Diabetes I and II Flashcards
1
Q
What is type I diabetes?
A
AI, idiopathic absolute insulin deficiency secondary to beta cell destruction.
2
Q
How may DM be diagnosed?
A
- Symptoms + RBG >11.1mmol/L
- FPG > 7.0 mmol/L
- HbA1C >48 mmol/mol (6.5%)
- OGTT @2h >11.1 mmol/L
3
Q
Range of impaired fasting glucose?
A
FPG 6.1 - 6.9 mmol/L
(Normal =
4
Q
Does TIIDM have a genetic component?
A
Yes:
- MZ twin concordance up to 80%
- 4/10 offspring and 1/3 siblings develop IGT or DM
- Polygenic; >250 genes
5
Q
How to distinuighs between TIDM and TIIDM?
A
- C-peptide (endogenous insulin production)
- Anti-GAD and anti-islet cell Abs (TIDM)
6
Q
What are the principles of TIIDM Mx?
A
- LoW / diet & exercise
- Oral hypoglycaemics
- Self BSL monitoring
- Regular surveillance microvascular complications
- Risk reduction macrovascular complications (BP, lipids, smoking)
7
Q
Principles of dietary management in DM?
A
- Refer dietician
- Weight loss (most cases)
- Low GI carbs
- Reduce sat fats
8
Q
Role of exercise in Mx DM?
A
- Increases glucose uptake into muscle
- Improved sensitisation can last 2-3/7
- May transiently increase (stress hormone); usually overall decrease in BSL
9
Q
Self BSL targets in DM monitoring?
A
Fasting: 6-8mmol/L
2h post prandial: 6-10mmol/L
10
Q
What determines HbA1C levels?
A
HbA1C is proportional to average BSL over previous 1-3 months.
11
Q
Prognosis pre-diabetes (impaired glucose tolerance)?
A
- 1-5% / year develop diabetes
- 50-80% revert to normal
12
Q
Diagnostic criteria impaired glucose tolerance?
A
-FBG 6.1-6.9mmol/L
OGTT 2h: 7.8 - 11.0 mmol/L
13
Q
What is TIIDM?
A
Syndrome of disordered metabolism and inappropriate hyperglycaemia secondary to absolute / relative deficiency of insulin, or a reduction in biological effectiveness of insulin or both.
14
Q
What are the macrovascular complications of diabetes?
A
- Ischeamic Heart Disease
- Peripheral Vascular Disease
- Cerebrovascular Disease
15
Q
What are the microvascular complications of diabetes?
A
- Retinopathy
- Neuropathy
- Nephropathy
16
Q
What is the risk of developing diabetic complications related to?
A
- Duration of diabetes
- DM Control (e.g. HbA1C)
- BP control
- Control of CV RFx (lipids, smoking)
- Genetic susceptibility
17
Q
How is diabetic eye disease classified?
A
- Non proliferative
- Pre-proliferative
- Proliferative
18
Q
What other eye conditions are more common in diabetics?
A
- Cataracts
- Glaucoma
19
Q
What is microalbuminura?
A
Albumin excretion rate 30-300mg / 24h.
20
Q
Screening test for diabetic neuropathy?
A
Albumin creatinine ratio:
N =
21
Q
Progression of untreated microalbuminura (type I and II)?
A
TIDM: albuminuria increases at 10-20% / year to over neprophathy in 10-15y.
TIIDM: 20-40% progress to overt nephropathy
22
Q
What is macroproteinuria?
A
Albumin excretion rate >300mg / 24h
23
Q
Natural history untreated macroproteinuria? (TI and TII)
A
- TI: ESRF 50% at 10y, 75% at 20y
- TII: 20% ESRF at 20y
24
Q
What are the most common types of neuropathy in diabetes?
A
- Distal symmetric polyneuropathy (glove and stocking)
- Autonomic
25
How does diabetes relate to other macrovascular risk factors?
Diabetes is a macrovascular RFx in itself BUT other macro RFx also more likely in diabetics (i.e. increased HTN, dyslipidemia etc)
26
Which areas are prone to ischaemia in DM patients with PVD?
-Great toe
-Medial surface 1st metatarsal head
-Lateral surface 5th metatarsal head
Secondary infection common
27
Why is exertion dsypnoea important to investigate in DM patients?
Myocardial ischaemia often silent; need high degree of clinical suspicion.
28
Prevention and treatment of diabetic retinopathy?
- Regular examination (asymptomatic until visual loss occurs)
- Laser treatment
- Meticulous BSL control
- Smoking cessation
- ?RAAS blockade
29
Treatment of diabetic nephropathy?
- Strict BP control (ACE, ARB)
| - Strict BSL control (HbA1C
30
Treatment of diabetic neuropathy?
- Control BSLs
- TCAs
- SNRI antidepressants
- Anti epileptics
- Opioid analgesics (e.g. tramadol)
- Capsaicin cream
31
How should foot ulcers be prevented in high risk feet?
- Foot care education
- Daily inspection
- Podiatry r/vs
- Early treatment skin injury
- Good footwear
- Callus detection and treatment
- Urea cream for dry feet
- Early referral for ulcers
32
What are the lipid targets for high risk patients?
- LDL: 1.0 mmol/L
| - TGs:
33
Features suggestive of LADA cf TIIDM?
- Lean build
- Anti islet Abs
- Rapid progression to insulin
34
Where are the highest rates of TIDM?
Finland and other Northern European countries
35
Which genes predispose to most genetic risk of TIDM?
HLA genes on Chr 6: highly polymorphic and modulate immune defence of body.
HIGH RISK = HLA:
-DR3 -DQ2
-DR4 -DQ8
36
Distinction between TIDM and TIIDM?
Key distinguishing feature (T1 v TII) is presence of auto-Abs against B-cell auto-ags:
- IAA: insulin reaction
- GADA: glutamic acid decarboxylase —> catalyses formation of gaba-aminobutyrate; located in B cells
- IA2A: insulinoma associated auto antigen 2 —> islet antigen 2, membrane bound in B cells
- ZnT8A: zinc transporters.
- C peptide
37
What are the four major determinants of TIIDM?
- Age
- Obesity
- Ethnicity
- FHx
38
Outline the inheritance component of TIIDM?
identical twins of DMII patients >50% chance of developing diabetes; siblings = 25%.Polygenic disorder: many susceptibilities e.g. TCF7-L2, KCNQ1.
39
Environmental factors predisposing to TIIDM development?
Low weight at birth and 12 months associated with glucose intolerance later in life. Poor early nutrition thought to impair B-cell development.
40
What is insulin resistance?
Failure of target tissue to respond normally to insulin (liver, muscle, adipose tissue major tissues in glucose regulation).
41
What does insulin resistance lead to?
- Failure to inhibit endogenous glucose production (gluconeogenesis) in liver.
- Failure of glucose uptake and glycogen synthesis in skeletal muscle following a meal.
- Failure to inhibit lipoprotein lipase in adipose tissue, leading to excess circulating FFAs.
42
Subacute presentation of DM?
SUBACUTE: clinical onset several months or years, esp older patients.
-Polydipsia
-Polyuria
-LoW
PLUS
-lack of energy
-visual blurring (owing to glucose induced changes in refraction)
-pruritus vulvae or balanaitis due to Candida infection
43
What is acanthosis ingrains?
Indicative of severe insulin resistance: blackish pigmentation of back of neck and axillae.
44
Outline pathophysiology of DKA.
- Occurs due to lack of insulin (first presentation, lack of compliance to insulin medication).
- Unrestricted hepatic glucose production —> hyperglycaemia —> osmotic diuresis —> dehydration and electrolyte disruption —> decreased Na+ (water shift to ECF).
- Fat mobilisation —> increased FFA —> ketoacids —> metabolic acidosis
- Severe hyperglycemia exceeds renal threshold for glucose and ketone resorption —> glucosuria and ketonuria.
- Total body depletion of K+, but serum K+ may be normal or elevated following a secondary shift from ICF to ECF due to lack of insulin —> increased plasma osmolality.
- Total body PO34- depletion
45
Ketoacidosis precipitating factors?
- New onset TIDM
- Inadequate / inappropriate insulin therapy
- EtOH abuse
- Infection
- Pancreatitis
- Drugs: corticosteroids and thiazides
46
Principles of ketoacidosis management?
1) Rehydration
2) Identify K+ level; correct imbalance (potassium)
3) Correct hyperglycemia: Insulin therapy
4) Identify precipitant
47
Fluids to be used in mx DKA?
-1L N saline over 30min - 2h
| Change to 5% dextrose when glucose
48
Principles of potassium treatment in Mx DKA?
Aim K+ 3.5 - 5mM:
| 1) K+ 5mM: withhold K+ but monitor levels
49
Insulin in Mx DKA?
-IM: 0.1 IU/kg/h
-IV infusion: 6-8 units hourly via pump THEN ADJUST to BSLs
Continue infusion until acidosis resolved then switch to s/c insulin (basal bolus).
50
How is effective osmolality determined?
2 (Na+) + glucose
51
What is hyperglycaemia hyperosmolar state?
AKA hyperosmolar nonketotic coma:
- severe hyperglycemia
- minimal ketosis
- profound dehydration
- depressed sensorium / coma
- efective osmolality >330 Osm/kg
52
Mx hyperglycemia hyperosmolar state?
- Fluids: 2L hypotonic saline (0.45%) over 1-2h
- Monitor urine output and CVP if indicated
- Insulin
- Potassium
- Prophylactic heparin
- identify cause
53
Broad pathogenesis of hyperosmolar state?
Relative lack of insulin --> hyperglycaemia --> glycosuria --> polyuria --> volume depletion --> renal insufficiency --> hyperosmolarity --> fluid shift from neutrons to ECF --> mental obtundation and coma.
54
Mx of hypoglycaemia?
- If possible: sugary fluids
- Unconscious / risk of aspiration:
- -> IV dextrose 50% (25-50mL)
- -> IM/SC glucagon 1mg
- Administer long acting carb
- Recheck glucose 20-30 min later
55
What may precipitate HHS?
-Sepsis / stroke / MI / CHF / renal failure / dialysis / recent surgery / burns
56
Why is dehydration more severe in HHS than DKA?
- More gradual onset =Increased duration of metabolic decompensation
- impaired fluid intake
57
What are the precipitants of DKA/
8Is precipitating DKA:
i) Infection
ii) Ischaemia / infarction
iii) Iatrogenic (glucocorticoids)
iv) Intoxication
v) Insulin missed
vi) Initial presentation
vii) Intra abdominal process
viii) Intra op / peri op stress
58
Pathophysiology of diabetic nephropathy?
- thickening of capillary BM and glomerular mesangium resulting in glomerulosclerosis and renal insufficiency
- diffuse glomerulosclerosis more common than nodular inter capillary glomerulosclerosis (Kimmelsteil- Wilson lesions)
59
Clinical features of peripheral neuropathy?
- Paresthesias (tingling, burning)
- Bilateral, symmetric
- Decreased perception of vibration / pain / temp
- Decreased ankle reflex
60
Clinical features in motor neuropathy of DM?
- Less common than sensory neuropathy
- Delayed motor nerve conduction w/ muscle weakness/ atrophy
- May involve one nerve trunk or more (mono neuritis complex)
- Diabetic amyotrophy
61
what is diabetic amyotrophy?
Pain, weakness, wasting of hip flexors or extensors
62
Clinical features of diabetic autonomic neuropathy?
- Postural hTN
- Tachycardia
- Decreased CV response to valsalva
- Gastroparesis / alternating diarrhoea constipation
- Urinary retention
- Erectile dysfunction
63
What is diabetic dermopathy?
Atrophic brown spots commonly in pretitibial region known as "shin spots".
Secondary to increased glycosylation of tissue proteins or vasculopathy.
64
Dermatologic manifestations of DM?
- Diabetic dermopathy
- Eruptive xanthomas
- Necrobiosis lipidoica diabeticorum
65
What is necrobiosis lipidoica diabeticorum?
Rare complication characterised by thinning skin over the shins allowing visualisation of subcutaneous vessels.
66
Bone and joint manifestations of DM complication?
- Juvenile cheiroarthropathy
- Dupuytyren's contracture
- Bone demineralisation
- Frozen shoulder
67
Clinical features of hypoglycemia?
1. Whipple's Triad:
| i) Serum glucose
68
What are symptoms of neuroglycopenia?
- Dizziness
- Headache
- Clouding of vision
- Mental dullness
- Fatigue
- Confusion
- Seizures / Coma
69
What are the common causes of hypoglycaemia due to hyperinsulinism?
- Exogenous insulin
- Sulphonylurea reaction
- AI hypoglycemia
- Pentamidine
- Insulinoma
70
What are the common causes of hypoglycaemia without hyperinsulinism?
- Severe hepatic dysfunction
- Chronic renal insufficiency
- Hypocortisolism
- EtOH
- non-pancreatic tumours
- inborn error of carb metabolism, glycogen storage deficiency
71
How is insulin infusion made up in DKA and Mx (i.e. rate and ongoing Mx)?
- 50units of insulin made up to 50mLs with 0.9%NSal ==> 1UN/mL.
- Rate of 0.1unit/kg/h up to 6 units / h.
- When glucose
72
Insulin in HHS?
-Initial dose insulin 0.05UN/kg (max 3 Units)
-Reduce insulin infusion when glucose 18mmol/L
Infuse 0.45% (half NS) at 250mL/h
