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LSB658 > Metabolism and diabetes mellitus > Flashcards

Metabolism and diabetes mellitus Flashcards

1
Q

Blood glucose control is dependent on what status?

A

Nutritional

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2
Q

When is insulin released, before or after a meal?

A

After, as blood glucose levels rise

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3
Q

What is stimulated by insulin?

A

Uptake and utilisation of glucose by cells

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4
Q

What three chemicals are released several hours after a meal as blood glucose levels fall?

A

Glucagon, cortisol, and adrenaline

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5
Q

What processes are stimulated as blood glucose levels fall several hours after a meal?

A
  • Glycogenolysis
  • Gluconeogenesis
  • Glucose is released from the liver
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6
Q

What pathways are stimulated when insulin signals the fed state?

A

Cellular uptake and storage

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7
Q

Which pathways are inhibited when insulin signals the fed state?

A

Fuel breakdown

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8
Q

List the four processes that occur when insulin signals the fed state

A
  • Uptake of fuel substrates into some cells (muscle, adipose tissue)
  • Storage of fuels (lipids, glycogen)
  • Inhibits gluconeogenesis
  • Biosynthesis of macromolecules (proteins, DNA)
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9
Q

Glucose utilisation causes BSL to fall to normal; what is the result of this?

A

Insulin secretion falls

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10
Q

Which pathwas are stimulated when glucagon signals the fasted state?

A

Fuel breakdown

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11
Q

Which pathways are inhibited when glucagon signals the fasted state?

A

Cellular uptake and storage

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12
Q

List the five processes that occur when glucagon signals the fasted state

A
  • Increasing glycogen breaking/inhibiting glycogen synthesis
  • Inhibiting fuel storage (lipids, proteins)
  • Stimulates gluconeogenesis
  • Enhances ketogenesis in liver (ketone body production from fatty acids)
  • Promotes protein breakdown in liver (does not effect muscle protein)
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13
Q

Between meals, ____ is released from the pancreas

A

Glucagon

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14
Q

Between meals, adipose tissues breaks down triglycerides into ____ ____ and ____.

A

Fatty acids; glycerol

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15
Q

Between meals, skeletal muscle is broken down to ____ ____.

A

Amino acids

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16
Q

What happens to the amino acids broken down from skeletal muscle when between meals?

A

The liver converts them to glucose which is exported to the blood

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17
Q

Between meals, the liver converts excess fatty acids to ____

A

Ketones

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18
Q

The brain can use ____% ketones during starvation

A

60%

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19
Q

Following a meal, ____ is released from the pancreas

A

Insulin (in response to a detected rise in BGL)

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20
Q

Following a meal, all tissues use ____ as an energy source.

A

Glucose

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21
Q

Following a meal, adipose tissues converts excess glucose to ____ ____ and then to ____.

A

Fatty acids; triglycerides

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22
Q

Following a meal, skeletal muscle converts excess glucose to ____.

A

Glycogen

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23
Q

Following a meal, the liver converts excess glucose and protein to glycogen, and further excess to ____ ____ and ____ to be transported to adipose tissue for storage.

A

Fatty acids; triglycerides

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24
Q

Following a meal, ____ ____ are used for tissue building and repair.

A

Amino acids

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25
Q

What is the meaning of ‘diabetes mellitus’?

A

Sweet urine — BGL is so high it overwhelms the ability of the kidneys to hold onto glucose so it is secreted in urine

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26
Q

In simple terms, diabetes mellitus is due to…

A

Lack of insulin secretion, action, or both

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27
Q

Diabetes mellitus is characterised by chronic ____.

A

Hyperglycaemia

28
Q

Briefly differentiate between IDDM and NIDDM

A

IDDM — cannot produce insulin

NIDDM — does not respond to insulin

29
Q

List and describe three overarching components of diabetes mellitus

A
  • Polydipsia — increased thirst (glucose in blood draws water out of cells)
  • Polyuria — increased urination (glucose in urine draws water into urine in kidneys)
  • Polyphagia — increased hunger (glucose remains in the blood rather than going into cells, ∴ body thinks it is starving)
30
Q

Differentiate between type 1 and 2 diabetes with regard to insulin secretion

A

Type 1: none

Type 2: normal/increased

31
Q

Differentiate between type 1 and 2 diabetes with regard to age of onset

A

Type 1: early

Type 2: late adult years/obesity trigger

32
Q

Differentiate between type 1 and 2 diabetes with regard to speed of onset

A

Type 1: rapid

Type 2: slow

33
Q

Differentiate between type 1 and 2 diabetes with regard to percentage of total diabetics

A

Type 1: 10-20%

Type 2: 80-90%

34
Q

Differentiate between type 1 and 2 diabetes with regard to pathophysiological defect

A

Type 1: destruction of β-cells

Type 2: insulin resistance

35
Q

Differentiate between type 1 and 2 diabetes with regard to treatment/management

A

Type 1: insulin, exercise, diet

Type 2: weight reduction, exercise, diet, drug therapies

36
Q

List the symptoms of diabetes mellitus

A
  • Hyperglycaemia
  • Polydipsia
  • Polyuria
  • Polyphagia
  • Weight loss (IDDM)
  • Slow healing
  • Blurred vision
  • Fatigue
37
Q

How does insulin deficiency lead to hyperglycaemia?

A
  • Decreased glucose uptake
  • Increased liver glycogenolysis
  • Increased gluconeogenesis
38
Q

Insulin deficiency causes decreased glucose uptake, resulting in an ____ ____ ____ and ∴ polyphagia

A

Intracellular glucose deficiency

39
Q

What are the effects of insulin deficiency on proteins?

A
  • Increased protein breakdown, leading to muscle wasting (∴ weight loss) and increased blood amino acids
  • Decreased amino uptake by cells, also increasing blood amino acids
  • Blood amino acids leads to increased gluconeogenesis and ∴ aggravating hyperglycaemia
40
Q

What is the osmotic effect of hyperglycaemia?

A

The hypertonic effect of hyperglycaemia causes water to be drawn from cells into ECF, then into blood then urine, causing dehydration

41
Q

Explain the link between pancreatic damage and free radicals

A
  • High glucose in pancreatic β-cells results in enhanced free radicals
    • Damage and loss of β-cell function
    • Reduced ability to secrete insulin
42
Q

Explain glycation/glycosylation of proteins

A

Glucose and proteins react together which causes the proteins to malfunction, resulting in vascular stiffening, hypertension, nephropathy, and retinopathy

43
Q

Why do diabetics have increased blood lipid levels?

A

Increased lipolysis leads to raised fatty acid levels. These are transported to the liver where they are converted back to triglycerides, which are carried by VLDL (very low density lipoprotein)

44
Q

Why might uncontrolled type 1 diabetics have increased ketone levels?

A

Lack of insulin leads to increased triglyceride breakdown. The fatty acids are transported to the liver and metabolised to acetyl CoA then ketones are formed.

45
Q

Why does uncontrolled type 2 diabetes rarely involve elevated ketones?

A

They have sufficient insulin to prevent ketogenesis

46
Q

What is acanthosis nigricans?

A

A skin disorder — dark patches of skin (often appearing in the armpits, groin, and neck) due to high levels of insulin in the blood (i.e. insulin resistance)

47
Q

How does forgotten insulin or drug use cause DKA?

A

Forgotten insulin/drug use leads to hyperglycaemia. There is no glucose inside cells, so fatty acids are metabolised and ketones (acidic) are produced.

48
Q

List some symptoms of DKA

A
  • Confusion
  • Dizziness
  • Dehydration
  • Polydipsia
  • Hyperglycaemia
49
Q

What is the rx for DKA?

A

Insulin and rehydration

50
Q

What is the diabetic emergency seen in NIDDM?

A

Hyperosmolar hyperglycaemic state (HHS)

51
Q

Why does HHS sometimes have more severe outcomes than DKA?

A

Underlying conditions (e.g. sepsis)

52
Q

List some symptoms of hyperglycaemia (>10mmol/L)

A
  • Dehydration
  • ALOC
  • Seizure
  • Hypotension
  • Tachycardia
  • Pale/cold unless fever is present
  • Kussmaul breathing (IDDM only) — hyperventilation to reduce CO2 in blood
53
Q

Explain the link between diabetes mellitus and hyperkalaemia

A

Insulin shifts K+ into cells; without it K+ remains in the blood.

54
Q

Explain how renal compensation for acidosis only exacerbates hyperkalaemia in diabetic pts

A

Kidneys attempt to remove H+ (acid) from blood by switching it with K+ in urine to be secreted. The K+ is returned to the blood, however insulin is not present to move K+ into cells, raising K+ levels in blood

55
Q

What is one of the most common causes of hyperkalaemia?

A

Renal failure

56
Q

List some possible outcomes of >5mmol/L serum K+

A
  • Cardiac arrrest
  • Wide complex tachycardia
  • Bradycardia
  • VF
  • Thrombus formation
57
Q

What is the effect of hyperkalaemia on cardiac muscle?

A

Initially increases frequency of depolarisation events as membrane potential is less negative; eventually leads to Na channel inactivation and ∴ slower conduction (bradycardia)

58
Q

List four ECG features indicative of hyperkalaemia

A
  • Peaked T waves
  • Flat/lost P waves
  • Wide QRS
  • Fusion with T wave (forming sine wave)
59
Q

Hyperkalaemia may present as what other cardiac emergency?

A

STEMI

60
Q

List and explain the rx for hyperkalaemia

A
  • Calcium gluconate 10%
    • Stabilises myocardium be reducing excitability
  • Sodium bicarbonate
    • Counteracts acidosis
  • Salbutamol
    • Stimulates movement of K+ into cells
    • Activates Na/K pump
  • Insulin + glucose
    • ​Insulin facilitates movement of K+ into cells
61
Q

What are two rx options for hyperkalaemia in the long term?

A
  • Dialysis (quickest way to remove K+ from blood)
  • Ion exchange resins (binds K+ in exchange for Na [contraindicated for HTN/CHF])
62
Q

Explain the link between long term diabetes/hyperglycaemia and the significant complications of vascular damage

A
  • Vascular cells can gather attached glucose after prolonged exposure (i.e. lesions form ∵ glycosylation)
  • This impaired blood flow can lead to tissue necrosis in the extremities, atherosclerosis, retinal damage, renal failure, and neuropathies
63
Q

What is neuropathy?

A

Damage to small blood vessels supplying nerves and preventing proper function, resulting in varies symptoms including diarrhoea, erectile dysfunction/impotence, incontinence, difficulty swallowing, speech difficulty, and drooping facial muscles

64
Q

What is nephropathy, and what are the long term results?

A

Damage to small blood vessels supplying the kidneys. Kidneys become ‘leaky’, causing hypertension and oedema, eventually resulting in renal failure.

65
Q

What is macrovascular disease?

A

Damage to large blood vessels supplying the heart and brain, leading to atherosclerosis and significantly increasing risk of MI and stroke.

LSB658 (11 decks)

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