Brainscape's Knowledge GenomeTM

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


See full index

Y2B1 - Endocrine πŸ“• > Physiology 🫁 > Flashcards

Physiology 🫁 Flashcards

1
Q

what is the definition of endocrine glands?

A

ductless glands, their secretion is not conveyed along ducts but pass directly into blood and lymphatic vessels

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

what are hormones?

A

specific chemical regulatory substances secreted by the endocrine glands in catalytic amounts into the blood stream and transported to specific target cells (or organs), where they elicit physiologic, morphologic and biochemical responses

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

what are the endocrine glands of the human body? and what do they secrete?

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

What are the organs with endocrine function? and what do they secrete?

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

what is the definition of local hormones?

A

They are hormones that act locally

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

what are paracrine hormones?

A

diffuse for a short distance through the interstitial space to affect neighbouring cells.

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

what are autocrine hormones?

A

which act on the same cells that produce them

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

what are juxtacrine hormones?

A

interact with specific receptor on juxta-posed cells.

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

what are examples of local hormones?

A

Prostaglandins, histamine, serotonin, bradykinin and GIT hormones

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

what is production and secretion of hormones determined by?

A

βœ“ Body requirements.
βœ“ Rate of hormone inactivation.
βœ“ Rate of hormone clearance from the body.

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

how are hormones transported?

A

Initially, all hormones enter the plasma pool, where they may circulate in 2 forms:

  1. Free (unbound) part: the active part which binds to receptor.
  2. Bound part: carried by specific albumins and globulins which are synthesized in the liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the plasma half-life of a hormone?

A

time needed for the concentration of the hormone to decrease to its half

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

what is the relation between plasma half-life of a hormone and the percentage of its protein binding?

A

positively correlated, (as the bound part is not metabolized nor excreted)

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

what are the factors that control hormone secretions?

A
  1. Neurohumor or neurosecretions
  2. Direct innervation
  3. Feed-back control
  4. Blood level of hormones
  5. Effect of cytokines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the definition of neurohumor or neurosecretions?

A

They are secretions released by a nerve cell or group of cells and reaches the endocrine glands via blood vessels or nerve fibres to control their secretions

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

what are examples of neurosecretions?

A
  1. Hypothalamic releasing and inhibitory factors or hormones
  2. Posterior pituitary hormones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

where are Hypothalamic releasing and inhibitory factors or hormones secreted from?

A

secreted from hypothalamic nuclei e.g. arcuate nuclei

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

how are Hypothalamic releasing and inhibitory factors or hormones transported?

A

transported via hypothalamohypophyseal portal circulation to control secretion of anterior pituitary gland hormone secretion

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

what are examples of Hypothalamic releasing and inhibitory factors or hormones?

A
  1. Growth hormone releasing hormone (GHRH) control secretion of GH
  2. Corticotropin releasing hormone (CRH) control ACTH secretion
  3. Thyrotropin releasing hormone (TRH) control TSH secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are examples of posterior pituitary hormones?

A

including oxytocin and ADH are secreted from hypothalamic nuclei (supraoptic and paraventricular)

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

how do posterior pituitary hormones reach the posterior pituitary?

A

reach the posterior pituitary via the hypothalamo-hypophyseal tract

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

give an example of a gland that secretes by direct innervation

A

activation of the sympathetic nerve fibers by stress β†’ directly stimulate secretion of adrenaline and noradrenaline from the adrenal medulla.

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

what is feed-back control?

A

It represents the relationship between a trophic hormone and its target gland hormone or its product

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are the types of feed-back control?

A

negative and positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

compare betweeen negative feedback and positive feedback according to incidence and significance

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

what is the definition of negative feedback? and give an example?

A
  • In which the trophic hormone stimulates the secretion of target gland hormone, which in turn inhibit the trophic hormone secretion
  • TSH stimulates the secretion of the target gland hormone e.g. thyroxine hormone which in turn inhibits the secretion of trophic gland hormone secreted from the pituitary gland e.g. TSH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is the definition of positive feedback? and give an example?

A
  • In which the trophic hormone stimulates the secretion of target gland hormone, which in turn stimulate the trophic hormone secretion.
  • An example of a +ve feed-back loop is that which exists between LH and estrogen 48 hrs before ovulation to induce ovulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what are the types of negative feedback?

A

according to the modes of action:

Long loop Feed-Back: It represents the relationship of trophic anterior pituitary hormones and their target gland hormones.

Short loop Feed-Back: The inter-relation between pituitary trophic hormones and the hypothalamic releasing and release- inhibiting hormones.

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

blood level control of hormones

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

what are cytokines?

A

Cytokines are proteins produced by various cell types in response to stimuli arising from different physiological and pathophysiological states.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

how do cytokines affect endocrine functions?

A

by acting on the endocrine glands and on the hormonally responsive tissues.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what are examples of cytokines affecting endocrine functions?

A

a) Inflammatory cytokines e.g. interleukin and tumour necrosis factors.

b) Immunomodulatory cytokines e.g. interferons.

c) Chemokines e.g. ciliary neurotrophic factors and oncostatin.

d) Growth factors e.g. platelet derived growth factor, epidermal growth factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is the definition of posterior pituitary?

A

Posterior pituitary is not a gland but a collection of nerve endings of cell bodies in the supraoptic and paraventricular nuclei of the hypothalamus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is the crude extract of posterior pituitary?

A
  • The crude extract of this posterior lobe is called pituitrin which contains 2 hormones:
  1. Antidiuretic hormone (ADH), also called vasopressin or pitressin.
  2. Oxytocin (or pitocin) hormone.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

process of formation of posterior pituitary hormones

A
  • The two hormones are formed in the hypothalamus and incorporated into granules with a binding protein (neurophysin).
  • neurophysin-1 for oxytocin and neurophysin-2 for antidiuretic hormone.
  • The granules (or neurosecretory vesicles) pass down the axons of the neurohypophyseal tracts to dilated nerve endings in the posterior pituitary, from which they enter the blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

release of hormones of posterior pituitary

A
  • When a nerve impulse is transmitted from the cell body in the hypothalamus down the axon, it depolarizes the neurosecretory vesicles within the terminal Herring body.
  • An influx of Ca into the neurosecretory vesicles then results in hormone enters the closely adjacent capillary.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what are the functions of ADH?

A
  1. The major action of ADH is on the distal convoluted tubules and collecting ducts that are responsible for reabsorbing free water from the glomerular filtrate.
  2. when administered systemically in large doses, ADH causes contraction of the smooth muscles particularly in the blood vessels leading to elevation of the blood pressure, coronary vasoconstriction and intense splanchnic vasoconstriction (control persistent, serious gastrointestinal bleeding).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Mechanism of action of ADH

A
  • ADH binds to V2 (vasopression-2) receptors.
  • The intracellular ↑cAMP causes the insertion of aquaporin-2 (AQP2) water channels in the apical (luminal) membrane.
  • Synthesis of the water channels also is increased, Removal of ADH removes the water channels from the membrane.
  • Basolateral membrane has AQP3 and AQP4 channels.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

control of secretion of ADH

A

Secretion of ADH is primarily regulated by osmotic and volume stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Osmotic regulation of ADH secretion

A
  • The hypothalamic supraoptic nuclei contain very sensitive osmoreceptors, being responsive to changes in osmolality of only 1% (normal plasma osmolality is 290 m osm/liter).
  • Minimal rise of plasma osmolality (dehydration, administration of solutes) leads to loss of intracellular water from osmoreceptor neurons and causes ADH release. As a result, ADH produces reabsorption of most of the water from tubular fluid, in the kidney, while electrolytes continue to be lost into the urine. This effect dilutes the extracellular fluids, returning them to a normal osmotic composition.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

how does blood volume affect the secretion of ADH?

A
  • ADH release is also stimulated by a decrease of 5% to 10% in total circulating blood volume, Haemorrhage decreases blood volume.
  • Hypovolaemia is perceived by a number of pressure (rather than volume) sensors:
  1. Carotid and aortic baroreceptors.
  2. Stretch receptors in the walls of the left atrium and pulmonary veins. Since the pressure receptors normally maintain tonic inhibition of ADH release, hypovolaemia decreases these inhibitory impulses and increases ADH release.
  3. Also, the release of renin from the juxtaglomerular apparatus leads to generation of angiotensin directly within the brain which stimulates thirst & mediates the release of ADH.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what other factors stimulate ADH secretion?

A
  • Sulfonylureas used in the treatment of diabetes mellitus
  • Nicotine
  • Increased temperature and opiates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what other factors inhibit ADH secretion?

A

Diuretics
Cold weather
ethanol
Chronic water loading

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what is the problem in Diabetes insipidus?

A

The problem is either
- a deficiency of ADH (central form)
- a lack of an effect of ADH on the collecting duct (nephrogenic form).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what are the characteristcs of diabetes insipidus?

A
  • the individual is forming a large volume of dilute urine (polyuria) along with polydipsia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what is the nature of oxytocin? and where is it secreted from?

A

polypeptide hormone, released by the paraventricular nuclei of the hypothalamus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what is the mechanism of action of oxytocin?

A

At the target cells, it combines with specific plasma membrane receptors and probably exerts its effects by increasing intracellular Ca++ content.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what are the functions of oxytocin?

A
  1. Milk-letting effect
  2. Suckling-reflex
  3. Powerful contracting action on the uterus
  4. Transport of the sperms into the uterus during intercourse
  5. Discharge of sperms in male
  6. Stimulation of sweat secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what causes the milk-letting effect by oxytocin?

A

by stimulation of the myoepithelial cells of the alveoli of the mammary glands.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what potentiates/inhibits the action of oxytocin (concerning milk letting effect)?

A
  • potentiated by estrogen
  • inhibited by catecholamines.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

mechanism of suckling reflex

A
  • Suckling of the breast by the infant stimulates touch receptors at the nipple and areola
  • which send afferent impulses into the hypothalamus to release both oxytocin and prolactin hormones.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

how does oxytocin cause powerful contractions on the uterus?

A
  • by lowering the threshold for membrane depolarization of the myometrial muscles

β€”β€”β€”

  • It plays an important role in labor, sustained post-partum contractions that help to:
    1. maintain haemostasis after evacuation of the placenta
    2. involution of the uterus after delivery.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

what potentiates/inhibits the action of oxytocin (concerning uterine contractions effect)?

A
  • potentiated by estrogen
  • inhibited by progesterone.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

how does oxytocin help in Transport of the sperms into the uterus during intercourse?

A

By the end of the act of intercourse (or matting), oxytocin is released giving the (orgasm) sensation due to uterine contractions which suck the sperms into the uterus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Discharge of sperms in male by oxytocin

A

Oxytocin leads to discharge of sperms from the seminiferous tubules and epididymis to vas deferens.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

stimulation of sweat secretion by oxytocin

A

from sweat glands at the axillae, nipples, groins and perineum which produce sex attraction especially in animals.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what is the shape of the pituitary gland?

A

ovoid structure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what is the weight of the pituitary gland?

A

500 and 600 mg in an adult.

β€œnot even 1 gm!”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what is the site of the pituitary gland?

A

at the base of the brain in a small cavity called (pituitary fossa or sella tursica)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

covering and connection of the pituitary gland

A
  • which is covered by an extension of the dura mater (the diaphragma sellae) through which passes the pituitary stalk connecting the gland to the hypothalamus.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what does the anterior pituitary gland represent? (relative to the whole pituitary gland)

A

accounts for 75% of the weight of the pituitary gland.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

what is the color of the anterior pituitary gland?

A

it is dark red colour is due to the presence of blood sinusoids in between the secretory cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what are the hormones secreted from the anterior pituitary gland?

A

Primary:
- GH (somatotropic or somatotropin)
- Prolactin (lactogenic or mammotropin)
- MSH (melanotropin or intermedin)

Trophic:
- TSH (thyrotropin or thyrotropic hormone)
- ACTH (corticotrophin)
- FSH
- LH (in male, it is called interstitial cell stimulating hormone).

Others:
- beta lipoproteins β€œanalgensic”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

what does the anterior pituitary gland control?

A

the adenohypophysis controls, through its trophic hormones, all other endocrine glands except the parathyroid, supra-renal medulla and pancreas.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what controls the secretions of the anterior pituitary gland?

A
  1. Hypothalamus
  2. Negative Feedback
  3. Others
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

explain the anatomy of the hypothalamo-hypophyseal portal circulation

A
  • The hypothalamus has a major influence on the release and the synthesis of the anterior pituitary hormones.
  • This is achieved by: hypothalamo-hypophyseal portal circulation. β€œ a path for hormones”
  • Internal Carotid Artery β€”> 2 Superior Hypophyseal Arteries β€”> 1st set of capillaries (In Median Eminence & Neural Stalk) β€”> Portal Veins β€”> 2nd set of capillaries (Sinusoids) (In Anterior Pituitary gland)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

hormone and hypothalamic control (Anterior pituitary gland)

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

negative feedback control of secretions of anterior pituitary gland

A

The activity of the anterior pituitary is also influenced by the hormones of the target glands:
- thyroxin
- cortisol
- gonadal steroids.

Thyroxin, GH —–> -ve FB on anterior pituitary
Cortisol, Estrogen β€”> -ve Fb on Hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

what other mechanisms could affect the secretions of the anterior pituitary gland?

A

Numerous other mechanisms influence the activity of the anterior pituitary such as:

  • physical and emotional stress β€œGH”
  • coitus β€œFSH & LH”
  • suckling β€œProlactin”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

what is the nature of GH? and where is it secreted from?

A
  • Growth hormone (GH) is a protein hormone secreted from specific acidophil cells in the adenohypophysis called somatotrophs which form 30-40% of the cell population of the gland.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

what is the basal blood concentration of GH?

A

less than 3 ng/ml.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

what are the functions of GH?

A
  • Growth Function
  • Metabolism Function
  • Others
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

growth Function of GH

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

effect of GH on protein metabolism

A

Stimulates protein synthesis by:
- Increase amino acid transport through the cell membranes.
- Increase of proteins synthesis by ribosomes.
- Increase formation of RNA.
- Inhibition of protein catabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

effect of GH on CHO metabolism

A

GH has anti-insulin action:

  • decreases glucose uptake by tissues. β€œwhich is mediated by hexokinase”
  • stimulates gluconeogenesis in the liver with more production of glucose.
  • stimulates the release of glucagon hormone by the pancreas with consequent increase in glycogenolysis in the liver.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

effect of GH on Fat metabolism

A
  • It has powerful lipolytic effect thus increasing the blood level of FFA which provides energy during stress conditions particularly hypoglycemia and starvation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

effect of GH on Electrolyte metabolism

A
  • Marked increase of Ca++ absorption from GIT.
  • Reduces Na+ , K+ and HPO4 - excretion by kidney
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

does GH have direct anabolic effects? and what mediates its growth promotimg actions?

A
  • Growth hormone has no direct anabolic effects.
  • Its growth promoting actions are mediated by a group of intermediary polypeptide substances called somatomedins.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

what is the nature of somatomedins? and where are they released from?

A

polypeptide, formed in the liver, in bone cells, and probably some other tissues.

80
Q

what is the structure of somatomedins similar to?

A

proinsulin

81
Q

how do somatomedins do their function?

A
  • Somatomedins bind to specific plasma membrane receptors.
  • IGF-I interacts with target organs to induce growth.
  • These receptors can also bind insulin and pro-insulin but with much less affinities.
  • They may also feedback on the pituitary to inhibit GH secretion.
82
Q

mention a case in which IGF-1 is independent of GH

A
  • In some cases, control of IGF-l can be independent of growth hormone.
  • For example, in a state of long-term stress (e.g., in starvation) growth hormone increases but IGF-I decreases
83
Q

what is the mechanism of GH action?

A
  • Growth hormone has no direct anabolic effects.
  • Its growth promoting actions are mediated by a group of intermediary polypeptide substances called somatomedins.
  • Somatomedins are formed in the liver, in bone cells, and probably some other tissues.
  • They are structurally similar to proinsulin.
  • they are called insulin-like growth factors (IGF), of which 2 types have been identified: IGF-I and IGF-II.
  • IGF-I interacts with target organs to induce growth.
  • They may also feedback on the pituitary to inhibit GH secretion.
  • Somatomedins bind to specific plasma membrane receptors.
  • These receptors can also bind insulin and pro-insulin but with much less affinities.
  • In some cases, control of IGF-l can be independent of growth hormone.
  • For example, in a state of long-term stress (e.g., in starvation) growth hormone increases but IGF-I decreases
84
Q

how is GH secretion controlled?

A
  1. Hypothalamus
  2. Others
85
Q

how does the hypothalamus affect the secretion of GH?

A
  • GHRH: ↑ GH secretion.
  • GHIH (somatostatin): ↓ GH secretion.
86
Q

3 nutrients, 3S, E

what stimulates the release of GH?

A
  • Hypoglycemia
  • ↓FFA
  • ↑A.A e.g. high protein diet or infusion of arginine
    β€”β€”β€”β€”
  • Starvation
  • Stress and Ξ±-adrenergic agonists
  • Sleep
    β€”β€”β€”β€”
  • Exercise
87
Q

what inhibits the relase of GH?

A
  • Hyperglycemia
  • ↑FFA
  • ↓A.A
    β€”β€”-
  • ↑Cortisol
  • ↑G.H
  • IGF-1
88
Q

when is most of the pulsatile release of GH take place? and is it suppressed by glucose?

A
  • Most (70%) of the pulsatile release of growth hormone occurs during slow wave sleep (stages 3 and 4) and this increases during puberty.
  • Nocturnal pulses are not suppressed by glucose.
89
Q

Disorders of GH secretion

A

↑ GH secretion
- If before union of epiphysis: gigantism
- If after union of epiphysis: acromegaly

——–
↓ GH secretion
- In adult: No physical signs but there’s loss of some proteins.
- In children: Dwarfism.

90
Q

what are the characters of GH release in cases of increased secretion?

A

Growth-hormone secretion remains pulsatile but nocturnal dominance is lost.

91
Q

what is the definition of gigantism?

A

A disease resulting from increased secretion of the growth hormone before the union of the epiphyses

92
Q

what are the symptoms of gigantism?

A
  • Marked elongation of different body bones but in a relative proportion (the span =the height).
  • Overgrowth of soft tissues e.g. the muscles and viscera.
  • Hyperglycemia and increased metabolic rate
  • These patients are often mentally subnormal and unless treated, usually die before the age of 20 yrs.
  • Headache and visual disturbances due to local pressure of the growing tumor on the sella tursica and optic chiasma
93
Q

what is the definition of acromegaly?

A
  • This disease is due to hyper secretion of growth hormone in adults after the epiphyses have fused
  • The bones become thicker and deformed; the muscles and viscera also enlarge
94
Q

what are the manifestations of acromegaly?

A
  • Generalized coarsening of the features due to:
    ➒Thickening of the skin and subcutaneous tissues.
    ➒Elevated supraorbital ridge
    ➒The lower jaw protrudes forward (prognathism), and the teeth become widely separated.
  • Kyphosis due to thickening of the vertebrae.
  • Raised BMR.
  • Hyperglycemia, glucosuria and Hypogonadism.
  • Some patients have defects in the visual fields because of the pressure of the tumor on optic chiasma.
  • headache and vomiting
95
Q

how is acromegaly treated?

A

requires surgical removal of the tumor or destruction by irradiation.

96
Q

what is the definition of dwarfism?

A

Deficiency of growth hormone in children

97
Q

what are the manifestations of dwarfism?

A

a) Short stature by rapid closure of the epiphyses.
b) Retarded growth of soft tissues but mild obesity is common.
c) normal mental and sexual growth

Treated by adminstrtion of GH

98
Q

what are other names of prolactin?

A

Lactogenic hormone or mammotropin

99
Q

what is the nature of prolactin?

A

polypeptide hormone.

100
Q

what is the structure of prolactin?

A

similar to growth hormone and human chorionic somatomammotropin (HCS).

101
Q

blood level of prolactin

A
  • Its normal plasma concentration is about 5 ng/ml in men and 8 ng/ml in women.
  • Prolactin circulates unbound, and in the basal state the plasma levels are the same in men and women.
102
Q

what are the Functions of prolactin?

A
  1. Prolactin participates in stimulating the development of breast tissue:
    - Prolactin is not involved in breast development during puberty but is involved in breast enlargement during pregnancy.
    - After parturition, prolactin stimulates milk synthesis and secretion.
  2. Hyperprolactinemia causes hypogonadism (infertility). It disrupts the GnRH-gonadotropin axis but does not affect the basal levels of LH and FSH

It affects exocrine gland

103
Q

what controls the secretion of prolactin?

A
  • Hypothalamic control
  • Pregnancy
  • Suckling
  • Drugs
  • Other factors
104
Q

Hypothalamic control of prolactin secretion (and mention what proves it)

A
  • The hypothalamus releases both prolactin releasing hormone (PRH) and prolactin release inhibiting hormone (PRIH) which is structurally similar to dopamine.
  • Section of the pituitary stalk leads to prompt increase in the plasma prolactin level, thus the effect of the hypothalamus is mainly inhibitory.
105
Q

Drugs effect on prolactin secretion

A

(Inhibit prolactin)

Drugs increasing the formation of dopamine or stimulate dopamine receptors:
- L-doppa
- Apomorphine
- bromocriptine

106
Q

suckling effect on prolactin secretion

A

Stimulation of the nipples as by suckling in lactation produces rapid increase of prolactin level through inhibition of PRIH release.

107
Q

pregnancy effect on prolactin secretion

A

prolactin secretion increases steadily during pregnancy, mediated by the large increase in estrogen.

108
Q

other factors affecting prolactin secretion

A

Increased release in response to rest and during sleep.

109
Q

what is sheehan syndrome?

A
  • Postpartum pituitary infarction: During pregnancy, the pituitary enlarges in response to estrogen stimulation of the lactotrophs, but there is no compensatory increase in vascularity. Thus, following delivery, the pituitary is more susceptible to blood loss and the ensuing hypotension.
  • Can result in partial or complete pituitary insufficiency.
110
Q

what is the first discovered thyroid hormone? and what % does it constitute of thyroid output?

A

Thyroxine hormone (T4) was the first to be discovered and constitutes about 90% of the thyroid output.

111
Q

what characterizes T3 hormone?

A

Although T3 is released in a smaller amount and persists in blood for a much shorter time than does T4, it appears to be the most active hormone at the cellular level, being 3-5 times more active than T4.

112
Q

what causes the biological effects of T4 hormones?

A

The biological effects of T4 are largely a result of its intracellular conversion to T3.

113
Q

what is T4 converted into?

A

T4 is converted to T3, Some of T4 is also converted to another iodinated tyrosine compound called β€˜reverse triiodothyronine (rT3) which has no apparent biological action.

114
Q

what are the functions of Thyroid hormones?

A
  1. Intracellular actions of thyroid hormones (mechanism of action).
  2. On the whole body.
115
Q

Intracellular functions of thyroid hormones

A

T3 and T4 appear to enter the cell freely by passive diffusion where they:

  • Bind directly to a specific nuclear receptor.
  • The hormone receptor complex interacts with DNA to stimulate the formation of mRNA β€”> increase synthesis of specific proteins β€”-> increase size and number of mitochondria and β€”> increase amount of plasma membrane Na+, K + -ATPase
116
Q

thyroid hormones effects on the whole body

A
  1. Growth and development
  2. Energy metabolism
  3. Gastro-intestinal tract
  4. Cardio-vascular system
  5. Respiratory system
  6. Gonads
  7. Skeletal muscles
  8. Vitamins and drugs
  9. Carbohydrate metabolism
  10. Protein metabolism
  11. Fat metabolism
  12. Haemopoietic system
117
Q

growth & development functions of thyroid hormones

A
  • Thyroid hormones stimulate physical, mental and sexual growth.

Physical growth:
- Has a permissive effect on GH & potentiate the effect of somatomedins.
- Eruption & development of teeth.
- Closure of fontannels.

Mental growth:
- Growth, development & function of CNS during fetal life & first few years after birth.
- Myelination of nerve fibers & development of synapses.

Sexual growth:
- Essential for normal menestrual cycle & spermatogenesis (fertility).
- Stimulates milk secretion during lactation.

118
Q

energy metabolism functions of thyroid hormones

A
  • Thyroid hormones stimulate the basal metabolic rate, oxygen consumption, heat production, and glucose uptake by cells.
  • One mg of thyroxin can raise heat production by about 1000 calories.
119
Q

GIT functions of thyroid hormones

A
  • inc. glucose absorption from the intestine and glycogenolysis.
  • inc. appetite and GIT motility.
120
Q

CVS functions of thyroid hormones

A
  • inc. heart rate and stroke volume.
  • The systolic blood pressure is high, while the diastolic remains normal or decreased due to dilatation of the peripheral arterioles which lead to a reduction in the peripheral resistance.
121
Q

Respiratory functions of thyroid hormones

A
  • inc. rate and depth of breathing with a consequent increase in pulmonary ventilation.
122
Q

functions of thyroid hormones on gonads

A
  • Normal level of thyroid hormones is essential for proper sexual functions.
  • Thyroid hormones increase sex steroid binding-globulin to decrease the metabolic clearance of estrogen and testosterone.
  • Both hyper and hypothyroid states lead to infertility.
123
Q

function of thyroid hormones on skeletal muscles

A

Normal skeletal muscle function also requires thyroid hormones.

124
Q

carbohydrate metabolism function of thyroid hormones

A

In physiologic amounts:
- thyroid hormones potentiate the action of insulin and promote glycogenesis and glucose utilization.

In large doses, induce hyperglycemia by:
1. inc. glycogenolytic effect of epinephrine.
2. inc. gluconeogenesis.
3. inc intestinal glucose absorption.

125
Q

protein metabolism function of thyroid hormones

A
  1. In physiologic amounts, they have protein anabolic effect.
  2. While in large doses,they enhance protein catabolism.
126
Q

fat metabolism function of thyroid hormones

A
  • Thyroid hormones stimulate all aspects of lipid metabolism, including synthesis, mobilization and utilization.
  • They dec. serum TG , phospholipids and cholesterol, mean while they inc. serum FFA and glycerol.
127
Q

functions of thyroid hormones on Haemopoietic system

A
  • Thyroid hormones inc. erythropoiesis with increase in RBCs.
  • They also facilitate the dissociation of O2 from haemoglobin by increasing the amount of 2,3 diphosphoglycerate (DPG) in the RBCs.
128
Q

what controls thyroid functions?

A
  1. TSH
  2. Thyroid stimulating immunoglobulin (TSI)
  3. All types of stress
  4. Age
  5. Pregnancy
  6. Antithyroid agents (Goitrogens)
  7. Blood iodine level
129
Q

TSH Control of thyroid function

A

TSH has the following effects on the thyroid gland:

  • Promotes hyperplasia of the gland cells.
  • Increases its uptake of iodide from the blood.
  • Stimulates synthesis and release of the thyroid hormones, T3 & T4.

There is a negative feedback mechanism between the plasma levels of the thyroid hormones and the output of TSH. Excess T3 and/or T4 suppresses the release of TSH by acting directly on the thyrotrope cells, and to a lesser extent on the anterior hypothalamus (site of release of TRH).

130
Q

TSI (Thyroid stimulating immunoglobulin) Control of thyroid function

A

TSI acts on the thyroid in a manner similar to TSH but is not affected by the level of T3 and T4 in the blood (no –ve feed back).

131
Q

stress Control of thyroid function

A

e.g exposure to cold environment stimulates the thyroid with consequent increase in metabolic rate and heat production to counteract the effects of low temperature.

132
Q

age Control of thyroid function

A

Although its effect is small, but there tends to be a decrease in activity with increasing age.

133
Q

pregnancy Control of thyroid function

A
  • Thyroid activity increases during pregnancy.
  • The placenta secretes a hormone called β€˜human chorionic gonadotropin’ or HCG which is structurally similar to TSH.
134
Q

Antithyroid agents (Goitrogens) Control of thyroid function

A
  • Such agents interfere with one or more steps in T3 and T4 synthesis.
  • Deficiency of thyroid hormones leads to a rise in TSH level which results in enlargement of the thyroid gland (goiter).
  • Primary goitrogens include thiocyanates such as those found in cabbage and inhibit the I - uptake by the thyroid gland.
135
Q

Blood iodine level Control of thyroid function

A

Iodine deficiency → dec. T3&T4 → inc. TSH→ goiter.

Excess iodine (Wolff-Chaikoff) results in:
1. dec. organic binding of iodine in the gland.
2. dec. proteolysis of thyroglobulin.

136
Q

What produces TSI?

A

This immunoglobulin is produced by lymphocytes in all cases of Grave’s disease (hyperthyroidism).

137
Q

what are examples of primary goitrens?

A

Primary goitrogens include thiocyanates such as those found in cabbage

138
Q

what are the disorders of thyroid hypofunction?

A

Cretinism & myxedema

139
Q

what is the definition of cretinism?

A

Hypothyroidism in human infants.

140
Q

what are the manifestations of Cretinism?

A
  • Retardation of physical , mental& sexual growth.
  • Low BMR and O2 consumption.
  • The skin:
    1. Yellowish due to carotinaemia.
    2. Scaly and thick with scanty coarse hair, due to failure of formation of vitamin A in the liver from carotins.
  • Facial features: puffy eye lids, Lips are thick and the tongue is swollen (macroglossia).
  • Abdomen is protuberant (potbelly) & umbilical hernia.
141
Q

what is the definition of Myxedema?

A

Hypothyroidism in adults.

142
Q

what are the manifestations of Myxedema?

A
  • Retardation of all mental processes e.g lack of concentration, slow thinking and speech, long reflex time and sleepiness.
  • Low BMR and O2 consumption leads to:
    1. Weight gain.
    2. Increased sensitivity to cold weather.
  • Bradycardia and hypotension.
  • Skin: becomes yellowish, cold and thicker due to the deposition of a protein substance (myxoedematus tissue)
  • Increased level of cholesterol
143
Q

what causes Hyperthyroidism or thyrotoxicosis?

A

due to excess thyroid hormones secretion resulting from thyroid tumor or over stimulation of the thyroid by TSH or TSI.

144
Q

what are the clinical features of Hyperthyroidism or thyrotoxicosis?

A
  • Excessive nervousness and irritability
  • Increased appetite.
  • Low serum cholesterol level.
  • Increased BMR and O2 consumption
  • The skin: Warm and moist, Hair is fine and silky.
  • Ocular signs include:
    1. Characteristic stare with widened palpebral fissure due to upward retraction of upper eye lid.
    2. Lid lag phenomenon i.e a delay in the downward movement of the upper eye lid on following a falling object.
    3. Exophthalmos (accumulation of exophthalmos producing factor’ which is probably a degradation product of TSH).
    4. Failure of convergence.
145
Q

what are the occular signs that indicate Hyperthyroidism or thyrotoxicosis?

A
  1. Characteristic stare with widened palpebral fissure due to upward retraction of upper eye lid.
  2. Lid lag phenomenon i.e a delay in the downward movement of the upper eye lid on following a falling object.
  3. Exophthalmos (accumulation of exophthalmos producing factor’ which is probably a degradation product of TSH).
  4. Failure of convergence.
146
Q

what is goiter?

A
  • Goiter means enlargement of the thyroid gland.
  • It is accompanied by either hypo, or hyperfunction.
147
Q

what causes goiter?

A
  1. Goitrogens
  2. Iodine deficiency
  3. Grave’s disease
  4. Nodular goiter
  5. Physiological goiter
148
Q

how do goitrens cause goiter?

A
  • These are substances that block synthesis of thyroid hormones, e.g. thiocyanates and thiocarbamides.
  • They lead to decreased T3 & T4 β†’ increased TSH β†’ increased gland size.
149
Q

how does iodine deficiency cause goiter?

A
  • it leads to decreased T3 & T4 β†’ increased TSH β†’ goiter
150
Q

how does grave’s disease cause goiter?

A

due to the presence of TSI which binds to TSH receptors on thyroid cells β†’ diffuse goiter.

151
Q

what is nodular goiter?

A

Irregular enlargement of the thyroid with varying numbers of discrete nodules, probably due to exposure to stresses.

152
Q

when could physiological goiter occur?

A

adolescence and pregnancy.

153
Q

effect of thyroid on Vitamins and drugs

A
  • inc. synthesis of vitamin A from carotenes in the liver.
  • Stimulate both the utilization and clearance of all vitamins.
154
Q

what is the normal blood glucose level?

A

70 - 110 mg / 100ml

155
Q

what controls the level of glucose in blood?

A

Pancreatic hormones:
- insulin
- glucagon
- somatostatin
- pancreatic polypeptide

Other Hormones: (All ↑ blood glucose level)
- Adrenaline.
- Glucocorticoid.
- Growth hormone.
- Thyroxine.

156
Q

what is the percentage of beta cells of islets of langerhans?

A

75% of islet mass

157
Q

what is the structure of insulin?

A

Peptide hormones.

158
Q

synthesis and release of insulin

A
  • A pre-proinsulin is first synthesized on the ribosomes.
  • 23 AA residue is rapidly cleared at the site of synthesis to yield a pro-insulin chain.
  • During its transport from the endoplasmic reticulum and its packaging into granules by the Golgi apparatus, pro-insulin is slowly cleaved by trypsin-like and carboxypeptidase-like enzyme.
  • The generated insulin and C-peptide molecules are stored in the granules and released by exocytosis in equimolar amounts.
  • C-peptide has no known function but because it is not removed by liver , C peptide is a better marker for insulin secretion than insulin itself.
  • Half life of insulin is 5-8 min , while C peptide is 3-4 times longer
159
Q

what is the importance of C peptide?

A
  • C-peptide has no known function but because it is not removed by liver , C peptide is a better marker for insulin secretion than insulin itself.
160
Q

what is the half life of insulin & C peptide?

A

Half life of insulin is 5-8 min , while C peptide is 3-4 times longer.

161
Q

what are the functions of insulin?

A

On glucose metabolism: Insulin tends to lower blood glucose level by:

  • Stimulation of Glycogenesis in the liver and muscles
  • Inhibition of glycogenolysis
  • Increasing the glucose uptake by the tissues
  • Inhibition of gluconeogenesis by decreasing the hepatic uptake
    of amino acids
  • Stimulate lipogenesis in adipose tissue

Anabolic action:

  • Stimulates the uptake of amino acids by muscle.
  • Stimulates the rate of protein synthesis, by stimulationg
    transcription followed by translation.
  • Anti-catabolic effects i.e. it inhibits proteolysis.
  • Certain peptides called insulin-like growth factors, have similar
    amino acid sequences, and cross react with insulin receptors.

Increases cellular uptake of potassium, phosphate , magnesium.

Increases reabsorption of potassium, phosphate and sodium by renal tubules.

162
Q

what regulates secretion of insulin?

A
  • CHO Compounds
  • FFA & Triglycerides
  • A.A
  • Gastric inhibitory polypeptide (GIP)
  • Glucagon & entero-glucagon
  • K & Ca
163
Q

effect of CHO compounds on insulin secretion

A
  • major regulation is the plasma glucose level.
  • No insulin is secreted below a plasma glucose level of 50
    mg.
  • A half maximum insulin secretory response occurs at a plasma glucose level of about 150 mg.
  • A maximum response at 300 to 500 mg.
164
Q

what causes most regulation of insulin?

A

plasma glucose level

165
Q

amount of insulin released in relation to blood glucose level

A
  • No insulin is secreted below a plasma glucose level of 50 mg.
  • A half maximum insulin secretory response occurs at a plasma glucose level of about 150 mg.
  • A maximum response at 300 to 500 mg.
166
Q

effect of FFA and Triglycerides on insulin secretion

A

increased FFA & Triglycerides Have little stimulatory effect on insulin release

167
Q

effect of Amino acids on insulin secretion

A

increased AA like oral protein intake stimulates insulin secretion

168
Q

effect of GIP on insulin secretion

A
  • Is the most important of these insulinogogues.
  • GIP is also called glucose dependent insulinotropic peptide.
  • It is released by duodenal mucosa in response to drop in pH of the contents and intake of sugars, to stimulate pancreas to release insulin.
  • When glucose is given orally, a greater insulin response is elicited than when plasma glucose is comparably elevated by intravenous administration.
169
Q

what is the most important insulinogogue?

A

GIP

170
Q

what gives a greater response of insulin, Oral or IV adminstration of glucose?

A

Oral

171
Q

effect of Glucagon & entero-glucagon on insulin secretion

A

Stimulates insulin secretion:
1. Directly by acting on B-cells (paracrine effect),
2. Indirectly by increasing blood glucose level.

172
Q

effect of K & Ca on insulin secretion

A

Both are essential for normal insulin responses to glucose

173
Q

what inhibits insulin secretion?

A

Somatostatin, Ξ±-Adrenergic stimuli, Fasting, Diazoxide, Phenytoin

174
Q

nature of Glucagon

A
  • a polypeptide of 29 AA , formed from pro-glucagon.
  • The only significant target site for glucogon is liver
  • skeletal ms is not a target tissue for glucagon.
175
Q

source of Glucagon

A
  • alpha cells of the pancreatic islets.
  • Small intestinal cells : secrete glycentin (glucagon-like peptides).
176
Q

what is the mechanism of action of Glucagon?

A
  • Glucagon binds to receptors in cell membrane
  • Second messenger is cAMP.
177
Q

what are the functions of glucagon?

A
  1. Glucagon is a hyperglycemic factor. It increases blood glucose level by:
    - It stimulates glycogenolysis through activation of glycogen phosphorylase.
    - It stimulates gluconeogenesis.
    - Glucagon has little or no effect on glucose utilization by
    peripheral tissues.
  2. Stimulate lipolysis by activation of lipase leading to increase FA which pass to tissue for oxidation.
  3. It decreases hepatic cholesterol synthesis.
  4. Natriuresis, by inhibition of renal tubular Na reabsorption.
  5. Activation of myocardial adenyl cyclase, causing a moderate
    increase of cardiac output.
  6. May act as a local CNS hormone for the regulation of appetite.
178
Q

what affects the secretion of Glucagon?

A
  • Amino acids release insulin and glucagon.
  • The CHO/protein content of the meal determines the rate of insulin to glucagon release (insulin/glucagon ratio) .
  • A mixed meal high in CHO releases mainly insulin.
  • A high-protein meal releases mainly glucagon. This is to protect the individual from the hypoglycemic effects of insulin following a protein meal.
179
Q

what stimulates the secretion of Glucagon?

A
  • Hypoglycemia.
  • Protein meal by amino acids such as arginine and alanine.
  • ↓plasma F.F.A.
  • Exercise of sufficient intensity and duration.
  • Stress.
180
Q

what inhibits the secretion of Glucagon?

A
  • Hyperglycemia.
  • ↑plasma free fatty acids.
  • Somatostatin.
  • Local insulin.
181
Q

what is the function of pancreatic polypeptide?

A

It inhibits secretion of insulin and somatostatin via a direct pancreatic effect.

182
Q

what are the sources and functions of somatostatin?

A
183
Q

what are the causes of DM?

A
  • Results from deficiency of insulin in type 1 diabetes.
  • insulin resistance in type 2 diabetes.
184
Q

what are the manifestations of DM?

A
  • Hyperglycaemia
  • Glucosuria
  • Polyuria
  • Polydepsia
  • Acidosis
  • weight Loss & asthenia
  • increased cholesterol & triglycerides
185
Q

what causes Hyper- glycaemia in DM?

A

Due to absence of the effects of insulin

186
Q

what causes Glucosuria in DM?

A
  • loss of glucose in urine.
  • This occurs when the blood glucose level becomes higher than the renal threshold (180 mg%).
187
Q

what causes Polydepsia in DM?

A

Intense thirst due to dehydration

188
Q

what causes Polyuria in DM?

A

Due to osmotic pressure of excreted glucose (osmotic diuresis).

189
Q

what causes Acidosis in DM?

A
  • Due to inhibition of CHO metabolism.
  • The body depends on the fat metabolism which leads to the accumulation of acetoacetic acid & beta hydroxy-buteric acid.
190
Q

what causes weight Loss & asthenia in DM?

A

Due to mobilization of fat and proteins for the supply of energy.

191
Q

what does increased cholesterol & triglycerides lead to?

A

due leads to early development of arteriosclerosis.

192
Q

How is DM diagnosed?

A
  • Diagnosis based on glucose intolerance
  • Hemoglobin A1C
  • Stress (counter regulatory) hormones
193
Q

Diagnosis based on glucose intolerance

A
194
Q

Hemoglobin A1C

A
  • Not recommended for diagnosing diabetes.
  • But remain the preferred method for monitoring the effectiveness of diabetes treatment.
195
Q

Stress (counter regulatory) hormones

A

In some cases can promote diabetes and, at the very least, aggravate the hyperglycemia of diabetes.

196
Q

how does pregnancy affect glucose level in blood?

A
  • Glucose intolerance can develop in late pregnancy.
  • Human placental lactogen (hPL) acts similarly to the stress effects of growth hormone. It decreases the peripheral uptake of glucose.
  • Most women revert to a normal glucose tolerance following delivery but have a higher risk of developing diabetes later in life .

Y2B1 - Endocrine πŸ“• (7 decks)

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