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REGUB > Diabetes (18, 19, 24, 25) > Flashcards

Diabetes (18, 19, 24, 25) Flashcards

1
Q

What does the HbA1C reflect? Why is it significant?

A
  • reflects average blood glucose concentration over preceding few months
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2
Q

Can glucose in the urine be used as a diagnostic test for diabetes?

A

NO. People easily spill glucose into urine - false positives

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3
Q

What 2 tests are done more frequently now to diagnose diabetes?

A
  1. Fasting Plasma Glucose

2. HbA1C

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4
Q

In which cases can HbA1C NOT be used to diagnose diabetes?

A
  • patient acutely unwell
  • haemoglobinopathy
  • haemolytic anaemia
  • iron deficiency anaemia
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5
Q

List the diagnostic values to diagnose someone with pre-diabetes

A

Impaired Fasting Glucose: b/w 5.6 - 6.9

Impaired Glucose Tolerance: b/w 7.8 and 11.0

HbA1C: b/w 37 - 48 mmol/mpl (5.7 - 6.4%)

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6
Q

What is an impaired fasting glucose?

A

high blood glucose despite fasting for 8 or more hours

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7
Q

What is an impaired glucose tolerance?

A

high blood glucose after 2 hour glucose tolerance test

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8
Q

List the criteria/values that can be used to diagnose diabetes (2hr OGTT, Fasting PG, HbA1C, Random PG)

A

2 hr OGTT: greater than 11.1 mmol/L

Fasting PG: greater than 7.0 mmol/L

HbA1C: greater than 48 mmol/mol or 6.5%

Random PG: PG greater than 11.1 w/ symptoms - only need 1 test

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9
Q

What is an oral glucose tolerance test (GTT)?

A

plasma glucose measured 2 hours after eating

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10
Q

What cells are insulin released from?

A

beta cells of islets of Langerhans

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11
Q

What is C-peptide? Why is it important?

A
  • proinsulin cleaved to insulin and c-peptide

- c peptide has a longer half-life (good measure of insulin secretory activity)

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12
Q

Which organs/components of the body do NOT need insulin to take up and use glucose as an energy source?

A
  • brain
  • RBCs
  • renal tubules
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13
Q

Which organs/components of the body NEED insulin to take up and use glucose as an energy source?

A
  • adipose tissue
  • skeletal muscle
  • liver
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14
Q

List the overall effects of insulin (be specific - try to list all)

A
  • anabolic hormone

GLUCOSE:

  • promotes glucose uptake
  • inhibits gluconeogenesis (in liver)
  • inhibits glycogenolysis (in liver)
  • promotes glycogen synthesis (in liver)

FATTY ACIDS:

  • promotes FA uptake (create fat)
  • inhibits lipolysis

PROTEINS:

  • promotes protein synthesis
  • inhibits protein breakdown

KETONES:
- inhibits ketone body formation

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15
Q

What are the counter-regulatory hormones of insulin? When are they stimulated/released?

A
  • stimulated by hypoglycaemia

- glucagon, adrenaline, cortisol, growth hormone

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16
Q

List the overall effects of the counter-regulatory hormones

A
  • increase blood glucose
  • glycogen breakdown
  • hepatic gluconeogenesis
  • fat breakdown (lipolysis)
  • inhibition of fat formation
  • formation of ketone bodies
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17
Q

How does hyperglycaemia cause blurred vision?

A

deposition of glucose within the lens of the eye

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18
Q

What is the most common form of diabetes mellitus?

A

Type 2

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19
Q

What is pre-diabetes?

A
  • a/w with T2DM

- preceding period of abnormal glucose homeostasis

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20
Q

What is the common presentation of T1DM?

A
  • silent progression in preceding months
  • clinically manifest when critical mass of beta cells lost
  • present with acute symptoms (hyperglycaemia, polyuria, polydipsia, polyphagia, weight loss, blurred vision)
  • can also present with DKA
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21
Q

What happens to the levels of C-peptide in T1DM?

A

c-peptide reflects insulin secretory activity

in T1DM, c peptide is absent (no insulin present)

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22
Q

T1DM has a genetic predisposition. What genes are a/w with T1DM and which are protective?

A

HLA-DR3 and DLA-DR4 (a/w T1DM)

Protective: HLA-DR2

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23
Q

T1DM may be associated with circulating auto-antibodies to islet cell components. List some of the auto-antibodies that may be present

A 
anti-GAD
anti-IA2
anti-insulin
anti-islet cell 
zinc transporter 8 antibodies
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24
Q

What is insulitis? Why does it occur?

A

Insulitis: lymphocytic inflammation of the islets cells of langerhans
– may be caused by T1DM

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25
Q

T1DM may be associated with other autoimmune diseases such as…

A
  • thyroid disease

- coeliac disease

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26
Q

What initially happens to the levels of C-peptide in T2DM?

A

high insulin release to compensate = high C-peptide levels

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27
Q

Why is DKA rare in T2DM?

A

b/c there is still some insulin secretion - this tends to inhibit lipolysis and prevent ketogenesis

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28
Q

What is metabolic syndrome? (What 3 things does it encompass + what can it cause?)

A
  1. Abdominal Obesity
  2. Abnormal Lipids
  3. Insulin Resistance

tends to cause pre-diabetes/T2DM and hypertension

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29
Q

What is the typical presentation of T2DM?

A
  • longer preceding period of hyperglycaemia

- usually presents with COMPLICATIONS (or complications occur soon after diagnosis)

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30
Q

List some of the risk factors for T2DM

A
  • physical inactivity
  • abnormal lipids
  • hypertension
  • known vascular disease
  • previous pre-diabetes
  • increasing age
  • raised BMI
  • family history
  • ethnicity
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31
Q

What is Maturity Onset Diabetes of the Young (MODY)? What genes are associated with it?

A
  • autosomal dominant + strong family history
  • consider if young, insulin-independent + no signs of insulin resistance
  • gene defects including:
    hepatic nuclear factors 1-alpha and 4-alpha
    glucokinase

treated w/ sulphonylureas

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32
Q

How is MODY treated?

A

Sulphonylureas - stimulates pancreas to make insulin

33
Q

What is a Hyperosmolar Hyperglycaemic State (HHS)? What is it associated with?

A
  • typical of T2DM
  • increase in glucose secreted in urine (which draws water out creating hyperosmolar state)
  • gross hyperglycaemia + dehydration, coma
34
Q

List the areas where macrovascular complications may be involved with [5]

A
  • coronary arteries (heart)
  • cerebrovascular (stroke)
  • peripheral vascular* (peripheral vascular disease)
  • abdominal aorta
  • renal arteries + branches
35
Q

Why do wounds not heal well/properly in diabetics?

A

hyperglycaemia impairs macrophage function (decreases their phagocytic ability)

36
Q

What are the 3 main microvascular complications of diabetes?

A
  1. nephropathy
  2. retinopathy
  3. neuropathy
37
Q

The intensity/extent of microvascular complications of diabetes is directly dependent on what 2 factors?

A
  1. Duration of Hyperglycaemia

2. Degree of Hyperglycaemia

38
Q

What does fibrosis mean? What does sclerosis mean?

A

Fibrosis: replacement of normal parenchyma with collagen

Sclerosis: “hardening” of arteries; becomes dense

39
Q

What is the main pathological process that causes the microvascular complications in diabetes?

A

Hyaline Arteriosclerosis - thickening of the wall of arterioles

40
Q

List some of the pathological/histological features of diabetic nephropathy

A
  • hyaline arteriosclerosis
  • diabetic glomerulosclerosis
  • – increased mesangial matrix
  • – Kimmelstiel-Wilson lesion
  • thickened glomerular BM
41
Q

What are Kimmelstiel-Wilson nodules characteristic of?

A

diabetic nephropathy (diabetic glomerulosclerosis)

42
Q

Diabetic nephropathy, a microvascular complication, has 4 sequential stages. List them and give specific values

A
  1. Normal
  2. Microalbuminuria (30 - 300 mg per day)
  3. Macroalbuminuria (Frank Proteinuria) (> 300 mg per day)
  4. End Stage Renal Disease
43
Q

What numerical value is considered microalbuminuria?

A

30 - 300 mg of protein in urine per day

44
Q

What numerical value is considered macroalbuminuria?

A

> 300 mg of protein in urine per day

45
Q

What is the treatment/management plan fo diabetic nephropathy?

A
  • intensive glucose control
  • treat hypertension (ACE inhibitors, Angiotensin Receptor Blockers)
  • avoid other damage to kidneys (e.g. UTI, drugs…)
46
Q

How is albumin in the urine (proteinuria/albuminuria) measured? (especially in the context of diabetic nephropathy)

A

Albumin to Creatinine Ratio (UACR) [in a spot urine sample]

47
Q

What is another name for an ophthalmoscopy?

A

Fundoscopy

48
Q

What are the progressive stages of diabetic retinopathy?

A
  1. Background [vascular damage, microaneurysms]
  2. Pre-Proliferative [ischaemia - infarcts, mild/moderate/severe]
  3. Proliferative [neovascularization]
  4. ± Maculopathy [oedema, exudates or ischaemia affecting macula; altered visual acuity]
49
Q

What is the treatment/management plan for treating diabetic retinopathy?

A
  • intense glucose control

- laser photo-coagulation

50
Q

What are the 2 types of diabetic neuropathy that may occur?

A
  1. Symmetrical Peripheral Sensorimotor Neuropathy

2. Autonomic Neuropathy

51
Q

What is the most common type of diabetic neuropathy to arise?

A

Symmetrical Peripheral Sensorimotor Neuropathy

52
Q

Diabetics have an increased risk of infection as diabetes alters phagocyte function. What organism may be increasingly colonised in these patients?

A

Staphylococcus aureus

53
Q

Diabetics have an increased risk of infection as diabetes alters phagocyte function. In these patients, their oral and genital mucosa may be colonised by which organism?

A

Candida

54
Q

What is the main adverse effect of intense glucose control?

A

hypoglycaemia

55
Q

What are the 3 main categories of treatment for T2DM

A
  1. Drugs (metformin, sulphonylureas, thiazolidinediodes, GLP-1 analogues, SGLT inhibitors)
  2. Insulin (usually in advanced T2DM)
  3. Bariatric Surgery
56
Q

If a diabetic women is pregnant, what are some of the complications that may occur?

A
  • foetal malformation
  • macrosomy (big baby)
  • delivery complications
  • pre-eclampsia
  • miscarriage
  • infection
  • intrauterine growth retardation
  • polyhydramnios
57
Q

What is polyhydramnios? What is it associated with?

A
  • there is too much amniotic fluid around the baby during pregnancy
  • a/w pregnancy occuring in diabetic women
58
Q

What is gestational diabetes mellitus? When does it normally occur? What is a possible complication?

A
  • transient hyperglycaemia induced by hormones of pregnancy
  • typically reverts to normal after delivery (but strong risk for mum developing T2DM)
  • emerges at 24-28 weeks of pregnancy
  • relationship b/w maternal blood glucose and fetal size (macrosomy)
59
Q

What are the 2 types of T1DM?

A
  1. Type 1A - autoimmune

2. Type 1B - non autoimmune/idiopathic

60
Q

List some examples of basal insulins

A
  • NPH or Insulatard
  • Glargine or Lantus
  • Levemir or Detemir
  • Degludec
  • Insulin Tuojeo
61
Q

What time of day are basal insulins usually given?

A

evening or bedtime

62
Q

List some examples of bolus insulins

A
  • Actrapid (regular)
  • NovoRapid (Aspart)
  • –FiAsp (fast-acting novorapid)
  • Humalog (Lispro)
  • Glulisine (Apidra)
63
Q

What are mixture insulins? Why may they be used?

A
  • mix of 2 insulins in one

- used in elderly patients b/c less # of injections (only 2)

64
Q

What are the disadvantages of mixture insulins [2]

A
  • inflexible regime

- high risk of hypoglycaemia

65
Q

What is the HbA1c target in T1DM?

A

< 7.0%

66
Q

Diabetic retinopathy proceeds through progressive stages. List some characteristics of the “background” phase

A
  • microaneurysms
  • exudates
  • “dot and blot” haemorrhages
67
Q

Diabetic retinopathy proceeds through progressive stages. List some characteristics of the “non-proliferative” phase

A
  • cotton wool spots (soft exudates - signs of ischaemia)
  • blot haemorrhages (bigger haemorrhages)
  • hard exudates (lipid/protein)
68
Q

Diabetic retinopathy proceeds through progressive stages. List some characteristics of the “proliferative” phase

A
  • ischaemia occuring
  • neovascularization
  • new vessels at disc (NVD)
  • new vessels elsewhere (NVE)
  • vitreal haemorrhage
69
Q

Diabetic retinopathy proceeds through progressive stages. List some characteristics of advanced diabetic retinopathy

A
  • vitreous haemorrhage
  • tractional retinal detachment (consequence of above)
  • rubeosis iridis
  • neovascular glaucoma
  • blindness
70
Q

What may cause retinal detachment?

A

vitreous haemorrhage

71
Q

What is rubeosis iridis?

A

blood vessels develop on the anterior surface of the iris (in response to ischaemia)
– a/w diabetic retinopathy [advanced stage]

72
Q

What is a hyphema? What can cause this condition?

A

Hyphema: blood in anterior chamber of the eye

- can be caused by rubeosis iridis (neovascularization of iris)

73
Q

What is Charcot’s Foot? What is it a complication of?

A
  • consequence of diabetic neuropathy
  • characterized by joint dislocations, fractures, debilitations, deformities
  • bones in feet unstable
74
Q

Compression neuropathy may occur as a consequence of diabetic neuropathy. What is a consequence of compression neuropathy?

A

muscle wasting

75
Q

ACE inhibitors should be carefully given to younger females as they are…

A

teratogenic - shouldn’t be given to pregnant women

76
Q

List the 3 criteria to make a diagnosis of DKA

A
  1. Ketonaemia > 3.0 mmol/L
  2. Blood Glucose > 11.0 mmol/L
  3. pH < 7.3 OR Bicarbonate < 17.0 mmol/L
77
Q

What is the management plan for DKA?

A
  • correction of volume deficits (fluids)**
  • insulin therapy**
  • potassium monitoring + replacement
  • acidosis correction
  • IV antibiotics
78
Q

In a pre-diabetic patient, which individual value - IFG or IGT - will most likely lead to T2DM in 5 years?

A

Impaired Glucose Tolerance (2 hr OGTT)

- 50% risk of T2DM

REGUB (22 decks)

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