Diabetes Flashcards

Day 4

1
Q

What are the types of diabetes ?

A

T1DM, T2DM, gestational-
Insulin resistance influenced by hormones released by placenta. diabetes insipidus -
deficiency in ADH which regulates fluid balance.

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2
Q

Describe normal blood glucose regulation

A

Pancreas produces insulin and glucagon which act on the cells in the liver. The liver acts on body’s glucose reservoir. When BG gets too high liver cells take in the glucose to store it. Some excess glucose stored as fat, other stored as glucagon in the liver and muscles.

The islets of Langerhans are in the pancreas - the 2 types (alpha and beta)
Beta produce insulin and prevents release of glucose from the liver
Alpha produce glucagon and releases stored glucose during hypoglycaemia.

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3
Q

Describe T1DM

A

Autoimmune destruction of beta cells Inflammatory condition- Beta cell fibrosis- Lack of insulin release.
Body doesn’t respond to raised blood sugar levels by producing insulin.
Activation of transporter proteins which move glucose into the cells from the blood across the cell membrane does not occur. The cells cannot utilise the glucose and the levels within the blood remain high.

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4
Q

Describe T2DM

A

Insulin resistance. Insulin is made in the pancreas by B cells, over time there is a malfunctioning of the B cells, so insulin is not secreted effectively. Insulin is the key that unlocks cells and allows glucose to flow through to provide the cells with energy. However with the malfunctioning B cells, tissues such as liver and muscle become less responsive to insulin so there is a decrease in glucose uptake.

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5
Q

What is DKA ?

A

Diabetic ketoacidosis. Acute metabolic complication of diabetes.
There is a shortage of insulin so inadequate utilisation of glucose in cells. The liver then rapidly breaks down fats into ketones as a source of fuel.
Triglycerides and amino acids will be metabolised into acidic ketone bodies. Kidneys are unable to filter all of the ketones from the blood, making it very acidic. Body will compensate by removing excess hydrogen ion through carbon dioxide conversion, which increases resp rate.
Acidosis - 6.8 - 7.35

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6
Q

What is the DKA triad ?

A

All factors need to be present to diagnose. The ‘D’ – a blood glucose concentration of >11.0 mmol/L or known to have diabetes mellitus
The ‘K’ – a capillary or blood ketone concentration of >3.0 mmol/L or significant ketonuria (2+ or more on standard urine sticks)
The ‘A’ – a bicarbonate concentration of <15.0 mmol/L and/or venous pH <7.3

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7
Q

What are the 3 types of ketones produced by the body ?

A

1) Acetoacetate
2) 3-Beta-hydroxybutyrate
3) Acetone

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8
Q

What is euglycaemic DKA ?

A

Body produces high levels of ketones but without high blood sugar levels.
Seen in Pregnancy, surgery, starvation.
Imbalance between insulin and glucagon, cortisol, epinephrine.
Leads to reduced insulin availability, increased break down of fats into free fatty acids and ketoacidosis.

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9
Q

What is a hyperosmolar hyperglycaemic state ?

A

Common in T2 diabetes.
When blood sugar levels very high.
Occurs over weeks.
Due to illness, and dehydration.
Causes hyperglycaemia, dehydration (kidneys work harder to remove excess glucose) blood becomes more concentrated.
Confusion, tachy, high RR, hypotension
Misdiagnosed as strokes and seizures.

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10
Q

Why does ketosis not occur during HHS ?

A

Ketosis does not occur due to the presence of endogenous insulin within the body which is sufficient to prevent ketogenesis however insufficient to reduce the blood glucose.

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11
Q

What is hypoglycaemia ?

A

Blood glucose below 4mmols.
Due to Liver failure – (raised lactate, deranged LFT’s)
Alcohol misuse - inhibit liver function
Addison’s disease, adrenal insufficiencies.

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12
Q

What is HbA1c ?
How does it develop and why do you test for it ?

A

Glycated haemoglobin. It develops when haemoglobin, a protein within RBC that carries oxygen throughout your body, joins with glucose in the blood, becoming ‘glycated’. Measuring HbA1c gives average picture of blood sugar over weeks/months. When the body processes sugar, glucose in the bloodstream naturally attaches to haemoglobin. The amount of glucose that combines with this protein is directly proportional to the total amount of sugar that is in your system at that time. Because red blood cells in the human body survive for 8-12 weeks before renewal, measuring glycated haemoglobin (or HbA1c) can be used to reflect average blood glucose levels over that duration, providing a useful longer-term gauge of blood glucose control.

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13
Q

What are the mol / % ranges for HbA1c ?

A

Normal - below 42mol and 6%
Pre diabetes - 42-47 mol and 6-6.4%
Diabetes - 48mol and over and 6.5% and over

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14
Q

What are the microvascular long term complications of diabetes ?

A

Eyes - high BG and BP damage blood vessels around eyes, causing retinopathy, cataracts and glaucoma
Kidney - High BP damages vessels and excess BG overworks kidneys resulting, in nephropathy.
Neuropathy - hyperglycaemia damages nerves in peripheral NS. Result in pain / numbness. Feet wounds go undetected - gangrene.

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15
Q

What are the macrovascular long term complications of diabetes ?

A

Brain - increased risk of stroke and cerebrovascular disease, transient ischemic attack, cognitive impairment.
Heart - high BP and insulin resistance increase risk of CHD.
Extremities - peripheral vascular disease results from narrowing of blood vessels increasing risk for reduced or lack of blood flow in legs. Feet wounds heal slower

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16
Q

Explain retinopathy

A

Hyperglycaemia cause damage to retinal cells – Pericytes – regulate the blood flow to the retina
Damaged Pericytes causes weaken of the capillary wall and increased blood flow – Aneurysms
Increase thicken in the basement membrane and increase permeability.
Proteins and fats leak out of the capillary forms hard exudate.
Narrowing of the capillary bed by proliferation of endothelium cells.
Reduced blood supply and ischemia causes vascular proliferation.
New blood vessels are weak and can haemorrhage.

17
Q

Explain nephropathy

A

Progressive kidney disease caused by damage to the capillaries
Inflammatory response
Thickening of the glomerular basement membrane
Micro aneurysm formation
Expansion of supporting tissues
Fibrotic changes in the renal arterioles
Leakage of albumin in into the filtrate presents as protein in the urine –proteinuria.
Most common cause of end stage renal failure

18
Q

What does macrovascular mean ?

A

Persistent hyperglycaemia causes endothelium cells to take up glucose.
Causes the release of Reactive oxygen species as a by product
Stimulates the inflammatory response
Increased permeability and monocyte release. LDL are able to enter the vessel more easily
LDL’s and monocytes = Foam cells = Atherosclerosis

19
Q

Describe neuropathy

A

Hyperglycaemia affects and damages the Schwann cells on the neuron.
Degeneration of Schwann cells.
Ischemic effect due to damage to capillaries that feed the neurons.
Damages the microvascular blood supply and impairs wound healing
Polyneuropathies -
Numbness tingling impaired pain and temperature vibratory sensation altered
Mononeuropathies-
Mixed nerve trunk loss of sensation, pain and motor weakness.

20
Q

List some of the effects of autonomic neuropathy

A

Impaired vasomotor function– postural hypotension
Impaired gastrointestinal function
Gastroparesis dumping syndrome- eat small and often
Impaired genitourinary function
Paralytic bladder
Incomplete voiding
Erectile dysfunction
Retrograde ejaculation
Cranial nerve
Impaired pupillary response – reduced response to light
Extraocular nerve paralysis