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Physiology > ENDO 1 > Flashcards

ENDO 1 Flashcards

1
Q

Endocrine Features: (2)

A 
• Provides “broadcast’ regulation of 
many tissues; specificity due to 
receptors
• Slower but longer lasting responses 
compared to the NS
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2
Q

We will discuss individual hormones and their specific physiological
functions, but, in general, all hormones regulate three types of things: (3)

A

(1) Maintenance of Homeostasis
- Thyroid Hormone, Insulin, PTH, Vasopressin, Aldosterone, etc.
(2) Growth and Differentiation
- Growth Hormone, Thyroid Hormone, etc.
(3) Reproduction
- LH, FSH, Estrogen, Progesterone, Testosterone, etc.

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3
Q

Specialized endocrine glands: (5)

A 
– Pituitary Gland
– Thyroid Gland
– Parathyroid Gland
– Adrenal Gland
– Pineal Gland
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4
Q 
SKIPPED
Some organs contain endocrine cells 
that secrete hormones even though 
their primary function is not endocrine 
regulation. (11)
A 
– Hypothalamus (TRH, CRH, etc.)
– Skin (Vitamin D)
– Adipose Tissue (Leptin)
– Thymus (Thymosin)
– Heart (Atrial Natriuretic Peptide)
– Liver (Insulin-Like GF1)
– Stomach (Gastrin)
– Pancreas (Insulin, Glucagon)
– Small Intestine (Secretin, CCK)
– Kidney (Renin, EPO, Vitamin D)
– Gonads (Testes, Ovaries)
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5
Q

Classes of Hormones (3)

A
  1. Proteins and Polypeptides
  2. Steroids
  3. Derivatives of Tyrosine
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6
Q

Protein and Polypeptide Hormones

Hormones from the (4)

A

Hypothalamus,
Anterior Pituitary,
Posterior Pituitary (ex. Antidiuretic Hormone – 9 Amino Acids),
Pancreas (ex. Insulin – 51 Amino Acids), etc.

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7
Q

process of protein activation

A 
Synthesized  first  as  a 
Preprohormone,  which 
isthen  converted  to  the 
Prohormone.  Upon 
packing into vesicles in the 
endocrine  cell,  the 
prohormone is cleaved into 
the  Active  hormone  and 
Inactive fragments that are 
then  secreted  by  the 
endocrine cell.
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8
Q

Steroid Hormones are from the (3)

A

adrenal cortex
ovaries
testes

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9
Q 
Steroid 
hormones 
are 
synthesized 
from
A

cholesterol

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10
Q

when are steroid hormones synthesized?

A

Hormones are synthesized upon demand rather

than being stored.

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11
Q

Amine Hormones are derived from

A

aa tyrosine

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12
Q

Amine Hormones includes (2)

A

thyroid hormone and adrenal medullary

neurohormones (epinephrine and norepinephrine).

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13
Q

when are amine hormones produced?

A

Amine hormones are produced and then stored until

secreted.

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14
Q

Thyroid
hormones bind
to the protein

A

thyroglobulin

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15
Q

Epinephrine
and
norepinephrine
are stored in

A

vesicles and
released by
exocytosis

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16
Q

Hormones released into the circulation can circulate either freely or bound to carrier proteins, also known as

A

binding proteins

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17
Q

The binding proteins serve as a reservoir

for the hormone and prolong the hormone’s

A

half-life, the time during which the

concentration of a hormone decreases to 50% of its initial concentration.

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18
Q

The (2) hormone is the active form of the hormone, which binds to the specific
hormone receptor

A

free or unbound

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19
Q

The majority of amines, peptides, and protein hormones circulate in their —
form.

A

free

20
Q

Steroid and thyroid hormones circulate bound to

A

specific transport proteins.
Some binding proteins are specific for a given hormone but some plasma
proteins, such as globulin and albumin can bind to hormones.

21
Q

Thyroid hormone travels in the plasma bound to: (3)

A

Thyroxine-binding Globulin (TBG), Transthyretin (TTR)

and Albumin

22
Q 
Because most binding proteins are 
synthesized in the liver, changes in liver 
function (ex. cirrhosis) may alter
A

binding
-protein levels and could indirectly affect
plasma hormone levels.

23
Q

Plasma levels of hormones
oscillate throughout the day,
showing peaks and troughs
that are — specific

A

hormone

24
Q 
This 
variable  pattern  of  hormone 
release  is  determined  by  the 
interaction  and  integration  of 
multiple  control  mechanisms, 
which  include
A 
hormonal, 
neural,  nutritional,  and 
environmental  factors  that 
regulate  the  constitutive 
(basal)  and  stimulated  (peak 
levels) secretion of hormones
25
Q

The location of the hormone receptor depends on the —

properties of the hormone (lipophobic/lipophillic).

A

chemical

26
Q

Ligand/Receptor binding demonstrates (3)

A

specificity, affinity and saturation.

27
Q

Plasma Membrane Hormone Receptors (4)

A
  1. G-protein Coupled
  2. Tyrosine Kinase: Insulin
  3. Serine Kinase
  4. Cytokine: Leptin
28
Q

Gs coupled Receptors (β Adrenergic, Calcitonin,
ACTH, Glucagon, TSH, Vasopressin) produce the
second messenger —.

A

cAMP

29
Q

Gq coupled Receptors (α Adrenergic,
Angiotensin II, TRH) activate the second
messengers (3)

A

IP3, DAG and Ca2+.

30
Q

Receptor numbers vary greatly in
different target tissues. This
provides a way to achieve specific

A

tissue activation

31
Q

Some receptors, such as (2) receptors,

are more widely distributed.

A

insulin

and thyroid hormone

32
Q

Nuclear Hormone Receptors

A

A large family of receptors that are located either in the cytoplasm or
nucleus. All act to increase or decrease gene expression.

33
Q 
The hormone receptor 
complex binds to a 
hormone responsive 
element in the 
promoter region of a 
gene, which leads to 
either
A

activation or
repression of
transcription. Forms
new proteins.

34
Q

Hormone Interactions

The effects of combined actions: (4)

A

– Antagonism
– Additive
– Synergistic
– Permissiveness

35
Q

Which hormone interaction is described in each of the
following situations?
A. Parathyroid increases plasma calcium levels; Calcitonin
decreases plasma calcium levels.
B. Glucagon, cortisol and epinephrine all increase blood
glucose more than the sum of their individual effects.
C. Thyroid hormone causes expression of B adrenergic
receptors in bronchiolar smooth muscle.

A
36
Q 
Tropic 
Hormones 
are 
hormones 
that have ---- as 
their 
targets.
A

other
endocrine
glands

37
Q

Hormone levels must be kept in balance
with negative feedback mechanisms. If this
doesn’t occur,— — occur.

A

endocrine disorders

38
Q

Primary Disorders

A

• Abnormality in the last
endocrine organ secreting the
hormone leading to either
hypo- or hyper-secretion.

39
Q

Causes of Primary Hyposecretion: (3)

A

(1) Partial destruction of the gland
(2) Dietary Deficiency
(3) Enzyme deficiency required for
hormone synthesis

40
Q

A tumor in an endocrine gland can

cause

A

Primary Hypersecretion.

41
Q

Secondary Disorders

A

• Abnormality in tropic hormone
leading to either hypo- or
hyper-secretion

42
Q

A lack of sufficient tropic hormone

leads to

A

Secondary Hyposecretion.

43
Q

A tumor (either in an endocrine gland
that secretes tropic hormones or in
non-endocrine tissue (lung)) can
secrete hormones and cause

A 
Secondary Hypersecretion
(Paraneoplastic Endocrine Syndrome)
44
Q

A PRIMARY endocrine
pathology is one where the
abnormality is in the

A 
endocrine organ secreting 
the hormone (ex. thyroid 
gland is either secreting 
too much or insufficient 
amount of TH.
45
Q

A SECONDARY endocrine
pathology is where the
abnormality is in

A 
one of the 
endocrine glands that 
secrete trophic hormones 
(Hypothalamus or Anterior 
Pituitary).
46
Q

SKIPPED
Diagnostic Tests of Endocrine
Function (7)

A
  1. Plasma hormone levels
  2. Autoantibodies: Hashimoto thyroiditis, type I diabetes, Graves disease, Addison disease, autoimmune hypoparathyroidism
  3. Urine hormone or hormone metabolite levels
  4. Stimulation tests by administration of a tropic or stimulating hormone (ex. ACTH to stimulate cortisol release, glucose load to stimulate insulin release)
  5. Suppression tests when hyperfunction of an endocrine organ is suspected (ex. response of GH to a glucose load or dexamethasone a synthetic glucocorticoid to suppress ACTH and Cortisol)
  6. Measurement of hormone receptor presence, number and affinity (ex. estrogen receptors in breast tumors)
  7. Imaging: Radioactive scanning of the thyroid and parathyroids; MRI of pituitary and hypothalamic imagine, CT scanning of adrenal and abdominal endocrine lesions, etc.

Physiology (53 decks)

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