHEA AND DHEA-S
35
Hormones produced from DHEA and DHEA-S:
estrogen
testosterone
androstenedione
5-dihydroestosterone
36
the principal adrenal androgen, is converted
to _____
DHEA TO ESTRONE
37
Principal medullary hormone
produced from norepinephrine and comes only from
the adrenal gland
EPINEPHRINE 80%
38
called the “ fight or flight” hormone (adrenaline)
regulates glucose metabolism (glycogenolysis)
HYPERGLYCEMIC AGENT
EPINEPHRINE
hypoglycemic- INSULIN
39
Best sample collection of epinephrine
indwelling catheter
40
Ratio of norepinephrine to
epinephrine in serum
9:1
41
also produced by the brain
because it is a neurotransmitter.
■ Produced by the CNS and sympathetic
nervous system (SNS)
○ ______ the serum
98% norepinephrine
42
The catecholamines are 50% protein bound.
TRUE
43
highest secretion is found in the brain
acts as a neurotransmitter in both CNS and
sympathetic nervous system (SNS)
NOREPINEPHRINE 20%
44
NOREPINEPHRINE
Metabolite in CNS
3-methoxy-4-hydroxyphenylglycol
45
major intact catecholamines present in the urine
DOPAMINE
46
present in highest concentration in the regions of the brain.
mobilize energy stores and prepare the body for
muscular activity and stressful conditions
DOPAMINE
47
Catecholamines should be rapidly eliminated in the body
TRUE
48
Major metabolite of medullary metabolies
vanillyl mandelic acid
49
Minor metabolites:
homivanilic acid
50
Sample for analysis for medullary metabolies
24 hour urine
51
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.
congenital adrenal hyperplasia
52
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
3B-HSD II
53
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
17a-hydroxylase
54
11-Deoxycorticosterone (DOC) will increase
11B-HYDROXYLASE
55
Increase progesterone and 17a-OH
progesterone
b. Can continue to form DHEA to form estradiol
21B-HYDROXYLASE
56
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.
ADDISON’S DISEASE
57
4. Aldosterone ↓
5. Cortisol ↓
6. Renin ↑
PRIMARY ADRENAL INSUFFICIENCY
58
PRIMARY = ORGAN
SECONDARY = PITUITARY
TERTIARY =HYPOTHALAMUS
TRUE
59
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.
CONN’s disease -overproduction
hypernatremia
hypokalemia
60
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
PRIMARY ALDOSTERONISM
61
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.
SECONDARY HYPERALDOSTERONISM
62
Problem is in the pituitary gland
Aldosterone ↑
Cortisol (N)
Renin ↑
SECONDARY ALDOSTERONISM
63
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
CUSHING DISEASE
64
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 ↓
GYNECOMASTIA
65
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
VIRILISM OR HIRSUTISM
66
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
PHEOCHROMOCYTOMA
67
●Adrenal medulla
○Increase in catecholamines
●Chromaffin cells
● Catecholamine
PHEOCHROMOCYTOMA
68
Fatal malignant condition in children in which cancer
of the nervous system causes excess production of Norepinephrine
NUEROBLASTOMA
69
diagnostic test for neuroblastoma
24 hour urine
vanillylmandelic acid or homovanillic acid test
70
Blackening and/or bulging of the eyes, problem in the
abdomen, neck, and head
Treated by surgery
neuroblastoma
71
Hypertension, hypokalemia, and metabolic
alkalosis
hyperaldosteronism
72
Hypertension, anxiety spells, palpitations,
dizziness, and diaphoresis
PHEOCHROMOCYTOMA
73
Hypertension, rapid unexplained weight gain,
red/purple stretch marks, and proximal muscle
weakness
cushing syndrome
74
Anorexia nervosa, unexplained weight loss, and
skin pigmentation
adrenal insufficiency
75
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
PANCREAS
76
glycogenolysis and gluconeogenesis
○ From alpha cells
GLUCAGON
77
glycogenesis, glycolysis, lipogenesis
○ From beta cells
INSULIN
78
From delta cells
somatostatin
79
causes secretion of HCl, pepsin, pancreatic enzymes by parietal cells;
relaxes iliocecal sphincter
GASTRIN
80
a tetradecapeptide with a disulfide bond
first isolated from the hypothalamus: originally
considered a hypothalamic hormone that inhibited
growth hormone secretion
SOMATOSTATIN
81
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)
SOMATOSTATIN
82
first isolated somatostatin peptide
Somatostatin - 14
83
84
with N-terminal extension; a more
potent inhibitor of other islet hormones.
somatostatin 28
85
37 amino acid protein
islet amyloid polypeptide
86
colocalized and cosecreted with insulin in response to
stimulation with nutrients
inhibits insulin secretion, slow gastric emptying, and
inhibit postprandial glucagon secretion
amylin
87
in hyperinsulinemic, pancreatic
cancer, insulin -resistant states, such as
impaired glucose tolerance and early type 2
diabetes (amyloid deposits, fibroid material
derived from IAPP)
HIGH LEVEL - TYPE2 DIABETES
88
type 1 diabetes
LOW LEVELS OF AMYLIN
89
Hypersecretion of insulin
May be due to tumor, insulinomia
a. Low blood glucose
b. Tumor in beta cells
hyperinsulinism
90
Caused by pancreatic cell tumors, which
overproduce gastrin, are called
GASTRINOMA
ZOLLINGER ELLISON SYNDROME
91
Hypersecretion of somatostatin by a tumor
Tumor in the delta cells
Low GH
somatostatinoma
92
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
GLUCAGONOMA
93
4D SYNDROME OF GLUCAGONOMA
diabetes
dermatosis
deep vein thrombosis
depression
94
(due to immune β-cell destruction,
usually leading to absolute insulin deficiency, including
latent autoimmune diabetes of adulthood)
TYPE 1
95
Due to a progressive loss of adequate β-cell insulin
secretion frequently on the background of insulin
resistance
TYPE 2 PROGRESSIVE
96
Diabetes diagnosed in the second or third trimester of
pregnancy that was not clearly overt diabetes prior to
gestation
GESTATIONAL DM
97
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
cystic fibrosis
98
manifestations: intestinal obstruction of the
newborn, excessive pulmonary infections in
childhood, or, uncommonly, as pancreatogenous
malabsorption in adults
cystic fibrosis
99
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
cystic fibrosis
100
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.
pancreatitis
101
no permanent damage to the
pancreas
acute pancreatitis
102
chronic (irreversible injury), or
relapsing/recurrent
chronic pancreatitis
103
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
pancreatic carcinoma
104
105
mineralocorticoid = aldosterone
ZONA GLOMERULOSA
