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Diabetes Flashcards

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1
Q

How many people diagnosed with diabetes in UK

A

3 million

4.9% of population

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2
Q

How much does DM lower life expectancy by

A

7 years

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3
Q

Insulin effect on liver

A

Inhibits gluconeogenesis

Promotes glycogen storage

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4
Q

Insulin effect on muscle

A

Glucose uptake

Promotes glycogen storage

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5
Q

Insulin effect on adipose tissue

A

Inhibits lipolysis

Increases fat synthesis

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6
Q

Type 1 onset

A

Usually juvenile onset (before 35)

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7
Q

Type 2 onset

A

Mainly after 35

More common in males

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8
Q

Which diabetes is prone to ketosis

A

Type 1

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9
Q

Which diabetes is prone to weight loss

A

Type 1

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10
Q

Type 1 Insulin

A

Insulin deficiency
Ketoacidosis
ALWAYS need insulin

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11
Q

Type 2 insulin

A

Insulin resistance - may have deficiency
Partial insulin deficiency initially and hyperosmolar state
Need insulin when Beta cells fail over time

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12
Q

Type 1 + autoimmune

A

GAD and ICA antibodies

Attack B cells

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13
Q

Type 2 + autoimmune

A

Non autoimmune

Associated with metabolic syndrome

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14
Q

Type 1 + HLA

A

HLA-DR3 and HLA-DR4 in more than 90%

Islet cell antibodies

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15
Q

Type 2 + HLA

A

No HLA relation

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16
Q

MZ Twins + Diabetes

A

50% concordance Type 1

100% concordance Type 2

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17
Q

Symptom duration

A

Type 1- weeks

Type 2- months/years

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18
Q

Ethnicity Type 1

A

Higher risk Northern European

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19
Q

Ethnicity Type 2

A

Higher risk Asian, African, poylnesian, native american

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20
Q

C peptide

A

Disappears in Type 1

Persists in Type 2

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21
Q

LADA

A

Latent autoimmune diabetes of adults

Type 1B DM

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22
Q

MODY

A

Maturity onset diabetes of the young

Rare autosomal form of T2DM

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23
Q

Secondary Diabetes- Pancreatic disease (diseases of exocrine pancreas)

A 
Acute + chronic pancreatitis
Trauma
Pancreatectomy
Neoplasia
Cystic Fibrosis
Haemochromatosis
Thalassaemia
Fibrocalculous pancreatopathy
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24
Q

Secondary Diabetes- Endocrine disease (diseases of endocrine pancreas)

A 
Acromegaly
Cushing's
Glucagonoma
Phaeochromocytoma
Hyperthyroidism
Conn's disease
Aldosteronoma
Somatostatinoma
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25
Drug-induced Diabetes
``` Immunosuppressive agents- glucocorticoids, cyclosporin, tacrolimus, sirolimus Beta blockers Beta adrenergic agonists Atypical antipsychotics (clozapine, olanzapine) Thiazide diuretics Phenytoin Levothyroxine Interferon alpha HIV treatment Niacin (B3) Pentamidine ```
26
Secondary diabetes- Genetic defects of:
``` Beta cell function Insulin action (receptor mutations) Genetic syndromes- Down's, Friedreich's ataxia, Huntington's chorea Klinefelter syndrome Prader- Willi Turner ```
27
Secondary diabetes- Infections
Congenital rubella | CMV
28
Secondary diabetes- uncommon forms f immune mediated diabetes
Stiff person syndrome | Anti-insulin receptor antibodies
29
Diabetes Investigations
Fasting plasma glucose (FPG) Random plasma glucose (RPG) 75g oral glucose tolerance test (OGTT) HbA1c
30
75g Oral glucose tolerance test
Fast for 9 hours Check fasting plasma glucose Give 75g of glucose Check 2 hour plasma glucose
31
HbA1c
Measure for average glucose control over 3 month period Normal- below 42 mmol/mol Generally below 53 indicates well controlled diabetes
32
Investigating with symptoms
1 diagnostic test
33
Investigating without symptoms
2 diagnostic tests OR 1 abnormal OGTT
34
Type 1 Aetiology
Polygenic Autoantibodies against pancreatic islets Pancreatic beta cell destruction --> absolute insulin deficiency
35
LADA
diagnosed in adulthood Usually non-acute --> can be diagnosed as T2DM ICA or GAD +ve Require insulin
36
T1DM environmental influences
Peak age onset 5-7 years Puberty Seasonal variation Predominantly European population
37
T1DM Genetic susceptibility
HLA genes on chromosome 6q (MHC)-HLA DR3/4 | Genes on chromosomes 2q, 15q and 11q
38
Pathogenic sequence of T1DM
Genetic susceptibility Environmental insult (virus) Development of insulitis (infiltration of activated T lymphocytes) Activation of autoimmunity Immune attack on Beta vells Development of DM (when more than 90% of Beta cells are destroyed)
39
When do you develop T1DM
When more than 90% of Beta cells are destroyed
40
Glucose toxicity
Beta cells have decreased functionality when exposed to high levels of glucose --> lowering glucose may increase beta cell function and promote greater insulin secretion
41
Alpha cells in T2DM
Increased | Leads to increased glucagon/insulin ratio
42
Classic Osmotic Symptoms
``` Polyuria Polydipsia Weight loss Nocturia Fatigue Pruritis Blurred Vision Recurrent UTI or GU infections DKA ```
43
HHS
Hyperosmolar Hyperglycaemic Syndrome
44
Diabetes complications
``` Skin infections Foot problems Retinopathy Erectile dysfunction Arterial disease ```
45
Factors in obesity contributing to insulin resistance
Adipokines Inflammation Lipids
46
Insulin resistance
Diminution in the response of the body’s tissues to insulin, so that higher concentrations of serum insulin are required to maintain normal circulating glucose levels; eventually the islet cells can no longer produce adequate amounts of insulin for effective glucose lowering, resulting in hyperglycaemia
47
Metabolic syndrome
``` Cluster of conditions that together increase risk of heart disease, stroke + T2DM Central obesity Dyslipidaemia Hypertension Impaired fasting glucose ```
48
Metabolic syndrome: Central obesity
``` BMI > 30 or Waist circumference of: Caucasian men- >94 Caucasian women- >80 South Asian men- >90 South Asian women- >80 ```
49
Metabolic syndrome: Dyslipidaemia
Increased Triglycerides >150mg/dL | Decreased HDL-cholesterol: <40mg/dL women, <50mg/dL men
50
Metabolic syndrome: Hypertension
Systolic >130 | Diastolic>85
51
Metabolic syndrome: Impaired fasting glucose
Fasting glucose >6.1mmol/L
52
Self monitoring blood glucose aims
Pre-prandial: 4-7mmol/L | Post-prandial (2hrs): 5-9mmol/L
53
Fructosamine
Another glycated protein- lasts around 2 weeks Can be used if HbA1c invalid e.g. haemoglobinopathy, increased RBC turnover Useful in glucose control in pregnancy
54
First line T2DM
Diet Physical activity- 3x30mins 3-5% weight reduction Smoking cessation
55
Smoking in diabetes
1 cigarette is equal to 5 cigarettes for non-diabetic
56
Diabetic BP control
Aim 140/80 | If CVD or renal disease too, 130/80
57
Diabetic cholesterol control
Diabetic>40 or Diabetic<40 + 1 risk factor= statin | Aim total cholesterol <4, LDL <2
58
Biguanides
Metformin
59
Biguanides function
1st line T2DM Decreases hepatic glucose production (gluconeogenesis and glycogenolysis) Improve insulin sensitivity in liver + muscle Doesn't affect insulin secretion, doesn't induce hypoglycaemia and doesn't predispose to weight gain
60
Biguanides SEs
``` Nausea Diarrhoea Abdominal pain Anorexia Hypoglycaemia ```
61
Biguanides STOP IF
Tissue hypoxia e.g. sepsis or MI General anaesthesia Before contrast medium containing iodine --> renal failure + subsequent lactic acidosis Restart no earlier than 48hr after test of renal function shows no deterioration
62
Insulin Secretagogues
Sulfonylureas | Meglitinides
63
Biguanides Contraindictions
Severe hepatic disease Severe renal disease (CKD stage 4 or eGFR<36ml/min) --> can cause lactic acidosis
64
Sulfonylureas examples
``` Gliclazide Tolbutamide Glibenclamide Glipizide Glimepiride Chlorpropamide ```
65
Sulfonylureas function
Oral hypoglycaemic Increases insulin release from pancreas Opens K+ channels in beta cells
66
Sulfonylureas side effects
Hypoglycaemia | Weight gain
67
Meglitinides examples
Repaglinide | Nateglinide
68
Meglitinide function
Opens K+ channels in Beta cells to increase insulin release | Short acting agents that promote postprandial release of insulin- Prandial Glucose Regulators (PGRs)
69
Thiazolidinediones (TZDs)/Glitazones example
Pioglitazone
70
TZDs MOA
PPAR-gamma agonist Modulates gene transcription of regions controlling lipid metabolism in the muscle, adipose tissue and liver --> decreases insulin resistance peripherally + increases insulin sensitivity
71
TZDs SEs
``` Hypoglycaemia Weight gain Fluid retention Heart failure Liver impairment Bladder cancer Mild anaemia Osteoporosis/fractures ```
72
TZDs contraindications
Past/present HF | Osteoporosis
73
Glucagon like peptide - 1 (GLP-1)
Incretin Gut peptide that augments insulin release when glucose is detected + decreases glucagon secretion Slows gastric emptying + induces satiety Stimulate + preserve Beta cells
74
GLP 1 receptor analogues examples
Exenatide Liraglutide Lixisenatide
75
GLP1 receptor analogues
Injected not oral | Only used in overweight patients (BMI > 35) with poor glucose control
76
GLP1 receptor analogues SEs
Nausea Diarrhoea Pancreatitis Pancreatic cancer
77
DDP4 inhibitors/gliptins examples
``` Sitagliptin Vildagliptin Alogliptin Linagliptin Saxagliptin ```
78
DDP inhibitors/gliptins
Oral 1x day Inhibit GLP1 breakdown Well tolerated, SEs uncommon
79
Alpha-glucosidase inhibitors examples
Acarbose
80
Alpha-glucosidase inhibitors
Decrease breakdown of starch into glucose
81
Alpha-glucosidase inhibitors SEs
Flatulence Diarrhoea Abdo pain/distension
82
Diabetes medication Prescribing Pathway
Step 1: Lifestyle, try and keep <48 Step 2: Metformin if gone above 48 Step 3: Metformin + Sulfonylurea if gone above 58, try and keep at around 53 Step 4: Triple therapy- metformin, SU + DDP4 inhibitor/insulin/pioglitazone Step 5: if not better, intensify insulin or add pioglitazone
83
Metformin dose CIs
Careful with dose if eGFR <45, if below 30 then stop Not tolerated if patient not overweight --> SUs instead
84
Sulfonylurea CIs
If hypoglycaemia a problem | --> DPP4 inhibitor/pioglitazone instead
85
If metformin is CI or not tolerated
2. SU/DPP4 inhibitor/pioglitazone 3. Combination of 2 of SU/DPP-4 inhibitor/Pioglitazone 4. Consider insulin regime
86
T2DM indications for insulin therapy
Inadequate glycaemic control on tablets or CI to tablets Symptomatic hyperglycaemia Pregnancy Infection/foot ulcers
87
Types of Insulin
Human | Analogue
88
Human Insulin types
Short acting Intermediate acting Biphasic
89
Humulin S
Short acting human insulin
90
Humulin I
Intermediate acting human insulin
91
Humulin M3
Biphasic human insulin (mixture of short and intermediate)
92
Analogue Insulin types
Rapid acting Long acting (basal insulin) Biphasic
93
Novorapid, Lispro
Rapid acting analogue insulin
94
Lantus, Levmir
Long acting analogue insulin (basal insulin)
95
Novomix 30
Biphasic analogue insulin
96
Insulin Injection Sites
Subcutaneous Abdomen Thighs Buttocks
97
Insulin Regimes
Once daily basal insulin Premixed insulin twice daily/biphasic Basal bolus/QDS regimen
98
Once Daily basal insulin
Once daily intermediate or long-acting insulin Given with tablets in T2DM Usually given before bed or 1st thing in morning
99
Premixed insulin twice daily/biphasic
30% short acting and 70% long acting Breakfast and lunch If once daily fails in T2DM
100
Basal bolus/QDS regimen
1 long acting injection + 3 short acting injections with each meal Mimics normal physiology Used primarily in T1DM
101
Sick Days
``` Illness causes stress and usually requires more insulin Drink lots of fluids (3L) Sugary fluids if unable to eat Regular glucose monitoring Never stop tablets or insulin ```
102
Diabetic Ketoacidosis
State of absolute or relative insulin deficiency resulting in hyperglycaemia and an accumulation of ketoacids in the blood with subsequent metabolic acidosis
103
Hyperosmolar hyperglycaemic state (HHS)
Hyperglycaemia resulting in high osmolarity without significant ketoacidosis
104
Hypoglycaemia
Below 3.6mmol/L
105
Hypoglycaemia causes
Imbalance between carb intake and insulin/oral hypoglycaemics Exercise with too much insulin/not enough carbs Alcohol Vomiting Breast feeding
106
Hypoglycaemia medical causes
``` Liver disease Progressive renal impairment Hypoadrenalism (T1DM) Hypothyroidism Hypopituitarism Insulinoma ```
107
Hypoglycaemia Autonomic Symptoms
``` Glucose around 3.6mmol/L Sweating Shaking Anxiety Palpitations Hunger Nausea ```
108
Hypoglycaemia Neuroglycopenic symptoms
``` Glucose around 2.7mmol/L Confusion Slurred speech Visual disturbance Drowsiness Aggression ```
109
Mild hypoglycaemia management
Conscious, lucid, able to self-treat Sugary drink 5-7 glucose tablets or 3-4 heaped tsp sugar
110
Moderate hypoglycaemia management
Conscious but can't self-administer and needs help Glucogel (1-2 tubes) or jam, honey, treacle IM Glucagon
111
Severe hypoglycaemia treatment
Unconscious- don't put anything in mouth + recovery position 0.5-1mg IM Glucagon In hospital, IV Glucose
112
Severe hypo treatment IV glucose
75ml of 20% glucose or 150ml of 10% glucose over 15 mins | 50ml of 50% glucose may be given with care as may cause extravasation leading to chemical burns
113
Post-hypo treatment
When glucose above 4mmol/L | Longer acting carbs needed- biscuits, bread, milk
114
Hypo + driving
Inform DVLA | Licence revoked following 1 or more severe hypos during driving
115
Nocturnal Hypo diagnosis
Rebound hyperglycaemia Headaches/hangover sensation 3am BM or CGMS (continuous glucose monitoring sensor) over 5 days
116
Nocturnal Hypo management
Analogue insulins Pre-bed snack Change of timing of insulin Insulin pump therapy
117
DKA MOA
Ketosis is pathway use in starvation states Acetone produced as by-product Cells can't take up glucose for metabolism Cells end up in starvation-like state --> ketoacidosis only form of energy production --> FFAs metabolised via Krebs cycle producing ketone bodies
118
DKA stands for
Severe acidosis Hyperglycaemia Ketones present
119
DKA triggers
``` Infection e.g. UTI Surgery MI Pancreatitis --> all 4 have glucocorticoid response, increasing levels of cortisol + blood glucose Chemo Antipsychotics Wrong insulin dose High exogenous steroids ```
120
DKA presentation
``` Abdominal pain Kussmaul respiration Drowsiness + confusion Polyuria Polydipsia Vomiting Ketones on breath Dehydration + tachycardia Severe- Na, Cl, K, Ca, Mg + phosphate losses due to osmotic diuresis ```
121
DKA Diagnosis
Acidosis- pH<7.30 Hyperglycaemia (usually >14mmol/L) Ketosis (serum + urine)
122
DKA investigations
Pregnancy test ECG, CXR Urine dip + MSU culture Bloods- CBG/biochem profile, plasma ketones, ABG/VBG, amylase, osmolality, FBC, blood culture, HbA1c
123
Plasma osmolality
2(Na) + urea + glucose
124
Assessing DKA severity
``` If one or more on admission, ITU: Blood ketones >6 Venous bicarb < 5 pH <7.1 K+<3.5 GCS<12 O2 sats<92% on air SBP<90 Pulse>100 or <60 Anion gap >16 ```
125
DKA monitoring
``` Consciousness BP Pulse Temp Glucose Urine output K+ Acidosis ```
126
DKA Fluid therapy
2 large bore cannulas NaCl 0.9% 5% or 10% glucose
127
DKA NaCl 0.9%
``` 1L start until SBP>90 1L in 1hr 1L in 2hrs (+20mmol KCl) 1L in 4hrs (+KCl) 1L in 4hrs (+KCl) ```
128
DKA 5/10% glucose
Start when CBG <12mmol/L and continue at 125ml/hour If using 10% glucose increase insulin infusion as needed Increase insulin infusion rate if glucose <6mmol/L
129
DKA K+
Do not give in first 2 bags because delivery ratio is too rapid On each subsequent bag of NaCl or glucose, add KCl dependent on serum levels <3.5- may need additional K+ and delay insulin 3.5-5.5- 20-40mmol/L >5.5- none
130
Normal DKA deficits
Typical fluid deficit= 100ml/kg | Typical K+ deficit= 3-5mmol/kg
131
Insulin during DKA
If known diabetic, continue Insulin infusion by IV syringe pump --> 50 units Actrapid made up to 50ml with 0.9% NaCl
132
DKA insulin infusion
50 units Actrapid made up to 50ml with 0.9% NaCl Fixed rate IV infusion --> 0.1units/kg/hr (around 6-8 units/hr) Aim for bicarb rise of 3mmol/hr and glucose fall 3mmol/L If not achieved, increase rate by 1 unit/hr
133
DKA treatment outcomes
Ketones <0.3mmol/L- use blood as urinary ketones persist after resolution Venous pH>7.3 Venous bicarb>18mmol/L
134
DKA complications
``` Aspiration pneumonia Hypo K+ Hypo Mg+ Hypo PO4- VTE Cerebral oedema ```
135
Most common cause of DKA death in children
Cerebral oedema Indicated by sudden CNS decline Treatment- dexamethasone or mannitol
136
DKA features
``` Increased plasma glucose Increased WBC Infection often apyrexial Increased creatinine HypoNa+- common due to osmolar compensation of hyperglycaemia, if increased or normal suspect severe Ketonuria Recurrent ketoacidosis Acidosis Serum amylase increased Non-specific abdo pain ```
137
Hyperosmolar Hyperglycaemic Syndrome (HHS)
``` Severe hyperglycaemia without significant acidosis Typically seen in T2DM Subacute history (1 week) with marked dehydration and hyperglycaemia ```
138
HHS and age
Old people experience thirst less acutely + become more dehydrated more readily Mild renal impairment associated with age --> increased urinary losses of fluid + electrolytes
139
HHS Features
``` Hyperglycaemia >40mmol/L Osmolality >420 Patient often hypernatraemic May or may not be ketonuria No ketoacidosis Severe dehydration ```
140
Normal osmolality
275-295
141
Calculating Osmolality
2(Na+K) + Ur + Glu
142
HHS clinical features
Dehydration --> stupor --> coma
143
HHS precipitating factors
Consumption of glucose-rich fluids Concurrent medication e.g. thiazide diuretics or steroids Intercurrent illness
144
HHS Complications
Occlusive events- stroke, MI, DIC, leg ischaemia/rhabdomyolysis, DVT/PE Give LMWH as prophylaxis
145
HHS Management
Rehydrate slowly over 48 hours with 0.9% NaCl IV No insulin bolus Replace K+ when urine starts to flow
146
HHS Rehydration
Typical deficit 110-220ml/kg | Avoid 0.45% NaCl
147
HHS Insulin
Only use insulin if blood glucose not falling by 5mmol/L/hr with rehydration or ketonuria Slow infusion of 0.05units/kg/hr (max 1unit/hr) Avoid in first 12 hours Rapid shifts in glucose should be avoided due to risk of rapid fluid/Na+ shifts and central pontine myelinosis
148
HHS K+
Replaces when urine starts to flow May need CVP monitoring K+ reduces rapidly Keep plasma glucose at 10-15mmol/L for 1st 24hrs to avoid cerebral oedema Look for cause, e.g. bowel infarct, drugs etc.
149
When choosing, giving + monitoring medication- BRAIN + AIMS
``` Benefits Risks Adverse effects Interactions Necessary prophylaxis Susceptible groups Administering Informing Monitoring Stopping ```
150
Diabetic mortality rate
Increased (x2-2.5) due to cardiovascular complications | 80% die of CVD
151
Long term hyperglycaemia leads to
Vessel closure- decreased supply of O2 and nutrients | Vessel permeability- damaged vessels dilate and leak unwanted substances
152
Diabetes chronic complications- Macrovascular (atherosclerosis)
Coronary Heart disease--> MI, CCF Cerebrovascular disease --> stroke Peripheral vascular disease --> ulceration, gangrene, amputation
153
Diabetes chronic complications- Microvascular
Nephropathy Retinopathy Neuropathy (peripheral sensorimotor, autonomic)
154
Diabetes chronic complications- Other
Skin Rheumatological Hepatic
155
Complications of Diabetes Risk Factors
Smoking- most potent Hypertension Dyslipidaemia Hyperglycaemia- least potent
156
Diabetic retinopathy
Common | Around 50% of people with diabetes for more than 10 years have it
157
Non-proliferative Retinopathy
Microaneurysms Dot and blot haemorrhages Hard exudates (lipid deposits) and soft exudates (cotton wool spots=retinal ischaemia- only in pre-proliferative- REFER) Macular oedema (leakage of macular blood vessel- main cause vision loss in this case) Mild, moderate, severe
158
Proliferative Retinopathy
Ischaemia of retina --> production of growth factors (GF) --> neovascularisation producing fragile vessels New vessels on disc and other places Vitreous haemorrhage --> vessels prone to haemorrhage, lead to fibrosis/scarring leading to loss of vision
159
Diabetic Maculopathy
Suspect if visual acuity decreased Occurs if retinopathy within 1 disc diameter of the macula Leads to oedema + vision loss Refer for laser photocoagulation, intravitreal steroids or anti-angiogenic agents
160
Focal or exudative maculopathy
Hard exudates around macula which leads to macular oedema and visual loss
161
Ischaemic maculopathy
Due to retinal vessel closure
162
Diff types of diabetic maculopathy
Focal or exudative Diffuse Ischaemic
163
Diabetic Maculopathy Pathophysiology
Capillary endothelial damage --> vascular leak --> microaneurysm -->
164
Diabetic Maculopathy Pathophysiology
Capillary endothelial damage --> vascular leak --> microaneurysm --> capillary occlusion --> local hypoxia and ischaemia --> neovascularisation Occurs due to increased blood flow in hyperglycaemia New vessels form on disc or ischaemic areas, proliferate, bleed, fibrose + can detach retina
165
Microvascular occlusion
Cotton wool spots
166
Maculopathy screening
Annual digital retinal screen BP, cholesterol, glycaemic control Laser photocoagulation
167
Diabetic Nephropathy
Most common cause of end-stage renal failure in UK 25-30% of T2DM have some degree of nephropathy Associated with atherosclerosis
168
Kidneys damaged in 3 main ways
Glomerular damage Ischaemia- resulting from hypertrophy of afferent and efferent arterioles Ascending infection
169
Diabetic Nephropathy RFs
``` Duration of diabetes Hypertension FH of hypertension Poor glycaemic control Smoking Gender-male Ethnicity- South Asians, Afro-Caribbeans ```
170
Diabetic Nephropathy Clinical Triad
Hypertension Albuminuria (preceded by microalbuminuria) Declining renal function --> on renal biopsy: "Kiemmelstein-Wilson" lesion
171
Microalbuminuria screening
Void urine in morning + measure urine albumin:creatinine ratio (ACR) Normal men <3.5mg/mmol, normal women <2.5mg/mmol If elevated, repeat twice- of 2 out of 3 positive, microalbuminuria present
172
Diabetic Nephropathy management
``` Maintain BP <130/80 HbA1c<53 Stop metformin eGFR <30 Refer to specialist eGFR<45 Consider renal replacement therapy Consider simultaneous pancreas and kidney transplant for T1DM ```
173
Diabetic Neuropathy
Peripheral neuropathy- injury or infection at pressure points (e.g. metatarsal heads) Ischaemia- critical toes and loss of pulses
174
Peripheral sensory neuropathy
Glove and stocking distribution High risk ulceration + amputations if blood supply poor Numbness, pins and needles, burning and shooting pain Loss sensation fine touch + proprioception Loss ankle reflexes, reduced muscle bulk, neuropathic deformity (pes cavus, claw toes, loss transverse arch, rocker bottom sole) Hands subject to median neuropathy/carpal tunnel
175
Autonomic Neuropathy- Genitourinary
``` ED Atonic bladder (difficulty voiding or incontinence) --> self catheterisation ```
176
Autonomic Neuropathy- GI
Gastroparesis (recurrent vom + early satiety due to poor gastric flow)- anti emetics, erythromycin, gastric pacing Chronic constipation/diarrhoea Gustatory sweating
177
Autonomic Neuropathy- Cardiovascular
Postural hypotension- fludrocortisone or alpha agonist midodrine Reduced cerebrovascular autoregulation Loss of respiratory sinus arrhythmia
178
Mononeuropathy
CN palsies Median nerve palsies --> carpal tunnel --> treat with immunosuppression
179
Proximal motor neuropathy
Painful atrophy of quads + pelvifermoal muscles
180
CV complications
Manage CV risks - smoking cessation - BP control - cholesterol control - glycaemic control
181
BP management
ACEI CCB Thiazide Alpha blocker or Beta
182
Cholesterol control
Total cholesterol <4 | Treat with statins- all diabetics > 40, all diabetics <40 +1 other RF
183
Acute MI - complication
4x increased risk May be silent because autonomic neuropathy Treatment- aspirin, angioplasty, glucose-insulin infusion, 2ndary prevention
184
Cerebrovascular disease- complication
If within 3 hours, consider thrombolysis | Aspirin, statins, glucose insulin infusion
185
Peripheral vascular disease complication
Intermittent claudication, rest pain, buttock pain | Aspirin, vasodilators
186
Skin complications
``` Oral/genital candidiasis Skin abscesses Diabetic dermopathy Necrobiosis Lipoidica diabeticorum Granuloma annulare acanthosis nigricans fungal nail infection ```
187
Rheumatological complications
Charcot neuropathy Adhesive capsulitis Diffuse idiopathic skeletal hyperostosis Flexor tendinopathy
188
Hepatic complications
NAFLD --> non alcoholic steatohepatitis/fibrosis/cirrhosis Increases ALT and AST more than 2x upper limit needs investigation Pioglitazone in reducing cirrhosis progression

Met 3b (21 decks)

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