Block 7 - Endocrinology

Front 1

what are symptoms of anxiety?

Back 1

trembling, sweating, flush/chills, nausea and palpitations

these people also have a higher HR, more rapid RR and high blood glucose and triglycerie concentration

Front 2

in an anxious state which hormones are increased

Back 2

corticotrophin releasing hormone (CRH - hypothalamus
adrenocorticotrophin hormone (ACTH) and prolactin from the anterior pituitary
Vasopressin from the posterior pituitary
cortisol and adrenaline - adrenals

Front 3

the anterior pituitary secretes which hormones

Back 3

FSH (follicle stimulating hormone)
LH (leutinising hormone)
ACTH
TSH
Prolactin
GH (gowth hormone)

CLUE: FLAT PiG

Front 4

the hypothalamus secretes which hormones

Back 4

CRH
GnRH

Front 5

What is the hormonal response of stress?

Back 5

increase in CRH for the hypothalamus --> increases in ACTH and prolactin fron the anterior pituitary as well as vasopressin from the posterior pituitary--> increase in cortisol and adrenalin release from the adrenal (cortisol is made cortex and adrenaline in the medulla)

Front 6

SNS stimulation in response to stress results in

Back 6

increased adrenalin (adrenal medulla) AND
increased noradrenaline (adrenal cortex) as a result of increased ACTH

Front 7

t/f. adrenaline and cortisol act to help insulin

Back 7

FALSE. they counter the actions of insulin by increasing glycogenenolysis (break down of glycogen) and increasing hepatic glucose output.
triglyceride breakdown is also excellerated

Front 8

t/f. increase in cortisol can cause immune suppression

Back 8

true!

Front 9

how is blood volume affected in anxiety

Back 9

blood volume increases due to a decrease in renal blood flow which triggers the increase in renin and vasopressin

Front 10

what is the Basal metobolic rate

Back 10

it is the energy expended by a human when completely at rest but not asleep in the absence of muscle movement and without SNS arousal

Front 11

what is resting metabolic rate

Back 11

is what we use in practice (instead of BMR) to measure the energy used by humans and is typically 10-15% higher than BMR

Front 12

what are some causes of energy expenditure?

Back 12

cold induced thermogenesis or thermoregulatory heat
thermic effects of exercise
thermic effects of food

Front 13

how is BMR measured?

Back 13

it is dependant on lean body mass - so while obseise people have a higher 'absolute ' BMR it is adjusted so that relatively we are all the same if we have normal functioning bodies

Front 14

what controls BMR

Back 14

the hypothalamus via the autonomic nervous system and genetic factors also contribute

Front 15

what are the two mechanisms of gain of body heat

Back 15

shivering and non-shivering

non-shivering is via biochemical reactions to produce heat

Front 16

what causes hypothermia?

Back 16

it is usually due to an acute illness

Front 17

name the 3 catecholamines

Back 17

adrenaline, noradrenaline and dopamine

Front 18

what is noradrenaline used for in the sympathetic nervous system

Back 18

it acts as a NT of the sympathetic nervous systen on postganglionic fibres

Front 19

t/f. beta adreno receptors are activated by dobutamine and blocked by metropolol

Back 19

true

Front 20

t/f. beta adrenoreceptors in the heart increase the force of contraction of the myocardium

Back 20

true

Front 21

what is an action of all beta adrenoreceotors

Back 21

they are activated by G proteins that result in stimulation of adenylate cyclase that then converts ATP to second messanger cAMP

Front 22

what are the grades of goitre

Back 22

0 none
1a not visible but palapalbe
1b palpable and visible on full neck extension
2 visible in the normal position
3 very large

Front 23

what are some of the classifications of a goitre

Back 23

difuse or nodular
single nodule or multinodular
toxic or non-toxic(simple)

Front 24

what is the most common goitre presentation

Back 24

non-toxic diffuse goitre

Front 25

what is the most common cause of endemic goitre?

Back 25

iodine deficiency

Front 26

what is the cause of sporadic goitre?

Back 26

due to heterogenoeous stimulation of the growth of thyroid epithelial cells by the growth fact such as TSH, insulin, insulin-like growth factor or moduate efects of TSH

Front 27

what is a cause of non-toxic diffuse or multinodular goitre?

Back 27

may be due to the presence of autoimmune changes within the thyroid gland due to hashimoto's thyroiditis

Front 28

a toxic multinodular goitre causes

Back 28

thyrotoxicosis

Front 29

a diffuse toxic goitre is often

Back 29

graves disease and accompanied by both the signs of thyrotoxicosis and the graves opthalmopathy signs

Front 30

what sre some effects of excessive thyroid hormone

Back 30

weight loss,
increased apeptite
increased heat production
heat intolerance
tachocardia
diarrhoea
tiredness
anxiety
irritability
tremour
muscle may become weak and wasted

Front 31

hypothyroid common signs include

Back 31

tiredness,
weight gain
loss of apetite
dry and brittle hair
cold intolerance
depression
slow HR
muscle may become painful and reflexes may be delayed in relaxing
puffy face and hands

Front 32

what is the autoimmune process in hashimoto's thyroiditis

Back 32

activated T cells

Front 33

what is the autoimmune process in Grave's Disease

Back 33

caused by thyroid autoantibodies, directed towards the thyroid hormone receptor TSH-R and stimulate it - that is stimulate thyroid hormone releases that is independent of the feedback loop with the pituitary gland. when T3/T4 levels are at a high enough level this negatively feeds back to the pituitary to stop TSH thus stop TH production

Front 34

in testing thyroid function if the TSH is normal does this warrant more testing?

Back 34

if TSH levels are normal this normally indicates that the patient is euthyroid

Front 35

if the TSH is high?

Back 35

this indicates there is a primary hypothyroidism

Front 36

if the TSH is low or undetectable what does this indicate?

Back 36

that there is thyrotoxicosis or a hypopituitary state

Front 37

when measure thyroid hormone explain what T3 and T4 should look like

Back 37

if the patient suffers thyroitoxicosis than there will be high free T3 and T4
in a hypothyroid patient T3 is not as important because it is very slow to fall; the T4 is useful in determining the thyroid state

Front 38

how long does it take TSH to reach a new equilibrium

Back 38

4 weeks

Front 39

what medications are there for thyrotoxicosis

Back 39

carbimazole and PTU = both block peroxidase activity
carbamazole has a longer half life of 8 hours
however PTU also converts T4 to T3
neither should be used in the first trimester of pregnancy - use Neomercazole

surgery is also an option

Front 40

what are the 3 growth phases in a human

Back 40

infantile
childhood
puberal growth spurt

Front 41

describe growth hormone in the body.

Back 41

GH is secreted in a pusatile fashion from the pituitary (anterior) gland. it is controlled by the hypothalamus - by somatostatin which negative controls it and by growth releasing hormone which has a positive effect

Front 42

what forms the roof of the pituitary fossa

Back 42

the roof of the pituitary fossa is formed by the sella diaphragm dura which stretched between clivoid processes
it has a small hole which the pituitary stalk travereses

Front 43

what does the pituitary stalk connect to?

Back 43

from the pituitary to the hypothalamus

Front 44

what lays just lateral to the pituitary gland

Back 44

the cavernous sinuses - which carry the carotid artery, III, IV, VI and V3

Front 45

name the parts of the anterior pituitary

Back 45

pars distalis
pars tuberalis
pars intermedia

Front 46

what are the secretory cells of the pituitary gland called

Back 46

acidophis and basophils

acidophils = lactotropes and samatotropes

Front 47

what do lactrotropes produce

Back 47

prolactin

which promotes mammary gland development and lactation in women. it stimulates testosterone in men by binding in the prostate

Front 48

what do basophils secrete

Back 48

gonadotrophs - FSH and LH,
thyrotropes - thyrotrophin and T4
adrenocorticotropes - stimulate adrenal cortex to produce glucocorticoids.

Front 49

what is the vascular pathway in the pituitary?

Back 49

supplied by the superior hypophyseal arteries and a single inferior artery = all are branches of the internal carotid

the superior hypophyseal supplies the infundibulum and the anterior pituitary via the portal system

Front 50

what is the definition of a microadenoma and a macroadenoma

Back 50

microadenoma is a pituitary tumour <1cm and macroadenoma is >1cm

Front 51

what are the pressure effects in a pituitary macroadenoma?

Back 51

compression or local invasion --> headache from stretching the dura, CSF obstruction and hydrocephalus.
can also get visual disturbances - bitemporal hemionopia - and III, IV, VI palsy

Front 52

compression of the pituitary stalk can cause?

Back 52

disruption to the delivery of factors from the hypothalamus to the anterior pituitary which typically occur in the following order
gonadotrophins,
GH
TSH
ACTH

Front 53

what is a craniopharyngeoma?

Back 53

a tumour arising from the remnants of Rathke's pouch which is the diverticulum at the roof of the mouth that gives rise to the antierior pituitary

Front 54

what is the most common type of pituitary tumour

Back 54

non-functioning adenoma (32%)

prolactinoma
growth hormone producing adenoma
corticotrope adenoma

Front 55

in a women what does a prolactinoma cause?

Back 55

galactorrhoea
menstral disturbance
infertility

NB: in a man there are no signifincat physiolgicaly side effects except for sexual dysfunction

Front 56

what would a growth hormone tumour do?

Back 56

prior to epiphyseal closure --> get gigantism; or after closure called acromegaly

Front 57

what is papilodoema?

Back 57

is due to transmision of ICP up the optic sheeth causing swelling and venous congestion of the optic nerve head, is almost pathogenic of increased ICP

Front 58

what does vasopressin do?

Back 58

controls water reabsorption in the kidney via V2 receptors that increase cAMP which increases the aquaporins in the apical membrane

its pressor effects via the V1 receptor increase DAG/IP3 and rise in Ca inside vascular smooth muscle causes peripheral vasoconstriction

Front 59

what does diabetes insipidus cause in the hypothalamus

Back 59

it causes destruction of cell bodies OR there is a mutation in the VP gene

Front 60

what does oxcytocin do?

Back 60

at birth it causes uterine contrations
it is involved in milk secretion: suckling --? signal to the SON and PVN to increase oxytocin --> mammary glands - contraction of myoepithelial cells around the alveoli

Front 61

what are the two most common groups of symptoms producing pituitary tumours

Back 61

primary tumour of adenohypophyseal origin (adults)
tumours of germ cell origin arising in the pituitary region though not of pituitary origin - seen in children

Front 62

t/f. all microadenomas of the pituitary will require treatment.

Back 62

false. many that become evident on autopsy never became clinically evident and therefore did not require treatment

Front 63

what do you treat a pituitary prolactinoma with

Back 63

carbergoline (DA agonist) which is efficacious in inhibiting the synthesis of prolactin and reducing serum prolactin

Front 64

which brain area is key in cirrcadian rhythm

Back 64

the anterior hypothalamus

Front 65

what is the supra nucleus

Back 65

is the cirrcadian pacemaker and resets everyday by the Zeitberger cues = light and dark

Front 66

what occurs in the pineal glad with respect to circadian rhythm

Back 66

SNS stimulation of the pineal gland --> darkness stimulates melatonin release and light inhibits SNS stimulation of malatonin
release of CRH --> pituitary gland --> ACTH --> adrenal cortex then releases cortisol

Front 67

when is cortisol the lowest?

Back 67

just before sleep


it is the highest early in the morning

Front 68

when is melatonin onset

Back 68

between 10 and midnight

the secretion of melatonin is independent of the sleep wake cycle and not affected by sleep deprivation

Front 69

what are steroid hormones synthesized from

Back 69

cholesterol

Front 70

names some synthetic glucocorticoids

Back 70

prednisolone, dexamethasone, betamethasone, budesonide and fluticasone

Front 71

how do glucocorticoids work?

Back 71

they act on intraellular steroid receptors in the cytoplasm forming a GCS-receptor compled that translocates to the nucleus binding to a target gene know as a glucocorticoid response element (GRE)

Front 72

do glucocortocoids modulated anything other that glucocorticoid activity?

Back 72

yes. some including hydrocortisone and prednisolone have mineralocorticoid activity as well although this is small, but can cause Na retention and K and Ca losses

Front 73

what is the mechanism of anti-inflammation in steroids?

Back 73

1. trasnactivation: glucocorticoid receptor complex translocates to the nucleus where it binds to GRE and causes the sythesis of anti-inflammatory proteins
2. transrepression: transcription factors such as activator protein 1 (AP-1) --> produce mRNA which codes for proinflammatory cytokines. the complex binds to transcription factors therefore suppressing the ability to stimulate mRNA products = less pro-inflammatory cytokines.

Front 74

t/f. steroids recruit HDAC to activate transcriptional complexes leading to deacetylation of histones that decrease transcription of pro-inflam.

Back 74

true

Front 75

what is a non-glucocorticoid use for dexamethasone

Back 75

treatment of cerebral oedema

Front 76

what is the half life of hydrocortisome

Back 76

8-12hours

Front 77

what is the half life of prednisolone

Back 77

12-36 hours

Front 78

what is the half life of dexamethasone

Back 78

36-72 hours

Front 79

which steroids are made in the adrenal cortex

Back 79

glucocorticoids
mineralocorticoids

Front 80

which steroids are made in the gonads

Back 80

androgens - testosterone and DHT
Oestrogen and Eostrodiol
progestogens

Front 81

which steroids are produced by fat cells

Back 81

testosterone and estridiol

Front 82

what are the 3 layers of the adrena cortex

Back 82

zona glomerulosa - aldosterone
zona fasiculata - cortisol
zona reticulata - androgens

Front 83

what do leydig cells snythesise?

Back 83

they are in the testes and they synthesise testosterone

Front 84

what stimulates testosterone production

Back 84

LH secreted by the antirior pituitary

LH is under the control of GnRH released by the hypothalamus

Front 85

what stimulates estridiol secretion

Back 85

FSH from the anterior pituitary

Front 86

what secretes estridiol in women

Back 86

the ovaries

Front 87

t/f. progesterone is a key intermediate in steroid synthesis - then converted to cortisol, aldosterone or a sex steroid

Back 87

true

Front 88

what is cushing's disease

Back 88

it is an ACTH secreting tumour which then leads to increased cortisol casing the steryotypic cushingoid appearence.

Front 89

addinson's disease is?

Back 89

an autoimmune atrophy of the drenal cortex --> decreased cortisol and increased ACTH which causes hyperpigmentation

because there is no cortisol beong procuded ACTH is upregulated in its secretions trying to stimulate cortisol release - however this is impossible as the area of the adrenal gland - the cortex - which synthesises and stores cortisol is now destroyed

Front 90

what impact do glucocorticoids have on glucose in the blood stream?

Back 90

they increase levels so that they are available to tissues more rapidly

Front 91

what happens in the muscle when cortisol is releasead?

Back 91

the muscle undergoes catabolism to realse amino acids into the blood stream. it also prevents reuptake of amino acids into muscle

Front 92

what effect does cortisol have on adipose tissue?

Back 92

it causes a breakdown of lipid stores

Front 93

what is the mechanism of cortisol and glucose including the hypothalamus and pituitary

Back 93

IACTH binds to receptors in the fasciculata and reticulata and produces cortisol which enters circulation and binds to a corticosteroid binding globulin and acts to increase glucose available.
cortisol is inhibiting ACTH from the pituitary. negatively feeding back on the system

Front 94

how is cortisol produced:

Back 94

cholesterol --> via p450 the pregnenelone -->p450 to cortisol

Front 95

what is the effect of cortisol on the muscles

Back 95

suppressed glucose oxidation leading to lactate build up
decreased glucose uptake (reduced sensitivity to insulin)
elevated proteolyses leading to release of animo acids

Front 96

what is the effect of cortisol on the liver

Back 96

lactate and amino acids released from muscle taken up by the liver and converted to glucose via gluconeogenesis --> this glucose is then stored as glycogen

Front 97

what is the effect of cortisol on carbohydrate metabolism

Back 97

cortisol and glucagon from the panceratic islet cells and circulating adrenaline (from the adrena medulla) act as key countrer regulatory hormones to insulin
cortisol increased plasma glucose and promotes production of hepatic glycogen where as glucagon and adrenalin promote gycogen break down

Front 98

what is the effect of cortisol on Protein metabolism

Back 98

cortisol enhances protein break down - antagonised by insulin and insulin-like growth factor 1 and testosterone

cortisol upregulates the small protein ubiquiton which is then attached to proteins marking them for degradation in proteosomes

Front 99

what is the effect of cortisol on fat metabolism?

Back 99

redistributes fat from the periphery to centreal sites.

promotes the enzymes hormone sensitive lipase in peripheral sites

Front 100

how long does it take for cortisol to have an effect

Back 100

may be several hours

Front 101

name the 3 enzymes that up regulate cortisol

Back 101

enzymes in the gluconeogenic pathway
glycogen synthase
hormon sensitive lipase

Front 102

give an example of a primary cause of adrenal insufficiency

Back 102

the adrenal glands have been ablated

Front 103

give an example of a secondary cause of adrenal insufficiency

Back 103

Pituitary ACTH is deficient or absent

Front 104

give an example of tertiary cause of adrenal insufficiency

Back 104

when the hypothalamus CRH is deficient or absent

Front 105

t/f. in a secondary or tertiary cause of adrenal insufficiency thre will be significant mineralocorticoid effect too

Back 105

FALSE. there will be none

Front 106

what is the most common cause of adrenal insufficiency?

Back 106

suppresion by exaogenous seteroids

Front 107

t/f. the first presentation of a primary adrenal insufficiency may be life thretening.

Back 107

true. an example of this may be an addisonian crisis.

Front 108

what is the replacement therapy for adrenal insufficiency

Back 108

~37.5mg ccortisone acetate and 100-200ug of fludrocortisone

Front 109

what would a patient with a secondary adrenal insufficiency look like.

Back 109

unlike in addison's disease they will have lost ACTH so they will be pale

Front 110

what is the blood supply to the adrenals?

Back 110

adrenal arteries: with small arteries that penetrate the capsule

capsular capillaries

fenestrated cortical sinusoidal capillaries that supply the cortex and dran into fenstarted medullary capillary sinusoids.

the medulla also supplied by medullary arterioles that travel with the trabeculae

Front 111

what embryonic structure does the adrenal gland belong to

Back 111

the mesoderm

Front 112

describe a typical steroid myopathy

Back 112

onset may be insidious by develops into a weakness in the proximal muscles of the limbs

Front 113

what dosage is required to induce steroid myopathy symptoms

Back 113

>30mg/day prednisone

Front 114

what is the main finding on muscle histology of steroid myopathy

Back 114

atrophy of the type II B fibres. these are the fast twitch fibres.

Front 115

where is insulin synthesised stored and released?

Back 115

in pancratic beta cells.

Front 116

what is the major stimulus for insulin secretion

Back 116

blood glucose <5mM concentration

Front 117

what is insulin synthesised from

Back 117

a large polypeptide pre-proinsulin

Front 118

how is the polypeptide pre-proinsulin transformed into insulin

Back 118

in the rough ER a 23 amino acid sequence is removed leaving proinsulin.

proinsulin has a C peptide cleaved and they are both secreted together. there will be no C peptide in the blood of a type I diabetic

Front 119

how is insulin secreted

Back 119

glucose --> beta cells --> taken up by glucose transporter GLUT-2
the glucose is then metabolised closing K channels on the beta cell surface: this destroys the membrane potential allowing Ca channels to open

Front 120

which are the key target organs for insulin

Back 120

liver, muscles and adipose tissue

Front 121

what does insulin inhibit?

Back 121

lipolysis and ketone body formation

Front 122

what occurs in starvation?

Back 122

starvation --> 0insulin: increase in cAMP --> liver activation of glycogon phosphytase which degrades glycogon to maintain glucose >4mM

Front 123

what is the consequence of prolongued exposure to hypoinsulinaemia.

Back 123

elicits massive lipolysis.
excess fatty acids are converted to ketone bodies in the liver so they can be transported in the blood
ketone bodies can be used by the brain although not that efficiently

Front 124

what is the cause of type 1 diabetes

Back 124

autoimmune attach that destroys beta cells in the pancreas

Front 125

at what level does glucose appear in the urine

Back 125

>10mM

Front 126

what do the osmotic change scaused by hyperglycaemia do?

Back 126

they mean that water is drawn out of tissues causing a cellular dehydration

Front 127

what are the key plasma glucose levels in hypoglycaemia

Back 127

<4mM glucose uptake and metabolism by the brain is compromised
<3mM symptoms appear
<2.7mM causes cognitive dysfunction

Front 128

what are the symptoms of a hypoglycemic episode

Back 128

tremous,
tachycardia
palpitations
sweating
weakness
usually becomes aware just before the symptoms come on

Front 129

what is hypoglycemic unawareness

Back 129

the symptoms of a hypo are due to sympathetic overdirve and secretion of adrenaline - after suffering DM1 for many years (>10years) this response becomes impaired or is dampened down --> meaning there is no warning signs before the life threatening reality of a hypoglycemic attack

Front 130

t/f. maintenance of near normal blood glucose levels is associated with significantly more hypos and thus a worse outcome.

Back 130

false. whilst it is accociated with more hypos, evidence now shows that those who maintain a lower blood glucose are less likely to suffer some of the common diabetic complications

Front 131

what are the characteristics of diabetic retinopathy?

Back 131

weakening, rupturem leakage and occlusion of the blood vessels manifest as miscraneurysms, blot haemorrhages and hard exudate (lipid deposits) and soft exudate (local ischemia and miscrovascular occlusion)

Front 132

what is diabetic nephropathy

Back 132

occurs in 30% of DM1
characterised by proteinuria, hypertension and oedema with renal insufficiency.

Front 133

what is the efficacy of ACEi in diabetic nephropathy?

Back 133

they can prevent it beyond their antihypertensive action.

Front 134

what is the name of very long acting insulin analogue

Back 134

Glargine and determir

Front 135

what are the genetic relationships of DM1

Back 135

concordance is only 50% between monocygotic twins

chanc eof inheriting diabetes is only ~5%

90% of type 1 diabetics have no relative affected

there is an association with the HLA locus at HLADR, 3, 4 and HLA DQ - these are important but not causative or sufficient.

at least 1 allele of DR3 or DR$ is present in 90-95% of caucations with DM1 and it is 50% in the general population.

Front 136

what autoimmune markers may be important in DM1

Back 136

antbody to insulin (IAA)
glutamic acid decarboxylase (GAD)
tryrosine phosphatase (IA-2)

Front 137

name a gene involved in obesity

Back 137

mutations in gene coding for MCR-4receptor or stop codon of leptin

Front 138

list some endocrine conditions that lead to weight gain?

Back 138

hyperinsulinaemia
DM2
acromegaly
cushing's disease/syndrome
hypothyroidism
raised prolactin

Front 139

what is the signal for insulin secretion from pancreatic beta cells?

Back 139

blood glucose > 5mM

Front 140

what is the primary role of insulin?

Back 140

to stimulate the use and storage or carbohydrates by promoting the synthesis of macromolecular fuel stores such as glycogen and lipids

Front 141

t/f. Insulin is pleiotropic.

Back 141

true. this is because it has effects within the nucleus of cells too affecting a wide variety of cellular processes

Front 142

what happens, with regards to insulin, after a meal?

Back 142

the blood glucose rises above 5mM stimulating pancreatic beta cells to secrete insulin.
the insulin then binds to its receptor forming a complex --> this stimulate the phosphorylation of signalling proteins within the cell.
these proteins modulate enzyme activity - in different ways in different tissues ---> causing the storage of energy in different forms in the liver, adipocytes and muscle.

Front 143

when insulin is stimulated by a rise in glucose what effect does this have in the muscles and adipose tissue?

Back 143

Golgi vesicles are stimulated to deposit GLUT4 on the cell surface --> this increases the rate of glucose transport.

Front 144

what is special about the liver and glucose transport?

Back 144

unlike in muscles and adipose tissue glucose transporters (such as GLUT 4 in the above tissues) do not need to be stimulated and recruited to the cell surface.

Front 145

what prevents the breakdown of carbohydrates and lipid stores with respect to insulin?

Back 145

cells binding to insulin decreased the concentration intracellularly of cAMP this prevents breakdown.

Front 146

what increases the amount of leptin in the body?

Back 146

high insulin, high glucocorticoids and increased nutritional intake

Front 147

name a gene involved in obesity

Back 147

mutations in gene coding for MCR-4receptor or stop codon of leptin

Front 148

list some endocrine conditions that lead to weight gain?

Back 148

hyperinsulinaemia
DM2
acromegaly
cushing's disease/syndrome
hypothyroidism
raised prolactin

Front 149

what is the signal for insulin secretion from pancreatic beta cells?

Back 149

blood glucose > 5mM

Front 150

what is the primary role of insulin?

Back 150

to stimulate the use and storage or carbohydrates by promoting the synthesis of macromolecular fuel stores such as glycogen and lipids

Front 151

t/f. Insulin is pleiotropic.

Back 151

true. this is because it has effects within the nucleus of cells too affecting a wide variety of cellular processes

Front 152

where is leptin synthesized?

Back 152

in the subcutaneous adipocytes mainly. more so than the visceral/omental adipocytes

Front 153

what is the role of leptin?

Back 153

plays a role in protection from starvation and in regulating T cell number and function

Front 154

what is the recommended intake of saturated fats and poly unsaturated fats?

Back 154

saturated fates is <10% of daily caloric intake
poly unsaturated is less than the % of saturated fat intake.

Front 155

what is an exchanger in the diet?

Back 155

not used anymore it represents a portion of food with 15g of carbohydrates.

Front 156

t/f. linoleic acid increases LDL in the body, this effect is not as bad with omega3 alpha-linoleic acid

Back 156

FALSE> linoleic acid is the most potent way to lower LDL and it is less effective in the omega 3 form

Front 157

what is the metabolic syndrome?

Back 157

also know as syndrome X it is associated with abdominal adipocity and may be related to insulin resistance. it represents increased hepatic glucose output, insulin resistance coupled with a defect in insulin secretion --> leads to impaired glucose tolerance and/or DM

Front 158

what is the first line drug treatment in type 2 DM

Back 158

metformin

Front 159

what is the second line drug treatment in DM2

Back 159

glitazones

Front 160

what is the mechanims of a sulphonylruea?

Back 160

it potentiates glucose stimulated insulin release by combining with its receptor on thebeta cell causing a depolarisation and therefore stimulation of insulin.

tends to stimulate appetite so is not recommended in obese patients

Front 161

what is the mechanism of action of biguanides

Back 161

an example is metformin.
increases glucose uptake into skeletal muscle and fat and surpresses appetite. 'it also decreases intestinal absorption of glucose and decreases gluconeogenesis

Front 162

what is a contra indication to metformin use?

Back 162

because it is excreted 100% by the kidneys it accumulates in renal failure
may cause a lactic acidosis which can be life threatening

Front 163

what is 'acarbose'?

Back 163

it is an alpha-glucosidase inhibitor.
it inhibits the enzyme that breaks down carbs and sugars so to decrease the amount of glucose available for absorption.

if often used in combination with other insulin related drugs such as metformin or sulphonylureas

Front 164

what is the mechanism of action of Glitazones?

Back 164

this is a thiazolidinedione
it acts on peroxisome proliferator receptors in fat cells. and efficetively lowers glucose however causes weight gain.

some indication it is linked to peripheral limb fractures in post menopausal women.

Front 165

what is periodontitis?

Back 165

it is a chronic bacterial infection of the supporting structures of the teeth.
common in diabetic patients.

Front 166

what product is implicated in the mechanism of chronic periodontitis?

Back 166

advanced glycation end-products (AGEs) which increase collagen X linking, alter the vascular walls and thicken capillary BM

Front 167

what are the 4 phases of intercourse?

Back 167

excitement
plateau
orgasm
resolution

Front 168

what are the two main functions of the testes?

Back 168

spermatogenesis and steroidgenesis (androgens)

Front 169

what is testosterone secretion regulated by?

Back 169

LH from the pituitary

Front 170

what controls the secretion of LH from the pituitary?

Back 170

GnRH

Front 171

where is FSH secreted from?

Back 171

the anterior pituitary?

Front 172

how do you describe the secretion of FSH

Back 172

pulsatile and under negative feedback from inhibin beta seccreted by mature sertoli cells.

Front 173

what are some hypothalamus related pathologies causing male infertility

Back 173

failure of GnRH stimulation of the pituitary LH and FSH
failure of testes to produce testosterone
Kallmann's syndrome: mutation of KAL gene causing failure of GnRH ceurons to migrate from the olfactory placode to the hypothalamus
severe weight loss --> hypotha dysfunction
anabolic steroids
tumour desrtoying GnRH
etc.

Front 174

what feedback system regulates LH secretion?

Back 174

negative feedback lop with testosterone production

Front 175

what are the normal figures in semen analysis

Back 175

15million sperm/ml
>40% with forward progression
>4% normal function
>58% alive
pH 7.2

Front 176

what does oligozoospermia mean?

Back 176

abnormal concentration of sperm

Front 177

what does asthenozoospermia mean?

Back 177

abnormal motility

Front 178

what does teratozoospermia mean

Back 178

morphological abnormalities

Front 179

what does globozoospermia mean?

Back 179

all sperm lacking an acrosome

Front 180

what are some exogenous causes of decreased fertility in men?

Back 180

genital infection
alcohol
smoking >40 cigarettes a day
left varicocele
exposure to toxins within 2 years

Front 181

what is fecundability?

Back 181

normal is around 20% - and that is the chance of getting pregnant in each months

Front 182

what is the fecundability of a couple who have not concieved after 2 years of trying?

Back 182

likely to be <5%

Front 183

what are some female causes of infertility?

Back 183

a blockage
endometriosis
female age - sterility precedes the menopause by up to 10 years

Front 184

for an amenorrhagic women what fertility test would be performed and why?

Back 184

a progestergen challenge test:
a positive test is vaginal bleeding after ceasing the progestogens within a few days and indicates chronic anovulation as the cause

a negative test will indicate a hypo-pituitary cause or if the FSH is high organ failure

Front 185

how many ova are created as the female genitalia rapidly develop?

Back 185

up to 7 000 000. however most degenerate

Front 186

t/f. at 6 weeks gestation the female and male genitalia are distinct looking and can be differentiated.

Back 186

false. they will appear identical containing mesonephritic and paramesonephritic ducts (without testosterone the meonephritc duct disappears)

they will appear identical as late as 12 weeks

Front 187

what does the paramesonephritic duct become in females?

Back 187

the upper part of the 2 ducts becomes the uterine tubes and the lower half becomes the uterus and upper vagina

note: the lower vagina has a different morphological origin to the rest of the genital tract.