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B8W4 > PBL 1 > Flashcards

PBL 1 Flashcards

1
Q

describe how glucagon interacts with its receptor?

A

it binds to G-protein coupled receptors in the liver which causes a conformational change that causes the G-protein within the cell to move and activate the adenylate cyclase. now ATP is converted to cAMP which can activate protein kinase A. this increases glycogen degradation, decreases glycogen synthesis, decreases glycolysis and increases gluconeogenesis

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2
Q

what happens when glucagon binds to adipose tissue?

A

stimulates the metabolism of TAG into fatty acids and glycerol

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3
Q

why does glucagon stimulate the production of fatty acids?

A

as they can be converted to ketone bodies which can be used as a source of fuel

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4
Q

what is glucagon’s effect on proteins?

A

it promotes metabolism to create amino acids which can help in gluconeogenesis

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5
Q

why doesn’t glucagon have any effect on skeletal muscle?

A

as they don’t have the correct receptor

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6
Q

what type of receptor is the insulin receptor?

A

a tyrosine kinase receptor

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7
Q

describe how insulin acts on its receptors?

A

2 insulin bind to the 2 alpha subunits which cause tyrosine kinase to phosphorylate the target protein within the cell to cause intracellular effects of insulin. this causes the glucose transporter to move to the cell surface membrane where it can acts as GLUT 2(liver) or GLUT4 (muscles and adipose tissue)

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8
Q

what are the effects of insulin?

A

glycogen synthesis, fat synthesis, protein synthesis, increases the expression of glucose transporters, promotes uptake of glucose into the liver and glycogenesis, amino acid absorbtion

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9
Q

when happens when glucose is converted to fats under the influence of insulin?

A

they can be packaged up as VLDLs and exported to adipose tissue

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10
Q

how does somatostatin regulate blood glucose?

A

it reduces gut motility and further absorption of nutrients
it also inhibits pancreatic exocrine secretions, suppresses the release of insulin, pituitary hormones, gastrin and secretin

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11
Q

where is somatostatin released from?

A

delta cells in islets in response to an increase in blood glucose and amino acids

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12
Q

how do gastrin and cholecystokinin regulate blood glucose levels?

A

GI tract releases these to stimulate the pancreas to secrete insulin in anticipation of absorption of nutrients

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13
Q

how do cortisol and adrenaline regulate blood glucose levels?

A

they increase blood glucose levels through glycogenolysis and suppressing the release of insulin

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14
Q

how does growth homrones regulate blood glucose?

A

by antagonising insulin (blood sugar levels stay high)

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15
Q

how does thyroxine regulate blood glucose?

A

it enhances the release of glucose from glycogen and enhances absorption of sugars from small intestine (increases blood glucose levels)

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16
Q

what is biguanides mechanism of action?

A

Lowers insulin resistance in skeletal muscle and liver through cAMP-mediated mechanisms- sensitizes the body to insulin.

Decrease glucose absorption in the intestines.
In the liver - decreases hepatic glucose by inhibiting gluconeogenesis and inhibiting glycogenolysis.
Sensitises body to insulin - increases uptake of glucose by skeletal muscle.

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17
Q

what is sulfonylureas mechanism of action?

A

Bind to ATP sensitive K+ channel on cell membrane of beta cells to prevent potassium efflux and electrical membrane potential becomes more positive.
Depolarisation opens voltage gates Ca2+ channels and rise in intracellular calcium leads to increased fusion of insulin granules within cell membrane. Increases insulin secretion.

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18
Q

what are thiazolidinediones mechanism of action?

A

PPAR gamma agonists which are insulin sensitizers
Modulate transcription of insulin sensitising genes.
Insulin sensitisers in liver, skeletal muscle, and adipose tissue.
Reduce HbA1c to approximately 1% (like metformin).
May have beta cell preservation effect.

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19
Q

what are GLP-1 receptor agonists mechanism of action?

A

they mimic the effects of incretin hormones to help lower post-meal blood sugar levels. They stimulate the release of insulin by the pancreas. These aren’t metabolised by the GPP-4 inhibitor, so it stays in the system for longer.

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20
Q

what are incretins?

A

a group of metabolic hormones that stimulate a decrease in blood glucose levels. e.g. GLP-1

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21
Q

what is DPP-4 enzyme inhibitor’s mechanism of action?

A

these mean GLP-1 is not metabolised and can stay in the system for longer

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22
Q

what are SGLT2 inhibitor’s mechanism of action?

A

SGLT2 is present in the proximal convoluted tubule in the kidney and is essential for reabsorption of glucose filtered through the glomeruli so blocking this transporter protein increases glucose excretion and the urine, reducing blood glucose concentrations.

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23
Q

what are the 4 types of diabetes?

A

type1
type 2
gestational
diabetes insipidus

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24
Q

what is gestational diabetes?

A

high blood sugar during pregnancy

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25
Q

what is diabetes insipidus?

A

when there’s low levels of ADH so you produce a large amount of urine and often feel thirsty

26
Q

what are some potential causes of insulin resistance?

A

genetics
family predisposition
bad eating habits
obesity

27
Q

what is insulin resistance?

A

the insulin receptors don’t work as effectively due to overstimulation or down-regulation of GLUT4 so we get high blood glucose levels

28
Q

describe how type 2 diabetes is an example of positive feedback?

A

as high blood glucose causes the pancreas to secrete more insulin even though levels are already high

29
Q

what are the effects of type 2 diabetes?

A

glucose is secreted out of the kidneys which results in osmotic diaresis which cause polyruea, losing water and electrlyes. this leads to dehydration and a hyperosmolar state. this dehydration stimulates the brain to drink more and eat more so regain the water and provide the glucose that the organs need.

30
Q

when might a type 2 diabetic have to go onto insulin injections

A

if, after a long time, beta cells atrophy due to the body not responding properly to insulin

31
Q

what are the symptoms of type 2 diabtes?

A

urinating more frequently, feeling thirstier, feeling more tired, unexplained weight loss, itching around the penis or vagina, cuts or wounds that heal slower, blurred vision

32
Q

what are some side efefcts of sulfonylureas?

A

hypoglycaemia, weight gain, headache, abdominal upset

33
Q

what are some side effects of thiazolidinediones?

A

weight gain, oedema and bone fractures

34
Q

what are some side efefcts of biguanide?

A

lactic acidosis, GI symptoms and B12 deficiency

35
Q

what are some reasons that certain groups might not go to the doctors?

A

because of stigmatisation of certain illnesses
gender issues
difficulty accessing services
language problems

36
Q

describe the relationship between social class and disease?

A

lower occupational groups are more vulnerable to all killer diseases

37
Q

describe the relationship between gender and disease?

A

men liver shorter lives
women are more likely to visit a doctor
women struggle the most from neurosis, psychossi, dementia and depressive disorders

38
Q

describe the relationship between ethnicity and disease?

A

Groups from India, Pakistan, and Bangladesh are more likely to die from heart disease that white population. This is due to poverty, stress of migration and racism, cultural deficit models.
One study has shown that between the ages of 60 to 70, ethnic minorities are 2x more likely than whites to have one of the four major chronic diseases specifically Diabetes, cancer, cardiovascular disease (CVD), and chronic lung disease.

39
Q

what are the principles of multidisciplinary team working?

A

identify a leader who gives clear direction
icorporate a set of values which are consistently portrayed
demonstrate a team culture of trust where all contributions are valued
ensure appropriate infrastructures are in place
provide patient-focussed services
utilise communication strategies
provide sufficient team stagging
recruit staff who demonstrate interdisciplinary competencies
promotes role interdependence and respect individual roles and autonomy
facilitate personal development through training

40
Q

how many of those with type 2 diabetes are overweight or have obesity?

A

90%

41
Q

why are those who are overwieght more likely to get type 2 diabetes?

A

abdominal fat causes fat cells to release ‘pro-inflammatory’ chemicals, cytokines and hormones which can make the body less sensitive to the insulin it produces by disrupting the insulin responsive cells and their ability to respond to insulin. (Induces insulin resistance)
obesity adds pressure on the body’s ability to properly control blood sugar levels through using insulin

42
Q

why can it be difficult to separate lifestyle risk and genetic risk for type 2 diabetes?

A

as lifestyle chices tend to run in the family e.g. parents with sedentry lives or unhealthy eating habits are likely to pass this on to their kids

43
Q

describe how TCF7L2 is associated with diabtes?

A

this gene makes you insensitive to incretin factors and so you produce insufficient amounts of insulin in response to blood glucose

44
Q

describe how ABCC8 is associated with diabetes?/

A

this gene provides instructions for making the sulfonylurea receptor 1 protein which controls the secretion of insulin out of the beta cells and into the blood. issues with this gene mean insulin is not released

45
Q

describe how CAPN10 is associated with diabetes?

A

it has a role in glucose metabolism and beta cell fucntion

46
Q

what is GLUT2?

A

a glucose transporter than helps move glucose into the pancreas

47
Q

what is GCGR?

A

the glucagon receptor involved in glucose regulation

48
Q

what is GLP-1?

A

glucagon like peptide 1

49
Q

what is GLP-1 action?

A

it slows stomach emptying
increase insulin production
and reduces glucose release from the liver

50
Q

what is statistical significance?

A

The strength of association gained from hypothesis testing. Implies that the difference seen in the sample also exists in the population.

51
Q

what is clinical significance?

A

Practical importance of a treatment effect - whether it has a real genuine, palpable, noticeable effect on daily life. It implies that the difference between treatments in effectiveness is clinically important and that clinical practice will change if such a difference is seen

52
Q

what are the Bradford Hill Criteria for?

A

a way of analysing any given association and assessing them for causation.

53
Q

what are the 9 Bradford Hill criteria?

A 
strength of association
temporal association
theoretical plausibility
consistency
coherence
specificity
dose-response relationship
analogy
experimental evidence
54
Q

what is ‘strength of association’ in the Bradford Hill criteria?

A

the larger the association, the more likely it is to be causal

55
Q

what is ‘temporal association’ in the Bradford Hill criteria?

A

the effect must occur after the cause

56
Q

what is ‘theoretical plausability’ in the Bradford Hill criteria?

A

there should be a plausible mechanism between cause and effect

57
Q

what is ‘consistency’ in the Bradford Hill criteria?

A

a relationship that is observed repeatedly is more likely to be causal

58
Q

what is ‘coherence’ in the Bradford Hill criteria?

A

the data should not seriously conflict with the generally known facts of the biology of the disease

59
Q

what is ‘specificity’ in the Bradford Hill criteria?

A

causation is likely if a very specific population at a specific site and disease with no other likely explanation

60
Q

what is ‘dose-response relationship’ in the Bradford Hill criteria?

A

greater exposure should generally lead to greater incidence of the effect

61
Q

what is ‘analogy’ in the Bradford Hill criteria?

A

if one virus causes a disease, it is plausible to say a similar virus might also cause a similar disease

62
Q

what is ‘experimental evidence’ in the Bradford Hill criteria?

A

is it possible to test it experimentall

B8W4 (7 decks)

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