Module 1 Flashcards

1
Q

what are the acute complications of diabetes mellitus

A
  • hypoglycaemia
  • hyperglycaemia in very unwell patients
  • diabetic ketoacidosis - type 1 DM
  • hyperosmolar hyperglycaemic state/syndrome - type 2 DM
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2
Q

complications of Type 1 and 2 DM

what is hypoglycaemia

A
  • defined as a BGL <4mmoI/L
  • can be fatal
    causes
  • medication overdose
  • not eating enough carbohydrates or skippin meals
  • excess alcohol consumption
  • excessive exercise
  • malnutrition
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3
Q

clinical manifestations

hypoglycaemia

A
  • BGL <4mmoI/L
  • sweating
  • pale
  • hunger
  • dizziness
  • anxiety
  • seizures
  • coma
  • death
  • vision changes
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4
Q

hypoglycaemia - management

A
  • if the person is unconciouss, drowsy - do not give them food
  • medical emegrency
  • check BGL <4mmoI/L
  • eat 15-20g of fast acting carbohydrates
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5
Q

complications of hyperglycaemia

A
  • acutely unwell
  • stress mehcanism
  • impaired insulin function
  • hyperglycaemia
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6
Q

what is diabetic ketoacidosis (DKA)

A
  • medical condition
  • related to hyperglycaemia
  • due to lack of insulin leading to glucose build up in blood
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7
Q

risk factors of DKA

A
  • new diagnosis
  • acute stress or illness
  • omission of inuslin
  • lack of access to medical care
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8
Q

DKA clinical manifestations

A

lab markers
* BGL >11mmoI/L
* ketones present in blood and urine
symptoms
* sunken eyes
* dry skin
* headache
* polyuria
* polydipsia
* abdo pain

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9
Q

DKA management

A
  • correction of dehydration
  • reverse ketosis
  • acid base and electrolyte corrections
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10
Q

complications

hyperosmolar hyperglycaemic state (HHS)

A
  • complications arising from T2D seen at initial presentation
  • severe dehydration
  • high serum osmality
  • very unwell
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11
Q

risk factor/ causes of HHS

A
  • elderly - reduced thirst or fluid intake
  • poorly controlled t2d
  • infection and illness
  • drugs that reduce insulin action
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12
Q

clinical manifestations of HHS

A

lab markers
* BGL >30mmoI/L
* ketones can be present/ absent
symptoms
* polyuria +
* polydispia +
* sunken eyes
* coma
* seizures
* abdo pain
* weakness
* cramps
* dry skin

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13
Q

HHS management

A
  • correction of dehydration
  • reverse hyperglycaemia
  • acid base and electrolyte corrections
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14
Q

whats the normal fasting BGL range

A

4-6 mmoI/L

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15
Q

what causes type 1 diabetes

A
  • autoimmune destruction of the beta cells
  • genetics
  • envrionmental factors - drugs, viruses
  • non immune mediated diabetes - secondary to other conditons (pancreas_
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16
Q

whats the pathophysiology of T1D

A
  1. genetic factors or viral infections cause
  2. immune response against beta cells which cause
  3. beta cell destruction
  4. lack of insulin released
  5. GLUT - 4s are not activated
  6. glucose unable to be taken up by cells leads to either
  7. hyperglycaemia which leads to T1D OR
  8. release of glucagon which leads to
  9. liver continuing to release glucose which leads to hyperglycaemia which leads to T1D
17
Q

clinical manifestations of T1D

A
  • 3 P’s (polyphagia, polyuria, polydispia)
  • fatigue
  • weight loss
  • blurred vision
  • confusion
  • abdo pain
  • nausea/ vomitting
  • coma
18
Q

treatment of T1D

A
  • insulin is the only teatment option for T1DM
  • protein based molecule
19
Q

risk factors of T2D

A
  • genetic factors/ family history
  • overweight/ obese
  • sedentary lifestyle
  • age 35> + overweight
  • history of gestational diabetes
20
Q

pathophysiology of T2D

A
  • characterised by insulin resistance
  • decreased insulin production
  • increased insulin resistance at the cell
  • decrease beta cell responsiveness
22
Q

what is the inflammatory response

A
  • response is rapid
  • limit the extent of injury
  • destroy contaminating infectious microorganisms
  • initate the immune response
  • begin healing process
23
Q

homeostaitic role in PGs, TXA2 and COX

A
  • COX enzymes are required to produce the mediators thromboxanes and prostaglandins
  • thromboxanes - involved in blood clotting function
  • PGI2- initate platlet activation
24
Q

what causes hypoglycaemia

A
  • excess alcohol consumption
  • exercise
  • insulin overdose
25
Q

what contributes to an increased insulin resistance and decreased production in T2D

A
  • a reduction in the number of insulin binding sites
  • a decrease in the amount of insulin binding to the receptors
  • decreased insulin production in the pancreas
26
Q

what can increase the risk of a person developing T2D

A

having both parents and a maternal grandmother diagnosed with T2D

27
Q

what is the role of insulin?

A
  • allows glucose uptake into the cells for ATP production
  • stimulate protein syntheis
  • inhibits liver production of glucose
28
Q

the role of insulin is to what?

A

reduce blood glucose levels

29
Q

after the consumption of carbohydrates, the pancreas releases what?

30
Q

when required for energy the liver breakdowns stored glycogen ans converts it to what?

31
Q

a BGL less than 4.0mmo/L is known as what ?

A

hypoglycaemia

32
Q

it is important to maintain fasting BGL between what?

A

4 to 6 mmo/L to prevent disease

33
Q

what can cause hypoglycaemia

A
  1. exercise
  2. insulin overdose
  3. excess alcohol consumption
34
Q

the role of insulin includes what

A
  • stimulates protein synthesis
  • allows glucose uptake into the cells for ATP production
  • inibits liver production of glucose
35
Q

what is the first line treatment for type 2 diabetes

A

increasing physical activity