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ENDO 100 Flashcards

all weeks revision

1
Q

Outline the transmission of effects, chemical mediators and distribution of effects of Direct communication, paracrine communication, endocrine communication and synaptic communication.

A

Direct
T= gap junctions
CM= ions, small solutes, lipid-soluble materials
E = limited to adj cell interconnected by connexions

Paracrine
T= ECF
CM = paracrine factors
E= local area where paracrine factors are high

Endocrine
T= bloodstream
CM= hormones
E= other tissues and organs with app receptors

Synaptic communication
T= across synaptic clefts
CM = NT
E= limited to specific area with app receptors

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2
Q

What are examples of lipophobic and lipophilic chemical messengers?

A

Lipophonic= Glycine, GABA and catecholamines

Lipophilic = steroid hormones

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3
Q

If a regulatory molecule is non-polar where will it bind?

A

It will bind to an intracellular receptor as it is lipid-soluble

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4
Q

What are the four classes of receptors and examples (at least 2) of ligands that can bind to them?

A

Ligand-gated (ionotropic) = ACh, ATP and Glutamate
GPCR (metabotropic) = Peptides, odorants and cytokines
Enzyme-linked = Insulin, erythropoietin, TGF-beta
nuclear- steroids, thyroid and prostaglandins

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5
Q

Describe the mechanism of Action for the cAMP second messenger pathway.

A

1- extracellular message binds to surface receptor activating G protein
2- a subunit dissociates and activates AC
3- AC converts ATP to cyclical AMP (cAMP)
4- cAMP activates PKA
5- PKA phosphorylates intracellular proteins
6- altered protein accomplishes cellular response

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6
Q

What are Phospholipases and what can they do?

A

Hydrolytic enzymes that split phospholipids

convert certain cell membrane phospholipids in second messengers

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7
Q

Describe the mechansim of action involving IP3.

A

1- hormone binds to GPCR
2- GTP exchanged for GDP
3- GTP causes subunits to dissociate and activate PLC
4- PLC generates PIP2 which activates IP3 (second messenger)
5-IP3 travels to ER where it activates Ca
6- 4 calcium bind to calmodulin to create a target response

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8
Q

Describe the mechanism of action for second messenger DAG.

A

GPCR acitiavtes PLC
PIP2 (from plasma membrane) generates DAG (and IP3) which activate PKC to generate cell response.

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9
Q

Name the 5 classes of chemical messengers and list their lipid solubility

A

Amino acids - lipophilic and lipophobic
Amines - lipophobic
peptides/proteins - lipophobic
steroids - lipophilic
eicosanoids - lipophilic

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10
Q

What is specificity spill over?

A

Hormones with similar structure may bind to one another’s receptors (ACTH and melanin)

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11
Q

What is down-regulation and how is it achieved?

A

when there are high levels of hormones so the cell decreases the number of target cell receptors

occurs via inactivation, decreased production, desruction and temporary sequestration of receptors inside

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12
Q

What factors affect the magnitude of a target cell’s response?

A

concentration of a ligand
number of receptors available
affinity for receptor

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13
Q

How are lipid soluble hormones transported? Describe

A

By binding transport proteins (in a loose and reversible manner)

transport proteins = albumin and globulins

this action increases the hormone’s half-life as they remain in the blood for longer and not easily broken down by enzymes.

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14
Q

Describe free hormones.

A

The only ones that can leave a blood capilarry and are physiologically active

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15
Q

name the first three steps of steroid hormone synthesis for different pathways.

A

Cholesterol –> pregnenolone –> progesterone

Cholesterol –> pregnenolone –> 1,7 Hydroxyprogesterone

Cholesterol –> androstenedione –> testosterone

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16
Q

what is the mechanism of action for Steroid hormones?

A

diffuses through membrane –> binds to intracellular receptor –> receptor/hormone comples enters nucleus –> binds to specific attachment site on DNA –> transcription of gene to mRNA –> mRNA directs protein synthesis –> proteins function as enzymes, transport proteins or structural proteins –> cell response

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17
Q

What is a long-loop feedback? Provide an example

A

Hypothalamic and pituitary hormones are inhibited by target glands’ hormones.

testosterone inhibition of GnRH and LH/FSH

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18
Q

What is a short-loop feedback? Provide an example

A

an anterior pituitary hormone inhibits release of hypothalamic hormone

GnRH inhibited by LH

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19
Q

What is ultrashort-loop feedback?

A

Sectertion of hypothalamic hormone is inhibited by same hormone.

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20
Q

Compare Hormonal Stimulus, Humoral stimulus and Neural Stimulus with examples.

A

Hormonal - release of hormone in response to another
- Hypothalamic hormones –> stimulate APG –> stimulate another gland (thyroid, adrenal, gonad etc) –> secrete other hormones from the endocrine gland

Humoral - changes in ECF
- capillary blood has low Ca concentration –> PTH secreted by PT

Neural - The nervous system stimulates
-preganglionic sympathetic fibre stimulates adrenal medulla –> secretes catecholamines

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21
Q

Differentiate between primary, secondary and tertiary disorders.

A

Primary = gland
secondary - Pituitary hormone is deficient (endocrine gland not damaged but has too little tropic hormone)
tertiary = Hypothalamic hormone is deficient

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22
Q

What is the median eminence?

A

where axon terminals of hypothalamic neurons release nuerpeptides

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23
Q

What are the two neurons that mediate endocrine function in hypothalamus?

A

Magnocellular (large cell body)
Parvocellular (small cell body)

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24
Q

What are the two nuclei of the hypothalamus and what do the produce large quantities of?

A

Paravenrticular and supraoptic

produce large quantities of neurohormones (oxytocin and AVP)

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25
Q

What is the Embryonic origin of the anterior and posterior pituitary glands respectively?

A

A= Cells form the roof of embryonic oral cavity

P= ectodermal cells of neural origin (from floor of 3rd ventricle in cerebrum)

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26
Q

The Anterior pitutary is highly vascular. Explain it’s blood system.

A

uses the Hypothamalc-hypophyseal portal system

Superior hypophyseal arteries –> primary capillary plexus –> long hypophyseal portal veirns –> secondary capilary plexus –> anterior pituitary

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27
Q

What are the hypothalamic hormones?

A

TRH, GRH, CRH, GHRE, Somatotstain and PIH (dopamine)

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28
Q

What are the predominant hypothalamic nuclei of the 6 hypothalamic hormones?

What are the predominant hypothalamic nuclei of the 2 posterior pituitary hormones?

A

TRH - paraventricular
LH - Anterior/medial hypothalamus
CRH - Parvicellular of paraventricular
GHRH - Arcuate nucleas close to median eminence
Somatostatin - Paraventricular
Dopamine - Arcurate nucleus

ADH - primarily supraoptic
Oxytocin - primarily periventricular

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29
Q

What are the functions of ADH?

A

produce more concentrated urine (increase water permeability in nephron)

Rehydrate

raise blood pressure

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30
Q

What happnes when a baby suckles on mother?

A

Oxytocin: Mechanoreceptors of nipples stimulated –> hypothalamus sends efferent impulsues via Periventruclar neurons –> posterior pituitary release oxytocin –> Oxytocin is secreted –> contraction of myoepithelial cells in small ducts –> milk forced into small ducts –> Milk collects in cisterns and flows out of nipples

Prolactin: Mechanoreceptors stimulated –> inhibition of hypothalamic hormones that release dopamine –> hypothalamus releases PRL releasing factors –> anterior releases PRL –> targets mammary glands –> increased milk production

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31
Q

What are the other actions of oxytocin?

A

Stress responses - stress activates catecholamine in medulla oblongata –> activates oxytocin –>

chronic/ acute administration –> attenuate hypothalamus-pituitary adrenal axis

analgesia
social behaviour

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32
Q

What regulates prolactin sectertion?

A

inhibits = dopamine
stimulayes = TRH

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33
Q

Describe the relationship between ACTH and MSH.

A

Both ACTH and MSH arise from post-translational processing of the POMC gene. = melanocortins

a-MSH acts on melanocytes which contain pigment called melanin. In times of hypersecretion of ACTH (Addisons disease), excess ACTH binds to MC1R receptor which activates these melanocytes

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34
Q

What are the stimulatory and inhibitory factors of prolactin release?

A

S= pregnancy, breast-feeding, sleep, stress, TRH and dopamine antagonists

I= dopamine, dopamine agonists, somatostatin and prolactin (negative feedback loop)

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35
Q

What is the functional unit of the thyroid gland? Describe this unit.

A

thyroid follicle = portion concerned with the production of TH

Each follicle is surrounded by a single layer of epithelial cells and filled with colloid

colloid = glycoprotein and TBG.

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36
Q

Compare the histology of inactive thyroid gland to an active one.

A

Inactive = colloid abundant, large follicles and flat-lining cells

Active= small follicles, cuboidal/ columnar cells, reabsorption lacunae allows site of colloid actively being reabsorbed

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37
Q

Outline the biosynthesis of thyroid hormone (simply)

A

TG synthesis in follicular lumen –> Na/I symporter brings in I into cell- –> pendrin takes I- to colloid –>oxidation of I- to I2 –> organification of I2 into MIT and DIT –> coupling –? Endocytosis of TG –> Hydrolysis of T4 and T3 –> residual MIT and DIT recycled.

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38
Q

How much of TH is bound to plasma proteins and how much of them are bound to TBG?

A

99%

70&

39
Q

Describe the affinity of T3 and T4

A

T4 = higher affinity to proteins (storage)
-67% of TBG is T4

T3= higher affinity for the receptor (active)

40
Q

Explain the effect of TH on fat metabolism.

A

increases all aspects but lipolysis increased more than lipogenesis

increased release of fatty acids from adipocytes

decreases plasma cholesterol

41
Q

Describe Graves Disease

A

Autoimmune disease as thyroid-stimulating-immunoglobulins activate thyroid gland.

42
Q

Explain how exophthalmos occurs.

A

Exophthalmos = protruding eyeballs: autoantibodies target orbital fibroblasts –> fibroblasts differentiate into adipocytes/myofibroblasts –> tissue behind eye becomes filled with immune cells –> inflammation –> expanded fat cells + inflamed muscles –> tissue behind eye swells –> eyeball pushed forwards.

43
Q

What receptor does GH use and what is required to activate it?

A

JAK2-STAT pathway

dimerization essential for activation

44
Q

What is the principal site of IGF-1 production and what are its actions?

A

liver

mediates anabolic effects of Gh
- regulates cell proliferation, differentiation and metabolism
-synergetic with cartridge and bone = stimulates bone, cartilage and soft tissue growth
-regulate cartilage forming cells
-stimulates osteoblasts replication and collagen and bone matrix synthesis

45
Q

Describe the IGF-1 receptor

A

2 extracellular spanning a-subunits and transmenenrabe B subunits

a-subunit has binding site and linked to B via disulfide bonds

B has a short extracellular domain, transmnebrane domain and intracellular domain

intracellular has the tyrosine-kinase domain = signal transdunction mechanism

46
Q

Describe laron dwarfism

A

plasma GH normal but receptors unrepsosnvie due to a genetic defect in GH receptor expression

no/low GH receptors
GH normal or elevated

reduced muscle strenth and endurance
hypoglycemia
delayed pubery
short limbs
obesity

47
Q

Describe African pygmies

A

normal plasma GH but low GH-binding protein and IGF-1 = no normal rise in IGF at puberty

lack pubertal serum IGF-1 surge and growth spurt

48
Q

describe the three forms of plasma calcium and the rough concentartions of each form for Ca and Pi.

A

ionised Ca
- 50%
- biologically active and diffuse through capillary membranes

Bound Ca
- 45%
- not diffusible

Complex form - ca + ions
- 5%
- combined to anionic substances of plasma and interstitial fluid

Pi
I = 84%
B = 10%
C= 6%

49
Q

Name some functions of calcium

A

structural integrity
synaptic transmission
coenzyme function
control of excitability of nerves
stimulus
regulation
second messenger

50
Q

What are the two phases in which calcium and phosphate are removed from the bone via PTH?

A

Rapid phase
- already existing bone cells activated –> ca and P removal from bone to ECF

Slower phase
- proliferation of osteoclasts –> greatly increased osteoclastic resorption of bone

51
Q

What organs have the greatest abundance of PTH 1R?

A

Kidney and bone

52
Q

will total removal of thyroid produce major alterations in Ca2+ homeostasis?

A

No
Calcitonin does not have a critical role in Ca homeostasis regulation

53
Q

Describe vitiman D biosynthesis in skin, liver and kidney

A

In skin: irridation of 7-dehydrocholestrol –> previtiman D –> Vitiman D3 (cholecalfierol)

In Liver: Cholecalciferol –> 25-hrydoxycholecaliferol using 25-hydroxylase

In kidney: 25-hydrox… –> 24,25 Dihydroxycholecalciferol OR 1,25 DHC (ACTIVE FORM)

54
Q

What are the effects of hypocalcemia?

A

tetany = increased neuromuscular excitability, laryngeal stridor, cardiac (delayed repolarisation and prolonged QT interval)

55
Q

What is the trousseau sign of late Tetany?

A

tetany in hand
- spastic contraction of skeletal muscle without relaxation

due to Ca channels not blocking Na from coming in

56
Q

What is Chvotek’s sign?

A

twitching of facial muscles when the facial nerve area tapped

57
Q

What are the two major tissue types of the pancreas

A

Acini - secrete digestive juices
islets of Langerhans - pancreatic hormones

58
Q

What are the five cell types of the endocrine pancreas and what do they secrete?

A

Alpha - glucagon
Beta-insulin and amylin
Delta - somatostatin
P cells - pancreatic polypeptide
Epsilon cells - ghrelin

59
Q

Describe the effects of glucagon on different organs

A

Liver
- increased glycolysis and gluconeogenesis
Adipose tissue
- increased lipolysis
pancreas
- decreased insulin

60
Q

What are incretins?

A

Digestive tract hormones that increase insulin secretion from beta cells

2 types= GLP-1 and GIP

61
Q

What hormones are released following ingestion of food?

What occurs upon the absorption of food?

What disease disrupts this?

A

release of incretins, insulin and amylin

GLP-1 + amylin = inhibitory effect on gastic emptying, glucagon release and appetite

Absorption of food = GLp-1 and GIP promote insulin sectertion

62
Q

Compare T1DM and T2DM.

A

1- beta cell destruction = insulin deficiency
2- progressive insulin secretory defect following insulin resistance

The 1-sudden onset of severe symptoms
2- insidious onset of tiredness, thirst, polyuria and nocturia

1-spontaneous ketosis
2- ketoacidosis

1- C peptide absent 2- C peptide detectable

63
Q

What are the insulin and anti-insulin-like activities of GH?

A

Insulin-like
- increased amino acid uptake, protein synthesis in muscle and protein and RNA synthesis in liver

Anti
- decreases muscle and adipose glucose uptake
- increased liver gluconeogenesis
- increased lipolysis in adipose

64
Q

What is the only corticol zone that can convert corticosterone to aldosterone?

A

Zone glom34ulosa because only zone that normally contains aldosterone synathse

65
Q

What are the first three steps of Aldosterone and cortisol synthesis?

A

Cholestrol –> pregneolone –> progesterone

66
Q

What is the biologically active state of cortisol and how much of the circulating cortisol does it make up?

A

free state = 10%

(other 90% is bound to CBG)

67
Q

What are the actions of aldosterone?

A

induces synthesis of proteins that are involved in Na transport (Na channels in the luminal membrane)

acts on distal convoluted and cortisol collecting ducts: increases Na Reabsoprion and increases K excretion

68
Q

How does the renin-angiotensin system regulate aldosterone?

A

Formation of ANG II –> stimulates aldosterone secretion

69
Q

How does K, Na, ACTH and ANP regulate aldosterone?

A

K
- increased K = increased Aldosterone
- K –> depolarises glomerulose –> opens Ca channel –> Ca influx –> increased aldosterone

Na
- increased Na inhbits

ACTH
stress -> CRH –> ACTH –> increased aldosterone (minimal effect)

ANP
- blocks renin and aldosterone

70
Q

How are NE and E formed respecively?

A

NE
- Hydroxylation + decarboxylation of tyrosine

E
- methylation of NE
- needs cortsiol!

71
Q

What is the enzyme used to make E from NE?

A

Phenyletanolamine-N-methyltransferase (PNMT)
- requires cortsiol

72
Q

what is the chemical stimulus for catecholamines?

A

ACh from sympathetic neurons

73
Q

What are the four types of Cushing’s disease and their determining features?

A

Pituitary Cusing’s syndrome
- functional adenoma –> excessive ACTH
- elevated ACTH
-lesions in the pituitary

Adrenal Cushing’s Syndrome
- one or both glands
-cortical hyperplasia
-low ACTH levels

Ectopic
-ACTH from region other than AP
- carcinoma of lung or pancreas secreting ACTH
-increased plasma ACTH

Iatrogenic
- prolonged therapeutic administration of high doses of glucocorticoids or ACTH

74
Q

name some symptoms of Cushing’s syndrome

A

Weight gain - truncal or central obesity
thin arms and legs
moon face
buffalo hump
wasting/thinning of muscles
purple straie on the abdomen enhanced bone resorption

75
Q

How does excess cortisol increase BP?

A

cortisol –> increases epinephrine and NE via permissive effects on the vasculature
at high conc cortisol binds to MCR –> Na reansotion increased –> increased ECF volume –> increased blood pressure

76
Q

What are the results of a Dexanethasone Supression Test for:
Adrenal Cushings syndrome
Pituitary Cushings Syndrome
Ectopic Cushing’s Syndrome

A

Adrenal Cushings syndrome
- not suppress cortsiol secretion as ACTH is already low
Pituitary Cushings Syndrome
-high ACTH causes cortisol therefore suppresses ACTH
Ectopic Cushing’s Syndrome
will not suppress as not from the HPA

77
Q

What ar ethe four starling forces?

A

Capillary pressure
Interstitial pressure
Capillary plasma colloid osmotic pressure
intertitial fluid colloidial osmotic pressure

78
Q

describe pressure at the arterial end vs venous end.

A

higher pressure at arterial end
= fluid leaves capillary at arterial end and then is reabsorbed at venous end

79
Q

What is the role of lymphatics in fluid movement?

A

picks up the excess fluid in interstitial space and eventually empty into the venous end

80
Q

What are the stimuli for thirst?

A

cellular dehydration via increased ECF osmolality

decreased blood volume

ANG II which act as a back up system for thirst

81
Q

Edema can occur as the result of imbalances in pressure. Describe what pressures cause edemas, how and what effects they can have.

A

Oncotic pressure
Reduction in colloid production –> plasma proteins –> reduced oncotic pressure = liver failure and malnutrition

increase in colloid loss –> reduced oncotic pressure = nephrotic syndrome and catabolic stress

increased interstitial pressure –> lymphatic construction

Hydrostatic pressure
increased capillary hydrostatic pressure –> heart failure, deep venous thrombosis and superior cava construction

82
Q

What is the cause of hypo-osmotic dehydration and what are its effects in Plasma Na, ECF and ECF v

A

adrenal insufficiency (duretic overdose)
decreased [Na] and ECF volume
increased ICF volume

83
Q

What is the cause of hyperosmotic overhydration and what are its impacts on plasma [Na], ECF V and ICF V

A

cushing’s syndrome
primary aldosetronism

increased NA and ECF V
decreased ICF v

84
Q

what are the actions of ADH and what receptor does it bind to?

A

V2 receptor

enhances cell permemability to water
increases water reabsoprtion –> increases urin osmolality

induces production and insertion of AQUAPORIN 2 into luminal membrane

85
Q

Outline features of AQUAPORIN 2

A

exclusively expressed in collecting ducts
only aquaporin regulated by ADH directly’
stimlauted by ADH binding to V2 receptor

86
Q

Outline ADH mechanism of action

A

V2 receptor coupled with GPCR –> activates Adenylate cyclase –> increases cAMP formation and AQP2 phosphorization.

high conc of ADH: binds to V1A receptor in liver, smooth muscle, brain and adrenal glands –> PLC –> hydrolysis of Phosphatidylionstiol –> increased intracellular calcium

87
Q

what are the four types of diabetes insipidus and their defining features.

A

Hypothalamic
- neurogenic/central/cranial
-parial/complete LACK of ADH secretion
- head injury/ trauma/ inflammation
-low ADH, large amounts of dilute urine

Nephrogenic
-inability for kidneys to respond to ADH
-CD unresponsive to ADH
-congential defect in V2
-urine output increased, ADH higher than normal

Gestational
-deficiency in pregnancy due to hormones

Disogenic
-increased thirst mechanism

88
Q

What is SIADH?

A

WHAT= Syndrome of Inappropiate ADH , inappropiate water retention and decreased blood Na

cause: brain injury or tumour

Symptoms:
low osmolality
concentrated urine in kidneys
inability to produce dilute urine –> water retention –> increased ECF –> hyponatermia

89
Q

what are the three types of hyperaldosteronism

A

Conns syndrome = overproduction of aldosterone

Primary = most common = from adrenal hyperplasia and aldosterone-producing adenomas low plasma renin

Secondary = high plasma renin –> stimulation of ANG II and alsoterone

90
Q

What is the effect of ANP on body fluid volume?

A

increase loss of body sodium –> decreased body water –> ECF decerased

91
Q

what are the central components of the stress system?

A

hypothalaus and brainstem

includes
-parvocellular CRH and periventricular AVP
catecholaminergic cell groups of medulla and pons

92
Q

What are the peripheral components?

A

peripheral limbs of HPA axis with efferent sympathtic/adrenomedullary system,

93
Q

How does sympo-adb=ranl activation impact cardipvacular system in times of stress

A

i ncreased heart rate
* Increased contractility
* Increased cardiac output [volume of blood pumped out of the heart]
* Increased venous return [volume of blood returned to the heart]
* Generalized vasoconstriction
* Diversion of blood flow to muscles, heart (myocardium) and the brain
* Increased blood pressure

94
Q

What are the three stages of GAS and what are each characterised by?

A

Alarm
-initial response
-catecholamines released (fight/flight)

Resistance
- stress continues –> the body mobilises to withstand stress
- adapts
-cortisol

Exhaustion
- ongoing extreme stressors
- body depleted of resources
-function at a lesser state

Endo (14 decks)

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