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Endocrinology > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is the role of insulin (6).

A

Skeletal muscles
- Stimulates glucose uptake & glycogen synthesis

Liver
- Supresses hepatic glucose output (inhibits glycogenolysis and gluconeogenesis)

Adipose Tissue

  • Stimulates lipogenesis (storage of fats)
  • Supresses lipolysis and proteolysis

Other
- Activates ATPase - uptake of K into cells

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2
Q

Cells and hormones secreted in the Islet of Langergans

A
  1. Alpha cells = glucagon
  2. Beta cells = insulin, amylin
  3. Delta cells = somatostatin
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3
Q

Role of glucagon

A
  1. Increases hepatic glucose output (via glycogenolysis, gluconeogenesis)
  2. Reduces peripheral glucose uptake
  3. Lipolysis
  4. Muscle glycogenolysis
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4
Q

What is glycogenolysis

A

Breakdown of glycogen into glucose

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5
Q

What is gluconeogenesis

A

Production of glucose

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6
Q

What is glycogenesis

A

Production of glycogen (using glucose)

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7
Q

What is glycolysis

A

Breakdown of glucose into pyruvate

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8
Q

What is lipogenesis

A

Synthesis and storage of FFA and triglycerides as fat in liver and adipose tissue

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9
Q

CHO metabolisms in fasting state

A
  1. Glucose from LIVER delivered to insulin-independent tissues (brain, RBCs)
  2. Insulin levels are low - this is sufficient to prevent breakdown of fat in insulin-sensitive tissues
  3. Muscles use FFA for energy
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10
Q

CHO metabolism after feeding state

A
  1. Rising BGL after eating stimulates insulin secretion and supresses glucagon
  2. Ingested glucose helps replenish glycogen stored in liver and muscle
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11
Q

What is Diabetes Mellitus?

A

Disorder of CHO metabolism characterised by hyperglycaemia

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12
Q

Name 8 complications of DM

A
  1. Microvascular (retinopathy, nephropathy, and neuropathy)
  2. Macrovascular (IHD, peripheral vascular disease, and CVD)
  3. DKA
  4. HHS
  5. Hyperglycaemia
  6. Other autoimmune disorders
  7. Opportunistic Infections
  8. Psychological complications, reduced QoL & life expectancy
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13
Q

Describe pathophysiology of DKA and why may you get hyperkalaemia

A

Ketoacidosis

  1. Shortage of insulin & hyperglycaemia
  2. Inc lipolysis (breaks down fat–>FFA)
  3. FFA is used as alternative energy source
  4. Liver uses FFA to produce ketone bodies
  5. Ketone bodies are used for energy but inc acidity of the blood (ketoacidosis)

Hyperkalaemia

  1. Extra H+ in blood goes to H/K pump and pumps K into blood
  2. Lack of insulin means reduced stimulation of ATPase so K is not pumped into cells
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14
Q

Signs, Symptoms, Investigations, Treatment of DKA

A

Signs and Symptoms

  1. hyperglycaemia related sx (polydipsia, polyuria, polyphagia, glycosuria)
  2. Osmotic diuresis
  3. GI upset - N+V, abdo pain, weight loss
  4. Fruit acetone breath
  5. Kussmaul breathing

Investigations

  1. Serum glucose and ketones
  2. U&E - look for hyperkalemia
  3. Urinalysis
  4. ABG - look for metabolic acidosis
  5. Others to consider - Chest Xray, ECG (any arrythmias)
Treatment and Management
Fluid, electrolyte, insulin replacement 
1. ABCDE + IV fluid must be done before insulin
2. IV insulin 
3. Replacement of electrolytes
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15
Q

What is DKA?

A

(1. ) It is a medical emergency characterised by hyperglycaemia, ketonemia, acidemia (remember DKA = Diabetes, Ketonemia, Acidemia)
(2. ) Failure of lipolysis –> breaking down fat at a rate that is much too fast. The liver processes the fat into a fuel called ketones, which causes the blood to become acidic.
(3. ) More common in type 1

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16
Q

What is HHS? and RF?

A
  1. High serum osmolarity with little/no ketosis and extreme dehydration.
  2. Common in Type 2
  3. RF = infections, medications (diuretics, Bb, steriods), CV event, non-adherence to insulin, overconsumption of CHO.
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17
Q

Symptoms, Investigations, Treatment of HHS

A

Symptoms

  1. Hyperglycaemia related symptoms
  2. Dry mucosus mb + poor skin tugor
  3. Cognitive impairment (lethargy, disorientation, stupor)
  4. Blurred vision
  5. Tachycardia + Hypotension

Investigations

  1. BGL, ketones (rule out DKA), serum osmolarity
  2. ABG

Treatment

  1. IV fluids
  2. IV insulin
  3. Correction of electrolytes
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18
Q

What hypoglycaemia? And how does the body respond to this in a non-diabetic and diabetic.

A
  1. low BGL <3.9mmol/L. More common in T1DM due to over-administration of insulin.
  2. Normal response to hypo = protective mechanisms kick -> ADRENALIN + GLUCAGON -> INHIBITION OF INSULIN
  3. DM response to hypo = altered threshold leading to impaired awareness of low BGL. Body resets to 2.5mmol/L for mechanisms to kick in.
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19
Q

Signs and Symptoms of hypoglycaemia - how would you differentiate between mild and severe hypo?

A
  1. mild = episode is self treated, severe = cognitive dysfunction
  2. Sympathoadrenal symptoms (<3.0mmol/L) = sweating, anxiety, tremor, palpitations due to inc glucagon, adrenaline, cortisol, GH.
  3. Neuroglycopenic symptoms (<2.8mmol/L) = blurred vision, dizziness, coma due to insufficient glucose supply to brain
20
Q

Causes of hypoglycaemia (6)

A
  1. Poor use of insulin therapy
  2. More exercise than normal
  3. Medication taken without eating
  4. Missing meal
  5. Alcohol on empty stomach
21
Q

Examination and Investigation of Hypoglycaemia

A

Examination
1. Are the following seen?: Altered consciousness, hypotension, tachycardia, visible tremor, sweaty, aggressive

Investigation

  1. Random plasma glucose
  2. HbA1c
  3. U&E
  4. GFR
  5. Urine albumin:creatine
22
Q

Treatment of Hypoglycaemia

A
  1. Fast release CHO e.g. dextro tablets
    - Retest BGL and repeat up to x3
    - Follow with long-acting carb
  2. IM glucagon
    - If BGL still low OR unable to swallow OR unconscious
    - Follow with long-acting carb
  3. IV glucose
    - if starved or intoxicated
23
Q

Management of hypoglycaemia

A
  1. Review insulin regime

2. Patient education - hypoglycaemic awareness

24
Q

What is Pre-diabetes?

A
  1. BGL is high but not high enough for Dx of diabetes. May also demonstrate: impaired fasting glucose or impaired glucose tolerance. This doesn’t usually cause symptoms
  2. Pts should should be educated regarding diabetes and implement lifestyle changes to reduce their risk of progressing to diabetes.
  3. They are not currently recommended to start medical treatment at this point.
25
Q

Pathogenesis of Type 1

A
  1. Insulin deficiency diabetes
  2. AI destruction of beta cells (type 4 hypersensitivity reaction), where HLA-antigens of b-cells are attacked by T-cells
  3. Loss of b-cells mean reduced insulin secretion
  4. Low insulin secretion results in:
    (a) Continued hepatic glucose output via glycogenolysis and gluconeogenesis
    (b) Supression of peripheral glucose uptake
    (c) Unrestrained lipolysis and muscle breakdown
    altogether they inc BGL –> hyperglycaemia
26
Q

Investigation of type 1 and 2

A

Two abnormal results are required for DM Dx:

  1. Random plasma glucose >11.1
  2. Fasting plasma glucose >7
  3. 2hr plasma glucose
  4. HbA1c >6.5%
  5. OGTT in pregnancy

Further tests for Type 1 only:

  1. Plasma or urine ketones
  2. Fasting C-peptides
  3. Autoimmune markers
27
Q

Random plasma glucose

A
  1. > 11.1mmol/L

2. Blood sample taken form pt and analysed for amount of glucose in blood, see if elevated or not

28
Q

Fasting plasma glucose

A
  1. Normal <7mmol/L

2. No calorie intake for 8h before test is taken

29
Q

2hr plasma glucose

A
  1. Blood sample taken and 75mg is given
  2. 2hrs later: another blood sample is taken to measure difference in glucose.
  3. PT must avoid activity as this can affect results
30
Q

HbA1c

A
  1. Diabetes HbA1c = >6.5%
  2. Measures average glucose levels for over 3 months
  3. Should not be used in:
    - under 18 years
    - Pregnant women or 2m postpartum.
    - Symptoms of diabetes for less than 2 months.
    - High diabetes risk who are acutely ill.
    - Taking medication that may cause hyperglycaemia (for example corticosteroids).
    - Acute pancreatic damage, including pancreatic surgery.
    - End-stage chronic kidney disease.
    - HIV infection.
31
Q

Treatment (&SE) and management for type 1

A
  1. Basal-bolus insulin therapy
    - mimics normal physiology
    - Bolus = Rapid acting used before meal, requires DAFNE approach
    - Basal (x2/day) = control BGL between meals and during the night

SE = weight gain, hypoglycaemia, hypokalaemia, localised lipoatrophy

Management

  1. Diet + exercise
  2. Dec alcohol + smoking cessation
  3. Regular BGL and HbA1c monitoring
32
Q

Signs and Symptoms of type 1 and 2

A

Hyperglycaemia related symptoms for both types:

  • Polyuria
  • Polydipsia
  • Glycosuria
  • Polyphagia
  • blurred vision

Type 1, DKA symptoms

  • Fruity acetone breath
  • Kussmaul breathing
  • GI upset (weight loss, nausea, vomitting)

Type 2
- Opportunistic infections

33
Q

Pathophysiology of Type 2 Diabetes

A
  1. B-cells makes insulin but cells are insulin resistant (due to repeated exposure to glucose & insulin) and do not respond
  2. There is no peripheral glucose uptake (translocation of GLUT-4 is impaired)
  3. B-cells compensate by producing more insulin. They undergo hyperplasia and hypertrophy in attempt to maintain normoglycemia.
  4. Beta cells also secrete amylin and over time this aggregates in the islets.
  5. B-cell compensation isn’t sustainable and over time become exhausted, dysfunctional and die off.
  6. Insulin levels dec and BGL inc leading to hyperglycaemia.
  7. Hyperglycaemia and extreme dehydration can result in HHS.
34
Q

Treatment and Management of Type 2 (1st, 2nd, 3rd, 4th line)

A
  1. Patient Education and lifestyle intervention (exercise, diet). If fail to control HbA1c proceed to anitdiabetic drugs:
  2. Metformin (1st line) if metformin CI/fail: DPP4i, GLP1, SGLT2i, SU, Pioglitazone
    - Metformin CI: DKA, renal impairment, low BMI, lactic acidosis risk
  3. Dual therapy (metformin + drug) [2nd line]
  4. Triple therapy (metformin + 2 drugs) [3rd line]
  5. Insulin therapy if triple therapy fails
35
Q

What antidiabetic treatment cause hypoglycaemia?

A

Sulfonyureas, Insulin

36
Q

What antidiabetic treatment is indicated and contraindicated in pregnancy

A
  • indicated = insulin

- contraindicated = sulfonyureas

37
Q

What antidiabetic treatment causes weight gain?

A
  1. Sulfonyureas
  2. Thiazolidinediones
  3. Insulin
38
Q

What are the SE, contraindications of metformin

A
  1. SE = Nausea, abdo pain, diarrhoea, wt loss

2. CI: DKA, renal impairment, low BMI, lactic acidosis risk

39
Q

What are the SE, contraindications of insulin?

A
  1. SE = hypoglycaemia, weight gain, hypokalaemia, localised lipatrophy
  2. Contraindicated = hypersensitivity, hypoglycaemia
40
Q

What are the SE, contraindications of thiazolidinediones

A
  1. SE = Inc CV risk, fluid retention, hepatotoxicity, wt gain
  2. CI = T1DM, hepatic disease, heart failure, bladder cancer
41
Q

What are the SE, contraindications, drug interactions of sulfonylureas?

A
  1. SE = wt gain, hypoglycaemia, CVD, GI problems

2. Contraindication = Renal and hepatic failure, pregnancy, breastfeeding

42
Q

Name a thiazolidinediones drug

A

Pioglitazone, glitazone

43
Q

Name a sulfonylureas drug

A

Gliclazide, glibenclamide

44
Q

What is mixed (biphasic) regime?

A
  • One, two or three short acting insulin mixed with intermediate acting insulin
  • Insulin preparation can be mixed by pt or can use premixed products
45
Q

What is basal-bolus regime

A
  1. Used to mimic normal insulin physiology
  2. Bolus = rapid or short acting insulin would be used before meals
  3. Basal = intermediate, long acting insulin would be taken once/twice and acts throughout the day
46
Q

What are the complications of insulin therapy?

A
  1. Hypoglycaemia
  2. Hypokalemia
  3. Lipodystrophy
  4. Weight gain
  5. Others: Headache, weakness, hunger, sweating, dizziness, anxiety, tachycardia

Endocrinology (9 decks)

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