Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Med Prep > endocrine - adrenal gland > Flashcards

endocrine - adrenal gland Flashcards

0
Q

Complex of N/NE with ATP, Ca and proteins inside the granules.

A

Chromogranins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Synthesis of epinephrine

A
  1. Transport of tyrosine into chromaffin cells cytoplasm
  2. Hydroxylation of tyrosine into DOPA
  3. DOPA to dopamine
  4. Transport of dopamine into chromaffin granules (secretory vesicles)
  5. Dopa to norepi within chromaffin granules as chromogranins
  6. Norepi diffuses out of granule thru facilitated diffusion
  7. Methylation of norepi to epi
  8. Transport of epi back into granules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Reduces osmotic burden of storing individual molecule of epi with chromaffin granules

A

Chromogranins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Important in biogenesis on secretory vesicles and organization of components within vesicles

A

Chromogranins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Secretion of noepi and epi is regulated by

A

Descending sympa signals in response to stress.
Hypothalamus and brain stem send a chemical signal as ACTH to bind to nicotinic receptor in chromaffin cells which increases acty of tyrosine hydroxylase and B-hydroxylase in which stimulates exocytosis of granules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Mechanism of action of catecholamine

A

Exerted thru adrenergic receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Tissue distribution and potency agonist:

a1 receptor

A

Adrenergic post synaptic nerve terminals

Norepi=epi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Tissue distribution and potency agonist:

a2 receptor

A

Adrenergic pre synaptic terminals

Norepi=epi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Tissue distribution and potency agonist:

B1 receptor

A

Heart

Epi=norepi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Tissue distribution and potency agonist:

B2 receptor

A

Liver

Epi>norepi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Tissue distribution and potency agonist:

B3 receptor

A

Adipose tissue

Norepi>epi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

2 primary degradation enzymes of catecholamine

A
  1. Monoamine oxidase MAO

2. Catechol-O-methyltransferae COMT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Degradation enzyme of catecholamine that predominates in neuronal mitochondria

A

MAO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Degradation enzyme of catecholamine that predominates as methylation of Norepi/epi in non-neuronal tissue

A

COMT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Degradation enzyme of catecholamine that is predominant

A

COMT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Metabolism of catecholamine

A

Draw!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Chromaffin cell tumor that produce, store, metabolize and secrete catecholamine (in excess).
Causing irregular secretion of epi and norepi leading to attacks of raised bp, palpitations, and headache.

A

Pheochromocytoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Pheochromocytoma is majorly bilateral/ unilateral?

A

90% unilateral and sporadic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Clinical features of pheochromocytoma

A 
Sweating 
Hypertension
Headaches
Anxiety/fear
Forceful heartbeat with or without tachycardia 
Flushing
Fatigue 
Tremors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

In pheochromocytoma, hypertension is mainly due to

A

Increased peripheral resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

In pheochromocytoma, lability of Bp is caused by

A

Episodic catecholamine release
Impaired Symphathetic reflex
Unrecognized chronic volume expansion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Biochemical diagnosis of pheochromocytoma

A

Catecholamine excess

Urinary fractionated metaphrenine or plasma free metaphrenine will predict size and location of tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How is blood collection done in diagnosis of pheochromocytoma?

A

Supine for 20min
Overnight fast
No nicotine, alcohol within 12hrs
Avoid acetaminophen, TCA and phrnoxybenzamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Imaging of choice for pheochromocytoma

A

CT scan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Imaging of choice in pheochromocytoma preferred for extra adrenal, pregnant, children and those allergic to contrast.
MRI
25
Imaging of choice in pheochromocytoma if there is metastasis, previous operation or for familial, multiple pheochromocytoma
MIBG - 1st choice, gets into cell but not metabolized in cell PET scan - metabolized further in cell
26
Largest and most Steroidogenic zone in adrenal Cortex
Zona fasciculata
27
Rate-limiting enzyme in Steroidogenesis
Cyp11A1
28
1st reaction in Steroidogenic pathway
Free cholesterol transported in inner mitochondria thru STAR protein, and converted into pregnenolone by CYP11A1
29
Reaction 2 in modification of FC to cortisol
Pregnenolone to progesterone by 3B-HSD or | Pregnenolone to 17-OH-pregnenolone by CYP17 (hydroxylase func)
30
Reaction 3 in modification of FC to cortisol
Progesterone to 17-OH-progesterone by cyp17(hydroxylase) or | 17-OH-pregnenolone (^5) to 17-OH-progesterone(^4) by 3B-HSD
31
Reaction 4 in modification of FC to cortisol
17-OH-progesterone to 11-deoxycortisol by CYP21B
32
Reaction 5 in modification of FC to cortisol
11- deoxycortisol to cortisol by cyp11B1
33
Reaction 4 in modification of FC to corticosterone
17-Oh-progesterone to 11-deoxycorticosterone by cyp21B
34
Reaction5 in modification of FC to corticosterone
11-deoxycorticosterone to corticosterone by cyp11B1
35
Mechanism of cortisol
Glucocorticoid receptor
36
In the absence of cortisol, GR stays I. Cytoplasm bound to molecular chaperone such as
Heat-shock protein 90 | Cyclophilin
37
Regulation of cortisol production
Thru Hypothalmus-ant. Pituitary-adrenal axis
38
ACTH binds to what receptor in zona fasciculata
Melanocortin-2 receptor
39
Acute effect of ACTH
1. Rapid transport of cholesterol to OMM 2. Increase STAR protein gene expression 3. Resulting to increase pregnenolone activity
40
Chronic effect of ACTH
1. Increase transportation of genes encoding Steroidogenic enzyme and coenzyme 2. Increase LDL and HDL receptor
41
Cortisol serves as negative feedback thru
1. Inhibition of pomc gen expression at corticotropes. | 2. Inhibition of pro-CRH gene expression at hypothalamus
42
Metabolic action of cortisol in response to stress
Increase cortisol Decrease insulin/glucagon ratio Increase epi and norepi from sympathoadrenal output
43
Metabolic action of chronically elevated cortisol in healthy individuals
Increase cortisol Increase insulin/glucagon ratio Decrease epi and norepi
44
Zona reticularis begins to appear after birth at..
5 year old
45
Adrenal androgens (DHEAS) appear in circulation at
6 year old
46
Steroidogenic pathway in zona reticularis
Pregnenolone to 17-OH-pregnenolone (CYP17) to DHEA (CYP17 -lyase) to DHEAS (SULT2A1) or DHEA to aldrostenedione (3B-HSD)
47
DHEAS/DHEA: has high affinity binding to albumin
DHEAS
48
DHEAS/DHEA: low affinity binding to protein
DHEA
49
Zona glomerulosa is primarily regulated by
RAS Extracellular K ANP
50
Zona glomerulosa is secondarily regulated by
ACTH
51
Unique features of zona glomerulosa
1. Absence of cyp17 | 2. Presence of cyp11b2 (aldosterone synthase)
52
Steroidogenic pathways in zona glomerulosa
Pregnenolone to progesterone (3B-HSD) to 11-doc (cyp21b) to corticosterone to 18-OH-corticosterone to aldosterone (cyp11B2)
53
Zona glomerulosa has low affinity binding to transport proteins
True
54
Zona glomerulosa almost all inactivated by
Liver (conjugated to glucoronide)
55
Mechanism of action of zona glomerulosa
Intracellular mineralocorticoid receptor
56
Presence of this enzyme converts cortisol to cortisone (inactivates)
11B-HSD2
57
Cortisone is converted back to cortisol in liver, skin and other tissues by
11B-HSD1
58
Physiologic action of aldosterone in kidney
Increase NA reabsorption | Increase K and H secretion
59
Results from continuous administration of aldosterone in 2-3days
Aldosterone escape
60
Regulation of aldosterone secretion
RAAS
61
Renin is produced by
Juxta glomerular cell
62
Renin is release in response to
Low bp | Low Na delivery to macula densa
63
Stimulators of aldosterone
Angiotensin II = increase STAR and cyp11b2 (potent vasoconstrictor) Extracellular K Acute elevated ACTH
64
Inhibitors of aldosterone
ANP (directly inhibits aldosterone production / indirectly inhibits renin release) Chronic elevated ACTH
65
What happens when there is Hypervolemia
Hypervolemia means high Na level, this will inhibit the renin release which will lower aldosterone secretion resulting back to normovolemia
66
Primary hyperaldosteronism | Usually due to aldosterone- secreting tumor
Conn's syndrome
67
Conn's disease results in
``` K depletion Na retention Ms weakness Hypertension Polyuria ```
68
Increase ACTH due to any enzyme block decreasing cortisol synthesis. May cause masculinization of female fetus or incomplete masculinization of male fetus
Congenital adrenal hyperplasia
69
Congenital adrenal hyperplasia usually due to
Cyp21

Med Prep (52 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions