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Fundamentals of P > Diabetes and Hypoglycaemia > Flashcards

Diabetes and Hypoglycaemia Flashcards

1
Q

How are blood glucose levels maintained

A

dietary carbohydrate
glycogenolysis
gluconeogenesis

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2
Q

Liver’s role in regulating glucose

A

after meals - stores glucose as glycogen

during fasting - makes glucose available through glycogenolysis and gluconeogenesis

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3
Q

Insulin function in adipose tissue

A

↑Glucose uptake
↑Lipogenesis
↓Lipolysis

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4
Q

Insulin function in liver

A

↓Gluconeogenesis
↑Glycogen synthesis
↑Lipogenesis

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5
Q

Insulin function in striated muscle

A

↑Glycogen synthesis
↑Glucose uptake
↑Protein synthesis

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6
Q

Diabetes Mellitus - define

A

…..a metabolic disorder characterised by chronic hyperglycaemia, glycosuria and associated abnormalities of lipid and protein metabolism:

the hyperglycaemia results from increased hepatic glucose production and decreased cellular glucose uptake

blood glucose > ~ 10mmol/L exceeds renal threshold – glycosuria

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7
Q

Diabetes Mellitus - type I vs type II

A

Type 1:
Insulin secretion is deficient due to autoimmune destruction of β-cells in pancreas by T-cells

Type 2:
Insulin secretion is retained but there is target organ resistance to its actions

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8
Q

Diabetes Mellitus - secondary vs gestational

A

Secondary:
chronic pancreatitis, pancreatic surgery, secretion of antagonists

Gestational:
Occurs for first time in pregnancy

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9
Q

Type 1 DM - cause

A

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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10
Q

Type 1 DM - onset

A

Sudden onset (days/weeks)

Appearance of symptoms may be preceded by
‘prediabetic’ period of several months

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11
Q

In type I DM circulating autoantibodies to various -cell antigens against:

A

glutamic acid decarboxylase
tyrosine-phosphatase-like molecule
Islet auto-antigen

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12
Q

HLA class II in type I DM

A

HLA class II cell surface present as foreign and self antigens to T-lymphocytes to initiate autoimmune response

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13
Q

Most common antibody in type I DM

A

The most commonly detected antibody associated with type 1 DM is the islet cell antibody

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14
Q

Destruction of pancreatic ß-cell causes

A

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

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15
Q

Amylin - function

A

Amylin, a glucoregulatory peptide hormone co-secreted with insulin.

lowers blood glucose by slowing gastric emptying, & suppressing glucagon output from pancreatic cells.

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16
Q

Effect of insulin deficiency in type I DM

A

INSULIN
DEFICIENCY → Hyperglycemia (leads to glycosuria) → Glycosuria → Polyuria → Volume depletion (polydipsia) = diabetic coma

INSULIN DEFICIENCY → Increased
lipolysis → Increased free fatty acids (FFA) → Increased FFA oxidation (liver) → Ketoacidosis
(DKA) = diabetic coma

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17
Q

Type 2 DM- Presentation:

A

Slow onset (months/years)

Patients middle aged/elderly – prevalence increases with age

Strong familiar incidence

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18
Q

Type 2 DM - pathogenesis

A

Pathogenesis uncertain – insulin resistance; β-cell dysfunction:

may be due to lifestyle factors - obesity, lack of exercise

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19
Q

Metabolic complications of Type 2 DM

A

Hyper-osmolar non-ketotic coma (HONK)
[Hyperosmolar Hyperglycaemic State (HHS)]

Development of severe hyperglycaemia

Extreme dehydration

Increased plasma osmolality

Impaired consciousness

No ketosis

Death if untreated

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20
Q

Diagnosis, Type 2 DM, in presence of symptoms

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

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21
Q

Diagnosis, Type 2 DM, in absence of symptoms

A

In the absence of symptoms:

test blood samples on 2 separate days

22
Q

Compare IGT vs IFG classification

A

IGT – impaired glucose tolerance
IFG – impaired fasting glycaemia

If impaired fasting glycaemia = increased risk of developing diabetes + developing cardiovascular disease is also increased

but this seems to be lower than if you have pre-diabetes (impaired glucose tolerance)

23
Q

OGTT should be carried out when

A

OGTT should be carried out:

in patients with IFG

in unexplained glycosuria

in clinical features of diabetes with normal plasma glucose values

24
Q

OGTT - process

A

75g oral glucose and test after 2 hour

Blood samples collected at 0 and 120 mins after glucose

Subjects tested fasting after 3 days of normal diet containing at least 250g carbohydrate

25
Q

Metformin - type II DM treatment
↑
↓

A

↓ gluconeogenesis and ↑ peripheral utilisation of glucose;

effective if residual functioning beta cells as acts only in presence of insulin

Helps respond better to own insulin, lower the amount of sugar created by the liver, and decreasing the amount of sugar absorbed by the intestines.

26
Q

Sulphonylureas - type II DM treatment

A

Stim the cells in the pancreas to make more insulin

They also help insulin to work more effectively in the body.

Dipeptidyl peptidase inhibitor (DPP-4; Gliptins): inhibitors work by blocking the action of DPP-4, an enzyme which destroys the hormone incretin.

27
Q

Incretins - type II DM treatment

A

Help the body produce more insulin only when it is needed

and reduce the amount of glucose being produced by the liver when it is not needed

28
Q

Monitoring glycaemic control - aim

A

Aim: to prevent complications or avoid hypoglycaemia

29
Q

Self-monitoring - describe types

A

Capillary blood measurement

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

30
Q

Long term complications in DM

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

Exact mechanisms of complications are unclear

31
Q

Hypoglycaemia - define

A

Defined as plasma glucose < 2.5 mmol/L

32
Q

Causes of hypoglycaemia + prevalence in types of DM

A

Drugs are the most common cause;

common in type 1 diabetes

Less common in type 2 diabetes taking insulin & insulin secretagogues

uncommon in patients who do not have drug treated DM:

33
Q

Why hypoglycaemia uncommon in pt w/DM that is not drug treated

A

In these patients hypoglycaemia may be caused by alcohol, critical illnesses such as hepatic, renal or cardiac failure, sepsis, hormone deficiency, inherited metabolic dx.

34
Q

Sulfonylureas - examples

A

Exogeneous insulin & insulin secretagogues such as glyburide, glipizide and glimepiride are examples of some of the more commonly used sulfonylureas.

35
Q

Stimulation of endogenous insulin - effect

A

Stimulation of endogenous insulin suppresses hepatic and renal glucose production and increase glucose utilisation

36
Q

List type II DM drugs that should not cause hypoglycaemia

A

Among drugs used to treat type 2 diabetes earlier in the disease, insulin sensitizers (metformin, Glitazones); glucosidase inhibitors; glucagon-like pepdide-1 (GLP-1) receptor antagonist and DDP-4 inhibitors should not cause hypoglycaemia.

37
Q

Drugs that cause hypoglycaemia

A

Drugs such as alcohol may cause hypoglycaemia;

Other drugs most commonly found to cause hypoglycaemia are quinolone, quinine, beta blockers, ACE inhibitors and IGF-1

38
Q

Hypoglycaemia in patients without diabetes - list

A

Endocrines disease; e.g. cortisol disorder

Inherited metabolic disorders, e.g. hereditary fructose intolerance.
Insulinoma

Others: severe liver disease, non-pancreatic tumours (beta cell hyperplasia), renal disease (metab. acidosis, reduced insulin elimination).

39
Q

Ethanol effect on glucose regulation

A

Ethanol: inhibit gluconeogenesis, but not glycogenolysis.

The hypoglycaemia will typically follow several days alcohol binge with limited food intake; resulting in hepatic depletion of glycogen.

40
Q

Sepsis effect on glucose regulation

A

Sepsis: relatively common cause of hypoglycaemia.

Cytokine accelerated glucose utilization and induced inhibition of gluconeogenesis in the setting of glycogen depletion

41
Q

CKD effect on glucose regulation

A

CKD: mechanism not clear, but likely to involve impaired gluconeogenesis, reduced renal clearance of insulin and reduce renal glucose production.

42
Q

Reactive hypoglycaemia - define

A

Also known as postprandial hypoglycaemia, drops in blood sugar are usually recurrent and occur within four hours after eating..

43
Q

Reactive hypoglycaemia - can occur in who

A

can occur in both people with and without diabetes,

thought to be more common in overweight individuals or those who have had gastric bypass surgery.

44
Q

Reactive hypoglycaemia - cause

A

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.

45
Q

Explain effect of plasma glucose level decline in fast state

A

When plasma glucose level decline in fast state pancreatic beta-cells secretion of insulin is decreased (1st defence);

hepatic glycogenolysis and gluconeogenesis is increased

there is reduced glucose utilisation of peripheral tissue, inducing lipolysis and proteolysis

46
Q

Counter-regulatory hormones function in response to hypoglycaemia

A

Counter-regulatory hormones are released:

Pancreatic alpha cells secrete glucagon to stimulate hepatic glycogenolysis (2nd defence)

Epinephrine release from adrenomedullary to stimulate hepatic glycogenolysis and gluconeogenesis; renal gluconeogenesis

If hypo is prolonged beyond 4 hours; cortisol and GH will support glucose production and limit utilisation.

47
Q

Epinephrine effect

A

Epinephrine has similar hepatic effect as glucagon; inhibits insulin secretion..

48
Q

Signs & Symptoms of hypoglycaemia - categories

A

Neurogenic (autonomic)

Neuroglycopaenia

49
Q

Neurogenic (autonomic) symptoms - describe characteristics

A

Neurogenic (autonomic):

triggered by falling glucose levels

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

50
Q

Neuroglycopaenia symptoms - describe characteristics

A

Neuroglycopaenia:

Due to neuronal glucose deprivation.

Sign &amp; symptoms include:
 confusion, 
difficulty speaking, 
ataxia, 
paresthesia, 
seizures, 
coma, 
death

Fundamentals of P (62 decks)

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