SUGER Flashcards

Question

what is standard bicarbonate

Answer 1

* absolute bicarbonate is affected by respiratory and metabolic components * standard bicarbonate is the bicarbonate concentration standardised to PaCO2 5.3kPa and temperature 37 * so standard bicarbonate represents the metabolic contribution to metabolic change * it's calculated not actually measured

Answer 2

* the quantity of acid required to return pH to 7.4 under standard conditions * standard base excess is corrected to Hb 50g/L * base excess is negative in acidosis

Answer 3

* arterial blood gas - it's what we can actually measure * it includes: * pH * pO2 * pCO2 * std HCO3- * std base excess

Answer 4

* henderson hasselbach * stewart's theory (strong ion difference)

Answer 5

pH = 6.1 + log([HCO₃^-]/0.03xpCO₂) blook has a pKa of 6.1

Answer 6

* The strong ion difference is the difference between the positively and negatively charged ions in plasma * So the principle is that pH and [HCO3-] are dependent on 3 factors: * pCO2 * concentration of weak acids * SID = [strong cations] – [strong anions] * = [Na+ + K+ + Ca2+ + Mg2+] – [Cl- + lactate-] * It's designed to help characterise the mechanism of the disorder rather than to simply catagorize it at metabolic or respiratory * basically it's too complicated to actually really use in practice * but theorhetically it's much more accurate than the HH abroach

Answer 7

1. Dilutional * rapid ECF volume expansion causes HCO3- to be diluted * but H+ is not diluted for some reason 2. Failure of H+ excretion * renal failure * type 1 renal tubular acidosis 3. Excess H+ load * lactic acidosis * ketoacidosis 4. HCO3- loss * diarrhoea * type 2 renal tubular acidosis

Answer 8

* Hyperventilation to increase CO2 excretion

Answer 9

* alkali ingestion * GI acid loss (vomiting) * renal acid loss

Answer 10

* hypoventilation but this is limited by hypoxic drivs * renal bicarbonate excretion

Answer 11

* CO2 retention leading to increased carbonic acid dissociation * The compensatory mechanism is renal H+ excretion and bicarbonate retention * but only if the acidosis is chronic * so if there's low pH and high CO2 with a partially raised HCO3- it means that there's some degree of renal compensation: chronic

Answer 12

* CO2 depletion due to hyperventilation * Causes: Type 1 respiratory failure, anxiety and panic Compensation: increased renal bicarbonate loss (if chronic)

Answer 13

* capillaries derived from the efferent arteriole that follow the nephron *

Answer 14

* this happens in the proximal tubule * the things that we want to re-absorb are the bicarbonate ions and the Na+ ions * the Na+ ions are antiported with H+ * That H+ is recycled * carbonic anhydrase in the luminal space allows us to re-absorb H2O and CO2 (from the H+ and luminal HCO3-) * In the tubular cells H2O and CO2 then form H2CO3 which dissociates to form H+ and HCO3- * HCO3- can be re-absorbed into the blood and the H+ is recycled for the same process * NB CA does H2CO3 --\> H2O and CO2 as well as the reverse reaction

Answer 15

* key component of altitude sickness is alkalosis due to the need to hyperventilate * they blow off all their CO2 * this can be treated with a CA inhibitor which promotes the excretion of HCO3- * one of these is called acetazolamide * i don't think you need to know that

Answer 16

* ANP is atrial natriuretic peptide * think of natriuretic as like a uretic triggered by high sodium * The JGA detects a fall in Na+ delivery to the distal tubule

Answer 17

* it's a steroid hormone * It affects cells in the collecting duct * Principal cells * these are the main Na+ reabsorbing cells * aldosterone increases PC expression of * ENaC (Na+ transporter into cell out of lumen) * Na/K ATPase (3Na+ into blood in exchange for 2K+) * net effect is reabsorbing Na+ and getting rid of K+ * K+ diffuses into the tubular lumen down an electrochemical gradient (because so much Na+ has been reabsorbed) * if the body needs to reabsorb Na+ due to low blood pressure, it sacrifices K+ * this could cause hypokalaemia * Intercalated cells * these reabsorb K+ in exchange for H+ * but doing too much of this would develop an alkalosis

Answer 18

* As aldosterone levels rise in response to volume contraction (low bp) the secretion of K+ (in exchange for Na+) will increase * this can cause hypokalaemia * the body may try to compensate by reabsorbing K+ in exchange for H+ * this can cause alkalosis * combined effect is hypokalaemic alkalosis * this is what happens in Barrter's when there is lots of salt wasting

Answer 19

* Hyperaldosteronism * Primary * disorder of the adrenal gland increases production * Secondary * the systems that control aldosterone production are aberrant * classic excample is renal artery stenosis * JGA recieves decreased Na+ and so thinks there's very low blood pressure when there isnt' * promotes increased aldosterone production unnecessarily * both cause hypokalaemic alkalosis as well as high blood pressure

Answer 20

* cortisol could activate the same nuclear receptor as aldosterone * it doesn't because it's broken down at the surface of the cell by an enzyme called * 11-beta hydroxysteroid dehydrogenase * don't think you need to know that * in some people this enzyme is deficient * this can cause secondary hyperaldosteronism and the associated hypokalaemic alkalosis and hypertension

Answer 21

* this is not uncommon in elderly diabetic patients * the problem here is a lack of aldosterone * there's a reduced generation of the electrochemical gradient that results in K+ of H+ secretion * so you develop a metabolic acidosis * the treatment is with diuretics

Answer 22

* not related to diabetes mellitus * diabetes just means weeing a lot * there's a defect in Vasopressin, its receptor or in aquaporin 2 itself * leads to the inability to concentrate urine

Answer 23

* prostaglandins * oxytocin * relaxin * progesterone * human chorionic gonadotrophin * oestrogen * prolactin

Answer 24

* stimulates the ovary to produce oestrogen/progesterone * it's the pregnancy test hormone * it diminishes once the pregnancy is mature enough to take over oestrogen and progesterone production

Answer 25

* produced throughout the pregnancy * regulates the levels of progesterone * prepares the uterus for the baby * prepares the breasts for lactation * drops dramatically at birth

Answer 26

* prevents miscarriage * builds up the endometrium for support of the placenta * prevents uterine contractions * drops dramatically at birth

Answer 27

* produced by the pituitary gland * increases cells that produce milk * after birth, levels of progesterone and oestrogen drop dramatically * this allows prolactin to stimulate production of milk * this is also controlled by suckling * it also prevents ovulation but unreliably

Answer 28

* this is high early in pregnancy * it limits uterine activity and softens the cervix in preparation for delivery

Answer 29

* trigggers 'caring' reproductive behaviour * it's responsible for uterine contractions during pregnancy and labour * it is the cause of the contractions felt during breast feeding * used as a drug to induce labour

Answer 30

* have a role in inducing labour * synthetic ones are used to induce labour

Answer 31

* CO increases * there is reduced total peripheral resistance * this reduces systemic blood pressure * there is much increased uterine blood flow * increased stroke volume * increased heart rate

Answer 32

* increased number of blood cells * increased clotting factors * increased fibrinolytic activtity

Answer 33

* diaphragm displaced superiorly * decreased functional reserve capacity * increased risk of apnea and dyspnea * hyperventilation

Answer 34

* Nausea and vomiting * heart burn and acidity

Answer 35

* varicose veins * linea negra * weight gain * foetal * amniotic * maternal * placental * breast size

Answer 36

* increase in size * nipples increase in size * areolas become larger and darker * montgomery's tubercles become more active and secrete substances to lubricate the nipples

Answer 37

* measured from the top of the uterys to the symphosis pubis with a tape measure * in cm it roughly corresponds to the age of the baby in weeks

Answer 38

* Malnutrition * extremes of maternal age * an underlying medical condition * drug misuse * hemorrhage

Answer 39

* Miscarriage * abnormal development * disordered foetal growth: * too big * too small * Premature birth and consequences of that

Answer 40

there's both hypertrophy and hyperplasia

Answer 41

smooth muscle cell bundles in the uterus that contract during parturition to expel the foetus

Answer 42

* it becomes the decidua which is the maternal part of the placenta * together with the chorion it forms the placenta

Answer 43

* this is the remodelling of the cervix in the final three months of pregnancy to prepare for labour * it is promoted by the release of prostaglandin, relaxin and placental oestrogen * collagen concentration drops

Answer 44

* phase 0: myometrial repression - no labour * promoted by progesterone * phase 1: myometrial activation - results in labour * promoted mainly by oestrogen * phase 2: biochemical activation - together with myometrial activation results in labour * promoted by cytokines and prostaglandins * phase 3: permanent changes associated with labour

Answer 45

* synthesised by all uterine tissues * main ones are E2 and F2alpha * they increase the sensitivity of the myometrium to oxytocin * positive feedback: as the head of the baby presses on the cervix this stimulates the production of PGEs

Answer 46

* joints of the skull are soft and sutures can overlap while the head is passing through the birth canal * the head also flexes to reduce its diameter

Answer 47

* there are braxton-hicks contractions throughout pregnancy that don't amount to labour * Ca2+ influx to the cell results in excitation relaxaction coupling * the uncoupling leads to relaxation * contractions must be coordinate to result in the safe birth of a baby * if they are inco-ordinate then it won't be as effective

Answer 48

* There are foetal, maternal and placental components to the initiation of labour * the drop in progesterone coupled with the rise in oestrogen results in increases in: * uterine sensitivity to oxytocin * increased release of prostaglandins * softening of the cervix * this all leads to uterine contractions and labour * oxytocin does the final job of ensuring that the uterus contracts

Answer 49

* the number of oxytocin receptors changes a lot throughout pregnancy * PGEs increase number of receptors on decidua and myometrium * Distention of uterus near term does the same thing * uterine contractions are elicited when the number of receptors reaches a critical point

Answer 50

Occipital-anterior position

Answer 51

* defined by the amount of cervical dilatation * there is a phase where there is not much dilation happening * this is the latant phase * then there is a phase when dilation begins to happen much more quickly * active phase * this is when you want to me managing the labour

Answer 52

* 1st stage: the time of established labour until the cervix is fully dilated * 2nd stage: the time between full dilation and delivery * 3rd stage: the time of full delivery of the baby until full expulsion of the placenta

Answer 53

* maternal surface: * cobblestone appearance * covered with maternal decidua basalis * embryonic side * umbilical cord attachment * umbilical vessels branch into chorionic vessels which anastomose within the placenta

Answer 54

* the outer layer of the blastocyst forms the trophoblastic cell mass (TCM) * The TCM infiltrates the endometrium and degenerates * implantation is the first stage of the development of the placenta * there's a differentiation of the cells forming: * trophoblast --\> placenta * embryoblast --\> baby

Answer 55

* two arteries out of baby * one vein into baby

Answer 56

* remember that the placenta has functional reserve so a lot of it needs to be damaged to cause problems * placenta has 3 main functions: * metabolism * synthesises glycogen, cholesterol and fatty acids * transport * endocrine * produces some important hormones

Answer 57

* hCG - which supports the corpus luteum * Relaxin * Progesterone * Oestrogen * Human chorionic somatommotropin (hCS)

Answer 58

abnormal adherance with absense of decidua basalis

Answer 59

* the placenta overlies the internal os of the uterus * blox exit * may cause abnormal bleeding

Answer 60

* If the testis are present: * leydig cells make testosterone * so the wolffian system develops into: * epididymis * vas deferens * seminal vesicles * ejaculatory ducts * sertoli cells secrete AMH which causes mullerian system to regress * If there are no leydig cells then the mullerian cells develop into: * fallopian tubes * uterus * upper third of the vagina

Answer 61

when oestrogen causes the epiphysis in the legs to fuse NB boys have oestrogen too they convert testosterone to oestrogen in fatty tissue

Answer 62

* its the growing bit of bone * each long bone has a growth plate at either end * growth from here is chondrogenesis * because building materials are needed every day, there is a direct effect of nutrition and calcium / phosphate supply on bone architecture

Answer 63

* GHRH cell bodies in the arcuate nucleus project into the portal capillaries of the anterior pituitary gland * Negative feedback is by: * IGF-1 (insulin like growth factor 1) * Somatostatin (SST) * GH

Answer 64

* Synthesized in the somatotroph cells * these are 40-50% of the anterior pituitary

Answer 65

* Pulsatile secretion (bursts) * mainly secreted at night * stimulates insulin like growth factor 1 * has a direct effect on the growth plate of bones * decreases glucose use * increases lipolysis * increases muscle mass

Answer 66

* aging * high carbohydrate meals * hyperthyroidism * hyperglycaemia

Answer 67

* hypoglycaemia * stress * high protein meals * perinatal development * fasting * exercise

Answer 68

* GH stimulates the production of Insulin like Growth Factor 1 * this is what mediates some of the growth * if there is IGF deficiency then there will be short stature

Answer 69

* Precocious puberty * menarche before 9 leads to short stature * congenital adrenal hyperplasia * Hyperthyroidism

Answer 70

* androgen/oestrogen deficiency * GH excess * Klinefelter syndrome (XXY) * Marfan syndrome

Answer 71

Girls: menarche Boys: ejaculation NB neither of these signify fertility

Answer 72

* Ovarian oestrogens control growth of breasts and female genetalia * Ovariana and adrenal androgens control pubic and axillary hair

Answer 73

* Testicular androgens control the development of: * external genetalia * pubic hair * enlargement of larynx

Answer 74

* genetics * nutrition * environment * leptin * adrenarche * the gradual maturation of the adrenal gland * comes with development of pubic hair, axillary hair, body odour and acne

Answer 75

* pseudopuberty doesn't have hypothalamus or anterior pituitary involvement and the gonadal effects are mediated by something else * the difference between them can be checked by stimulating them with GnRH and seeing how much gonadotropin (LH and FSH) they produce * if it's true puberty they should produce lots

Answer 76

it's an oestrogen precursor

Answer 77

* at the junction of the foregut and the midgut, 2 pancreatic buds (dorsal and ventral) are generated and fuse to form the pancreas * exocrine functions begin after birth (pancreatic juices etc) * Endocrine functions (hormones) begin from 10-15 weeks

Answer 78

* retroperitoneal * posterior to the greater curvature of the stomach * 12-15cm long * head tucks into the C portion of the duodenum * has 5 parts * uncinate process * head * neck * body * tail * exocrine secretions pass from small ducts into two larger ducts * these larger ducts join the common bile duct and enter the duodenum as the hepatopancreatic ampulla * aka the ampulla of Vater * this ampulla has a sphincter (sphincter of Oddi)

Answer 79

* 98-99% of cells are in clusters called acini * exocrine activity secretes pancreatic juice which includes: * amylase - carbs * trypsin, elastase - protein * Lipase - triglycerides * all become active once in lumen of small gut * endocrine activity is performed by islet cells * hormones secreted into the portal vein

Answer 80

* Beta cells are the most common (60-70%) * secrete insulin * Alpha cells (20%) * secrete glucagon * Delta cells (5%) * secrete somatostatin * there's cross talk between alpha cells and beta cells * i.e. insulin secretion inhibits glucagon secretion

Answer 81

* suppresses hepatic glucose output * inhibits glycogenolysis * inhibits gluconeogenesis * increases glucose uptake by somatic cells * GLUT4 on transport vesicles is transported to the membrane when insulin binds the membrane receptors * suppresses use of bodily stores for energy * inhibits lipolysis * inhibits ketogenesis * inhibits muscle breakdown

Answer 82

* increases hepatic glucose output * activates glycogenolysis * activates gluconeogenesis * reduced peripheral glucose uptake * stimulates release of gluconeogenic precursors * this includes amino acids and glycerol * activates lipolysis

Answer 83

* glucose crosses GLUT2 transporters on B cells at a rate that reflects the blood glucose concentration * intracellular metabolism of this glucose results in production of ATP * ATP closes a potassium channel on the cell which stops the efflux of K⁺ * the membrane is depolarised which results in the opening of voltage-dependent Ca²⁺ channels * rapid influx of calcium triggers exocytosis of insulin from secretory granules

Answer 84

* the presence of C peptide * a peptide that linked A and B chains of pro-insulin * they are secreted together in equimolar concentrations * helps physicians to distinguish between endogenous and exogenous insulin

Answer 85

1. rapid release of stored insulin 2. slower process of synthesising and releasing insulin

Answer 86

* these are hormones secreted by sensory cells in the gut wall that also stimulate insulin release * insulin response is greater following oral glucose than IV glucose * this difference is due to the incretin effect * incretins to remember: * Glucagon-Like Peptide 1 (GLP-1) * Glucose-dependent insulinotrophic peptide (GIP)

Answer 87

* Glucagon-Like peptide-1 * has a short half life as it is cleaved by protein DPPIV * this prevents hypoglycaemia

Answer 88

* all glucose comes from the liver through: * breakdown of glycogen * gluconeogenesis * from alanine, lactate or glycerol * this glucose is then delivered to the tissues * muscles use FFA for fuel * insulin levels are low * glucose is delovered

Answer 89

* Rising glucose causes increase in insulin and suppression of glucagon * ingested glucose replenishes glycogen stores in the muscle and the liver * excess glucose is converted to fat * lipolysis is inhibited and level of FFAs falls

Answer 90

* there's an outer capsule, a cortex and a medulla * the cortex has three layers: * the zona glomerulosa * mineralcorticoids (aldosterone) * the zona fasciculata * glucocorticoids (cortisol) * the zona reticularis * androgens (DHEA) * the medulla produces catecholamines

Answer 91

* includes mineralocorticoids and glucocorticoids * cholesterol is the precursor for them all * they're lipid soluble * bind specific intracellular receptors * alter gene transcription * directly or indirectly * some key ones are cortisol and aldosterone

Answer 92

* it massively stimulates it * in ACTH excess the adrenal gland becomes enlarged

Answer 93

* synthesised int he zona fasciculata and reticularis * essential for life * important for homeostasis * increase glucose metabolism * increased lipolysis * augment gluconeogenesis * maintain circulation * salt/water balance * vascular tone * immunosuppression

Answer 94

* these proteins are heavily bound * 90% to corticosteroid-binding globulin (CBG) * 5% to albumin * 5% free * only the free ones are bioavailable * CBG is cleaved during inflammation * so when CBG decreases due to inflammation (e.g. due to sepsis) the % free cortisol increases * more glucocorticoid can enter cells

Answer 95

* ACTH does!!! * it acutely stimulates cortisol release * it also stimulates corticosteroid synthesis * it does this by binding a receptor on the surface of a cell in the zona fasciculata * this produces a cAMP response within the cell that triggers steroidogenesis * CRH from hypothalamus stimulates ACTH release from pituitary * cortisol in turn has a negative feedback mechanism on the ACTH and CRH production

Answer 96

* just know it's quiet when you're asleep and then released mainly between waking up and breakfast * also know that stresses such as trauma or sepsis will heighten it * CBG is broken down so more free cortisol

Answer 97

* Aldosterone and DOC are the main ones * they're synthesised in the zona glomerulosa * they're essential for life

Answer 98

* acts on the distal conveluted tubule and the cortical collecting duct * it acts on intracellular receptors * these upregulate transcription of proteins that modulate the activity of ion transport systems in the apical and basolateral membranes *

Answer 99

* ENaC on apical surface * more Na+ out of lumen and into cells * Na+K+ATPase on basolateral surface * more Na+ out of cell and into interstitium * more K+ into cell and out of interstitium * this then leaves the cell and enters the urine through ROMK * Plasma: sodium up, potassium down * Urine: sodium down, potassium up

Answer 100

* e.g. aldosterone * not regulated via the hypothalamus, pituitary, adrenal system * YOU DO NOT GET SALT LOSS AS A SYMPTOM OF SECONDARY ADRENAL INSUFFICIENCY * the juxtoglomerular apparatus sense the bp of the afferent arterioles * if blood pressure drops they secrete renin * this kicks off RAAS

Answer 101

* secretion of renin by JGA can be activated by: * drop in bp * prostaglandins * beta adrenergic action * renin cleaves angiotensinogen (produced by the liver) into angiotensin I * angiotensin I is cleaved by ACE (angiotensin converting enzyme) in the lung to angiotensin II * angiotensin II binds angiotensin II receptor in the adrenal leading to the synthesis and release of aldosterone from the zona glomerulosa * aldosterone works on the kindey by binding the mineralocorticoid receptor * once extracellular potassium drops there's a direct negative feedback on the adrenal to halt aldosterone production

Answer 102

* pancreas * sweat glands * colon in these places there is the same effect of sodium retention

Answer 103

* the inactive form of cortisol * cortisol is present at high levels but can also bind the mineralocorticoid receptor * this is a problem because aldosterone is present at very low levels * so in order for aldosterone to be able to bind its receptor and be effective, cortisol must be inactivated * so every tissue that expresses the mineralocorticoid receptor also expresses the enzyme which inactivates cortisol to cortisone * if you inhibit this enzyme then you induce severe hypotension because aldosterone can no longer bind

Answer 104

* androgens are produced in the ovaries and the testis too * females have them but at lower levels * in women the adrenal is a major source of androgen * adrenal androgens * Dehydroepiandosterone (DHEA) is the most abundant adrenal steroid but it is a very weak androgen * Androstenedione is stronger but still only a 1/10th as strong as testosterone * production is regulated by ACTH not gonadotrophins

Answer 105

* produces catecholamines like adrenaline * is part of the autonomic nervous system * has specialised ganglia supplied by preganglionic neurones from the spinal cord * these preganglionic neurons produce noradrenaline * the medulla has the enzyme to convert noradrenaline to adrenaline but the neurons don't * so catecholamine synthesis is regulated by the sympathetic nervous system

Answer 106

* they are synthesised from tyrosine * sympathetic stimulation is important for some of the enzymes * cortisol stimulates the final enzyme which makes adrenaline from noradrenaline * so without cortisol you will not produce adrenaline

Answer 107

* gluconeogenesis in liver and muscle * lipolysis in adipose tissue * tachycardia and increased cardiac contractility

Answer 108

* through the hypothalamic hypophysial tract * from the paraventricular nucleus and the supraoptic nucleus of the hypothalamus * the hormones are transported in the large neurons of these nuclei to the posterior pituitary where they are released

Answer 109

* Vasopressin * AKA ADH * stimuli from supraoptic nuclei * Oxytocin * promotes onset of labour * promotes expression of milk * stimuli is from the paraventricular nuclei

Answer 110

* Na+ * Ca2+ * Cl- * HCO3-

Answer 111

* K+ * Mg2+ * PO^3-₄

Answer 112

* binds V₂ receptors on the renal collecting duct principal cells * it triggers and intracellular signalling cascade that results in the transport of AQP2 containing vesicles to the apical surface of the cell * aquaporins are transmembrane channel proteins for water * this results in net movement of water into the cell and through into the blood stream * this decreases plasma osmolality

Answer 113

* concentration of particles per kilo of liquid * v similar to osmolarity in plasma * size of particle is not relevant, just the numbers of them

Answer 114

* synthesised in both sexes but well known effects are only in women * action * secretion of milk * contraction of myometrium * onset of labour * together with oestrogen it causes cervical dilation * both suckling and uterine contraction have a positive feedback effect on the PVN to produced more oxytocin

Answer 115

* mainly to rid the body of nitrogenous waste * it does this by converting ammonia and ammonium to the less toxic urea * urea is water soluble and can be excreted through the kidneys

Answer 116

* bulk reabsorption * Na+ * Cl- * amino acids * HCO3-

Answer 117

* Oxytocin: paraventricular nucleus * Vasopressin (AKA ADH): supraoptic nucleus

Answer 118

* Tri-iodo-thyronine (T3): major thyroid hormone * Thyroxine (T4): reservoir for T3 * Calcitonin: involved with Ca²⁺ homeostasis

Answer 119

* increasing plasma Ca²⁺levels causes the thyroid gland to produce calcitonin. * Calcitonin has two effects to reduce plasma calcium 1. It inhibits bone resorption by osteoclasts 2. it decreases reabsorption of calcium in the kidneys.

Answer 120

* it is the active form of vitamin D * sunshine converts 7 dehydroxy cholesterol in the skin into vitamin D3 * In the liver this vitamin D3 is converted to 25, hydroxy VD3 * aka calcidiol * Calcidiol is converted to 1,25 dihydroxyvitamin D3 (Calcitriol) in the kidney by enzyme 1 alpha hydroxylase

Answer 121

* even though osteoblasts are principally responsible for building bone, they have an important role in activating osteoclasts which are responsible for bone resorption * Parathyroid hormone binds to PTH receptor on osteoblasts and mediates 3 effects on it: 1. osteoblast proliferation 2. upregulation of cell surface RANKL 3. stops production of OPG * OPG inhibits activity of RANKL binding * This means that RANKL can now bind RANK on pre-osteoclasts. * RANK-RANKL binding allowsthe pre-osteoclast to proliferate and differentiate into a mature osteoclast * This will result in increased bone resorption

Answer 122

* Reduced glucose produced by the liver * less glycogenolysis * les gluconeogenesis * Increases movement of glucose to tissues * Glycogen and protein synthesis in the muscle * Triglyceride synthesis in the adipocytes * Suppresses: * ketogenesis * lipolysis * muscle breakdown * Insulin also draws potassium into cells

Answer 123

distal conveluted tubule and the collecting duct

Answer 124

1. acts on the principle cells of the collecting duct and the distal tubule to up regulate the Na⁺/K⁺pump * more Na+ enters the interstitium * therefore more Na+ reabsorbed down concentration gradient * K+ is pumped into the urine in exchange 2. upregulates ENaC Na+ transporter on the apical surface of cells lining the collecting duct and the colon

Answer 125

1. Metabolism * Protein --\> amino acids * Triglyceride --\> glycerol and fatty acids (lipolysis) * Glycogen --\> glucose (gluconeogenesis) 2. Circulation * increases vasoconstriction 3. Decreases inflammation and the specific immune response 4. Decreases non-essential functions like reproduction and growth

Answer 126

Through the hypothalamic-hypophyseal portal system into which the neurosecretory neurons secrete releasing hormones.

Answer 127

thyrotropin releasing hormone (TRH) released from hypothalamus

Answer 128

Corticotropin releasing hormone (CTH) released from the hypothalamus

Answer 129

it is released by neurosecretory neurons in the hypothalamus. It travels in the hypothalamic-hypophyseal portal system to the anterior pituitary where it causes the release of follicle stimulating hormone (FSH) and Leutenising Hormone (LH)

Answer 130

growth hormone releasing hormone (GHRH) released by the hypothalamus GH release is inhibited by somatostatin

Answer 131

dopamine release by the hypothalamus causes inhibition of prolactin release

Answer 132

primary is always a problem with the final gland (i.e. with cortisol it would be a problem with the adrenal) secondary is always a problem with the pituitary tertiary is always a problem with the hypothalamus

Answer 133

growth hormone

Answer 134

* GnRH release from hypothalamus * GnRH causes release of LH and FSH * LH stimulates leydig cells in interstitium to produce testosterone * FSH stimulates sertoli cells to produce androgen binding globulin and inhibin * ABG binds testosterone and localises it to the seminiferous tubules for spermatogenesis * Inhibin supports spermatogenesis and inhibits FSH, LH and GnRH production

Answer 135

* Hypothalamus secretes GnRH * The AP releases FSH and LH * LH and FSH reach the ovaries where they cause the production of oestrogen, progesterone and inhibin * Inhibin inhibits activin which is responsible for stimulating GnRH

Answer 136

* Low levels * stimulates FSH release * inhibits LH release * High levels * stimulates LH release * inhibits FSH release

Answer 137

* Metabolism * protein --\> amino acids * triglycerides --\> FFAs and glycerol (lipolysis) * glycogen --\>glucose (glycogenolysis) * Circulation * vasoconstriction * Inhibits inflammation and specific immune response * Inhibits non-essential functions like reproduction and growth