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ENDO 100 Flashcards

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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
What is the Embryonic origin of the anterior and posterior pituitary glands respectively?
A= Cells form the roof of embryonic oral cavity P= ectodermal cells of neural origin (from floor of 3rd ventricle in cerebrum)
26
The Anterior pitutary is highly vascular. Explain it's blood system.
uses the Hypothamalc-hypophyseal portal system Superior hypophyseal arteries --> primary capillary plexus --> long hypophyseal portal veirns --> secondary capilary plexus --> anterior pituitary
27
What are the hypothalamic hormones?
TRH, GRH, CRH, GHRE, Somatotstain and PIH (dopamine)
28
What are the predominant hypothalamic nuclei of the 6 hypothalamic hormones? What are the predominant hypothalamic nuclei of the 2 posterior pituitary hormones?
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
29
What are the functions of ADH?
produce more concentrated urine (increase water permeability in nephron) Rehydrate raise blood pressure
30
What happnes when a baby suckles on mother?
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
31
What are the other actions of oxytocin?
Stress responses - stress activates catecholamine in medulla oblongata --> activates oxytocin --> chronic/ acute administration --> attenuate hypothalamus-pituitary adrenal axis analgesia social behaviour
32
What regulates prolactin sectertion?
inhibits = dopamine stimulayes = TRH
33
Describe the relationship between ACTH and MSH.
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
34
What are the stimulatory and inhibitory factors of prolactin release?
S= pregnancy, breast-feeding, sleep, stress, TRH and dopamine antagonists I= dopamine, dopamine agonists, somatostatin and prolactin (negative feedback loop)
35
What is the functional unit of the thyroid gland? Describe this unit.
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.
36
Compare the histology of inactive thyroid gland to an active one.
Inactive = colloid abundant, large follicles and flat-lining cells Active= small follicles, cuboidal/ columnar cells, reabsorption lacunae allows site of colloid actively being reabsorbed
37
Outline the biosynthesis of thyroid hormone (simply)
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.
38
How much of TH is bound to plasma proteins and how much of them are bound to TBG?
99% 70&
39
Describe the affinity of T3 and T4
T4 = higher affinity to proteins (storage) -67% of TBG is T4 T3= higher affinity for the receptor (active)
40
Explain the effect of TH on fat metabolism.
increases all aspects but lipolysis increased more than lipogenesis increased release of fatty acids from adipocytes decreases plasma cholesterol
41
Describe Graves Disease
Autoimmune disease as thyroid-stimulating-immunoglobulins activate thyroid gland.
42
Explain how exophthalmos occurs.
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
What receptor does GH use and what is required to activate it?
JAK2-STAT pathway dimerization essential for activation
44
What is the principal site of IGF-1 production and what are its actions?
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
Describe the IGF-1 receptor
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
Describe laron dwarfism
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
Describe African pygmies
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
describe the three forms of plasma calcium and the rough concentartions of each form for Ca and Pi.
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
Name some functions of calcium
structural integrity synaptic transmission coenzyme function control of excitability of nerves stimulus regulation second messenger
50
What are the two phases in which calcium and phosphate are removed from the bone via PTH?
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
What organs have the greatest abundance of PTH 1R?
Kidney and bone
52
will total removal of thyroid produce major alterations in Ca2+ homeostasis?
No Calcitonin does not have a critical role in Ca homeostasis regulation
53
Describe vitiman D biosynthesis in skin, liver and kidney
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
What are the effects of hypocalcemia?
tetany = increased neuromuscular excitability, laryngeal stridor, cardiac (delayed repolarisation and prolonged QT interval)
55
What is the trousseau sign of late Tetany?
tetany in hand - spastic contraction of skeletal muscle without relaxation due to Ca channels not blocking Na from coming in
56
What is Chvotek's sign?
twitching of facial muscles when the facial nerve area tapped
57
What are the two major tissue types of the pancreas
Acini - secrete digestive juices islets of Langerhans - pancreatic hormones
58
What are the five cell types of the endocrine pancreas and what do they secrete?
Alpha - glucagon Beta-insulin and amylin Delta - somatostatin P cells - pancreatic polypeptide Epsilon cells - ghrelin
59
Describe the effects of glucagon on different organs
Liver - increased glycolysis and gluconeogenesis Adipose tissue - increased lipolysis pancreas - decreased insulin
60
What are incretins?
Digestive tract hormones that increase insulin secretion from beta cells 2 types= GLP-1 and GIP
61
What hormones are released following ingestion of food? What occurs upon the absorption of food? What disease disrupts this?
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
Compare T1DM and T2DM.
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
What are the insulin and anti-insulin-like activities of GH?
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
What is the only corticol zone that can convert corticosterone to aldosterone?
Zone glom34ulosa because only zone that normally contains aldosterone synathse
65
What are the first three steps of Aldosterone and cortisol synthesis?
Cholestrol --> pregneolone --> progesterone
66
What is the biologically active state of cortisol and how much of the circulating cortisol does it make up?
free state = 10% (other 90% is bound to CBG)
67
What are the actions of aldosterone?
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
How does the renin-angiotensin system regulate aldosterone?
Formation of ANG II --> stimulates aldosterone secretion
69
How does K, Na, ACTH and ANP regulate aldosterone?
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
How are NE and E formed respecively?
NE - Hydroxylation + decarboxylation of tyrosine E - methylation of NE - needs cortsiol!
71
What is the enzyme used to make E from NE?
Phenyletanolamine-N-methyltransferase (PNMT) - requires cortsiol
72
what is the chemical stimulus for catecholamines?
ACh from sympathetic neurons
73
What are the four types of Cushing's disease and their determining features?
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
name some symptoms of Cushing's syndrome
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
How does excess cortisol increase BP?
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
What are the results of a Dexanethasone Supression Test for: Adrenal Cushings syndrome Pituitary Cushings Syndrome Ectopic Cushing's Syndrome
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
What ar ethe four starling forces?
Capillary pressure Interstitial pressure Capillary plasma colloid osmotic pressure intertitial fluid colloidial osmotic pressure
78
describe pressure at the arterial end vs venous end.
higher pressure at arterial end = fluid leaves capillary at arterial end and then is reabsorbed at venous end
79
What is the role of lymphatics in fluid movement?
picks up the excess fluid in interstitial space and eventually empty into the venous end
80
What are the stimuli for thirst?
cellular dehydration via increased ECF osmolality decreased blood volume ANG II which act as a back up system for thirst
81
Edema can occur as the result of imbalances in pressure. Describe what pressures cause edemas, how and what effects they can have.
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
What is the cause of hypo-osmotic dehydration and what are its effects in Plasma Na, ECF and ECF v
adrenal insufficiency (duretic overdose) decreased [Na] and ECF volume increased ICF volume
83
What is the cause of hyperosmotic overhydration and what are its impacts on plasma [Na], ECF V and ICF V
cushing's syndrome primary aldosetronism increased NA and ECF V decreased ICF v
84
what are the actions of ADH and what receptor does it bind to?
V2 receptor enhances cell permemability to water increases water reabsoprtion --> increases urin osmolality induces production and insertion of AQUAPORIN 2 into luminal membrane
85
Outline features of AQUAPORIN 2
exclusively expressed in collecting ducts only aquaporin regulated by ADH directly' stimlauted by ADH binding to V2 receptor
86
Outline ADH mechanism of action
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
what are the four types of diabetes insipidus and their defining features.
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
What is SIADH?
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
what are the three types of hyperaldosteronism
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
What is the effect of ANP on body fluid volume?
increase loss of body sodium --> decreased body water --> ECF decerased
91
what are the central components of the stress system?
hypothalaus and brainstem includes -parvocellular CRH and periventricular AVP catecholaminergic cell groups of medulla and pons
92
What are the peripheral components?
peripheral limbs of HPA axis with efferent sympathtic/adrenomedullary system,
93
How does sympo-adb=ranl activation impact cardipvacular system in times of stress
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
What are the three stages of GAS and what are each characterised by?
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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