Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

endocrinology lectures phase 2 > intro to diabetes > Flashcards

intro to diabetes Flashcards

1
Q

where does glucose come from in the fasting state

A

all glucose comes from the liver (and a bit from kidney)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how do you get glucose in the fasting state

A

breakdown of glycogen

gluconeogenesis - uses 3 carbon precursors - lactate, alanine and glycerol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

which cells is glucose delivered to in the fasting state

A

insulin indepdent tissues

brain

red blood cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

are insulin levels low or high in the fasting state

A

low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what does muscle use for fuel in the fasting state

A

FFA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

in the fasting state are processes sensitive to insulin?

A

some processes are very sensitive to insulin, even low insulin levels prevent unrestrained breakdown of fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what happens after feeding

A

postprandial state

there is a physiological need to dispose of a nutrient load

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

when does glucose rise

A

5-10 mins after eating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what does rising glucose stimulate

A

stimulates insulin secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

where does ingested glucose

A

40% goes to the liver

60% goes to the periphery - mostly muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what do high insulin and glucose levels cause

A

they suppress lipolysis and levels of non-esterified fatty acids fall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the site of insulin and glucagon secretion the endocrine pancreas

A

islets of langerhans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what do beta cells do

A

secrete insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what do alpha cells do

A

secrete glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what do delta cells do

A

paracrine ‘crosstalk’ between alpha and beta cells is physiological

ie local insulin release inhibits glucagon

an effect lost in diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

insulin action in muscle and fat cells

A
  • insulin receptor
  • intracellular signalling cascades
  • glut 4 vesicle mobilisation to plasma membrane
  • glucose entry into cell via GLUT 4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are hormonal regulators of carbohydrate metabolism

A

insulin

counterregulatory hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

give examples of counterregulatory hormones

A

glucagon, adrenaline, cortisol, growth hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how does insulin regulate carbohydrate metabolism

A

suppresses hepatic glucose output
- decrease glycogenolysis
- decrease gluconeogenesis

increases glucose uptake into insulin-sensitive tissues (muscle fat)

suppresses
- lipolysis
- breakdown of muscle

20
Q

how does glucagon regulate carbohydrate metabolism

A

increases hepatic glucose output
- increase glycogenolysis
- increase gluconeogenesis

reduce peripheral glucose uptake

stimulate peripheral release of gluconeogenic precursors (glycerol, AAs)
- lipolysis
- muscle glycogenolysis and breakdown

21
Q

define diabetes mellitus

A

a disorder of carbohydrate metabolism characterised by hyperglycaemia

22
Q

how does diabetes mellitus cause morbidity and mortality

A
  1. acute hyperglycaemia - untreated can lead to acute metabolic emergencies diabetic ketoacidosis (DKA) and hyperosmolar coma
  2. chronic hyperglycaemia - leading to tissue complications
  3. side effects of treatment - hypoglycaemia
23
Q

what serious complications is diabetes associated wirh

A
  1. diabetic retinopathy
  2. stroke
  3. diabetic nephropathy
  4. cardiovascular disease
24
Q

6 types of diabetes

A
  1. type 1
  2. type 2
  3. maturity onset diabetes of youth (MODY)
  4. pancreatic diabetes
  5. endocrine diabetes
  6. malnutrition related diabetes
25
pathogenesis of type 1 diabetes
- an insulin deficiency disease characterised by loss of beta cells due to autoimmune destruction - beta cells express antigens of HLA histocompatibility system perhaps in response to an environmental event - activates a chronic cell mediated immune process leading to chronic insulitis
26
what does failure of insulin secretion lead to
- continued breakdown of liver glycogen - unrestrained lipolysis and skeletal muscle breakdown providing gluconeogenic precursors - inappropriate increase in hepatic glucose output suppression of peripheral glucose uptake
27
what does rising glucose concentration result in
increased urinary glucose losses as renal threshold (10mM) is exceeded
28
what does failiure to treat type 1 diabetes with insulin lead to
- increase in circulating glucagon (loss of local increases in insulin within the islets leads to removal of inhibition of glucagon release), further increasing glucose - perceived stress leads to increased cortisol and adrenaline - progressive catabolic state and increasing levels of ketones
29
aetiology of type 2 diabetes
impaired insulin secretions and insulin resistance leads to impaired glucose tolerance
30
what does impaired insulin action in type 2 diabetes lead to
- reduced muscle and fat uptake after eating - failure to suppress lipolysis and high circulating FFAs - abnormally high glucose output after a meal
31
describe ketone production in type 2 diabetes
even low levels of insulin prevent muscle catabolism and ketogenesis so profound muscle breakdown and gluconeogenesis are restrained and ketone production is rarely excessive
32
effects of absent insulin secretion in type 1 diabetes
no hepatic insulin effect no muscle/fat insulin effect leads to unrestrained glucose and ketone production hyperglycemia + raised plasma ketone leads to impaired glucose clearance + muscle/fat breakdown leads to glycosuria/ketonuria
33
pathophysiology of type 1 diaberes
severe insulin deficnecy due to autoimmune destruction of beta cell
34
pathophysiology of tyoe 2 diabetes
insulin resistance and impaired insulin secretion due to a combination of genetic predisposition and environmental factors
35
principles of treatment for diabetes
- control of symptoms - prevention of acute emergencies, ketoacidosis, hyperglycaemia hyperosmolar states - identification and prevention of long term microvascular complications -HbA1c 50mmol/mol
36
real life treatment of type 2 diabetes
weight loss and excercise if substantial will reverse hyperglycaemia also management usually consists of medication to control BP, blood glucose and lipids
37
what does sulphonylureas do
stimulate insulin release by binding to B cell receptors improves glycaemic control at the expense of weight gain but can cause hypoglycaemia
38
what does thiazolidinediones do
bind to the nuclear receoptor PPAARy activate genes concerned with glucose uptake and utilisation and lipid metabolism improves insulin sensitivity need insulin for a therapeutic effect
39
what would an ideal drug in type 2 diabetes do
- reduce appetite and induce weight loss - preserve b cells and insulin secretion - increase insulin secretion at meal time - inhibit counterregulatory hormones which increase blood glucose such as glucagon - not increase the risk of hypoglycaemia during treatment
40
when and where is GLP-1 secreted
upon ingestion of food From L cells in the intestine
41
modes of action of GLP-1
- stimulates insulin secretion - suppresses glucagon secretion - slows gastric emptying - reduces food intake - increases B cell mass and maintains B cell function - improves insulin sensitivity - enhances glucose disposal
42
what do SGLT2 inhibitors do
block the reabsoptriyon of glucose in the kidneys increase glucose exctreion lower blood glucose levels
43
first line of oral agents
metformin
44
why doesnt DKA occur in type 2 diabetes
its rare becausr the low insulin leveks are sufficein to suppress the catabolism and prevent ketogeneiss
45
why does obesity cause type 2 diabetes
obiesty imparies insulin action
46
why does insulin secretion becoe impared in type 2 diabetes
possibly related to - genetic predeposition - glucotoxicity hyperglycaemia inhibits insulin secretion main factor is lipid deposition in the pancreatic islets which prevent normal secretion of insulin

endocrinology lectures phase 2 (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions