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Physiology > ENDO 2 > Flashcards

ENDO 2 Flashcards

1
Q

The — is a true endocrine gland.

A

anterior pituitary gland

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2
Q

The posterior pituitary

gland contains

A

axon
terminals of hypothalamic
neurons

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3
Q

The pituitary gland weighs ~600

mg and is located within the

A

sella
turcica ventral to the diaphragma
sella.

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4
Q

Anterior Pituitary (6) peptide hormones

A 
• Growth Hormone
• Adrenocotricotropin (ACTH)
• Thyroid-Stimulating 
Hormone (TSH)
• Follicle-Stimulating 
Hormone (FSH)
• Luteinizing Hormone (LH)
• Prolactin
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5
Q

Somatotrophs secrete

A

GH (30-40% of cells)

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6
Q

Corticotrophs secrete

A

ACTH (20% of cells)

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7
Q

Thyrotrophs secrete

A

TSH (3-5% of cells)

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8
Q

Gonadotrophs secrete

A

LH and FSH (3-5% of cells)

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9
Q

Mammotrophs secrete

A

Prolactin (3-5% of cells)

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10
Q

Posterior Pituitary (2) peptide hormones

A

• Antidiuretic Hormone
(ADH)/Vasopressin
• Oxytocin

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11
Q 
Adenomas (benign) 
involving somatotropic 
cells can cause 
--- if occurring in 
children before closure 
of the long bones’ 
epiphyseal plates or 
--- in adults, 
with musculoskeletal, 
neurologic, and other 
medical consequences.
A

gigantism

acromegaly

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12
Q 
Neurons in the hypothalamus 
synthesize and secrete 
hypothalamic releasing and 
inhibiting hormones that 
control the
A

endocrine cells in

the anterior pituitary.

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13
Q

The hypothalamic hormones are

released into the

A

primary
capillary plexus in the median
eminence.

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14
Q

Hypothalamic-Hypophyseal
Portal Blood Vessels carry the
hypothalamic hormones to the

A

sinuses of the anterior pituitary

gland

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15
Q

The hypothalamic regulatory hormones bind to G-protein coupled receptors in
the various endocrine cells of the

A

anterior pituitary. Then, through generation of
second messengers (ex. cAMP via Adenylate Cyclase, IP3 and DAG via
Phospholipase C), they either stimulate or inhibit AP hormone secretion.

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16
Q

GH,

A 
a peptide hormone, 
acts directly on target 
tissues and as a tropic 
hormone to the liver, 
which releases insulin-
like growth factor-1 (IGF-
1).
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17
Q

Normal concentration of

GH is the adult is

A 
1.6-3 
ng/ml it is higher in 
children (~6 nmg/ml). 
Levels can increase to 
50 ng/dl during 
prolonged starvation.
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18
Q

Regulation of Growth Hormone Secretion:

Pulsatile secretion;

A

lower
concentrations during the day
with highest levels a few hours
after sleep.

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19
Q 
Regulation of Growth Hormone Secretion:
Stimulated by (5)
A 
starvation (protein deficiency), 
fasting (hypoglycemia), 
stress, 
exercise, and 
excitement.
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20
Q

Regulation of Growth Hormone Secretion:

High secretion in

A 
neonatal 
period but decreases in 
childhood. Peak levels during 
puberty and then they decline 
with age.
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21
Q

stimulation of GH release (5)

A 
GHRH
dopamine
catecholamines
excitatory aa 
thyroid hormone
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22
Q

inhibition of GH release (4)

A

somatostatin
IGF1
glucose
FFA

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23
Q

Many of the growth and
metabolic effects of GH
are mainly produced by

A

IGFs (also called

somatomedins).

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24
Q

IGF-1 is produced in most
tissues and acts on
neighboring cells in a
— manner.

A

paracrine

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25
Q

The — is the major

site of IGF-1 synthesis.

A

liver

26
Q

There are – different IGF
binding proteins (ex.
IGFBP-1 and IGFBP-3).

A

6

27
Q

Mechanisms
of Action of
GH and IGF-1 (4)

A
  1. Growth in nearly all tissues in the body (increased size of cells, mitosis and differentiation of bone and muscle cells) mainly via IGF-1
  2. Amino acid uptake and protein synthesis in most cells.
  3. Reduced glucose utilization- decreased uptake, increased hepatic glucose production and increased insulin secretion (insulin resistance; diabetogenic)
  4. Mobilization of fatty acids from adipose tissue (lipolysis) resulting in increased FFA in blood and use of FFA for energy
28
Q

Before fusion of the epiphyseal plates,

GH and IGF-1 stimulate

A

chondrogenesis
and widening of the epiphyseal plates,
followed by bone matrix deposition
stimulating linear growth.

29
Q

In adults, GH and IGF-1 play a role in
regulating the normal physiology of
bone formation by

A 
increasing bone 
turnover (increasing bone deposition 
via the activation of OSTEOBLASTS and 
also  increasing  bone  resorption  via 
activation of OSTEOCLASTS, though to 
a lesser extent).
30
Q

Growth Hormone Excess

  • – in Children
  • – in Adults
A

Gigantism

Acromegaly

31
Q

An MRI shows a pituitary tumor in 90% of
acromegalic patients. These tumors
ordinarily involve the (2); rare ectopic tumors may arise in the
— bone

A

sella and cavernous sinus

sphenoid

32
Q

Growth Hormone Excess features (6)

A 
Coarse facial features, large fleshy nose, frontal bossing, jaw malocclusion.
Diabetes Mellitus
Coronary Heart Disease 
Kyphosis 
Hyperhidrosis and oily skin
Paresthesias
33
Q

Treatment for a Pituitary Microadenoma

A

Surgical resection of the tumor (adenomectomy)
via transphenoidal approach followed by
medication (somatostatin (GHIH) receptor ligand
or GH receptor antagonist).

34
Q

Oral Manifestations of GH Excess (7)

A

 Thick rubbery skin, enlarged nose, and thick lips
 Macrocephaly
 Macrognathia
Disproportionate mandibular growth
o Mandibular Prognathism
o Generalized Diastemata
 Anterior open bite and malocclusion
(macrognathia and tooth migration)
 Macroglossia, Dyspnea, Dysphagia, Dysphonia, Sialorrhea
 Hypertrophy of the pharyngeal and laryngeal tissues  sleep apnea

35
Q

Manifestations of Acromegaly/Gigantism; will also show enlarged (2)

A

frontal sinuses

pituitary fossa

36
Q

Growth Hormone Deficiency

Causes (5)

A
  • Hypothalamic disorders
  • Mutations: GHRH receptor, GH gene, GH receptor, IGF-1 receptor
  • Combined pituitary hormone deficiencies (panhypopituitarism)
  • Radiation
  • Psychosocial deprivation
37
Q

Growth Hormone Deficiency
Clinical manifestations
Depend on the time of onset and the severity of hormone deficiency.
Complete GH deficiency: (4)

A
  • slow linear growth rates
  • normal skeletal proportions
  • pudgy, youthful appearance (decreased lipolysis)
  • in the setting of cortisol deficiency  hypoglycemia
38
Q

— is the most common form of dwarfism

A

Achondroplasia

39
Q

Achondroplasia

A

autosomal dominant condition
that results from a mutation of FGF-3 receptor in cartilage and brain. This mutation makes
the receptor overly active and it inhibits cartilage growth at growth plates so limb growth is
reduced (growth of the trunk of the body is not impacted).

40
Q

Oral Manifestations of GH Deficiency (4)

A

• Disproportionate delayed growth of the skull & facial skeleton leading to small facial appearance.
• Tooth formation & growth of the alveolar regions of the jaws are
abnormal and may be disproportionately smaller than adjacent
anatomic structures
• Solitary Median Maxillary Central Incisor
• Eruption of primary and secondary dentition and shedding of deciduous teeth are delayed.

41
Q

• Tooth formation & growth of the alveolar regions of the jaws are
abnormal and may be disproportionately smaller than adjacent
anatomic structures (4)

A

 tooth crowding and malocclusion
 a high tendency for plaque accumulation
difficulty maintaining good oral hygiene
 prone to gingivitis and periodontal disease

42
Q

Eruption of primary and secondary dentition and shedding of deciduous teeth are delayed.
Management:

A

correct dental & skeletal malocclusions

43
Q

The Posterior Pituitary/Neurohypophysis
Contains ~100,000 unmyelinated
axons of neurons whose cells
bodies are in the

A

hypothalamus
(Paraventricular nucleus and
Supraoptic nucleus).

44
Q

The Posterior Pituitary/Neurohypophysis secretes (2)

A

(1) Antidiuretic Hormone (ADH)/Arginine Vasopressin (AVP)

(2) Oxytocin

45
Q

Both neurohormones are polypeptides of – amino acids.

A

nine

46
Q

Both neurohormones are polypeptides of nine amino acids.
While each nucleus synthesize one predominate neurohormone, each can
synthesize and secrete

A

some of the other neurohormone.

47
Q

ADH/AVP Mechanism of
Action
Blood Vessels:

A

– Contraction of vascular
smooth muscle via V1
receptors

48
Q

ADH/AVP Mechanism of Action

Renal Tubules:

A 
– Binds to V2 receptors in 
the late distal tubule and 
collecting duct. 
– Aquaporin-2 (AQP-2) 
proteins are then 
inserted into the apical 
membrane of tubular 
epithelial cells, allowing 
for water reabsorption 
(along with AQP-3 and 
AQP-4 on the 
basolateral membrane).
49
Q

Stimuli for ADH Secretion (3)

A

Decreased Blood Volume (Isotonic)
Increased Osmolarity (Isovolemic)
Decreased Blood Pressure

50
Q

Normally changes in Osmolarity stimulate

— Secretion by the Posterior Pituitary

A

ADH

51
Q

Hypodipsia (2)

A
  • Decreased or absent feeling of thirst, which results in reduced intake of water and can cause Hypernatremia.
  • A common problem in elderly people, but is also associated with lesions in the hypothalamus (thirst center), head trauma, occult hydrocephalus or subarachnoid hemorrhage.
52
Q

ADH Imbalances (2)

A
  • Diabetes Insipidus (DI)

* Syndrome of Inappropriate ADH (SIADH)

53
Q

• Diabetes Insipidus (DI) (2)

A

– Neurogenic/Central

– Nephrogenic/Peripheral

54
Q

DI:

Due to either

A 
insufficient production (Neurogenic/Central) or lack 
of kidney response (Nephrogenic/Peripheral) to ADH.
55
Q

DI:

Presentation with

A

Polyuria

56
Q

Polyuria

A

Excretion of a large volumes of

urine that is hypotonic and tasteless (insipid)

57
Q

DI:

Diagnostic test includes a

A

dehydration test in a controlled

environment.

58
Q

Other causes of polyuria include:

A
  1. Primary ingestion of excess fluid: Primary Polydispia

2. Increased metabolism of ADH (ex. pregnancy)

59
Q

Syndrome of Inappropriate ADH (SIADH)

A

Increased and uncontrolled secretion of ADH that causes

volume expansion and hyponatremia.

60
Q

Syndrome of Inappropriate ADH (SIADH) can result from (3)

A

surgery, pain, stress,

temperature changes,
tumor, TB, Pneumonia, positive pressure breathing,
Hydrocephalus, Meningitis, HIV, etc.

61
Q

Mechanisms of Action of Oxytocin (2)

A 
• Stimulates 
contraction of the 
uterus towards the 
end of gestation. 
• Causes milk 
ejection from the 
breasts in lactation.

Physiology (53 decks)

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