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molecular basis of disease > Diabetes and hypoglycemia > Flashcards

Diabetes and hypoglycemia Flashcards

1
Q

How are glucose levels maintained?

A
  • dietary carbohydrate
  • glycogenolysis
  • gluconeogenesis
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2
Q

What metabolic changes occur in fed state?

A
  • when you eat a meal
  • insulin levels increase
  • liver glucose production decreases
  • peripheral catabolism decreases
  • peripheral uptake increases
  • liver nutrients uptake increases
  • decrease in catabolism
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3
Q

What metabolic changes occur in fasting state?

A
  • insulin levels decrease
  • liver gluconeogenesis
  • plasma glucose levels increase
  • peripheral uptake decreases
  • lipolysis/ proteolysis increases
  • increase in catabolism
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4
Q

Why is it important to have plasma glucose regulation?

A
  • enough glucose to fuel the body , specially the brain

- too high plasma glucose can cause pathological changes in cells

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5
Q

What happens at high glucose levels?

A
  1. promotes beta cells in pancrease to release insulin
  2. insulin stimulates glucose uptake from blood into muscle and adipose tissue
  3. this will lower blood glucose levels
  4. glucose -> glycogen for storage
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6
Q

What happens at low glucose levels?

A
  1. promotes glucagon release from alpha cells in pancreas
  2. Glucagon stimulates glycogen -> glucose breakdown in the liver
  3. this will increase blood glucose levels
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7
Q

What is the role of insulin in the adipose tissue?

A
  • increase glucose uptake
  • increase lipogenesis
  • decrease lipolysis
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8
Q

What is the role of insulin in striated muscles?

A
  • increase glucose uptake
  • increase glycogen synthesis
  • increase protein synthesis
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9
Q

What is the role of insulin liver?

A
  • decrease glucogenesis
  • increase glycogen synthesis
  • lipogenesis
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10
Q

What is diabetes mellitus?

A
  • a metabolic disorder characterised by chronic hyperglycemia, glycouria and associated abnormalities of lipid and protein metabolise,
    Prevalence:
  • globally 422 million people have diabetes
    -In UK 2018 ~ 3.8 million diagnosed with DM
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11
Q

What are classifications of diabetes?

A
  1. type 1 : deficiency in insulin secretion
  2. type 2: insulin secretion is retained but there is target organ resistance to its actions
  3. secondary: chronic pancreatitis, pancreatic surgery, secretion of antagonists
  4. Gestational: Occurs for first time in pregnancy
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12
Q

Type 1 diabetes

A
  • predominantly in children and young adults
  • sudden onset
  • appearance of symptoms may b preceded by ‘prediabetic’ period of several months
  • commonest cause is autoimmune destruction of B- cells;
    => interaction between genetic and environment factors.
    => strong link with HLA genes within the MHC region on chromosome 6.
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13
Q

What are pathogenesis of type 1 DM?

A

Destruction of B-cells starts with autoantigen formation
- autoantigens are presented to T-lymphocytes to initiate autoimmune response
- there would be circulating autoantibodies to various- cell antigens against glutamic acid decarboxylase :
=> tyrosine -phosphatase -like molecule
=> islet auto-antigen
-the most commonly detected antibody associated with type 1 DM is the islet cell antibody.

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14
Q

How does destruction of pancreatic beta cell lead to hyperglycemia?

A
  • destruction of pancreatic beta cell causes hyperglycemia due to absolute deficiency if both insulin and amylin.
  • amylin is glucoregulatory peptide hormone co-secreted with insulin
  • lowers blood glucose by slowing gastric emptying, & suppressing glucagon output from pancreatic cells.
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15
Q

what are metabolic complications of type I diabetes?

A
  • insulin deficiency will lead to increased plasma glucose levels = hyperglycemia
  • due to hyperglycemia polyphagia (excessively eating)
  • glycosuria = due to there being excess glucose, kidney is not able to filter it all
  • polyuria = more water gets into kidney
  • volume depletion = due to polyuria
  • polydipsia = body tries to compensate by drinking more water.
  • diabetic coma
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16
Q

how does insulin deficiency lead to ketoacidosis?

A
  • increased lioplysis
  • increased free fatty acids (FFAs)
  • increase FFA oxidation (liver)
  • ketoacidosis
17
Q

Type 2 diabetes

A
  • slow onset
  • patients middle aged/elderly prevalence
  • strong familiar incidence
  • pathogenesis uncertain - insulin resistance; beta cell dysfunction
18
Q

What is pathophysiology of type 2 diabtetes?

A
  • genetic predisposition and lifestyle factors can lead to insulin resistance
  • compensatory eta cell hyperplasia
  • beta cell failure (early) = impaired glucose tolerance
  • beta cell failure (late) = diabetes.
19
Q

What are metabolic complications of type 2 diabetes?

A 
-low insulin leads to 
=> increased gluconeogenesis 
=>glycogenolysis 
-this leads to hyperglycemia 
=>glucosuria
=>osmotic diuresis 
=>loss of water and electrolytes (increased blood viscosity =thrombosis)
=> dehydration
20
Q

how do you diagnose diabetes?

A
  1. In the presence of symptoms:
    (polyuria, polydipsia, & weight loss for type 1)
    => random plasma glucose >/= 11.1 mmol/l(200mg/dl)
    => fasting plasma glucose >/= 7.0 mmol/l (126 mg/dl) fasting is defined as no caloric intake for at least 8 hrs
    =>oral glucose tolerance test(OGTT) - plasma glu >/=11.1 mmol/l
  2. In the absence of symptoms:
    =>test blood samples on 2 separate days.
21
Q

How do you diagnose pre-diabetes?

A
  1. impaired glucose tolerance (IGT)

2. impaired fasting glycaemia (IFG)

22
Q

How is oral glucose tolerance test carried out?

A
  1. to check body’s ability of metabolising glucose
    - in patients with IFG
    - in unexplained glycosuria
    - in clinical features of diabetes with normal plasma glucose values
  2. 75g oral glucose and test after 2 hour
  3. blood samples collected at 0 and 120 mins after glucose.
23
Q

What are treatments for T2D stepwise?

A
  1. diet and exercise
  2. oral monotherapy
    - metformin
  3. oral combination
    - sulphonylureas
    - gliptins
    - GLP- 1 analogues
  4. insulin + oral agents.
24
Q

What is the aim of monitoring glycemia?

A
  • to prevent complications or avoid hypoglycemia
    1. self -monitoring to be encouraged:
  • capillary blood measurement
  • urine analysis : glucose in urine gives indication of blood glucose concentration above renal threshold
25
Q

What is the aim of monitoring glycemia?

A
  • to prevent complications or avoid hypoglycemia
    1. self -monitoring to be encouraged:
  • capillary blood measurement
  • urine analysis : glucose in urine gives indication of blood glucose concentration above renal threshold
    2. 3-4 months: blood HbA1c (glycated Hb; covalent linkage of glucose of residue in Hb.
    others: urinary albumin (index of risk of progression to nephropathy)
26
Q

What are long term complications of type 1 and type 2 diabetes?

A
  1. occur in both T1D and T2D
  2. micro-vascular disease
    - retinopathy
    - nephropathy
    - neuropathy
  3. macro-vascular disease
    - related to atheroscelerosis heart attack/stroke
  4. exact mechanisms of complications are unclear.
27
Q

Define hypoglycaemia

A

-plasma glucose <2.5 mmol/L in both diabetic and non diabetic patients.

28
Q

What are causes of hypoglycemia?

A

Drugs are most common cause

-more common in T1D than T2D

29
Q

What are some common insulin secretagogues used in sulfonylureas that cause hypoglycemia?

A
  1. glyburide
  2. glipizide
  3. glimepiride
    => used to treat type 2 diabetes
30
Q

What causes hypoglycemia in patients without diabetes?

A
  1. drugs such as alcohol
    - quinolone, quinine, beta blockers, ACE inhibitors and IGF-1
  2. endocrine disease: eg. cortisol disorder
  3. inherited metabolic disorders, eg: heriditary fructose intolerance
  4. insulinoma (tumour)
31
Q

How does ethanol cause hypoglycemia?

A
  • inhibits glucogenesis
    -but not glycogenolysis
    (several days of alcohol binge and limited food intake will result in hepatic depletion of glycogen)
32
Q

How does sepsis lead to hypoglycemias?

A

cytokines accelerated glucose utilisation and induced inhibition of gluconeogenesis in the setting of glycogen depeletion.

33
Q

How does CDK lead to hypoglycemias?

A

-mechanism not clear, but likely to involve impaired gluconeogenesis, reduced renal glucose production.

34
Q

What is reactive hypoglycemia (aka postprandial hypoglycemia)

A

=> drop in blood sugar are usually recurrent and occur within 4hrs after eating.
=> cause is unclear but could possibly be:
- benign tumour in the pancreas leading to overproduction of insulin
-too much glucose used up in tumour
- deficiencies in counter-regulatory hormones eg: glucagon.

35
Q

What is the counter-regulatory response to hypoglycemia?

A
  1. brain : needs glucose for function so low levels are sensed by hypothalmus and activates the autonomic nervous system.
  2. ANS stimulates b cells in pancreas to decrease insulin production to decrease glycolysis.
  3. ANS stimulates alpha cells to increase glucagon production for glycogen -> glucose.
  4. ANS causes the adrenal gland to increase cortisol levels and noradrenaline levels will stimulate gluconeogenesis and glycolysis in liver.
36
Q

What are signs and symptoms of hypoglycemia?

A
  1. neurogenic (autonomic)
    - triggered by falling glucose levels
    - activated by ANS & mediated by sympathoadrenal release of catecholamines and Ach
37
Q

What is neuroglycopenia and what are signs and symptoms?

A
  • due to neuronal glucose deprivation

symptoms:
- confusion, difficulty speaking, ataxia, paresthesia, seizures, coma, death.

molecular basis of disease (29 decks)

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