Brainscape's Knowledge GenomeTM

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


See full index

Physiology > ENDO IV > Flashcards

ENDO IV Flashcards

1
Q

The two adrenal glands
each weighs ~4 grams.
They are located

A

superior

to each kidney

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

adrenal glands consist of (2)

A

outer cortex

inner medulla

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

Adrenal cortex is essential for

A

life

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

Adrenal cortex secretes (3)

A 
Corticosteroids (ex. Cortisol)
 Mineralocorticoids (ex. Aldosterone)
 Sex hormones (ex. DHEA)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Adrenal medulla

•–% of gland tissue

A

20-30

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

Adrenal medulla secretes (2)

A

E and NE in response to SNS stimulation

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

Adrenal medullary hormones are not

essential for —, but help to

A

life

prepare the individual to deal with emergencies

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

The adrenal cortex secretes hormones that are made from –

A

cholesterol

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

The cortex has three layers: (3)

A 
Zona Glomerulosa (~15%), 
Zona Fasciculata (~75%), 
Zona Reticularis (~10%).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Mineralocorticoids

Secretion regulated by the

A 
renin-angiotensin-
aldosterone system (RAAS).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Glucocorticoids

Secretion regulated by the

A

hypothalamic-pituitary-adrenal

axis (HPA) – CRH, ACTH

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

Androgens

Secretion is regulated by the

A

HPA

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

The adrenal medulla is related to the sympathetic nervous system and
chromaffin cells secrete (2) into the blood.

A

the catecholamines epinephrine (EPI) and

norepinephrine (NE)

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

aldersterone increases

A

renal tubular reabsorption of Na+ and secretion of K+.

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

aldosterone leads to an increase in (2)

A

EC fluid volume and Mean Arterial Pressure

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

Aldosterone has similar effect on sweat glands and

salivary glands as

A

renal tubules

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

Aldosterone greatly increases reabsorption of (2) by gland ducts

A

sodium and secretion of potassium

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

Effect on sweat glands important to conserve body — in hot environments

A

salt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Effect on salivary gland conserves — during high rates of salivary secretion

A

sodium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q 
In addition to 
hyperkalemia, 
--- causes 
secretion of 
Aldosterone.
A

Angiotensin II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q 
--- is an enzyme 
released by the cells in 
the kidneys in response 
to a variety of stimuli (ex. 
Sympathetic Nervous 
system).
A

Renin

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

Angiotensin Converting
Enzyme (ACE) is
produced by the —

A

endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q 
Primary Hyperaldosteronism (Conn’s Syndrome)
Causes:
A 
adrenal adenoma (benign), adrenal hyperplasia, adrenal 
carcinoma (malignant)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

SKIPPED
Primary Hyperaldosteronism (Conn’s Syndrome)
Signs and Symptoms

A
  • Hypertension
  • Hypernatremia
  • Headaches
  • Potassium depletion
  • Weakness
  • Fatigue
  • Polyuria
  • Hypokalemic alkalosis
  • Low plasma renin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q 
Primary Hyperaldosteronism (Conn’s Syndrome)
Tx options (2)
A

– Surgical removal of the tumor or most of the adrenal tissue when hyperplasia is
the cause.
– Pharmacological antagonism of the mineralocorticoid receptor (ex.
spironolactone) is another option

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Secondary Hyperaldosteronism

Caused by

A 
decreased blood flow & pressure in renal artery
– CHF
– Cirrhosis
– Nephrosis
– Renal artery stenosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Secondary Hyperaldosteronism

Signs and Symptoms (5)

A

• High plasma renin activity
• Hypernatremia w/extracellular volume expansion
• Edema
• Decreased cardiac output
• Similar clinical findings as Primary Hyperaldosteronism-hypertension
etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

cortisol is secreted with any

A

stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

cortisol causes

A

mobilization of energy stores and

suppresses the immune response.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Types of stress that increase

cortisol release include:

A
  • Trauma of almost any type
  • Infection
  • Intense heat or cold
  • Injection of norepinephrine
  • Surgery
  • Hypoglycemia
  • Psychological stress
  • Almost any debilitating disease
31
Q

Cortisol secretion also

peaks in the

A

AM – it is

secreted in a circadian

32
Q

When ACTH is secreted from the AP, several other hormones are secreted as well because the gene for ACTH forms a larger protein -

A

a preprohormone called Proopiomelanocortin (POMC).

33
Q

When ACTH is secreted from the AP, several other hormones are secreted as
well because the gene for ACTH forms a larger protein - a preprohormone
called Proopiomelanocortin (POMC). (3)

A

– Melanocyte stimulating hormone (MSH)
– β-endorphin
– β-lipotropin

34
Q 
The specific proteins produced 
depend on the --- enzymes 
found in the cell. Many tissues 
express the POMC gene beside the 
anterior pituitary (hypothalamus, 
melanocytes).
A

processing

35
Q

• Melanocytes have processing
enzymes that form — which
stimulates formation of melanin
pigment.

A

MSH

36
Q

Cortisol is found in 1000-fold higher circulating
conc. (compared to aldosterone), which could
potentially cause symptoms of

A

mineralocorticoid

excess.

37
Q

11beta-hydroxysteroid dehydrogenase (11betaHSD)
converts cortisol to — in aldosterone-
responsive tissues.

A

cortisone

38
Q

Cortisone does not bind GC or

MR receptors with as high of an affinity as

A

Cortisol

39
Q

A Genetic deficiency of 11β-HSD leads to the syndrome

A

AME (Apparent Mineralocorticoid Excess).

40
Q

Glycyrrhetinic acid, a compound of licorice, inhibits the activity of

A

11β-

hydroxysteroid dehydrogenase.

41
Q

HIGH circulating — levels (such as in Cushing’s Syndrome) can overwhelm
this enzyme.

A

cortisol

42
Q

Effects of Cortisol on Metabolism

Carbohydrate (3)

A
  1. Stimulation of both gluconeogenesis and glycogenolysis in liver (increase
    plasma glucose)
  2. Anti-insulin action - decreases glucose uptake in muscle and fat but not
    brain and heart
  3. Makes diabetes worse by increasing glucose levels, lipid levels, ketone
    body formation and insulin secretion.
43
Q

Effects of Cortisol on Metabolism

Protein (2)

A
  1. Inhibits protein synthesis and increases proteolysis especially in skeletal
    muscle (provides source of AA for glycoenogenesis)
  2. Cortisol excess leads to muscle weakness, pain due, thin skin and abdominal
    striae due to protein catabolic effect.
44
Q

Effects of Cortisol on Metabolism

Lipid: (2)

A
  1. Promotes lipolysis; shifts energy system from utilization of glucose to fatty
    acids in times of stress.
  2. Causes lipid deposition in certain areas (abdomen, interscapular “buffalo
    hump” and a rounded “moon face”.
45
Q

95% of the glucocorticoid activity of the adrenal cortex

due to the secretion of

A

cortisol

46
Q

Absence of cortisol contributes to circulatory failure
due to loss of — action of catecholamines on
blood vessels.

A

permissive

47
Q

Lack of cortisol also prevents mobilization of energy
sources (glucose & free fatty acids) during stress &
can result in

A

fatal hypoglycemia

48
Q

Anti-inflammatory Actions of Cortisol: (5)

A
  1. Stabilizes the lysosomal membrane
  2. Decreases capillary permeability
  3. Decreases WBC migration and phagocytosis
  4. Suppresses T lymphocytes proliferation
  5. Decreases IL-1 secretion from WBCs
49
Q

Glucocorticoid treatment can

cause osteoporosis. (3)

A

1) Stimulates bone resorption (via increased RANK-L expression)
2) Inhibits osteoblastic maturation and
activity
3) Promotes apoptosis of osteoblasts
and osteocytes

50
Q 
Due to their anti-inflammatory 
properties, glucocorticoids 
can be used to treat patients 
with diseases/conditions that 
involve
A 
an inflammatory 
process (ex. rheumatoid 
arthritis, glomerulonephritis, 
rheumatic fever, 
anaphylaxis).
51
Q 
The Zona Reticularis begins to 
secrete adrenal androgens 
around age 8 (adrenarche) 
peaking in the early 20s and 
then falling with age. (3)
A
  1. Dehydroepiandrosterone
    (DHEA)
  2. Androstenedione
  3. Testosterone
52
Q

Normally, the adrenal androgens have only weak effects in

— but contribute ~50% of active androgens in —

A

males

females

53
Q

Growth of the pubic and axillary hair and libido in females are due
to

A

adrenal androgens

54
Q

Conditions resulting from excess androgen production by the

adrenal gland: (3)

A

– In pre-pubertal boys, it can cause precocious pseudopuberty (not
due to the hypothalamic- pituitary-adrenal axis)
– 21-hydroxylase deficiency can result in virilization in newborn
females and pseudo-hermaphroditism
– Androgen secreting tumors producing excess androgen result in
virilization and precocious pseudopuberty in females

55
Q 
DHEA and DHEA sulfate are 
secreted in greater quantities but 
--- is more important 
because it is more readily converted 
peripherally to testosterone. 
Conversion  to testosterone and 5-
dihydrotestosterone occurs in 
peripheral tissues.
A

Androstenedione

56
Q

In adults, hormonally active benign adrenal adenomas usually secrete (2)

A

aldosterone or cortisol.

57
Q

Virilizing tumors in women are more likely to be caused by

A

ovarian tumors.

58
Q

Virilizing adrenal tumors are rare, and virilization is usually due to

A

hypersecretion of adrenal androgens.

59
Q

SKIPPED
Signs and symptoms of
virilization include:

A 
• hirsutism, 
• male-pattern baldness,
• acne, 
• deep voice, 
• male musculature, 
• irregular menses or 
amenorrhea,
• clitoromegaly, 
• increased libido. 
• rapid linear growth with 
advanced bone age is 
common in children
60
Q

Primary adrenal insufficiency (Addison’s) (4)

A

– Primary atrophy or injury of adrenal cortex
– In about 80% of US cases, atrophy caused by
autoimmune destruction of all cortical zones
– High ACTH and low corticosteroid production
– Loss of glucocorticoid, mineralcorticoid and
adrenal androgen secretion

61
Q

Secondary adrenal insufficiency (4)

A

– Pituitary gland unable to secrete enough ACTH
– Often Iatrogenic due to abrupt cessation of
steroid therapy
– Low ACTH and cortisol production
– Mineralcorticoid secretion not affected

62
Q 
Adrenal insufficiency from 
--- ----
treatment (which 
suppresses the HPA axis) is 
much more common, 
occurring in 0.5–2% of the 
population in developed 
countries.
A

exogenous glucocorticoid

63
Q

ORAL MANIFESTATIONS OF ADRENAL INSUFFICIENCY (Addison’s
disease)
Orofacial features:

A 
• skin pigmentation
o mucocutaneous junctions lips
o intraoral mucosal surfaces
o buccal mucosa
o palate
o lingual surface of the tongue
64
Q

ORAL MANIFESTATIONS OF ADRENAL INSUFFICIENCY (Addison’s
disease)
Treatment:

A 
corticosteroids
o immunosuppression 
o susceptibility to oral candidiasis
o recurrent herpes labialis 
o herpes zoster infections
o gingival and periodontal diseases
o impaired wound healing
65
Q

ACTH-dependent Cushing’s Disease (Secondary

Disorder) (3)

A
  1. Adenoma of anterior pituitary secretes large
    amounts of ACTH
  2. “Ectopic secretion” of ACTH by non-pituitary
    tumor such as the lungs
  3. “Ectopic secretion” of corticotropin-releasing
    hormone (CRH) by non-pituitary tumor
66
Q

ACTH-independent Cushing’s Syndrome (Primary

Disorder) (2)

A
  1. Adenomas of the adrenal cortex overproducing
    Cortisol
  2. Primary nodular hyperplasia of the adrenal
    gland causing overproduction of Cortisol.
67
Q

Manifestations of Cushing Syndrome/Disease (2)

A

Moon facies with erythema
and telangiectases of cheeks
and forehead

Increased fat deposition in
the supraclavicular fossae
and dorsocervical area
(buffalo hump).

68
Q

Oral Manifestations of Hypercortisolism (Cushing
Syndrome/Disease)
Orofacial features:

A

 Round, moon face (muscle wasting & fat accumulation)
 Fragile surface capillaries  susceptible to hematomas after
mild trauma
 Acne and excessive facial hair (hirsutism)
 Delayed growth and development (skeletal and dental
structures)
 Increased pigmentation of buccal mucosa if due to ACTH
excess

69
Q

Oral Manifestations of Hypercortisolism (Cushing
Syndrome/Disease)
 Immunosuppression:

A
  • oral candidiasis
  • Recurrent herpes labialis
  • herpes zoster infections
  • gingival and periodontal diseases
  • impaired wound healing
70
Q

Adrenal Disease (3)

A 
Conn’s Syndrome
(Mineralocorticoids)
Pheochromocytoma
(Catecholamines)
Cushing’s Syndrome/Disease
(Glucocorticoids)
71
Q

Pheochromocytoma

A

• Sudden releases of hormone causing sudden “attack” due to chromaffin cell
tumor in the Adrenal Medulla resulting in excessive secretion of EPI and NE.

72
Q

SKIPPED

Signs and Symptoms of excess NE & EPI

A

– Hypertension, Tachycardia, Palpitations,
Headache, Sweating, Tremors, Weight
Loss, Hyperglycemia, Orthostatic
Hypotension

73
Q

Pheochromocytoma

Occurs in

A

2-8 in 1 million person per year. Mean age of diagnosis is 40 but
tumors can occur from each childhood to late in life.

74
Q 
Its clinical presentation is so variable that pheochromocytoma has been 
termed “the great masquerader”. Among the presenting manifestations, 
episodes of (3) are typical, and 
these manifestations constitute a classic triad.
A

palpitation, headache, and profuse sweating

Physiology (53 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions