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WorksheetsEndo Exam 1 - Adrenal - Khan
Total questions: 77
Worksheet time: 1hrs 17mins
Name
Class
Date
1.
What are the types of adrenal steroids are approved for therapeutic replacement
a)
glucocorticoids
b)
mineralcorticoids
c)
androgen
d)
estrogen
e)
progestogens
2.
What are characteristics of glucocorticoids
a)
replacement therapy
b)
anti-inflammatory
c)
immunosuppressant
d)
widely used in therapy
e)
hypoaldosteronism
3.
What are characteristics of mineralcorticoids
a)
replacement therapy
b)
anti-inflammatory
c)
immunosuppressant
d)
widely used in therapy
e)
hypoaldosteronism
4.
Where are the adrenal glands located
a)
above the kidneys
b)
below the kidneys
c)
next to the kidneys
5.
What is another name for the adrenal gland
(a)
6.
Where is the medulla on the adrenal gland
a)
inside
b)
outside
7.
Where is the cortex on the adrenal gland
a)
inside
b)
outside
8.
What does the medulla secrete
a)
epinephrine (a catecholamine)
b)
glucocorticoids
c)
mineralcorticoids
d)
adrenal androgen (DHEA)
9.
What does the cortex secrete
a)
epinephrine (a catecholamine)
b)
glucocorticoids
c)
mineralcorticoids
d)
adrenal androgen (DHEA)
10.
What is the adrenal steroid that is important in carbohydrate metabolism
a)
glucocorticoids
b)
mineralcorticoids
c)
adrenal androgen
11.
What is the adrenal steroid that is important in mineral homeostasis
a)
glucocorticoids
b)
mineralcorticoids
c)
adrenal androgen
12.
What is the most important natural glucocorticoid
a)
aldosterone
b)
DHEA
c)
cortisol
13.
What is the most important naturally occuring mineralcorticoid
a)
aldosterone
b)
DHEA
c)
cortisol
14.
What are the 3 zones of the adrenal cortex
a)
Zona glomerulosa
b)
Zona fasciculata
c)
Zona reticularis
d)
Zona adrenal
15.
What adrenal cortex zone secretes aldosterone
a)
Zona glomerulosa
b)
Zona fasciculata
c)
Zona reticularis
d)
Zona adrenal
16.
What adrenal cortex zone is regulated by angiotensin II and K
a)
Zona glomerulosa
b)
Zona fasciculata
c)
Zona reticularis
d)
Zona adrenal
17.
What adrenal cortex zone secretes cortisol and androgen
a)
Zona glomerulosa
b)
Zona fasciculata
c)
Zona reticularis
d)
Zona adrenal
18.
What adrenal cortex zone is regulated by ACTH and CRH
a)
Zona glomerulosa
b)
Zona fasciculata
c)
Zona reticularis
d)
Zona adrenal
19.
In the absence of the pituitary gland
a)
Zona glomerulosa will not undergo atrophy
b)
Zona glomerulosa will undergo atrophy
c)
Zona fasciculata/reticularis will undergo atrophy
d)
Zona fasciculata/reticularis will not undergo atrophy
20.
Where are adrenal steroids synthesized from
a)
water
b)
fat
c)
cholesterol
21.
What is the rate limiting step between cholesterol and adrenal steroids
a)
Pregnenolone to Progesterone
b)
Pregnenolone to 17alpha-Hydroxypregnenolone
c)
Cholesterol to Pregnenolone
d)
Progesterone to 17alpha-Hydroxyprogesterone
22.
Which structure is the common precursor for all adrenocortical hormones
a)
Progesterone
b)
Pregnenolone
c)
Cortisol
d)
Corticosterone
e)
Aldosterone
23.
If a stress stimulus occurs, what hormone is released in the hypothalamic hormone
a)
ACTH
b)
Cortisol
c)
GCCs
d)
CRH
24.
If a stress stimulus occurs and CRH is released, what hormone is triggered from the pituitary hormone
a)
ACTH
b)
Cortisol
c)
GCCs
d)
CRH
25.
If a stress stimulus occurs and CRH and ACTH has been released, what hormone is triggered from the endocrine gland hormone
a)
ACTH
b)
Cortisol
c)
GCCs
d)
CRH
26.
What adrenal steroid uses the hypothalamic-pituitary-axis pathway
a)
glucocorticoids
b)
mineralcorticoids
c)
adrenal androgen
27.
What is synthesized from the precursor molecule proopiomelanocortin (POMC)
a)
β-Endorphin
b)
β-LPH
c)
ACTH
d)
MSH
28.
Where is ACTH synthesized
a)
anterior pituitary
b)
posterior pituitary
c)
thalamus<br />
29.
Where are limited expression mineralcorticoid receptors located
a)
wide cellular distribution
b)
saliva
c)
colon
d)
kidney
30.
Where are glucocorticoid receptors located
a)
wide cellular distribution
b)
saliva
c)
colon
d)
kidney
31.
Which adrenocorticoid receptors are ligand-activated transcription factors
a)
glucocorticoids
b)
mineralcorticoids
c)
adrenal androgen
32.
How much of the steroids in ciculation are bound to CBG (corticosteroid binding protein)
a)
0.6
b)
0.7
c)
0.8
d)
0.9
33.
What do corticosteroids bind to in order to regulate transcription in the nucleus
a)
CBG
b)
GRE
c)
ligand receptor dimerization
34.
How do steroids enter the nucleus and what is it called
a)
nuclear translocation
b)
binds to GRE
c)
binds to receptor in cytoplasm that allows it to enter the nucleus
d)
binds to glucocorticoid response elements and regulates transcription
35.
How do glucocorticoids affect transcription
a)
it can increase transcripton
b)
it can decrease transcription
c)
it does not affect transcription
36.
When taking oral glucocorticoids, during intermediate metabolism of carbohydrates and proteins, what gets converted to glucose in the liver
a)
amino acid
b)
glycerol
c)
glycogen
d)
lipids
37.
What effect does oral glucocorticoids have on the periphery during carbohydrate and protein intermediary metabolism
a)
diminish glucose utilization
b)
increase protein breakdown
c)
lipolysis
d)
synthesis of glutamine
e)
amino acid and glycerol used in gluconeogenesis in the liver
38.
Oral glucocorticoids ultimately causes
a)
elevated blood glucose
b)
can worsen glycemic control in diabetic patients
c)
precipitate onset of hyperglycemia in susceptible patients
d)
lower blood glucose
e)
can increase glycemic control in diabetic patients
39.
What effect does glucocorticoids have on intermediary metabolism of lipids
a)
redistribution of fat
b)
increase fat in buffalo hump and moon face
c)
decrease fat in extremieites seen in hypercorticism
d)
increase fatty acid release after glucocorticoid administration
e)
decreased fatty acid release after glucocorticoid administration
40.
What is the cause of hypercorticism
a)
endogenous
b)
pharmacological
41.
What are characteristics of steroid myopathy and what is it caused by
a)
characterized by weakness of proximal limb muscles
b)
myopathy occurs in respiratory muscles in patients with asthma or COPD
c)
recovery from myopathy is slow
d)
caused by excessive glucocorticoids
42.
What effect does glucocorticoids have on the number of blood cells in the immune system
a)
increase the number of blood cells in circulation
b)
decrease the number of blood cells in the circulation
c)
does not have an effect on the number of blood cells
43.
What effect does GCC have on the PG and LT production in the immune system
a)
increase PG and decrease LT
b)
decrease PG and increase LT
c)
increase PG and LT
d)
decrease PG and LT
44.
What are characteristics of the effects GCC has on the immune system and the decrease in PG and LT production
a)
induces expression of lipocortin to inhibit PLA2
b)
decreases the expression of COX-2 enzyme
c)
inhibition of permeability, pain sensation, extravasation
d)
inhibits expression of lipocortin to induce PLA2
e)
increases expression of COX-2 enzyme
45.
What does PLA2 acting on membrane phospholipids release
a)
arachidonic acid
b)
amino acid
c)
folic acid
d)
ascorbic acid
46.
What serves as the precursor of PG and LT biosynthesis
a)
arachidonic acid
b)
amino acid
c)
folic acid
d)
ascorbic acid
47.
What effects does GCC have on the expression of cytokines in the immune system
a)
increased expression of certain cytokines involved in inflammation (IL-2, TNF-alpha)
b)
decreased expression of certain cytokines involved in inflammation (IL-1, TNF-alpha)
c)
increased expression of anti-inflammatory proteins
d)
decreased expression of anti-inflammatory proteins
48.
What is the overall effect of GCC on the expression of cytokines in the immune system
a)
increased leukocyte activation
b)
decreased leukocyte activation
c)
no change in leukocyte activation
49.
What are the effects that GCC have on mast cells and basophil degranulation in the immune system
a)
inhibits mast cell and basophil degranulation
b)
induces mast cell and basophil degranulation
c)
decrease in IgE-mediated histamine and LT release
d)
increase in IgE-mediated histamine and LT release
e)
decrease inflammation, increase bronchodilation
50.
What are the effects that GCC have on adhesion of leukocytes
a)
decreased expression of ICAM-1 and ECAM-1 molecules
b)
increased expression of ICAM-1 and ECAM-1 molecules
c)
Leukocytes bind to endothelial cells via these molecules and move to the site of inflammation
d)
reduced influx of leukocytes
e)
increased influx of leukocytes
51.
Excessive glucocorticoid secretion produces hypertension in
a)
hyperaldosteronism
b)
Cushing's syndrome
c)
some patients who are taking synthetic GC
d)
osteoporosis
52.
What effects does excessive glucocorticoid secretion produce in hyperaldosteronism
a)
hypertension
b)
atrial fibrillation
c)
stroke
d)
MI
53.
What are the GI effects of excessive glucocorticoids
a)
increased gastric acid
b)
decreased gastric acid
c)
increased pepsin
d)
decreased pepsin
54.
What side effects do glucocorticoids have on a patient
a)
hypertension
b)
increased gastric acid and pepsin
c)
cataract formation
d)
behavioral changes
55.
What are the different types of CNS behavioral changes that occur from glucocorticoids
a)
nervousness
b)
insomnia
c)
psychosis
d)
mood swings
e)
bipolar disorder
56.
What effects do glucocorticoids have on bone function
a)
decreased gastrointestinal absorption of Ca
b)
increase Ca excretion
c)
suppressive effect on osteoblast activity (decrease anabolic effect)
d)
increase osteoclast activity (increase catabolic effect)
e)
can cause osteoporosis and bone fracture
57.
What are some characteristics of the effects of mineralcorticoids
a)
site of action is in the distal tubules and collecting ducts of the kidneys
b)
enhances reabsorption of Na+ from tubular fluid
c)
increases urinary secretion of K+
58.
What diagnosis is given when the adrenal cortex is selectively destroyed by an autoimmune disorder and leads to decreased synthesis of cortisol, aldosterone, sex hormone, weakness, fatigue, hypotension, hypokalemia, hyperpigmentation
a)
primary adrenal insufficiency
b)
secondary adrenal insufficiency
c)
congenital adrenal hyperplasia
d)
Cushing's syndrome
e)
aldosteronism
59.
What diagnosis is given when a patient has prolonged/high-dose therapy with glucocorticoids where the aldosterone secretion is not altered and hyperpigmentation is not seen
a)
primary adrenal insufficiency
b)
secondary adrenal insufficiency
c)
congenital adrenal hyperplasia
d)
Cushing's syndrome
e)
aldosteronism
60.
What diagnosis is given to a group of disorders characterized by specific defects in synthesis of cortisol and aldosterone; with the most common defect being 21 hydroxylase deficiency
a)
primary adrenal insufficiency
b)
secondary adrenal insufficiency
c)
congenital adrenal hyperplasia
d)
Cushing's syndrome
e)
aldosteronism
61.
What happens when there is a defect in 17-hydroxyprogesterone in excess
a)
hyperplasia
b)
the synthesis pathway is diverted to the adrenal androgen pathway
c)
virilism (masculinization)
d)
hirsutism
62.
What are causes of Cushing's syndrome
a)
adrenal hyperplasia secondary to an ACTH secreting-pituitary adenoma
b)
adrenal tumor
c)
ectopic ACTH secreting tumor of small cell lung cancer
d)
adrenal carcinoma
63.
What are some characteristics of Cushing's syndrome
a)
hypofunction of adrenal gland
b)
hyperfunction of adrenal gland
c)
chronic presence of excessive glucocorticoids
d)
acute presence of excessive glucocorticoids
64.
What are some symptoms of Cushing's syndrome
a)
founded face, trunk obesity, muscle wasting
b)
purple color striae, easy bruising, poor wound healing
c)
osteoporosis, mental problems
d)
diabetes
e)
hypertension
65.
What diagnosis is given when there is an abnormal secretion of aldosterone from the hyperplastic gland or a tumor
a)
primary adrenal insufficiency
b)
secondary adrenal insufficiency
c)
congenital adrenal hyperplasia
d)
Cushing's syndrome
e)
aldosteronism
66.
What are symptoms of aldosteronism
a)
hypertension
b)
weakness
c)
tetany (due to increased Na and decreased K)<br />
d)
decreased plasma renin
e)
decreased Angiotensin II
67.
What can you use replacement therapy for
a)
primary adrenal insufficiency
b)
secondary adrenal insufficiency
c)
congenital adrenal hyperplasia
68.
Which replacement can be used for CAH
a)
glucocorticoids
b)
mineralcorticoids
69.
Why do we use fludrocortisone as the mineralcorticoid replacement therapy for CAH
a)
it is a glucocorticoid with significant mineralcorticoid activity
b)
it has significant salt retaining properties
c)
use with a glucocorticoid
70.
What are the side effects of fludrocortisone
a)
HTN
b)
hypokalemia
c)
edema
d)
GI
e)
hypotension
71.
Which glucocorticoid is used most often
a)
inhaled glucocorticoids
b)
systemic glucocorticoids
c)
topical glucocorticoids
72.
What are the reasons for using systemic glucocorticoids for treatment
a)
increased GCC activity more than cortisol
b)
decreased GCC activity less than cortisol
c)
decreased MCC activity
d)
increased MCC activity
73.
What are common systemic glucocorticoids
a)
cortisone, hydrocortisone
b)
dexamethasone
c)
methylprednisolone, prednisolone
d)
triamcinolone<br />
e)
prednisone
74.
What are common adverse effects following systemic therapy
a)
mood disturbances, increased appetite
b)
loss of glucose control, weight gain
c)
fluid retention, HTN
d)
masking of infections
e)
peptic ulcer
75.
Long term systemic use of glucocorticoids cause HPA suppression. How can a pateitn restore endogenous hormone production
a)
no change, cortisol will return to normal continuing glucocorticoid therapy
b)
taper dose down
c)
completely stop, cortisol will automatically return to normal
76.
What is the precursor of glucocorticoids
a)
cholesterol
b)
hydrocortisone
c)
mineralcorticoids
77.
What are characteristics of cortisone
a)
inactive form of cortisol
b)
active form of cortisol
c)
enzymatic activation in the liver to cortisol
d)
enzymatic activation in the kidney to cortisol
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