Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Physiology 2 > Adrenal Gland Physiology > Flashcards

Adrenal Gland Physiology Flashcards

1
Q

Zona glomerulosa

A 
Produce mineralcorticoids (aldosterone)
Regulate mineral/electrolyte balance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Zona fasciculata

A

Glucocorticoids (cortisol)

Regulate glucose metabolism

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

Zona reticularis

A

Androgens
Stimulate masculinization
dehydroepiandrosterone

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

Medulla

A

Stress hormones
Sympathetic ANS
epi and norepi

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

HPA axis

A

Hypothalamus -corticotropin releasing hormone->
Anterior pituitary -Adrenocorticotropic hormone
Adrenal cortex- cortisol

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

Mineralcorticoids

A

Aldosterone

Stimulated mainly by signals from the kidneys but also hypothalamic (CRH) and pituitary (ACTH)

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

Glucocorticoids and androgens

A

Cortisol and dehydroepiandrosterone

Stimulated mainly by signals from the hypothalamus (CRH) and pituitary (ACTH)

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

Catecholamines

A

Epi

Stimulated by signals from the sympathetic nervous system

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

Andrenal cortex hormone synthesis

A

Produces steroid hormones- derived from cholesterol
In the first step- cholesterol is used to form pregnenolone
This step is common to all arden-cortical hormones
Occurs in the mitochondrion
This step is regulated by ACTH- limits the rate of synthesis of all adrenocortical hormones

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

Mineralocorticoid overview

A

These are corticosteroids that influence salt and water balances (electrolyte and fluid balance)
Aldosterone is the primary mineralocorticoid
Acts on distal tubules in kidneys to provide:
-active reabsorption of Na
-active secretion of K
-active secretion of protons
-passive reabsorption of water

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

Adrenal cortex aldosteron

A

Closely linked to a renin (enzyme) and angiotensin (hormone, which create RAAS.

Primary regulators: decrease in blood volume or BP will activate RAAS. Also an increase in K in blood
Leads to zona glomerulosa enhanced secretion of aldosterone which leads to increase blood volume and BP

Main stimulants are low blood Na or high blood K or low blood volume and pressure
Major function- regulate NA and K through the distal tubules in kidneys
-active reabsorption of Na, active secretion of K and passive reabsorption of water
Negative feedback primarily via restoration of electrolyte balance

Weakly binds to plasma transport proteins.
-bound 10% to transcortin and 50% to albumin
-40$ is free or bioactive
Action on target tissue
-via cytoplasm or nuclear receptors- mineralocorticoid-receptor complex on DNA
half life iin circulation 20 minutes
metabolized in liver
-sulfates and glucuronides reduce bioactivity and increase water solubility
-secreted in urine

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

Steroid hormones bind to intracellular receptors

A
  1. most hydrophobic steroids are bound to plasma protein carriers. Only unbound hormones can diffuse into target cell
  2. Steroid hormon receptors are in the cytoplasm or nucleus
  3. The receptor-hormone complex binds to DNA and activates or represses one or more genes
  4. Activated genes create new mRNA that moves back to the cytoplasm
  5. Translation produces new proteins for cell processes
  6. Some steroid hormones also bind to membrane receptors that use second messenger systems to create rapid cell response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Glucocorticoids overview

A

These are corticosteroids that have broad effects but are primarily involved in metabolic (carbohydrate) and immunologic (antiinflammatory) responses
Cortisol- the most important glucocorticoids- considered stress hormoen
Circadian or diurnal rhythm- higher blood concentrations in morning than afternoon/evening
Regulation is via hypothalamic (CRH)- pituitary (ACTH) adrenal (cortisol) axis in response to low blood glucose and other stressors

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

Adrenal cortex: Cortisol

A

Stress is a biological response to external or internal stimuli or a bodys reaction to change to maintain homeostasis

  • hypoglycemis
  • physical trauma
  • inflammation
  • pathogenic
  • disease

Glucocorticoids, stress and diurnal rhythm can influence the axis

Metabolic enhancer: Stimulated in response to low blood sugar or glucose

  • Increases glucose via countering insulin and inhibiting glucose uptake and storage in muscle and adipose tissue, except brain
  • Simulates liver enzymes to increase gluconeogenesis and glucogenolysis
  • mobilize aas and FFAs to serve as substrates for gluconeogenesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Cortisol actions on carbohydrate metabolism

A

Stimulates synthesis of enzymes involves in gluconeogenesis
Antagonizes insulins effects to inhibit gluconeogenesis in liver
Decrease glucose utilization be cells
Potentiates the action of glucagon and epic on glucose metabolism
Can cause diabetes mellitus
-increased gluconeogenesis + reduction in glucose utilization

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

Cortisol actions on protein metabolism

A

Stimulate catabolism of protein in muscle
Cause mobilization of aa from the extra hepatic tissues
-mainly from muscle
-serves as substrate for enzyme manufacturing

17
Q

Cortisol actions on fat metabolism

A

Increase mobilization of FAs from adipose tissue
-shift the metabolism from glucose to fat utilization
-enhance the oxidation of FFAs in cells- reduced glucose transport into fat cells
Can cause obesity- depletion peripheral fat while increasing visceral (abdominal) fat

18
Q

Cortisol actions on immune system

A

Immune system suppressant:
Immunosuppresive and anti-inflammatory effects
-decrease formation of prostaglandins and leukotrienes production
-reduce secretion of histamine by mast cells
-decreases phagocytosis and surpasses antibody formation

Down regulates a variety of pro-inflammatory factors
Up-regulates a variety of anti-inflammatory factors- inhibits inflammation

Inhibits secondary functions not necessary for survival

19
Q

Cortisol

A

Cortisol transported in plasma by binding proteins
-bound 75% to transcortin and 15% to albumin
-10% free or bioactive
Half life in circulation 66 minutes
Metabolized in liver
-sulfates and fllucuronides reduce bioactivity and increase water solubility
Secreted in urine

20
Q

Androgens overview

A

Hormones that interact with male sex hormone receptors
DHEA converted to DHEA-sulfate
DHEA concertes to androstenedione released into the blood stream and taken up by testis or ovaries to produce testosterone and estogerns

21
Q

Adrenal medulla: Catecholamines

A

Chromaffin cells-neuroendocrine cells -modified post-ganglionic sympathetic neurons
-lack dendrites and axons
–stimulated by acetylcholine from pre-ganglionic sympathetic neurons that binds with nicotinic receptors on the chromatin cells
Produce and secrete epic (80%) norepinephrine (20%) and dopamine

22
Q

Short term stress response

A

increased HR
increased BP
liver converts glycogen to glucose and releases to blood
Dilation of bronchioles
Changes in blood flow patterns leading to decreased digestive system activity and reduced urin output
Increased metabolic rate

23
Q

Long term stress response

A

Mineralocorticoids
Retention of Na and water by kidneys
Increased Blood volume and BP

Glucocoricoids
Proteins and fats converted to glucose or broken down for energy
Increased blood glucose
suppression of immune system

24
Q

Catecholamines

A

Acetylcholin release from pregangionic nerve fibers initiates the synthesis

The synthesis inside of the cells begins with conversion of tyrosine to DOPA by the enzyme tyrosine hydrozylase
End products of tyrosine metabolism include DOPA, dopamine, epic, and norepi
-DOPA concerted to dopamin in the cytosol
-dopamine is concerted tonorepi within the chromatin granules –dopamine beta-hydroxylate
-in cells that secrete epinephrin, NE returns to cytosol where is converted to epic– EPI moves to granules for storage before release

25
Q

Fight or flight

A

EPI and NE
increases energy availability and overall metabolism
Bind to adrenoceptors which are cell surface GPCR on target tissues
Two major types of adrenergic receptors:
alpha, a1 and a2
Beta, B1 and B2

26
Q

Adrenergic receptors

A

Alpha
a1= smooth muscle contraction, mydriasis
a2= mixed smooth muscle effects

Beta
B1= increased cardiac chronotropic (Increase HR) and inotropic (increase contractibility) effects
B2= bronchodilation

27
Q

Medulla: catecholamines

A

Half-life in circulation about 2 minutes for NE and less for EPI
Liver and kidney metabolism
-degraded primarily by methylation by catechol-o-methyltransferases
Ecreted in urine

28
Q

Disorders of adrenal gland

A

Hyperadrenocorticism- cushings
Hypoadrenocorticism- addisons
Hyperaldosteronism- conns syndrome

29
Q

Adrenal dysfunction: In primary hyperadrenocorticism there is an overproduction of cortisol caused by a tumor…

A

In zona fasciculata

30
Q

Hyperadrenocorticism is an overproduction of cortisol. What part of HPA axis or adrenal cortex is responsible for secondary hyperadrenocortiscism

A

Anterior pituitatry

31
Q

Adrenal cortex dysfunction: hyperadrenocorticism

A

Overproduction of cortisol
-primary= adrenal gland tumor (20%)
-secondary= pituitary gland tumor (80-85%). Tumor secretes ACTH which stimulates overproduction of cortisol
-cushings disease=pituitary-dependent hyperadrenocorticism
Common in dogs, rare in cats
Increased rate of lipolysis results in redistribution of fat into the liver and abdomen -classic potbelly

32
Q

Adrenal cortex dysfunction: hypoadrenocorticism

A

Deficiency of cortisol and or aldosterone= addisons disease
Most common in young to middle age dogs and occasionally horses
Deficiency can be result in dysfunctional adrenal gland (primary) or pituitary gland (secondary)
Primary : endogenous plasma ACTH are increased due to lack of negative feedback. Reduced response to exogenous ACTH
Secondary: Endogenous ACTH are typically decreased
Mya or may not be a reduced response exogenous ACTH

33
Q

Adrenal cortex dysfunction: Hyperaldosteronism

A

Overproduction of aldosterone= Conn’s syndrome
Diagnosed in older cats and occasionally dogs
Hypersecreting adrenal tumor or bilateral adrenal hyperplasia
Classic electrolyte changes: decrease in blood K, increase Blood Na and pH
Diagnosis: increased plasma aldosterone, low to undetectable plasma renin, increased plasma aldosterone-to-plasme renin concentration
Ultrasonographic imaging: unilateral or bilateral or adrenal hyperplasia or enlargement
Treatment: K supplementation
Surgical removal of adrenal tumor- tumors of adrenal gland usually benign

Excessive production of aldosterone- the most common form of adrenal disease in cats
caused by hyperplasia or neoplasia of zona glomerulosa

34
Q

Adrenal cortex dysfunction: Hypoaldosteronism

A

Very rare

35
Q

Pheochromocytoma

A 
Neoplasm of adrenal medullary chromatin cells
-catecholamine-secreting tumor
Signs can be absent/sporatic
Hypertension
-blindness
Collapse
Tachypnea
Arrithmia

Physiology 2 (12 decks)

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