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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)

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2
Q

how do you get glucose in the fasting state

A

breakdown of glycogen

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

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3
Q

which cells is glucose delivered to in the fasting state

A

insulin indepdent tissues

brain

red blood cells

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4
Q

are insulin levels low or high in the fasting state

A

low

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5
Q

what does muscle use for fuel in the fasting state

A

FFA

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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

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7
Q

what happens after feeding

A

postprandial state

there is a physiological need to dispose of a nutrient load

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8
Q

when does glucose rise

A

5-10 mins after eating

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9
Q

what does rising glucose stimulate

A

stimulates insulin secretion

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10
Q

where does ingested glucose

A

40% goes to the liver

60% goes to the periphery - mostly muscle

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11
Q

what do high insulin and glucose levels cause

A

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

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12
Q

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

A

islets of langerhans

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13
Q

what do beta cells do

A

secrete insulin

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14
Q

what do alpha cells do

A

secrete glucagon

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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

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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
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17
Q

what are hormonal regulators of carbohydrate metabolism

A

insulin

counterregulatory hormones

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18
Q

give examples of counterregulatory hormones

A

glucagon, adrenaline, cortisol, growth hormone

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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
Q

pathogenesis of type 1 diabetes

A
  • 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
Q

what does failure of insulin secretion lead to

A
  • 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
Q

what does rising glucose concentration result in

A

increased urinary glucose losses as renal threshold (10mM) is exceeded

28
Q

what does failiure to treat type 1 diabetes with insulin lead to

A
  • 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
Q

aetiology of type 2 diabetes

A

impaired insulin secretions and insulin resistance

leads to impaired glucose tolerance

30
Q

what does impaired insulin action in type 2 diabetes lead to

A
  • reduced muscle and fat uptake after eating
  • failure to suppress lipolysis and high circulating FFAs
  • abnormally high glucose output after a meal
31
Q

describe ketone production in type 2 diabetes

A

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
Q

effects of absent insulin secretion in type 1 diabetes

A

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
Q

pathophysiology of type 1 diaberes

A

severe insulin deficnecy due to autoimmune destruction of beta cell

34
Q

pathophysiology of tyoe 2 diabetes

A

insulin resistance and impaired insulin secretion due to a combination of genetic predisposition and environmental factors

35
Q

principles of treatment for diabetes

A
  • control of symptoms
  • prevention of acute emergencies, ketoacidosis, hyperglycaemia hyperosmolar states
  • identification and prevention of long term microvascular complications
    -HbA1c 50mmol/mol
36
Q

real life treatment of type 2 diabetes

A

weight loss and excercise

if substantial will reverse hyperglycaemia

also management usually consists of medication to control BP, blood glucose and lipids

37
Q

what does sulphonylureas do

A

stimulate insulin release by binding to B cell receptors

improves glycaemic control at the expense of weight gain

but can cause hypoglycaemia

38
Q

what does thiazolidinediones do

A

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
Q

what would an ideal drug in type 2 diabetes do

A
  • 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
Q

when and where is GLP-1 secreted

A

upon ingestion of food

From L cells in the intestine

41
Q

modes of action of GLP-1

A
  • 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
Q

what do SGLT2 inhibitors do

A

block the reabsoptriyon of glucose in the kidneys

increase glucose exctreion

lower blood glucose levels

43
Q

first line of oral agents

A

metformin

44
Q

why doesnt DKA occur in type 2 diabetes

A

its rare becausr the low insulin leveks are sufficein to suppress the catabolism and prevent ketogeneiss

45
Q

why does obesity cause type 2 diabetes

A

obiesty imparies insulin action

46
Q

why does insulin secretion becoe impared in type 2 diabetes

A

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)

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