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Y2S2 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is homeostasis?

A

The relative constancy of the body’s internal environment

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2
Q

What is the central process for the NS?

A

Detect- Intergrate- Respond

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3
Q

What are the three categories of the Peripheral NS?

A

Sensory system
Autonomic system
Somatic system

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4
Q

What does the somatic NS innervate to?

A

Skeletal muscle (voluntary responses)
Alpha motor neurons

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5
Q

What does the autonomic NS innervate to?

A

Preganglionic fibre->ganglion->postganglioinc fibre-> smooth, cardiac muscles/ glands and neurones

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6
Q

What are oligodendrocytes and where are they found?

A

Forms myelin sheath around axon in CNS, insulates and increases speed of transmission

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7
Q

What are the three categories in the autonomic NS?

A

Sympathetic (fight/flight)
Parasympathetic (rest/digest)
Enteric (neural network surrounding the gut)

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8
Q

What are Schwaan cells and where are they found?

A

The same as the oligodendrocyte but found in the peripheral NS

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9
Q

What is an astrocyte?

A

Provides structural and metabolic support in neurones
Take up excess neurotransmitters
Have foot processes which sit at junction of epithelial cells and protect them (blood brain barrier)

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10
Q

What are microglia?

A

Immune cells of the NS

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11
Q

What does the cell body contain?

A

Nucleus, mitochondria, RER- to make membrane proteins

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12
Q

What does an axon do?

A

Nerve fibre extending from axon hillock
Carries the action potentials
1µm-1m
Contains microtubules-which move proteins through neuron body

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13
Q

What do dendrites do?

A

Receive input from other neurons
Outgrowths from cell body
1-500000 per cell

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14
Q

What does the axon terminal do?

A

Synapse, release of neurotransmitter

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15
Q

Name sensory neurons and what do they do?

A

Afferent, transmit info to CNS, have sensory receptors at peripheral end

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16
Q

Name motor neurons and what do they do?

A

Efferent, transmit info from CNS to effector to organs or to other neurons

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17
Q

Name relay neurons and what do they do?

A

Interneurons – only in CNS and transmits from neuron to neuron, 99% of all neurons

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18
Q

What is a ganglia?

A

Collection of cell bodies of neurons

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19
Q

What does the peripheral NS consist of?

A

43 pairs of nerves
12 cranial pairs (brain)
31 spinal pairs

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20
Q

Name an important cranial nerve and what does it do?

A

Cranial nerve 10, vagus nerve
Parasympathetic supply from CNS to the thoracic organs (heart, lungs etc)

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21
Q

What is a nerve fascicle?

A

Many axons bundled in connective tissue

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22
Q

Describe the neuroendocrine mechanism:

A

The endocrine system works in coordination with the nervous system to maintain homeostasis

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23
Q

What is a hormone?

A

A chemical substance used to carry info from one part of the body to another via the blood

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24
Q

How is hormone secretion controlled?

A

Negative feedback

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25
Q

How can an action of a hormone be controlled?

A

An antagonistic hormone

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26
Q

Give the antagonistic hormone for insulin:

A

Glucagon

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27
Q

Why is glucose very important for the body?

A

Its the source of energy for the brain, 120g per day

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28
Q

What is the normal BG levels?

A

3.5-5.8mmol/L

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29
Q

What can amino acids be made into and where does the excess go?

A

Made into proteins (structural/ secretory)
Excess:
-can be made into glucose/ fat
-excreted via urea (urine)

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30
Q

What can glucose be made into and where does the excess go?

A

Most glucose used in respiration and expired for ATP
Excess:
-made into glycogen storage in liver/muscles
-can be made into fatty acids

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31
Q

What can fatty acids be made into?

A

Made into triglycerides stores in adipose tissue
Most produce ATP

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32
Q

What is the synthesis and breakdown of glycogen called?

A

Synthesis= glycogenesis
Breakdown= glycogenolysis

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33
Q

How much glycogen can be stored?

A

A limited amount

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34
Q

What is the synthesis and breakdown of fat called?

A

Synthesis= lipogenesis
Breakdown= lipolysis

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35
Q

How much fat can be stored?

A

Store as much as need, major energy store

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36
Q

What is the name for glucose being made by a.a and what is the name for protein breakdown?

A

Glucose synthesis= gluconeogenesis
Protein breakdown= proteolysis

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37
Q

What is glucagon and where is it secreted from?

A

Antagonistic to insulin, secreted from alpha cells in the islets of Langerhans

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38
Q

What is cortisol and where is it secreted from?

A

Glucocoticoid from adrenal cortex
Increase energy sources as part of stress response

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39
Q

What is adrenaline and where is it secreted from?

A

Increase blood glucose and fatty acids
Secreted from adrenal medulla

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40
Q

What is growth hormone and where is it secreted from?

A

Major effect in protein synthesis in muscles
Secreted from anterior pituitary, can elevate BG

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41
Q

What is somatostatin and where is it secreted from?

A

Inhibits digestion and absorption
Secretion of pancreatic hormones
Secreted from delta cells of endocrine pancreas in response to raised glucose or a.a

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42
Q

What is pancreatic polypeptide and where is it secreted from?

A

Appetite reduction
Secreted form F cells (pp cells) in response to raised a.a

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43
Q

What is amylin and where is it secreted from?

A

Delays gastric emptying
Secreted from B cells

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44
Q

Describe insulin:

A

Two polypeptide chains joined by disulphide bridges
A peptide hormone consists of alpha and beta chains
Acts as a tyrosine kinase receptor

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45
Q

Where is insulin secreted from and where does it target?

A

It is secreted from the B cells in the islets of Langerhans in endocrine pancreas into hepatic portal vein (liver being target)

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46
Q

How is insulin synthesised?

A

Synthesised as a pro peptide by ribosomes on the RER
Processing in the Golgi involves:
-folding and formation of disulphide bonds
-removal of the C peptide (31aa) to give 2 chains, A-21aa and B30aa linked by disulphide bonds
C peptide aswell as insulin is secreted, insulin is stored until secretion is stimulated

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47
Q

How can you indirectly measure the level of insulin secretion?

A

Plasma C peptide level is a measure of insulin secretion as it isn’t cleared rapidly from the blood

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48
Q

Describe the basic negative feedback mechanism for blood glucose control:

A

After a meal, BG increases
Glucose diffuses into pancreatic B cell via GLUT2
Increase in glucose conc in the cell causes secretion of insulin
Insulin decreases BG
Decreased glucose in the B cell decreases insulin secretion

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49
Q

Describe 3 other factors which can influence insulin secretion:

A

Some a.as (leucine, arginine) increase a.a secretion
Autonomic NS (parasympathetic increases, sympathetic decreases)
Some gut hormones (incretins- GLP1) secreted in the GI tract in response to food

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50
Q

Describe the pharmacological mechanism of how insulin is secreted from glucose:

A

Glucose enters the cell by diffusion via GLUT2
Glycolysis and the Krebs cycle forms ATP
ATP can gate a K+ channel which closes the K+ channel (ATP gated K+ channel) and this causes depolarisation as less K+ moves out
Depolarisation causes activation of voltage gated Ca2+ channels to open and Ca2+ enters the cell
Causes Ca2+ induced calcium release from the ER, causes exocytosis of secretory granules (containing insulin) causes insulin release

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51
Q

In which way does a.a cause the release of insulin?

A

The same way as glucose

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52
Q

How does the parasympathetic NS cause an increase in insulin?

A

Ach acting at muscarinic receptors, increase Ca2+ via Gq-> PLC->IP3-> Ca2+

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53
Q

How does the sympathetic NS cause a decrease in insulin?

A

Adrenergic agonists like somatostatin inhibits cAMP, so a decrease in insulin

54
Q

How does GLP1 cause an increase in insulin?

A

Acts via the Gas, increases activity of adenylate cyclase, increases cAMP via PKA + Epac and increases calcium induced exocytosis

55
Q

Describe the insulin dependent uptake of glucose:

A

Down the concentration gradient inside the cell via the GLUT4 facilitated glucose transporter
GLUT 4 is abundant in skeletal muscle and adipose tissue

56
Q

Describe the insulin independent uptake of glucose:

A

Mainly in the liver with GLUT2 transporters

57
Q

Describe what occurs when insulin binds to the receptor:

A

Subunit come together and cross phosphorylate:
-RAS complex- actions on DNA/RNA
-Phosphorylation of IRS (insulin receptor substrate) and acts via SH2 domains
Both lead to activation/inactivation of proteins and leads to recruitment of glucose transporters so more uptake

58
Q

Describe the actions of insulin on fats:

A

Insulin lowers blood fatty acids and increases triglycerides synthesis
Increases uptake into adipose
Increase uptake of glucose in adipose -> synthesis of fatty acids +glycerol
Decrease in lipolysis

59
Q

Describe the action of insulin on a.as and proteins:

A

Insulin lowers a.a and increases protein synthesis
Increases uptake of a.a into cells (esp skeletal muscle)
Decreases protein degradation

60
Q

Describe glucagon and how does it work:

A

31 a.a peptide, hydrophilic, receptors at cell surface
Act by stim of a GPCR (Gas) and increases cAMP within the cell
Promotes the breakdown of energy stores
Secreted between meals

61
Q

What effect does glucagon have on protein metabolism?

A

LIVER only
No sig effects on blood a.a levels as no effect on skeletal muscle

62
Q

Name the primary diabetes Mellitus:

A

Type 1
Type 2

63
Q

Name the secondary diabetes Mellitus:

A

1-2 % of cases
Caused by an underlying cause:
-liver diseases
-pancreatic disease
-endocrine disease
*mainly drug induced e.g thiazides, corticosteroids

64
Q

What is gestational diabetes?

A

Diabetes during pregnancy usually in the 2nd or 3rd trimester
It is closely monitored
Caused by insulin resistance
Usually managed by diet, may need insulin
Risk of large birth weight baby
Usually return to normal following delivery

65
Q

What ethnicity has the highest and lowest rate of T1D?

A

Highest in caucasians
Lowest in Japan and pacific area

66
Q

What is the age range in developing T1D?

A

Any age but prominent disease of childhood peaking at puberty
50-60% <20 years

67
Q

What ethnicity increases the risk of T2D?

A

3-4x more with African/ Caribbean
4-7x more with hispanic American + south Asia/ Arabian with western lifestyles

68
Q

What is the age range in developing T2D?

A

Increases with age and obesity
Mostly over 40

69
Q

What is the aetiology of T1D?

A

HLA- associated immune-mediated disease
more than 90% carry HLA-DR3 and/or DR4 marker
Autoantibodies versus pancreatic cells
Islet cell antibodies in more than 70% at point of diagnosis and appear in circulation several years before clinal presentation
Not genetically predetermined but may increases susceptibly to disease may be inherited

70
Q

What is the aetiology of T2D?

A

Stronger genetic relationship than type 1
Obesity occurs in 80%
Increase in insulin resistance, decrease in number of B cells

71
Q

What is metabolic syndrome?

A

Combination of medical disorders when occurring together increases risk of CVD and T2D
e.g Increase in BP, BG, cholesterol, central abdominal obesity:
-men ≥102cm
-women ≥88cm

72
Q

How many B cells are remaining in T1D?

A

5-10%

73
Q

How many B cells are remaining in T2D and why does this cause T2D?

A

50%
Down regulation of insulin receptors which leads to insulin resistance

74
Q

What causes hyperglycaemia in diabetes due to B cells?

A

Unregulated hepatic glycogenolysis and gluconeogenesis

75
Q

How can a metabolic disturbance such as an acute illness cause diabetic ketoacidosis?

A

Increase in counter regulating hormones (glucagon, cortisol etc) cause a further increase in hepatic glucose production
At the same time an increase in lipolysis:
-fatty acids taken up by liver to produce acetyl-CoA and metabolism by liver exceeded so release of ketone bodies (acetoacetate and hydroxybutyrate) released into circulation

76
Q

Describe and explain the common symptoms in diabetes:

A

Polyuria- due to osmotic diuresis when blood glucose exceeds renal threshold
Polydipsia- due to resulting fluid and electrolyte loss
Weight loss- due to fluid depression and increase breakdown of fat and muscle
Fatigue- due to bodies inability to get glucose from blood into cells to meet energy needs
Blurred vision- glucose induced changes in refraction

77
Q

What can cause diabetic ketoacidosis in a T1D?

A

Can be first presentation if diagnosis is not made from common symptoms
Interruption of insulin supply in a diagnosed diabetic
Intercurrent illness

78
Q

What are symptoms of DKA?

A

Hyperventilation, N&V, dehydration, weakness, ketone breath, reduced consciousness, potentially fatal

79
Q

Describe explanations as to why there are specific symptoms in DKA:

A

Increase in BG ->osmotic diuresis= dehydration and hypotension
Increase ketone bodies-> metabolic acidosis = H2O2, ketone breath and air hunger so hyperventilation
Hyperosmolarity= dehydration
Potassium loss through urine
Muscle catabolism and generalised weakness

80
Q

Why are there chronic skin infections in T2D and give examples?

A

Increase in glucose impairs phagocyte function e.g UTI, thrush

81
Q

What does HONK stand for?

A

Hyperosmolar non-ketotic syndrome

82
Q

What is HONK?

A

Medical emergency
Similar to DKA but no significant ketosis and no acidosis due to endogenous insulin level being sufficient to inhibit hepatic ketogenesis, but hepatic glycogenolysis and gluconeogenesis still occur

83
Q

What are the symptoms of HONK?

A

Same as DKA but no ketone breath or air hunger:
N&V, dehydration, weakness, reduced consciousness, potentially fatal

84
Q

What is the value for the random venous plasma glucose that indicates diabetes with symptoms:

A

More than 11.1mmol/L

85
Q

What is the value for the fasting venous plasma glucose that indicates diabetes with symptoms:

A

More than 7mmol/L

86
Q

What is the glucose tolerance test and why is it used?

A

If greater than 11.1mmol/L after 75g of anhydrous glucose from an oral administration
Only used for borderline cases and diagnosis of gestational diabetes

87
Q

What should occur if the patient has no symptoms but has a high glucose value:

A

Two separate measurements of either random or fasting or two hours post GTT
If fasting or random non diagnostic, the GTT value should be used

88
Q

How can an official diagnosis be made for diabetes?

A

A venous blood sample in the lab

89
Q

Apart from a venous blood sample, what is another diagnostic factor for T2D?

A

Glycated HbA1c blood test

90
Q

What is the HbA1c value for a diagnosis of T2D?

A

more than 48mmol/mol (6.5%)

91
Q

What should be the aim for HbA1c value for type 1 and how often should it be measured?

A

48mmol (6.5%) or lower
Every 3-6 months

92
Q

What are CGMs and name the 2 types:

A

Continuous glucose monitoring
-real-time continuous glucose monitoring
-intermittently scanned continuous glucose monitoring (flash
Monitors interstitial fluid

93
Q

What are other factors that could indicate diabetes?

A

Glucose, urea, creatinine eGFR
Arterial pH pO2
Blood pressure, urine analysis, renal/liver function

94
Q

Why could the body’s immune response be problematic to insulin?

A

Mount an immune response
Bovine is the most problematic
Human is the least

95
Q

What are the problems with injection insulin?

A

Local at injection site:
-Lipohypertrophy
-Bruising/ redness/ scarring (as injecting in IM rather than SC)
-Rare allergic reactions
Weight gain
Hypoglycaemia

96
Q

What is the BG value which indicates hypoglycaemia?

A

Less than 4mmol/L

97
Q

What BG level should T1D achieve when waking?

A

5-7mmol/L

98
Q

What BG level should T1D achieve at other times?

A

4-7mmol/L

99
Q

What are mild symptoms of hypoglycaemia?

A

Palpitations, tremor, hunger, sweating (all adrenergic mediated through B receptors, if put on B blockers may not experience this)
Perioral numbness tingling, blurred vision, fatigue, headache

100
Q

What are moderate symptoms of hypoglycaemia?

A

Behaviour change, restlessness, agitation, irritability, drowsiness (but rousable), confusion, slurred speech

101
Q

What are severe symptoms of hypoglycaemia?

A

Very agitated/ aggressive, unconscious, unresponsive, seizures, coma

102
Q

What is the treatment for mild hypoglycaemia?

A

15-20g of rapidly absorbed sugar
e.g 2 teaspoons of sugar, Glucogel, 120ml lucozade
If necessary repeat after 10-15 mins
After snack or next meal of sustained carbs

103
Q

What is the treatment for moderate hypoglycaemia?

A

1.5-2 tubes of GlucoGel (oral) or 1mg glucagon (IM)

104
Q

What is the treatment for severe hypoglycaemia?

A

1mg Glucagon (IM) or 10-15 mins of 10% IV glucose (150ml)

105
Q

What can be the causes of hypoglycaemia?

A

Incorrect dosing of insulin at night
Delayed/ missed meals
Alcohol (inhibits gluconeogenesis)
More exercise than usual
Heat
Stress

106
Q

Name and describe the two major categories of diabetic complications:

A

Microvascular: small BV damage
-retinopathy (eyes)
-nephropathy (kidneys)
-neuropathy (nerves)
Macrovascular: large BV damage
-hypertension (BP)
-hyperlipidaemia (blood lipids)

107
Q

What is the most common macrovascular and microvascular complication in T2D?

A

Micro= retinopathy
Macro=hypertension

108
Q

What does an increase in the HbA1c mean?

A

There’s an increase in CV risk

109
Q

Why is it only the eyes, kidneys and nerves get damaged due to glucose and not other organs?

A

The endothelial cells of the retina, kidney and peripheral nervous system allows glucose to enter the cells even in the absence of insulin, other cells need insulin, so no control as to how much enters

110
Q

What are some types of diabetic eye disease?

A

*retinopathy
Blurred vision (diplopia = double vision)
Cataracts at an earlier age than usual
Glucoma (increase pressure of fluid inside eye) which is resistance treatment

111
Q

What is retinopathy?

A

Within 20 years of diagnosis
Starts with small haemorrhages and abnormal spots of hardened exudates (leaked fluids of proteins and lipids)
Progresses to infarction of retina- areas with little or no blood supply
Eventually new blood vessels form but they are fragile so tend to bleed and destroy the retina (blindness) unless treated early enough

112
Q

What are the risk factors of retinopathy?

A

Main ones: hyperglycaemia, hypertension
Increase duration of diabetes, if have diabetic nephropathy, pregnancy, increase blood triglycerides, smoking, rapid improvement control of BG

113
Q

How can a rapid improvement of control of BG cause retinopathy?

A

Insight threatening disease, must stabilise retina before improving BG levels as can make it worse

114
Q

How can you prevent diabetic retinopathy?

A

Good glycaemic control
Effective management of hypertension
Avoidance of smoking
Regular screening (annually)
Laser treatment to seal off the leaking blood vessels

115
Q

Describe what nephropathy is:

A

Leading cause of end-stage renal failure in the western world
Occurs around 15–25 years after onset of diabetes
Responsible for more than one third of patient starting renal replacement therapy (dialysis)
Once dialysis is required, most patients also have other complications

116
Q

Describe proteinuria in nephropathy:

A

Presence of protein (mainly albumin) in urine
Common signs of renal disease
Presents detected using urine dipsticks
Repeated positive needs a 24 hour urine collection and quantify how much protein in it

117
Q

Describe microalbuminuria in nephropathy:

A

Presence of small amount of albumin in urine
Detected with specialist dipsticks
Early indicator of diabetic nephropathy
Check albumin:creatinine ratio (ACR)
Need treatment to prevent progression, ACE inhibitor

118
Q

What is the ACR value which indicates treatment is needed in nephropathy?

A

Men > 2.5mg/mmol
Women > 3.5mg/mmol

119
Q

What is the treatment for nephropathy in both types of diabetics?

A

Improve control of diabetes
Aim for HbA1c of less than 7%, target 6%
Aggressive control of BP
T1D= less than 130/80
T2D= less than 140/90, 150/90 (if 80+)
Also treat any other CV risk factors like smoking cessation

120
Q

What is the treatment for hypertension in patients with diabetes?

A

Start with an ACE inhibitor regardless of age/ethnicity as renoprotective
If target BP not achieved add other drugs
If using CCB use amlodipine or felodipine as additional renoprotective action (additive effect with ACEi)
Restrict dietary sodium intake to 100mmol per day

121
Q

What are the symptoms of diabetic neuropathy?

A

Numbness occurs in both legs
Pain may/may not be present
Accompanied by unusual feelings without any obvious causes e.g tingling, itching
Impaired sense of position leading to pt being unsteady on their feet

122
Q

What are the symptoms in motor neuropathy?

A

Neuropathy in the autonomic nerves leads to:
ED in men
Low BP when pt is standing- orthostatic hypotenstion
Delayed emptying of the stomach causing bloating, occasional N&V- gastroporesis
Diabetic diarrhoea

123
Q

What is the treatment in motor neuropathy?

A

Optimise control of BG- possible worsening of symptoms initially but then improvement
Pain modifying agents:
-simple analgesics like paracetamol
-analgesics for nerve pain e.g amitriptyline, gabapentin

124
Q

What can be the outcomes of diabetic foot disease?

A

Consequence of neuropathy and Macrovascular
Deep ulceration
Uncontrollable infection
Cellulitis
Gangrene
Amputation

125
Q

What are the causes of diabetic foot disease?

A

*Peripheral vascular disease
Poor circulation and ischaemia (low blood flow) of lower limb causes:
-problems with healing of infection
-problems getting antibiotics to site of infection insufficient conc to be effective as no blood supply
*Peripheral neuropathy
Reducent sensation to pain means that the ulcer can be very severe and the patient may be totally unaware

126
Q

What increases the risk of getting diabetic foot disease?

A

Previous foot ulcerations
Presence of callus or deformity of joint, foot or nail
Orthopaedic problems such as arthritis
Visual impairment or poor mobility preventing self-care
Increase duration of diabetes
Poor control of BG or BP
Poor fitting footwear

127
Q

Describe the management of diabetic foot:

A

Wound management, cleaning/dressings
Reduce the risk of recurrence:
-check foot wear
-no products containing acids E.g. salicylic acid, don’t use OTC foot treatment
-no abrasive products designed to remove hard skin

128
Q

When should you refer to a diabetic foot care team?

A

If patient has ulceration, swelling, cellulitis or discolouration of the skin

129
Q

What should be given to diabetic patients to reduce CV risk? (over 40)

A

All patients aged over 40 with diabetes are considered at high CV risk and receive a statin
Atorvastatin 20mg

130
Q

What should be given to a patient with diabetes to reduce CV? (under 40)

A

If they have one of the following risk factors then they should have atorvastatin 20mg:
-retinopathy
-nephropathy
-Persistent poor glycemic control (HbA1c >9%)
-Elevated BP needing antihypertensives
-Total serum cholesterol <6mmol/L
-Premature CVD in first degree relative
-Features of metabolic syndrome

131
Q

Should you give aspirin to a diabetic?

A

Don’t offer to them unless they have established CV disease

132
Q

What is the lifestyle advice to give to diabetic patients to reduce CV risk:

A

Weight reducing
Diet, oily fish 2x week, 5 fruit/veg a day
Exercise 30mins 5x week
Stop smoking
Alcohol max 14 units week

Y2S2 (14 decks)

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