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MIMS > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Full name of diabetes

Give meaning and reason for name

A

Diabetes mellitus

“Siphon of honey” - one feature of the disease is passing large volumes of urine containing glucose (when there are high levels of blood glucose)

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2
Q

What is diabetes

A

A disease in which blood glucose concentration is inappropriately raised

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3
Q

What are normal blood glucose levels

A

4mM(fasting) - 7mM (fed)

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4
Q

Does insulin affect all tissues in the same way

A

No

It is required for efficient uptake of glucose in muscle and fat but not in liver or brain, which respond to it in other ways

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5
Q

Insulin is a ____ by function and a ____ by structure

A

Hormone

Protein

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6
Q

What is the % of diabetics who are type one

A

5%

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7
Q

What causes type 1 diabetes

A

Environmental: could be a virus or chemical
Genetic: several genes have been identified which can predispose or protect

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8
Q

How might type 1 diabetes be cured

A

Transplant of islets or stem cells

Vaccine?

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9
Q

How much of diabetics are type 2

A

90%

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10
Q

What are the genetic and environmental components that affect type 2 diabetes

A

Genetic: no simple inheritance: different genes might contribute, runs in families

Environmental: low birth weight and adult obesity are major risk factors

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11
Q

Treatment for type 2 diabetes?

A

Mild: lifestyle (diet and exercise)
Moderate: drugs that stimulate insulin secretion or improve insulin sensitivity
Severe: insulin injection

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12
Q

What kind of drugs increase insulin secretion

A

Sulphonylureas

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13
Q

What kind of drugs improve insulin sensitivity?

A

Thiazolidinediones

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14
Q

What are the rarer forms of diabetes

A

MODY (mature onset diabetes of the young)
Severe insulin resistance (mutation in insulin receptor)
Gestational diabetes (pregnancy associated hormone disturbance, affecting insulin)
Secondary diabetes (as a consequence of a pancreatic disease or hormone disturbance)

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15
Q

What happens in the short term for type 1 diabetes generally

A

Glucose uptake into muscle and fat is impaired, causing hyperglycaemia
Glucose spills over into urine, requiring water for excretion
Body fat and protein are broken down as alternative fuels
Production of ketoacids from fats is increased

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16
Q

What happens if food intake doesn’t match insulin therapy

A

Hypoglycaemia, leading to trembling, sweating and potentially a coma (due to a lack of glucose to the brain)

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17
Q

Long term complications of diabetes

A

Micro vascular: eyes and kidney
Neuropathy: particularly deer
Macro vascular: increased risk of stroke and heart attack

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18
Q

How many amino acids does insulin have? Is every one necessary?

Briefly describe its structure

A

51

No

2 polypeptide chains linked by disulphide bonds between C residues

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19
Q

Who discovered insulin’s primary structure

A

Sanger in Cambridge in 1955

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20
Q

What is glucagon

A

A polypeptide, produced by alpha cells in pancreatic islets of Langerhans

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21
Q

How does [insulin] compare to [glucose]

A 
[insulin]= 0.1-1nM
[glucose] = 5-10 mM
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22
Q

In insulin anabolic?

A

Yes

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23
Q

How does insulin affect muscle

A

Increases glucose uptake
Increases conversion of glucose to glycogen
Increases protein synthesis
Decreases proteolysis

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24
Q

How does insulin affect fat

A

Increases glucose uptake
Increases lipogenesis
Decreases lipolysis
Increases protein synthesis

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25
Q

How does insulin affect

The Liver

A

No effect on glucose uptake
Increases conversion of glucose into glycogen and lipid
Decreases gluconeogenesis and glycogenolysis

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26
Q

How does insulin affect the CNS

A

No effect on glucose uptake or metabolism
Suppressed appetite
Promotes fertility

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27
Q

How does insulin affect pancreatic beta cells

A

Promotes insulin synthesis and secretion

Promotes proliferation

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28
Q

What subcellular compartments does insulin act on

A

Stimulation of glucose uptake involves trafficking vesicles to plasma membranes

Stimulations of glycogen synthesis involves effects in cytosolic enzymes

Stimulation of lipogenesis involves effects on mitochondrial and cytosolic enzymes

Inhibition of gluconeogenesis involves effects in gene transcription in the nucleus

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29
Q

3 reasons all cells need a constant supply on energy

A

Biosynthetic reactions in maintenance and division

Maintain correct ionic and chemical balance of intracelleular environment

Specialised functions eg muscle contraction

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30
Q

How do mammalian cells obtain energy from derivatives of food

A

Oxidation

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31
Q

What does an ATP molecule contain

A

A heterocyclic base, ribose and 3 phosphates

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32
Q

How many pathways exist in mammals to convert fat into glucose

A

None

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33
Q

When are catabolic pathways active

A

Always

May be accelerated to meet energy demand

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34
Q

When are storage pathways most active?

A

Fed state, whereas mobilisation occurs during fasting or exercise

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35
Q

When does lipogenesis occur

A

Fed state

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36
Q

When does gluconeogenesis mainly occur

A

Fasting

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37
Q

What are the main regulators and consumers of the body’s fuel supply

A

Regulators: liver and fat
Consumers: Muscle and Brain

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38
Q

What metabolic processes occur mainly in the liver

A

Lipogenesis
Gluconeogenesis
Ketogenesis

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39
Q

Where does lipogenesis occur

A

Liver

Fat

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40
Q

What does insulin do in fed state

A

Promotes uptake and storage of products of digestion by muscle and fat

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41
Q

What does glucagon do in fasting state

A

Promotes gluconeogenesis (in liver) and lipolysis in fat

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42
Q

What does Adrenalin do I’m stressed state

A

Promotes glycogenolysis in muscle and lipolysis in fat

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43
Q

Where is insulin secreted and what is it originally

A

Pancreatic β cells

A larger precursor, proinsulin, which is then directed into vesicles and cleaved by proteases

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44
Q

What happens to insulin after proinsulin is cleaved

A

Remains stored in vesicles until the cell receives signals to secrete insulin. Excretion occurs via exocytosis

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45
Q

What conc of glucose is required to stimulate insulin release

A

Above 5mM

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46
Q

What does glucokinase do

A

Converts glucose into glucose-6-phosphate

It also acts as a glucose sensor, beginning the process of glucose metabolism

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47
Q

How does ATP affect β-cells

How does this relate to drugs

A

Regulates their ion channels

Drugs to stimulate insulin secretion act on the same channels

48
Q

How does insulin act to lower blood glucose in muscle

A

Stimulates glucose uptake and conversion to glycogen

49
Q

How does insulin act to lower blood glucose in fat

A

Stimulates glucose uptake and conversion into triacylglycerol

50
Q

How does insulin act to lower blood glucose in liver

A

Stimulates glycogen synthesis and inhibits glucose production

51
Q

How does insulin act to lower blood glucose in brain

A

Suppresses appetite and may influence centres controlling peripheral glucose utilisation

52
Q

How do insulin receptors work

A

Extra cellular part of receptor has a special recognition site to bind insulin.
Intracellular part is a protein tyrosine kinase which is activated upon bonding, initiating a signalling cascade

53
Q

What are the different ways protein phosphorylation is a regulatory mechanism

A

Simultaneous and coordinated control of several enzymes

Activation or inhibition

Distinct kinases can induce phosphorylation at different sites on same protein thus integrating the effects of different primary signals

54
Q

How many times does the glucose transporter polypeptide span the membrane

A

12 time’s, forming a transport pore through which glucose can enter by diffusion

55
Q

What does stimulation of glycogen synthesis involve

A

De phosphorylation of glycogen synthase

56
Q

How does a decrease in the number of insulin receptors affect someone

A

Meh unlikely to be of great importance

Subtle changes in the level and activity of proteins are more important

57
Q

Give BMI classifications for
Normal
Overweight
Obese

A

Normal: 20-25
Overweight: 26-30
Obese: >30

58
Q

True or false:

All type 2 diabetics are obese and most obese people are diabetic

A

False:

Most T2 diabetics are obese but most obese people are not diabetic

59
Q

How does risk of diabetes increase with BMI for men and women

A

Women: 5x at 25; 30x at 30, 100x at 35

Men; 2x at 25, 25x at 30, 40x at 35

60
Q

How does obesity increase chance of T2 diabetes

A

Obesity causes insulin resistance

61
Q

What is the lipotoxicity theory for how obesity causes insulin resistance

A

Lipid overload: increases flux of FFA and TAG leads to lipid accumulation, antagonising insulin signalling by lipid related protein serine kinases

62
Q

Is T2 Diabetes a disorder of metabolism of lipids or carbohydrates?

A

Both

Adipose tissue is increasingly seen as playing a central role in disease progression

63
Q

How does Type 2 diabetes ensue

A

Insulin sensitivity decreases with age and in obesity so insulin production increases to compensate for this.

Insulin secretion is later impaired by hyperglycaemia and hyperlipidaemia resulting from insulin resistance

Type 2 diabetes occurs when pancreas can no longer cope with The increased demand

64
Q

What happens in the absence of effective insulin action

A

Muscle is not able to take up sufficient glucose to satisfy energy requirements

Breakdown of fat and protein is increased as they are no longer being inhibited

65
Q

What happens during persistent elevated blood glucose

A

Renal threshold is exceeded and glucose is lost in urine

66
Q

What happens in untreated extreme T1 diabetes

A

Fat breakdown exceeds capacity of tissues to utilise fatty acids and ketone bodies are formed leading to acidosis

67
Q

Why are sub classes important

A

Treatment maybe effective for one sub group but not another’s

68
Q

Before modern medicine what did disease sub division rely on

Eg?

A

Clinical observation

Diabetes used to be subdivided into insipidus and mellitus depending on the urine

69
Q

What did Himsworth propose in 1936

A

Diabetes mellitus had 2 sub types :

Insulin deficiency and insulin resistance

70
Q

What made measuring insulin in blood possible

A

Radioimmunoassay technology

71
Q

What is the typical age of onset for type 1 and 2 diabetes

A

1: early age
2: 40-70

72
Q

How does type 2 diabetes develop

A

Slowly and with variable severity

May be asymptomatic for years

73
Q

Is type 2 diabetes a specific diagnosis

A

No it is more of a clinical label (to aid management and decision making)

74
Q

What is ketosis prone diabetes

A

Observed in African American population and in sub Sahara

Male predominant

Presents acutely with metabolic decompensation and diabetic ketoacidosis

Requires insulin acutely but β cells recover and insulin isn’t needed in the long run

75
Q

What is MODY

A

Maturity onset diabetes of the Young

A heterogeneous group of disorders that result in β cell dysfunction

76
Q

How many genes are currently know to be associated with MODY

Which 5 are most common

Why is this important

A

9

HNF-4a
Glucokinase
HNF-1a
IPF-1
HNF-1b

To Inform prognosis and treatment

77
Q

Does diabetes usually appear in the first 3 months of life

A

No

Patients with this form have previously been treated with insulin for life

78
Q

What can neonatal diabetes be caused by

A

Mutation in Kir6.2 subunit of ATP sensitive K+ channel which mediates glucose stimulated insulin secretion in the β cell

79
Q

What can mitochondrial disease be caused by

A

Mutations is nuclear DNA or in mitochondrial DNA

80
Q

What can a mutation in m.3243 cause

What is the mutation

A

MIDD and MELAS syndrome

A>G

81
Q

What is MIDD

A

Maternally Inherited Diabetes and Deafness

82
Q

What is MELAS syndrome

A

Mitochondrial Encephalomyopathy with Lactic Acidosis and Stroke like episodes

83
Q

What is metformin

A

An oral hypoglycaemic agent

84
Q

4 ways to further stratify disease

A

Moving from studying rare genetic mutations to common polymorphisms

Stratification by response to medication

Stratification by response to lifestyle

Aetiological Stratification on the basis of gene-environment interaction

85
Q

What might response to metformin by affected by

A

Genetic variation at the ATM locus

86
Q

What is the strongest common locus variant for type 2 diabetes

A

TCF7L2

87
Q

CCK:

a) structure
b) where is it secreted
c) what does it act on and what is the effect (3)

A

a) a mixture of peptides, where the octapeptide is the most active
b) secreted in duodenum and jejunum when exposed to protein and fat digestion products by I cells
c) acts on gall bladder, stimulating contraction; acts on pancreases to stimulate release of enzymes; acts on Vagal afferents to medulla oblongata causing satiety

88
Q

Ghrelin:

a) structure
b) where is it secreted
c) what does it act on and what is the effect (2)

A

a) 28 amino acids
b) secreted by stomach endocrine cells in response to fasting
c) acts on hypothalamus to stimulate feeding; counteracts effects of leptin and PYY-3-36

89
Q

Neuropeptide Y (NPY)

a) structure
b) where is it secreted
c) what does it act on and what is the effect (3)

A

a) 36 amino acids
b) secreted by neurons in hypothalamus
c) Potent feeding stimulant and causes increased storage of ingested food as fat; also blocks transmission of pain signals to the brain

90
Q

PYY 3-36

a) structure
b) where is it secreted
c) what does it act on and what is the effect (3)

A

a) 34 αα with 21 residues identical time sequence in NPY
b) released by intestinal cells after meals, amount secreted increases with calories ingested

c) acts on:
•hypothalamus to suppress appetite
• pancreas to regulate exocrine secretion
• gall bladder to stimulate contraction

91
Q 
Which of the following works tastes to suppress appetite:
CCK 
leptin
PYY
(Fastest to slowest)
A

CCK>PYY> leptin

92
Q

What are IL6 and TNF

How do these affect obesity related diseases

A

Inflammatory factors (cytokines) secreted by adipose

These may contribute to disease: without TNF, might develop obesity but not insulin resistance or Type II diabetes

93
Q

How do the levels of adiponectin vary

A

Levels fall as fat mass increases

94
Q

What is BMR

A

The metabolic rate of a resting fasted adults in a Thermo neutral environment

95
Q

What are the proportions of oxygen consumption of the BMR

A 
65%= mitochondrial production of ATP
20%= intrinsic H+ leakiness in mitochondria

The rest are non mitochondria based

96
Q

What are the proportions of ATP expenditure

A 
Na/K pump: 25%
Protein synthesis: 25%
Ca+ pump: 5% 
Actinomysin ATPase: 5%
Gluconeogenesis: 7% 
Urea formation: 2%
DNA/ RNA synthesis: 30-40%
97
Q

How efficient is obviously phosphorylation in terms of ATP production

A

70%

98
Q

What is DIT

A

Diet induced thermogenesis

The increase in energy expenditure above basal fasting level
————————————-
Energy content of ingested food

99
Q

What happens in malignant hyperthermia

A

Calcium leakage from the SR and increased activity of ATP calcium pumps to return it

There is a consequent rise in oxygen consumption and CO2 output leaving to acidosis, tachycardia and heat generation

100
Q

Give a simplified summary of the formation and release of thyroid hormones

A

Iodide ions are concentrated by the thyroid gland using the Na/I co-transporter

Synthesis occurs in The space outside follicle cells
Eight peroxidase complex uses hydrogen peroxide to conjugate iodide to tyrosine residues of the protein thyroglobulin

Thyroglobulin enters the cell by endocytosis and is broken down into secondary lysosomes to release T4 and T3

101
Q

How much of T3 and T4 are dissolved in blood

A

V little

99% are protein bound

102
Q

What is the effect of thyroid hormones on energy metabolism

A

They stimulate metabolic rate by increasing expression of genes that include proteins involved in oxidative metabolism and thermogenesis

103
Q

How does T3 affect the expression of genes

A

T3 easily enters cells due to being lipid soluble and attaches to a receptor protein in the nucleus and also bunds to the retinoids X receptor

The resulting heterodimer which binds to DNA sequences in promoter regions

104
Q

What is myxoedema?

A

Hypothyroidism

105
Q

Which thyroid problem causes facial swelling

A

Hypothyroidism

Due to a build up of glycoproteins

106
Q

Why does a goiter form in hypothyroidism

A

T4 normally inhibits TSH secretion so TSH rises when T4 is low and stimulates growth of the thyroid gland

107
Q

What is diabetes

A

Dis regulation of blood glucose

108
Q

Difference between symptom and sign

A

Symptom: subjectively described
Sign: objective

109
Q

What is diabetes insipidus

A

Too little ADH/ insensitive to ADH

110
Q

What causes XS urination in diabetes

A

Increases osmotic pressure in tubules due to excess glucose

This increased osmotic pressure leads to micro-vascular damages which can lead to blindness etc

111
Q

Are you born with type 1 diabetes

A

No

112
Q

Do you get comas for hypoglycaemia or hyperglycaemia

A

Both

Hypo is more unpleasant as the body shuts down and nervous control is lost

113
Q

What causes a coma in ketosis

A

Low pH in the brain

114
Q

What does genetic determinism mean

A

Their genes mean they WILL get the disease

115
Q

What is HBA1c

A

Tests levels of glycated Hb

116
Q

Which GLUT receptor is insulin dependent

A

GLUT4

117
Q

In 1 person how many genes cause MODY

A

1 gene mutation

MIMS (12 decks)

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