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History
HbA1c
Microalbuminuria
Dyslipidaemia
Thyroid dysfunction
Risk factors
-
Diabetes type 2
Pathogenesis
Central obesity
-
Glycaemic control
Comprehensive eye examinations
Renal complications
-
Disease progression
-
Type 2
-
Treatment
Screening of microalbuminuria
Ophthalmic
-
Renal testing
-
Microalbuminuria
Serum creatinine
Estimate GFR
Neuropathy
50% of individuals is as with other complications it is
related to duration and glycaemic control, BMI and
smoking.
Polyneuropathy/mononeuropathy
-
Treatment
Avoidance of neurotoxins such as alcohol and
smoking.
Supplementation with B12 and folate.
Pain management
-
Antidepressants
Anticonvulsants
Tricyclic antidepressant
Diagnosisketoacidosis
Diabetic
Management
of Type
1 Diabetes
diabetic
ketoacidosis
Gastrointestinal/genitourinary
is
to control
blood
glucose
concentration
and
Mainly
occurs
in DM1
but
can occur
in nonglucose,
Confirm
diagnosis
with
Increased
plasma
- Target
Gastroparesis,
constipation,
diarrhea
complications.
immunological
features
of typeacidosis
1 + obese
serum
ketones
and metabolic
+ GCS
- minimize
Anorexia,
nausea,
vomiting,
early
satiety
and
individuals
with
DM2 of Hispanic and African
abdominal
bloating
assessment
of
American
descent.
Management
is similar.
- Ongoing
Cystopathy,
erectile
dysfunction,
female
sexual
dysfunction
1. Serum
electrolytes K, Na, Mg, CL,
- Symptoms
Urinary
hesitancy,
voiding
bicarbondate, decrease
phosphate
frequency,
incontinence,
recurrent
urinary
2. Acid base
state pH Bicarb,
PCO2
and ketones
tract(B-hydroxybutyrate)
infection
3. Renal function (Creatinine and output)
Cardiovascular
Treatment
Treatment
Control
risk factors
Replace
fluids:
23 Lbackground
of 0.9% saline
1. Basal
insulin
insulinover first
- Dysplipidemia,
hypertension, obesity,
13 h (1520
mL/kg of
per
hour); subsequently,
0.45%
independent
carbohydrate
intake. 40-50%
physical
activity,mL/h;
smoking
saline
at
change
5% glucose
and
of250500
total daily
insulin
dose to
through
once or
0.45%(see
saline
at 150250
mL/h when acting
plasmainsulin
twice
daily
long/intermediate
Treatment
cardio)
glucose
reaches
200 mg/dL (11.2 mmol/L)
2. Bolus
insulin
Prandial
insulin
cover carohybdrate
- GPIIb.IIIaa.platelet
inhibit
hastoimproved
GIVE POTASSIUM
IF REQUIRED
using
short or very short
outcomes inintake
diabetic
patients
acting
insulin
- Short
Use acting
of B blockers,
ACE
inhibitors or ARB
insulin
b.
Correction
doses of insulin to return
- Antiplatelet therapy (aspirin)
- IVLDL
0.1units/kg
increasing
if no response
high
blood
glucose2-3x
to acceptable
- Lower
as
a focus
Serum
glucose
can initially
but only
- by
Nausea
and
vomiting
most common
2-4 hours
levels
- Hypertension
treatment
choice
Abdominal
pain
=
DDx
pancreatitis?
- oEnsure
serum
K isacute
<3.3mmol/L
= do
minimally
elevated
ACEi initial
that
are
glucose/lipid
beneficial
Typical
starting
islow
0.3-0/4
units/kg
per is
day
administer
insulin
until
- onot
Bicarb
isdose
often
(below
10mmol)
Ruptured
viscus?
Calcium
channel
blockers,
B this
blockers
pHand
can
vary
with the
acidosis
- corrected
Cerebral
oedema
= are
serious
vasodilators
lipid complication
and glucose of
Treatment
types
- If
initial
serum
K
is
>5.2mmol/l
do not
Dehydration
results
in
DKA
and
frequently
seen
in
children
neutral
supplement
K+
until
potassium
isCl,
corrected.
o
Inaccurate
reading
of
Na,
K and
Multiple
daily
injection
regime
o B blockers and thiazide diuretics
can
PrecipitatorsMg
of which
DKA are decreased
increase
insulin+
resistance
= not60%
good.
Secondary
assessment
- Basal
(once)
bolusand
(meals)
o 40%
Increased
in BUN
creatinine
Sympathetic
inhibits
and
a-adrenergic
- oInfection
(patients
should
increase
their
Based on carbohydrate intake, expected
- precipitated
Leukocytosis
What
the
episode
blockers
= worsen
orthostatic
insulin
illness)
level
ofduring
physical
activity,
blood glucose
- Hypertrigylceridemia
-- concentration
Tissue
hypotension
ischaemia
(brain
or heart)
at
that
time
Noncompliances,
infection
trauma, infarction
- Hyperlipoproteinaemi
Monitor
potassium
and renal.
- oOmission
ofserum
insulin
due to eating
disorder
cocaine
use
Mixed
insulininfusion
regimen
Insulin
device
mechanical
failure
Ketones
can bestate
detected via capillary ketone,
- Mental
Dermatology
Cultures,
urinary
or serum.
- Mixture
ofCXR,
shortECG
acting and intermediate
Pathophysiology
acting
to
be
given
- On-going
Poor wound
healing andtwice
skin daily
ulceration.
assessment
Differentials
Minimal
role
in
type
1 diabetes
decrease
glucagon/catecholeamines
- Insulin
Diabetic
skin spots
(pigmented
pretibial
increase
promotes
papules)
1.
Capillary
glucose
1-2
hours
If
hyperamylasemia
+
abdominal
pain
can suggest
Continuous subcutaneous insulin infusions
- pancreatis
Acanthosis
nigricans
hyperpigementation
2. Measure
electrolytes
(K+, bicarbondate,
-- Gluconeogenesis
phosphate
and
anion
gap).
K+axilla
repletion
velvety
plaques
seen
on the
neck,
or as
Pump
therapy
(high
cost)
-- Glycogenolysis
soonsurfaces.
as
urine output
and
normal
Need
to adequate
monitor
and count
extensor
regularly
severe
insulin
resistance
- Ketone
body formation
liverinsulin doses
serumannulare
K+.
carbohydrates
to
selectin
bolus
- Grauloma
is erythematous
plaques
3.
Continue
replacement
of
treatment
until
on
extremities
or
trunk
Ketosis
is dueoftoblood
increase
in FFA release from
Monitoring
glucose
patient
is
stable
- adipocytes
Sclerodema
thinkinginsulin
on back
or neck
dueskin
to reduced
levels.
These are
4. Long acting insulin as soon as patient is
- and
Performed
4-6 times each
day, usually
acidic
are
physiologically
decreased
by
eating
before and
after main meals,
before
bicarbonates.
As bicarbonate
decreases
exercise, when hypo is suspected and before
Extra notes:
Infection
driving.
SC insulin
can
be usedand
in mild
DKAof
- Periods
ofcolonization
unwell
Hyperglycaemia
aids
growth
Acidosis
and
ketosis
resolves
slower
than
After
treatment
of
hypoglycaemia
organisms. But they also have impaired white cell
hyperglycaemia
During
times
of
increased
activity
function. Watch for
Potassiuminisinsulin
decreased
due to insulin,
- Changes
regimen
- Skin resolution
infections of acidosis and urinary loss.
should should
also bebe
monitored
if symptoms
- Glucose
ADDED when
plasma or
- Ketones
Otitis
externa
low
blood
glucose
or
acute
illness
- UTI glucose hit 8.3-13.9 mmol/L and insulin
infusion continued (possibly decreased
slightly)
- Ketones improve slower and as it improves B
hydroxybutyrate is converted to
acetoactetate
Treatment of HHS
Choice of therapyHyperglycaemic hyperosmolar state
Similar patient
to DKA in
that
there
is need
for careful
Elderly
with
Type
2 DM
and history
of
Generally a HbA1c of less than 53 or 7% is Metformin is first choice
of antihyperglycaemic
drug
monitoring
of
patients
polyuria,
weight
loss
and
decreased
oral
intake
+
recommended but glycaemic target should be
in type 2.
mental
confusion
leathgy
or
coma.
individualized to ensure hypoglycemia is avoided.
- Fluid state
No lifestyle changes met + max metformin dose =
6.5% in a younger person. 8% in an older if they
Laboratory
This- is due
to drug values
add second antihyperglycaemic
(Sulfonylurea).
have risk of hypoglycaemia
- Insulin infusion rate
Basal insulin or incretin- based
therapies
are new
Profound dehydration
second line treatment
HHS-approaches.
has
more pronouched fluid loss and
Hyperosmoalility
dehydration
due to longer duration of illness
- Hypotension
Sulfonylureas can cause
hypoglycaemia. The
Tachycardia
other medication when
used
with
sulfonylureas
Mental
state
and
changes should also be noted.
Altered mental state
have increased riskHHS
of -hypoglycaemia.
has higher moratlity rate than DKA
This is NOT DKA = no nausea, vomiting, abdominal
1. Fluid replacement 1-3L 0.9% saline over first
pain or KLussmaul respiration.
2-3 hours
2. Ensure there
isnt too rapid repletion as it
Precipitating
factors
can worsen neurological function
-3. Concurrent
illness
(sepsis, pneumonia)
Serum sodium
> 150mmo/L
= usue 0.45%
- Myocardial
infarction
saline
-4. Stroke
Free water deficit
- Social
stroke or dementia
causes
a. situation
After haemodynamically
stable
decreased
water
intake
b. 0.45%
saline
c. Then 5% dextrose in water
Pathology
5. Potassium repletion usually necessary
6. deficiency
Insulin bolus then constant infusion rate. If
Insulin
glucose does not fall increase 2x
-7. Hepatic
production
Glucose glucose
should be
added when plasma
- Impaired
glucose
utilization
in and
skeletal
glucose fall 13.9-16.7
mmol/L
insulin
Diet
muscles
decreased.
Management of Type 2 DIabetes
Dehydration
-
Hyperglycaemia ( >55.5mmol/L)
Hyperosmolality (>350mosmol/L)
Prerenal azotaemia
Gastrointestinal intolerance
Lactic acidosis (rare and adverse)
Kidney excretion (dose reduction in those with
poor kidney function)
Insulin
Basal insulin with metformin/
+sulfonylurea
Combination insulin with
metform
Gastrointestinal
- Flatulence
- Bloating
- diarrhoea
Used when
glycaemic targets
are not met.
Eventually require
Hypoglycaemia
insulin due to
progressive beta cell
failure.
Thiazolidinediones (pioglitazone, rosiglitazone)
Peroxisome
- Heart failure due to fluid retention
- Fracture risk in postmenopausal women
proliferator- Bladder cancer with pioglitazone
activated receptor
- Macular oedema
gamma agonists.
Only
used in those with severe insulin resistance or
Promotes glucose
hypoglycaemia
avoidance is paramount
utlisation in
peripheral tissues,
suppress
gluconeogenesis in
liver and reduce
adipocyte lipolysis.
Sodium glucose cotransporter 2 inhibitor (Dapagliflozin)
New drug
Increases urine
output of glucose
Other considerations
Alcohol intake
-
Travel
-
Carry a letter of introduction with their diabetes history and letter for customs (syringes, blood testing
equipment, insulin vails and other drugs)
Driving
-
Test BGL
DM 1 Summary