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Dysfunction > DH > Flashcards

DH Flashcards

1
Q

During fasting how does the liver make glucose?

A

→Glycogenolysis: - breakdown of glycogen store to glucose

→ Gluconeogenesis:- making glucose from non-glucose sources, e.g. lactate, alanine, fatty acids

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2
Q

Which cells in the pancreas release glucagon?

A

→ alpha cells

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3
Q

What are the roles of insulin on adipose tissue?

A

→ glucose uptake
→ lipogenesis
→ reduced lipolysis

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4
Q

What is the effect of insulin on muscle?

A

→ increased glucose uptake
→ increased glycogen synthesis
→ increased protein synthesis

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5
Q

What is the role of insulin in the liver?

A

→ reduced gluconeogenesis
→ increased glycogen synthesis
→ increased liponeogenesis

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6
Q

What are the functions of adrenaline in metabolism?

A

→ Mobilises fuels in acute stress
→ stimulates glycogenolysis;

→ stimulates fatty acid release

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7
Q

What are the functions of cortisol on metabolism?

A

→ Changing long term
→ amino acid mobilization

→ gluconeogenesis

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8
Q

What are the functions of GH in metabolism?

A

→ Inhibits insulin action

→ stimulates lipolysis

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9
Q

Define diabetes

A

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

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10
Q

What are the 4 classifications of diabetes?

A

→ Type 1
→ Type 2: Insulin secretion is retained but there is target organ resistance to its actions

→ Secondary: chronic pancreatitis, pancreatic surgery, secretion of antagonists

→ Gestational

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11
Q

What is the most common cause of Type1 DM?

A

→ autoimmune destruction of B-cells

→ strong link with HLA genes within the MHC region on chromosome 6

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12
Q

Which demographic is Type 1DM predominant in?

A

→ children and young adults

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13
Q

Describe 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

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14
Q

What is the most commonly detected antibody associated with Type 1 DM?

A

→ the islet cell antibody

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15
Q

What are the three antigens that antibodies work against in Type 1 diabetes

A

→ glutamic acid decarboxylase (GAD);
→ insulin;
→ a tyrosine-phosphatase-like molecule

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16
Q

What is amylin?

A

→ 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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17
Q

What does amylin suppress?

A

→ glucagon output

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18
Q

What leads to ketoacidosis in Type 1 DM?

A

→ increased lipolysis
→ Increased free fatty acids (FFA
→ Increased FFA oxidation (liver

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19
Q

Describe the steps to diabetic coma

A 
→ Hyperglycemia
→ Glycosuria
→ Polyuria
→ Volume 
depletion
20
Q

What can lead to polyphagia?

A

→ hyperglycaemia

21
Q

What can lead to polydipsia?

A

→ Volume

depletion

22
Q

What are the presentations 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 can lead to HONK state?

A

→ increased gluconeogenesis

→ increased glycogenolysis

24
Q

What is involved in the diagnosis of HONK state?

A

→ increased glucose
→increased osmolarity
→ reduced pH

25
Q

What is involved in the diagnosis of diabetes in the presence of symptoms?

A

→ Random plasma glucose
→ Fasting plasma glucose
→ Oral glucose tolerance test (OGTT)

26
Q

What is involved in the diagnosis of diabetes in the absence of symptoms?

A

→ test blood samples on 2 separate days

27
Q

What is fasting defined as?

A

→ no caloric intake for at least 8 h

28
Q

When should OGTT be carried out?

A

→ in patients with IFG

→ in unexplained glycosuria

→ in clinical features of diabetes with normal plasma glucose values

29
Q

When are blood samples collected in OGTT?

A

→ at 0 and 120 mins after glucose

30
Q

What is the stepwise treatment for T2D?

A

→ diet and exercise
→ oral monotherapy
→ oral combination
→ insulin +- oral agents

31
Q

What are incretins?

A

→ help the body produce more insulin only when it is needed

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

32
Q

What are GLP-1 agonists?

A

→ work by copying, or mimicking, the functions of the natural incretin hormones in your body that help lower post-meal blood sugar levels

33
Q

What are the drug treatments of T2DM?

A 
→ Metformin:
→ Sulfonylureas
→ Thiazolidinediones:
→ SGLT2 inhibitors:
→ Incretin targeting drugs:
DPP-4 inhibitors (prevent breakdown of natural incretins)
→ Synthetic GLP-1 analogues
34
Q

What is the aim of monitoring glycaemic control?

A

→ to prevent complications or avoid hypoglycaemia

35
Q

What is involved in self monitoring in DM?

A

→ Capillary blood measurement

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

36
Q

What is HbA1C?

A

→ glycated Hb;

→ covalent linkage of glucose to residue in Hb.

37
Q

Define hypoglycaemia

A

→ Defined as plasma glucose < 2.5 mmol/L

38
Q

What are the causes of hypoglycaemia?

A

→ Drugs are the most common cause;

→ quinolone, quinine, beta blockers, ACE inhibitors and IGF-1

→ endocrine disease

→ inherited metabolic diseases eg hereditary fructose intolerance

→ sepsis

39
Q

What are some secretagogues that can cause hypoglycaemia?

A

→ glyburide,
→ glipizide
→ glimepiride

40
Q

How does ethanol cause hypoglycaemia?

A

→ inhibit gluconeogenesis, but not glycogenolysis.

41
Q

How does sepsis cause hypoglycaemia?

A

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

42
Q

How does CKD cause hypoglycaemia?

A

→ impaired gluconeogenesis,
→ reduced renal
clearance of insulin

→ reduce renal glucose production.

43
Q

What is reactive hypoglycaemia?

A

postprandial hypoglycaemia

44
Q

What are some causes of reactive hypoglycaemia?

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

What are the neurogenic symptoms of hypoglycaemia?

A

→ triggered by falling glucose levels

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

46
Q

What are neuroglycopenic symptoms of hypoglycaemia?

A 
→ result of brain neuronal glucose deprivation
→ confusion, 
→ difficulty speaking, 
→ ataxia, 
→ paresthesia, 
→ seizures, 
→ coma, 
→ death

Dysfunction (29 decks)

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