Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Molecular Basis of Disease - SGUL (Sem 4) > Diabetes & Hypoglycaemia > Flashcards

Diabetes & Hypoglycaemia Flashcards

1
Q

How are blood glucose levels maintained

A
  • Dietary carbohydrates
  • Glycogenolysis
  • Gluconeogenesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Explain the FED state

A

When we eat there is an increase in blood glucose levels.
There is a rise in insulin levels to counter that increase.
There is less liver glucose production and increased liver nutrient uptake

  • Increased peripheral uptake
  • Decreased peripheral catabolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Explain the fasting state

A
  • Decreased insulin production
  • Increased liver gluconeogenesis
  • decreased peripheral uptake and increased lipolysis and proteolysis
  • Increased glucose production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the mechanism for when there is high blood sugar

A
  • Increased insulin release from the pancreas
  • Insulin stimulates glucose uptake from blood
  • Stimulates glycogen formation in the liver and glucose uptake in muscle and tissue cells
  • Lowers blood sugar
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the mechanism for when there is low blood sugar

A
  • Increased glucagon release from the pancreas
  • Glucagon stimulates glucose release into the blood
  • Stimulates glycogen breakdown in the liver
  • Increases blood sugar
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the effects of insulin on adipose tissue

A
  • Increased glucose uptake
  • Increased lipogenesis
  • Deceased lipolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the effects of insulin on striated muscle

A
  • Increased glucose uptake
  • Increased glycogen synthesis
  • Increased protein synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the effects of insulin on the liver

A
  • Decreased gluconeogenesis
  • Increased glycogen synthesis
  • Increased lipogenesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the function of insulin and what are its major metabolic pathways

A
  • Promotes storage - stimulates glucose storage in muscle, liver
  • Promotes growth - Stimulates protein and fatty acid synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the function of glucagon and what are its major metabolic pathways

A
  • Mobilises fuel - activates gluconeogenesis and glycogenolysis
  • Maintains blood glucose in fasting - activates fatty acid release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the function of Adrenalin and what are its major metabolic pathways

A
  • Mobilises fuels in
    stimulates - glycogenolysis; acute stress, stimulates fatty acid release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the function of cortisol and what are its major metabolic pathways

A
  • Changing long term - amino acid mobilization gluconeogenesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the function of growth hormone and what are its major metabolic pathways

A
  • Inhibits insulin action - stimulates lipolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is diabetes mellitus

A

A metabolic disorder characterised by chronic
hyperglycaemia, glycosuria and associated abnormalities of lipid and protein metabolism

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

What is the prevalence of DM

A
  • Globally 422 million people have diabetes (WHO, 2014); estimated to increase by 2035
  • In UK 2018 ~ 3.8 million diagnosed with DM.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the types of diabetes

A
  • Type 1: deficiency in insulin secretion
  • Type 2: Insulin secretion is retained but there is target organ resistance to its action
  • Secondary: chronic pancreatitis, pancreatic surgery, secretion of antagonist
  • Gestational: Occurs for first time in pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the characteristics of type 1 DM

A

Predominantly in children and young adults; but other
ages as well.

Sudden onset (days/weeks)

Appearance of symptoms may be 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.
18
Q

What is the 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

19
Q

What is the role of amylin in diabetes

A

More than 90% of newly diagnosed persons with type 1 DM have one or another of these antibodies.

Destruction of pancreatic ß-cell causes hyperglycaemia
due to absolute deficiency of both insulin & amylin:

  • Amylin, a glucoregulatory peptide hormone co-secreted
    with insulin.
  • lowers blood glucose by slowing gastric emptying, & suppressing glucagon output from pancreatic cells.
20
Q

Describe how insulin deficiency can cause Diabetic coma

A
  • Even with high blood sugar there is still a feeling of hunger therefore we eat more - Polyphagia
  • High blood glucose causes it to leak into urine in the kidneys - Glycosuria
  • Increased glucose concentration draws more water into the urine in the nephron causing more ruin and more frequent urination - Polyuria
  • Water leaving causes volume depletion and causes feelings of thirst and drinking more water to compensate - Polydipsia
  • If not able to keep up with volume depletion with drinking more water can lead to diabetic coma
21
Q

Describe how insulin deficiency can cause Ketoacidosis

A
  • Increased lipolysis to make glucose within cells
  • There is an increase in free fatty acids
  • Increased free fatty acid oxidation in the liver
  • Increased production of ketone bodies leading to ketoacidosis
22
Q

What are the characteristics of type 2 DM

A
  • Slow onset (months/years)
  • Patients middle-aged/elderly – prevalence increases
    with age
  • Strong familiar incidence
  • Pathogenesis uncertain - insulin resistance; β-cell dysfunction
23
Q

what is the pathophysiology of type 2 DM

A
  • Both genetic predisposition and Obesity lifestyle factors can cause Insulin resistance
  • Beta cells compensate by producing more insulin which results in temporary normoglycemia
  • When there is beta cell failure there is impaired glucose tolerance
  • Full beta cell failure leads to diabetes
  • Primary beta cell failure can cause diabetes straight away
24
Q

How do we diagnose diabetes

A

In the presence of symptoms: (polyuria, polydipsia & weight loss for Type I):

  • Random plasma glucose ≥ 11.1mmol/l (200 mg/dl ).
    OR
  • Fasting plasma glucose ≥ 7.0 mmol/l (126 mg/dl) Fasting is
    defined as no caloric intake for at least 8 h OR
  • Oral glucose tolerance test (OGTT) - plasma glu ≥ 11.1 mmol/l

In the absence of symptoms:

  • test blood samples on 2 separate days
25
Q

What is the Glycated Haemoglobin (HbA1c) test

A
  • Glycated haemoglobin (HbA1c) was initially identified as
    an “unusual” Hb
  • It reflects average plasma glucose over 8 to 12 weeks
  • It can be performed at any time of the day
  • Initially used as glycaemic control, but now used for
    diagnosis, ≥6.5% (48mmol/mol) is diagnostic for diabetes
  • However, HbA1c may be affected by a variety of
    genetic, haematologic disorders, e.g. haemoglobinopathies, certain anaemias, accelerated
    red cell turnover as with malaria
26
Q

What is IGT (pre-diabetes)

A

Impaired Glucose Tolerance (IGT):

  • Fasting plasma glucose >7mmol/L**
  • OGTT value of 7.8 – 11.1 mmol
27
Q

What is IFG (pre-diabetes)

A

Impaired Fasting Glycaemia (IFG):

  • Fasting plasma glucose 6.1 to 6.9 mmol/L,
  • OGTT value of < 7.8mmol/L
28
Q

What is the oral glucose tolerance test

A

OGTT should be carried out:

  • To check body’s ability of metabolizing glucose.
  • in patients with IFG
  • in unexplained glycosuria
  • in clinical features of diabetes with normal plasma
    glucose values.

75g oral glucose and test after 2 hour

Blood samples collected at 0 and 120 mins after
glucose

29
Q

How can we treat type 2 DM

A
  • Lifestyle changes
  • Drug treatments
30
Q

What are some drugs used to treat type 2 DM

A
  • Metformin: Increases insulin sensitivity, reduces hepatic glucose production
  • Sulfonylureas: stimulates the release of insulin, can cause hypoglycaemia
  • Thiazolidinediones: Increases insulin sensitivity, reduces hepatic glucose production
  • SGLT2 inhibitors: inhibit the reuptake of glucose
  • Incretin targeting drugs: DPP-4 inhibitors (prevent breakdown of natural incretins)
    GLP-1 agonist
31
Q

How do we monitor blood glucose concentration

A

Aim: to prevent complications or avoid hypoglycaemia

Self-monitoring to be encouraged:

  • Capillary blood measurement
  • Urine analysis: glucose in urine gives indication of blood
    glucose concentration above renal threshold

2-3 months: blood HbA1c (glycated Hb; covalent linkage of glucose to residue in Hb.

Others: urinary albumin (index of risk of progression
to nephropathy).

32
Q

What are the long term implication of diabetes

A

Occur in both type 1 and type 2 DM

Micro-vascular disease:

  • retinopathy
  • nephropathy
  • neuropathy

Macro-vascular disease:

  • related to atherosclerosis heart attack/stroke

The exact mechanisms of complications are unclear

33
Q

What is hypoglycaemia

A

Defined as plasma glucose of < 4.0 mmol/L:

  • Hypoglycaemia in diabetes
  • Hypoglycaemia in patients without diabetes
34
Q

What are the causes of hypoglycaemia

A
  • Drugs are the most common cause;
  • common in type 1 diabetes
  • Less common in type 2 diabetes taking insulin & insulin secretagogues
35
Q

What can cause hypoglycaemia in a patient with diabetes

A

Exogeneous insulin & insulin secretagogues such as glyburide, glipizide and glimepiride.

36
Q

What drugs an cause hypoglycaemia in patients without diabetes

A
  • alcohol, by inhibiting gluconeogenesis;
  • other drugs most commonly found to cause hypoglycaemia are quinolone, quinine, beta blockers, ACE inhibitors and IGF-
37
Q

What are other causes that can lead to hypoglycaemia in patients without diabetes

A
  • endocrines disease; e.g. cortisol disorder
  • inherited metabolic disorders, e.g. hereditary fructose intolerance.
  • Insulinoma
  • Sepsis, due to cytokine accelerated glucose utilization.
  • CKD
38
Q

What is reactive hypoglycaemia

A
  • Drops in blood glucose level after eating are. usually
    recurrent and occur within four hours after eating, (aka postprandial hypoglycaemia.)

Cause is unclear:

  • possibly a benign (non-cancerous) tumour in the pancreas
    may cause an overproduction of insulin,
  • too much glucose may be used up by the tumour itself
  • deficiencies in counter-regulatory hormones: e.g. glucagon.
39
Q

What are Neurogenic signs and symptoms of hypoglycaemia

A

triggered by falling glucose levels

activated by ANS & mediated by sympathoadrenal release
of catecholamines and Ach

  • Shaking
  • Cold sweats
  • Anxiety
  • Nausea
  • Palpitations
  • Numbness.
40
Q

What are Neuroglycopaenia signs and symptoms of hypoglycaemia

A

Due to neuronal glucose deprivation

Sign & symptoms include:

  • confusion,
  • difficulty speaking,
  • ataxia,
  • paresthesia,
  • seizures,
  • coma,
  • death

Molecular Basis of Disease - SGUL (Sem 4) (29 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions