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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
T1DM may be associated with other autoimmune diseases such as...
- thyroid disease | - coeliac disease
26
What initially happens to the levels of C-peptide in T2DM?
high insulin release to compensate = high C-peptide levels
27
Why is DKA rare in T2DM?
b/c there is still some insulin secretion - this tends to inhibit lipolysis and prevent ketogenesis
28
What is metabolic syndrome? (What 3 things does it encompass + what can it cause?)
1. Abdominal Obesity 2. Abnormal Lipids 3. Insulin Resistance tends to cause pre-diabetes/T2DM and hypertension
29
What is the typical presentation of T2DM?
- longer preceding period of hyperglycaemia | - usually presents with COMPLICATIONS (or complications occur soon after diagnosis)
30
List some of the risk factors for T2DM
- physical inactivity - abnormal lipids - hypertension - known vascular disease - previous pre-diabetes - increasing age - raised BMI - family history - ethnicity
31
What is Maturity Onset Diabetes of the Young (MODY)? What genes are associated with it?
- 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
32
How is MODY treated?
Sulphonylureas - stimulates pancreas to make insulin
33
What is a Hyperosmolar Hyperglycaemic State (HHS)? What is it associated with?
- typical of T2DM - increase in glucose secreted in urine (which draws water out creating hyperosmolar state) - gross hyperglycaemia + dehydration, coma
34
List the areas where macrovascular complications may be involved with [5]
- coronary arteries (heart) - cerebrovascular (stroke) - peripheral vascular* (peripheral vascular disease) - abdominal aorta - renal arteries + branches
35
Why do wounds not heal well/properly in diabetics?
hyperglycaemia impairs macrophage function (decreases their phagocytic ability)
36
What are the 3 main microvascular complications of diabetes?
1. nephropathy 2. retinopathy 3. neuropathy
37
The intensity/extent of microvascular complications of diabetes is directly dependent on what 2 factors?
1. Duration of Hyperglycaemia | 2. Degree of Hyperglycaemia
38
What does fibrosis mean? What does sclerosis mean?
Fibrosis: replacement of normal parenchyma with collagen Sclerosis: "hardening" of arteries; becomes dense
39
What is the main pathological process that causes the microvascular complications in diabetes?
Hyaline Arteriosclerosis - thickening of the wall of arterioles
40
List some of the pathological/histological features of diabetic nephropathy
- hyaline arteriosclerosis - diabetic glomerulosclerosis - -- increased mesangial matrix - -- Kimmelstiel-Wilson lesion - thickened glomerular BM
41
What are Kimmelstiel-Wilson nodules characteristic of?
diabetic nephropathy (diabetic glomerulosclerosis)
42
Diabetic nephropathy, a microvascular complication, has 4 sequential stages. List them and give specific values
1. Normal 2. Microalbuminuria (30 - 300 mg per day) 3. Macroalbuminuria (Frank Proteinuria) (> 300 mg per day) 4. End Stage Renal Disease
43
What numerical value is considered microalbuminuria?
30 - 300 mg of protein in urine per day
44
What numerical value is considered macroalbuminuria?
> 300 mg of protein in urine per day
45
What is the treatment/management plan fo diabetic nephropathy?
- intensive glucose control - treat hypertension (ACE inhibitors, Angiotensin Receptor Blockers) - avoid other damage to kidneys (e.g. UTI, drugs...)
46
How is albumin in the urine (proteinuria/albuminuria) measured? (especially in the context of diabetic nephropathy)
Albumin to Creatinine Ratio (UACR) [in a spot urine sample]
47
What is another name for an ophthalmoscopy?
Fundoscopy
48
What are the progressive stages of diabetic retinopathy?
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
What is the treatment/management plan for treating diabetic retinopathy?
- intense glucose control | - laser photo-coagulation
50
What are the 2 types of diabetic neuropathy that may occur?
1. Symmetrical Peripheral Sensorimotor Neuropathy | 2. Autonomic Neuropathy
51
What is the most common type of diabetic neuropathy to arise?
Symmetrical Peripheral Sensorimotor Neuropathy
52
Diabetics have an increased risk of infection as diabetes alters phagocyte function. What organism may be increasingly colonised in these patients?
Staphylococcus aureus
53
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?
Candida
54
What is the main adverse effect of intense glucose control?
hypoglycaemia
55
What are the 3 main categories of treatment for T2DM
1. Drugs (metformin, sulphonylureas, thiazolidinediodes, GLP-1 analogues, SGLT inhibitors) 2. Insulin (usually in advanced T2DM) 3. Bariatric Surgery
56
If a diabetic women is pregnant, what are some of the complications that may occur?
- foetal malformation - macrosomy (big baby) - delivery complications - pre-eclampsia - miscarriage - infection - intrauterine growth retardation - polyhydramnios
57
What is polyhydramnios? What is it associated with?
- there is too much amniotic fluid around the baby during pregnancy - a/w pregnancy occuring in diabetic women
58
What is gestational diabetes mellitus? When does it normally occur? What is a possible complication?
- 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
What are the 2 types of T1DM?
1. Type 1A - autoimmune | 2. Type 1B - non autoimmune/idiopathic
60
List some examples of basal insulins
- NPH or Insulatard - Glargine or Lantus - Levemir or Detemir - Degludec - Insulin Tuojeo
61
What time of day are basal insulins usually given?
evening or bedtime
62
List some examples of bolus insulins
- Actrapid (regular) - NovoRapid (Aspart) - --FiAsp (fast-acting novorapid) - Humalog (Lispro) - Glulisine (Apidra)
63
What are mixture insulins? Why may they be used?
- mix of 2 insulins in one | - used in elderly patients b/c less # of injections (only 2)
64
What are the disadvantages of mixture insulins [2]
- inflexible regime | - high risk of hypoglycaemia
65
What is the HbA1c target in T1DM?
< 7.0%
66
Diabetic retinopathy proceeds through progressive stages. List some characteristics of the "background" phase
- microaneurysms - exudates - "dot and blot" haemorrhages
67
Diabetic retinopathy proceeds through progressive stages. List some characteristics of the "non-proliferative" phase
- cotton wool spots (soft exudates - signs of ischaemia) - blot haemorrhages (bigger haemorrhages) - hard exudates (lipid/protein)
68
Diabetic retinopathy proceeds through progressive stages. List some characteristics of the "proliferative" phase
- ischaemia occuring - neovascularization - new vessels at disc (NVD) - new vessels elsewhere (NVE) - vitreal haemorrhage
69
Diabetic retinopathy proceeds through progressive stages. List some characteristics of advanced diabetic retinopathy
- vitreous haemorrhage - tractional retinal detachment (consequence of above) - rubeosis iridis - neovascular glaucoma - blindness
70
What may cause retinal detachment?
vitreous haemorrhage
71
What is rubeosis iridis?
blood vessels develop on the anterior surface of the iris (in response to ischaemia) -- a/w diabetic retinopathy [advanced stage]
72
What is a hyphema? What can cause this condition?
Hyphema: blood in anterior chamber of the eye | - can be caused by rubeosis iridis (neovascularization of iris)
73
What is Charcot's Foot? What is it a complication of?
- consequence of diabetic neuropathy - characterized by joint dislocations, fractures, debilitations, deformities - bones in feet unstable
74
Compression neuropathy may occur as a consequence of diabetic neuropathy. What is a consequence of compression neuropathy?
muscle wasting
75
ACE inhibitors should be carefully given to younger females as they are...
teratogenic - shouldn't be given to pregnant women
76
List the 3 criteria to make a diagnosis of DKA
1. Ketonaemia > 3.0 mmol/L 2. Blood Glucose > 11.0 mmol/L 3. pH < 7.3 OR Bicarbonate < 17.0 mmol/L
77
What is the management plan for DKA?
- correction of volume deficits (fluids)** - insulin therapy** - potassium monitoring + replacement - acidosis correction - IV antibiotics
78
In a pre-diabetic patient, which individual value - IFG or IGT - will most likely lead to T2DM in 5 years?
Impaired Glucose Tolerance (2 hr OGTT) | - 50% risk of T2DM

REGUB (22 decks)

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