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Module 203 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Microvascular complications of Diabetes

A

Retinopathy
Neuropathy
Nephropathy

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2
Q

Macrovascular complications of Diabetes

A

Ischaemic heart disease
Coronary heart disease
Peripheral vascular disease

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3
Q

Presentation of microvascular disease

A

5yrs after T1DM

May be presentation for T2DM

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4
Q

Diabetic eye disease

A

Diabetic retinopathy
Macular oedema
Cataract
Glaucoma

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5
Q

Diabetic retinopathy

A

Damage to retinal capillaries in retina due to high glucose levels in the blood
2nd commonest cause of blindness
When looking at the retina, hard exudate, blot haemorrhages and microaneurysms may develop

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6
Q

Pathological findings for diabetic retinopathy

A

Loss of pericytes therefore reduced regulation of blood flow to retina
Thickening of basement membrane
Ischaemia - VEGF production and increased capillary permeability to promote angiogenesis
Capillary closure

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7
Q

Clinical stages of retinopathy

A

Non-proliferative (mild, moderate, severe) - ischaemia
Proliferative - angiogenesis
Macular oedema

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8
Q

Treatment of retinopathy

A

Diabetic control and blood pressure control
Panretinal photocoagulation
Focal laser treatment
Intravitreal anti-VEGF antibodies

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9
Q

Panretinal photocoagulation

A

Laser treatment used to prevent new blood vessels from forming in ischaemic areas and causes old blood vessels to scar up –> reduces oxygen demand to reduce angiogenic factors
Prevents vitreous haemorrhage and neovascular glaucoma
Used to treat diabetic retinopathy
Side effect: peripheral visual field constraints

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10
Q

Focal laser treat

A

A laser is used to burn areas of retinal leakage to slow leakage and reduce the amount of fluid in the retina
Used to treat diabetic retinopathy

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11
Q

Intravitreal anti-VEGF antibodies

A

Antibodies target VEGF to reduce angiogenesis and improve diabetic retinopathy

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12
Q

Diabetic neuropathy

A

High blood glucose causes damage to the small blood vessels which supply the nerves therefore the nerve fibres are damaged or disappear
Only symptom relief available, and improve blood glucose control

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13
Q

Types of neuropathy

A

Mononeuropathy - affects a single nerve or group of nerves e.g. carpal tunnel syndrome
Peripheral neuropathy - damage to nerves of the extremities e.g. charcot foot, neuropathic ulcer and callus
Entrapment neuropathy/nerve compression syndrome

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14
Q

Peripheral neuropathy

A

Divided into:
Autonomic neuropathy - nerves to organs affected so can cause gastroparesis, postural hypotension, erectile dysfunction, etc.
Motor neuropathy
Sensory neuropathy

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15
Q

Charcot foot

A

Bones in foot are weakened and repeated use causes fractures but neuropathy causes loss of sensation (including touch and pain) and results in further damage causing distortion of the shape of the foot

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16
Q

Nephropathy

A

Common cause of end-stage renal failure requiring dialysis
High blood glucose causes damage to the glomerular basement membrane and results in leakage of proteins and glucose into the urine (albuminuria and glycosuria)

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17
Q

Pathological findings of the diabetic nephropathy

A

Basement membrane thickening - due to ROS and proteins accumulating
Loss of glomerular podocytes - loss of filtration barrier
Glomerular sclerosis - scarring of the glomerular capillaries
Mesangial expansion to clear the ROS and proteins accumulating on the basement membrane of the glomerulus

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18
Q

Management of diabetic nephropathy

A 
Blood pressure control
Blood glucose control
RAS system blocker
Reduce CVD risk
Possible renal transplant
19
Q

Preventing macrovascular complications

A

Address modifiable risk factors e.g. blood pressure, lipids/cholesterol, smoking, glucose control

20
Q

Metabolic syndrome

A 
Central/visceral obesity
Insulin resistance (pathophysiological mechanism)
BMI>30kg/m2
Dyslipidaemia
Hyperglycaemia
Hypertension
21
Q

Complications associated with obesity

A

Increased blood volume, viscosity and vascular resistance
Hypertension, Left ventricular hypertrophy, Coronary artery disease, Stroke
Obstructive sleep apnoea, hypercapnia/hypoxia, pulmonary hypertension
Non-alcoholic fatty liver disease (steatohepatitis/NASH), cirrhosis, portal hypertension, hepatocellular cancer, gallstones, reflux
Breast, endometrial, oesophageal, colon, gallbladder, renal and thyroid cancer
PCOS, male hypogonadism, subfertility
Osteoarthritis, gout
Depression and eating disorders

22
Q

Genes associated with T1DM

A

HLA DR3-DQ2 and HLA DR4-DQ8

23
Q

Foetal programming

A

Epigenetic modification of gene expression in response to stimuli or insult during critical periods resulting in persistent biological effects

24
Q

Slow-acting hormones regulating body weight

A

Insulin and Leptin

25
Q

Rapid-acting hormones regulating meal size

A

Cholecystokinin - stop eating
Ghrelin - increase eating/hunger
PYY hormone - sateity

26
Q

roux-en-Y gastric bypass

A

A small pouch is created at the top of the stomach with staples and this is attached to the intestines lower down to bypass the rest of the stomach
Limits the amount eaten by altering hormone levels produced by the gut
May lead to micronutrient deficiencies, irreversible

27
Q

Laparascopic adjustable banding

A

A balloon and soft silicone ring with saline fluid are used to create a smaller top part of the stomach to limit the amount of food eaten
Reversible

28
Q

Physiological changes seen in T2DM

A

Increased levels of leptin and leptin resistance resulting reduced satiety and increased feeding
Gut microbiota changes - possible reduction in bacterial variety

29
Q

Type 1 Diabetes

A

Reduced secretion of insulin or absence of insulin secretion due to autoimmune destruction

30
Q

Type 2 Diabetes

A

Insulin resistance with a lack of beta cell reserve
Pt may initially appear hyperinsulinaemic and euglycaemic as there is a rise in insulin production initially when resistance develops but, as resistance continues, the beta cells are unable to keep up resulting in hyperglycaemia

31
Q

Absence of insulin

A 
Body enters starvation state to cause:
Gluconeogenesis
Reduced glycogenesis
Increased glycolysis
Increased lipolysis
Ketogenesis in liver
32
Q

How to the typical symptoms of Diabetes present?

A

High levels of glucose exceeds renal threshold (10mM) so glycosuria occurs which draws water as well causing polyuria with large volumes of urine passing during the day and night
Polyuria leads to polydipsia

33
Q

Diabetic ketoacidosis

A

Occurs in T1DM

Starvation state due to absence or low insulin causes ketogenesis which accumulate to cause ketoacidosis

34
Q

A&E presentation of patient with T1DM

A

Confusion and apparent breathlessness due to ketoacidosis

Pt is breathing deeper and faster (tachypnoea) to reverse the metabolic acidosis

35
Q

Treating DKA

A

Rehydrate to correct dehydration due to polyuria

Insulin to stop ketogenesis and cause GLUT4 translocation

36
Q

Hyperosmolar Hyperglycaemic State

A

Severe hyperglycaemia occurring in T2DM
High glucose takes water with it causing more sodium retention (hypernatraemia) leading to high osmolality
Can cause confusion or coma

37
Q

Normal fasting plasma glucose level

A

4.0 to 5.4 mmol/L

38
Q

Diabetic plasma glucose

A

Fasting plasma glucose >7.0mmol/L
HbA1c > 6.5% or 48mmol/L
GTT > 11.1mmol/L

39
Q

Impaired fasting glucose

A

Fasting plasma glucose between 6.0-7.0mmol/L

40
Q

Hypoglycaemic stress

A

Glucose falls to between 2mM and 4mM

Patients develop symptoms of sympathetic overactivity e.g. increased heart rate, sweating

41
Q

Neuroglycopenia

A

Blood glucose falls below 1.5mM so there is not enough glucose provision for the brain so the patient becomes unconscious

42
Q

Treating hypoglycaemia

A

Intravenous insulin and subcutaneous glucagon

43
Q

Glycation

A

Bonding of glucose to proteins or lipids e.g. glycated Hb (used to detect levels of glucose)
Glycation of endothelial proteins results in micro- and macrovascular complications

Module 203 (10 decks)

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