Brainscape's Knowledge GenomeTM

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


See full index

PMP 101 Health, Disease and Patient > Endocrine system > Flashcards

Endocrine system Flashcards

You may prefer our related Brainscape-certified flashcards:
Physics 101 flashcards Psychology 101 flashcards Chemistry 101 flashcards Biology 101 flashcards Organic Chemistry 101 flashcards Sociology 101 flashcards
1
Q

Examples of

Neurotransmitters

A

Noradrenaline and acetylcholine

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

Examples of

Neuroendocrine

A

Oxytocin & ADH

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

Endocrine

A

Insulin, TSH, thyroxine, cortisol

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

Example of

Paracrine

A

Glucagon and somatostatins

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

Example of

Autocrine

A

Prostoglandins

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

Hormones

A
  • Arouses or exicte cells
  • Glands secretes hormones directly into blood stream
  • Carried to target cells away from the endocrine glands
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Types of hormones

A
  • Peptide hormones
  • Steroidal hormones
  • Tyrosine hormone
  • Eicosanoids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Structure and examples

Peptide hormones

A
  • Chains of amino acids
  • Small chains such as TRH that contains 3 AAs
  • Large chains such as FSH and LH that have 80 AAs
  • They are secreated by hypothalmus, pituitary, pancreas and GIT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Peptide hormone synthesis and transport

A
  • Transcription and translation occour
  • Preprohormone (coiled) to prohormone to hormone to secreatory granules to vesicales
  • Released by exocytosis
  • Hydrophilic so free chains that circulate in the blood (no binding to protien)
  • short half life (minutes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Structure and examples

Steroidal hormone

A
  • Cholesterol as the base
  • Cortisol
  • Aldosterone (adrenal cortex)
  • Sex hormones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Steroidal hormones synthesis and transport

A
  • Enzymatic conversion of percursor (cholesterol base) molecules into hormone
  • Stimulus increases percursor level of enzyme activation and diffusion occour across the membrane
  • Is lipophilic so binds with plasma protien albumin if bound to protien it is active
  • Half life is hours to days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Struture

Tyrosine Hormone

A

Tyrosine base in the thyroid hormone and catecholamines (adrenal medulla)

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

Tyrosine synthesis and transport

A
  • From thyroxine to tyrosine to epinephrine
  • Stimulus required and it diffuses across the membrane
  • Are lipophilic and binds with plasma protein
  • Half life from hours to days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Structure

Eicosanoids

A
  • Polyunsaturated fatty acids derivatives
  • e.g prostaglandins, leukotrienes, prostacyclins and thromboxanes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Eicosanoids synthesis

A
  • Precursor are arachidonic (lipids)
  • Enzyme lipase dictates the production of various eicosanoids
  • Synthesised by stereo- and regio-specific peridoxation of arachidonic acid by 3 enzyme families
  • lipoxygenases, cyclooxygenases, and cytochrome P450
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Transport and release of eicosanoids

A
  • Stimulus required and poorly diffuses through cell membrane
  • Requires transporter which as it is anionic
  • Half life is seconds and hormone is inactivated rapidly to limit autocrine and paracrine effects
16
Q

Peptide hormone functions

A
  • Hydrophilic hormone bind to receptor act on G-protien couple receptor which stimulates the effector (ACTH and glucagon)
  • Elswhere the hormone binds with receptor which stimulates tryosine kinase (insulin growth hormone)
  • Causes signal conduction and a physological reponse occours
17
Q

Simple feedback axis

A
  • Target cells see more glucose automatically sends signal to stimulate insulin and close the receptor for glucagon
18
Q

Insulin secreation

A
  • Release of insulin via endocrine glands by a stimulus
  • The insulin activates the target cells to increase its uptake of substrates to produce protien synthesis and glycogen storage
  • Negative feedback between target cells to endocrine glands
19
Q

Hypothalamus pituitary axis

A
  • Hypothalamus releases Releasing hormone which acts on the anterior pituitary gland
  • Trophic hormones are released from the anterior pituitary which can act on the target tissue directly
  • Trophic hormones can also send a signal to the peripheral edocrine glands
  • Then hormone released from the peripheral endocrine glands act on the target cells
20
Q

Complex feedback axis

(cortical)

A
  • The cortisol releasing hormone is released from the hypothalamus
  • Stimulates the signal of the antiror pituitary gland to release ACTH
  • Acts on peripheral endoctrine gland (adrenal gland) this systhesis the steroidal hormmone cortisol
21
Q

Negative feedback axis

(cortical)

A
  • Too much cortisol send signal to adrenal gland to stop sysnthesising release of cortisol in adrenal cortex
  • Long fedback axis to anterior piturity gland to stop producing the ATCH
  • Send signal directly to the hypothalmus to stop producing CRH
22
Q

Neuroendocrine reflex centres

A
  • Emotion control infulence HP acess
23
Q

Metabolism of hormones

A
  • Largely in blood liver and kidney some are in target cells and it is exreated by urine
24
Q

Endocrine disorders

Hypersecreation

A
  • Excess amount of hormone secreated e.g. Graves disease
25
Q

Endocrine Disorder

Hyposecreation

A
  • Tumour in glands may cause hyposecreation as less hormone is released
  • Type 1 diabetes or immunological distruction
26
Q

Type 1 diabetes

A
  • Autoimmune conditions and genetic conditions
  • insulin producing cells can’t produce insulin due to antibodies being generated that stop insulin production so hyposecreation occours
27
Q

Primary defect

A
  • Non-funtional peripheral endocrine gland (tumour) in hyposecreation
  • Stimulates Antierior pituitary and Hypothalmus more therefore increased secreation of CRH and ACTH
28
Q

Secondary defect

A
  • Pituitary tumor could cause hypo or hypersecreation
  • if hyper then lots of ACTH is being produced therefore more cortisol is being produced
  • Low levels of CRH produced at hypothalamus
29
Q

Ectopic deffect

A
  • Signal external to the HPA axis
  • Tumour produce ACTH which increases its level
  • Increase ACTH stimulate release of cortisol
  • Scan to check where tumour is
30
Q

Defect with target cells

A
  • Type 2 diabetes where the muscle cells adipose cells and liver cells become insulin resistant due to signal unrecognised by receptor on cell
31
Q

diagnose defective hormones

A
  • Dynamic and provocative tests this checks for the integrity of feedback control ( primary secondary or target)
  • Stimulation test - suspective hyposecreation
  • Supression test - suspective hypersecreation
32
Q

Treatment for hyposecreation, hypersecreation and impared target cell

A
  • Replace hormone supplements - hyper
  • Block synthesis and release of drugs - hypo
  • enhance drug cellular respose to hormone

PMP 101 Health, Disease and Patient (64 decks)

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