ALWAYS GIVE PPI (OMEPRAZOLE) when giving dexamethasone to
provide protective effect against dexamethasone induced gastric
muscosal damage and ulcers!
NEVER EVER WITHOLD BASAL INSULIN IN T1DM! EVEN WHEN
FASTING FOR SURGERY etc! May precipitate DKA
• If BSL>18, check ketones
• If ketones >1, do VBG to exclude DKA
• To titrate long acting, look at the fasting sugar levels
• Always think about when the insulin is active at which point in
time!
Hassall's corpuscles are the concentric ring of epithelial cells seen in
the medulla of the thymus.
An FNA should be considered in all thyroid nodules with normal or
elevated TSH
Remember that in Type 1 diabetics, your main complication concern is
diabetic ketoacidosis or Hypoglycemia, BUT in type 2 diabetics, you are
more concerned with the micro and macrovascular changes.
Note that thyroxine, aripiprazole and other antipsychotics in standard
dosing can augment the SSRI antidepressant activity, especially for
female patients for which pharmacotherapy has yet to be very effective.
Hypothyroidism Tiredness, husky voice, cold intolerance, physical slowing, menta
slowing, facial puffiness
Hyperthyroidism Anxiety, weight loss, muscle weakness, sweaty hands, loose frequent
bowel motions, palpitations
Acromegaly Nasal problems , fitting problems (shoes, gloves, rings), weakness,
sweating
Addison disease Fatigue, weakness, anorexia, nausea, dizziness, weight loss, loos
bowels, abdominal pain, skin discolouration
Cushing disease Plethoric moon face, thin extremities, muscle weakness, hisutism,
abdominal striae, hypertension
Hypopituitarism Female: amenorrhoea, loss of axillary and pubic hair, breast atrophy
Male: reduced libido, impotence, loss of body hair
Diabetes insipidus Weakness, polyuria, polydipsia (intense craving for ice cream)
Hypercalcemia Weakness, constipation, polyuria (primary parathyroidism)
Hyperparathyroidism: bones, moans, stones, abdominal moans
Hypocalcemia Cramps, cognitive dysfunction, confusion, tetany
Hyperprolactinemia Common to both sex: reduced libido, galactorrhea, subfertility
Females: amenorrhoea/oligomenorrhoea
Males: erectile dysfunction, reduced facial hair
Diagnosis of diabetes:
• If asymptomatic: 2 separate occasions of diabetes range results
needed (includes OGTT)
• If symptomatic: 1 occasion of diabetes range results needed
, • HbA1c ≥ 6.5%
o HbA1c measures the long term sugar control by measuring amount of
glycated Hb. If RBC life is shortened, then shorter times are reflected and
hence range of HbA1c is falsely low. Causes Include:
§ Erythropoietin
§ Blood transfusion
• Steroid induced hyperglycaemia: Steroids usually given in early
morning
o You shoud measure BSL in the evening at 5pm (anecdotal),
around 6-8 hours after the dose
o Steroids should not be given in the evening because it can be
quite stimulating, leading to insomnia etc
Differentiating investigations
• C-peptide with paired glucose (shows how much C peptide and
what the sugar is responding to)
o High In T2DM, low in T1DM
• Diabetic autoantibodies (anti GAD, anti islet cell/Anti IA2)
BSL home monitoring only needed if insulin dependent (using insulin to treat
diabetes)
Whipple triad: to suggest hypoglycemia caused by insulinoma
1. Symptoms known or likely to be caused by hypoglycemia after fasting
or heavy exercise
2. Low plasma glucose at times of symptoms
3. Relief of symptoms when glucose is raised to normal
Isoenzymes catalyse the same reaction but have different amino acid
sequences
Note: about 50% of diabetes goes undiagnosed in many individuals
• Increased BSL associated with:
o Longer hospital stay
o Increased infection
o More disability post hospital discharge
o Death
Factors leading to hyperglycemia:
• Increased counter regulatory hormones/cytokines, stress
hyperglycaemia
• Enteral/parenteral feeds
• Medications including steroids, anti-psychotics
• Reduced physical activity
• Peritoneal dialysis
T-TREKS: regarding events
• Type of diabetes (T1 or T2)
• Time of Day
• Usual regime
, • Eating
• Ketones
• Sugars
Diabetes type 1
Syndrome of disordered metabolism and inappropriate hyperglycaemia secondary to relative
absolute/ relative deficiency of insulin, or a reduction in biological effectiveness of insulin, or
both
Type:
1. 1A: cell medited autoimmune destruction of beta islet cells
2. 2A: rare non-immune variation, unknown cause
Normal sugar levels = 2(HbA1c) – 5
False elevation of HbA1c:
• Splenectomy
• Alcohol
• Iron deficiency: less iron bind with haem groups and hence more hb can be glycated
• Steroids use, surgery, illness, stressful periods
Falsely lowered HbAc:
• Blood transfusion
• Recovery fcute Blood loss
• Chronic blood loss
• Hemolytic anemia: HS, elliptocytosis, AIHA, MAHA
• Chronic renal failure: Dialysis or due to the prolonged problem of anaemia
Questions to ask
• What is your diagnosis?
• When was it diagnosed?
• How is it being controlled?
o On insulin? What medications?
• Are you taking your sugar levels regularly? What are the readings? (4 times a day is
best)
• What complications? Eye: cataracts, glaucoma, macular degeneration and hence
driving? Renal: dialysis? Peripheral neuropathy: tingling, shooting burning pain,
amputations? Autonomic: gastroparesis, postural hypotension, erectile dysfunction?
o Peripheral: use pin prick and test pulses
• Podiatry/optometry review?
• Hypoglycaemic episode (BSL <3.2)? How often? Do you get it? What happens
o Neuroglycopenic symptom: light headedness, irritabile, altered conscious
state
o Adrenergic effect: Tachycardia, sweating, tremors
• Any diabetes educator?
Epidemiology
• Usually <30 yo
• More common in caucasians
• Account for 5-10%
• Less genetic concordance
Aetiology
• Autoimmune caused by autoimmune antibodies (islet cell Ab up to 60-85%, often
against glutamic acid decarboxylase and insulin Ab up to 60%)
• Just to note: after initial presentation, honeymoon period often occurs where glycemic
control is achieved with little or no insulin as residula cells are still abel to produce
insulin
, • Disease results from some level of genetic predisposition and an environmental
trigger
Risk Factors:
• Personal or family history of autoimmune conditions: Hashimoto thyroiditis, graves,
coeliac disease
• Family history (less so)
o If father has T1DM: kids have 5% risk of T1DM
o If mother has T1DM: kids have 1% risk of T1DM
Pathophysiology
• Synergistic effects of genetic, immune, environmental factor causing B cells
destruction
• Autoimmune process triggered by environment (e.g virus, bovine milk protein,
urea compound)
• Pancreatic cells infiltrated with lymphocytes causing destruction
• 80-90% of islet B cells destroyed before DM signs appear
• HLA-DR3/DR4 in >90% of patients (confers about 50% of genetic susceptibility)
• In DKA, ketones are produced because sugars remain in blood vessels and are
not intracellular for cells to use. As such, fat metabolism takes over and
produces Acetyl CoA units. Usually these acetyl CoA will be burnt for energy
and removed. However, in DKA, oxaloacetate will be used up for
gluconeogenesis in the liver and no longer available to combine with acetyl
CoA and as a result, acetyl CoA forms Acetoacetate and B-hydroxybutyrate
(ketone bodies). Ketotic breath will be acetone
• Symptoms of abdo pain, feeling unwell are all due to the ketone bodies within
the body as well as the stress response from a sudden release of cortisol to
activate the sympathetic nervous system
Clinical Presentation
• Inspection: polyuria, polydipsia, weight loss (may not be apparent in obese),
Abnormal endocrine facies (cushing/acromegaly), Bronze pigmentation
(haemachromatosis), LOC (comatose in hyperosmolar hyperglycemic state, vitiligo
(also seen in Grave disease, addison’s, hashimoto thyroiditis and T1DM, loss of
skin pigments)
• Peripheral neuropathy
• Sometimes polyphagia due to sugar not being metabolized
• Lower limb: Charcot’s knees, Ulcers, non-healing wounds, cellulitis, fungal infections,
absensce of hair, atrophy of legs, necrobiosis lipoidica diabeticorum, Peripheral
neuropathy
• Upper Limb: candida infection in fingers Autonomic neuropathy (postural
hypotension), diabetic cheiroarthropathy: cutaneous condition characterized by
thickened skin and limited mobility and lead to flexion contractures
• Eye: cataract, rubeosis iridis, Argyll Robertson pupil, absent light reflex,
proliferative/non-proliferative changes
• Face: otitis externa and oral candidiasis
• When severely high sugars, you get DKA. The ketones has to be >0.6 for it to be
considered DKA: N/V, Kussmaul breathing (deep labored brethig pattern), abdominal
pain, warm dry skin, sweet-smelling breath
• Hypoglycemia: hunger, stomachache, wobbly feeling, pallor, cold sweat, tremor,
pounding heartbeat, tachycardia
• DKA: fatigue, nausea, vomiting, abdominal pain (due to gastric dilation and
ileus), kussmaul breathing, confusion
o Hyperglycemia, keotsis acidosis (pH<7.3, HCO3<15)
o Beware fluids, low K+, low BGL and cerebral edema
• In absence of adequate of insuin
o Polyuria, polydipsia
• Alterative fuel souce:
o Lipolysis causing ketosis
provide protective effect against dexamethasone induced gastric
muscosal damage and ulcers!
NEVER EVER WITHOLD BASAL INSULIN IN T1DM! EVEN WHEN
FASTING FOR SURGERY etc! May precipitate DKA
• If BSL>18, check ketones
• If ketones >1, do VBG to exclude DKA
• To titrate long acting, look at the fasting sugar levels
• Always think about when the insulin is active at which point in
time!
Hassall's corpuscles are the concentric ring of epithelial cells seen in
the medulla of the thymus.
An FNA should be considered in all thyroid nodules with normal or
elevated TSH
Remember that in Type 1 diabetics, your main complication concern is
diabetic ketoacidosis or Hypoglycemia, BUT in type 2 diabetics, you are
more concerned with the micro and macrovascular changes.
Note that thyroxine, aripiprazole and other antipsychotics in standard
dosing can augment the SSRI antidepressant activity, especially for
female patients for which pharmacotherapy has yet to be very effective.
Hypothyroidism Tiredness, husky voice, cold intolerance, physical slowing, menta
slowing, facial puffiness
Hyperthyroidism Anxiety, weight loss, muscle weakness, sweaty hands, loose frequent
bowel motions, palpitations
Acromegaly Nasal problems , fitting problems (shoes, gloves, rings), weakness,
sweating
Addison disease Fatigue, weakness, anorexia, nausea, dizziness, weight loss, loos
bowels, abdominal pain, skin discolouration
Cushing disease Plethoric moon face, thin extremities, muscle weakness, hisutism,
abdominal striae, hypertension
Hypopituitarism Female: amenorrhoea, loss of axillary and pubic hair, breast atrophy
Male: reduced libido, impotence, loss of body hair
Diabetes insipidus Weakness, polyuria, polydipsia (intense craving for ice cream)
Hypercalcemia Weakness, constipation, polyuria (primary parathyroidism)
Hyperparathyroidism: bones, moans, stones, abdominal moans
Hypocalcemia Cramps, cognitive dysfunction, confusion, tetany
Hyperprolactinemia Common to both sex: reduced libido, galactorrhea, subfertility
Females: amenorrhoea/oligomenorrhoea
Males: erectile dysfunction, reduced facial hair
Diagnosis of diabetes:
• If asymptomatic: 2 separate occasions of diabetes range results
needed (includes OGTT)
• If symptomatic: 1 occasion of diabetes range results needed
, • HbA1c ≥ 6.5%
o HbA1c measures the long term sugar control by measuring amount of
glycated Hb. If RBC life is shortened, then shorter times are reflected and
hence range of HbA1c is falsely low. Causes Include:
§ Erythropoietin
§ Blood transfusion
• Steroid induced hyperglycaemia: Steroids usually given in early
morning
o You shoud measure BSL in the evening at 5pm (anecdotal),
around 6-8 hours after the dose
o Steroids should not be given in the evening because it can be
quite stimulating, leading to insomnia etc
Differentiating investigations
• C-peptide with paired glucose (shows how much C peptide and
what the sugar is responding to)
o High In T2DM, low in T1DM
• Diabetic autoantibodies (anti GAD, anti islet cell/Anti IA2)
BSL home monitoring only needed if insulin dependent (using insulin to treat
diabetes)
Whipple triad: to suggest hypoglycemia caused by insulinoma
1. Symptoms known or likely to be caused by hypoglycemia after fasting
or heavy exercise
2. Low plasma glucose at times of symptoms
3. Relief of symptoms when glucose is raised to normal
Isoenzymes catalyse the same reaction but have different amino acid
sequences
Note: about 50% of diabetes goes undiagnosed in many individuals
• Increased BSL associated with:
o Longer hospital stay
o Increased infection
o More disability post hospital discharge
o Death
Factors leading to hyperglycemia:
• Increased counter regulatory hormones/cytokines, stress
hyperglycaemia
• Enteral/parenteral feeds
• Medications including steroids, anti-psychotics
• Reduced physical activity
• Peritoneal dialysis
T-TREKS: regarding events
• Type of diabetes (T1 or T2)
• Time of Day
• Usual regime
, • Eating
• Ketones
• Sugars
Diabetes type 1
Syndrome of disordered metabolism and inappropriate hyperglycaemia secondary to relative
absolute/ relative deficiency of insulin, or a reduction in biological effectiveness of insulin, or
both
Type:
1. 1A: cell medited autoimmune destruction of beta islet cells
2. 2A: rare non-immune variation, unknown cause
Normal sugar levels = 2(HbA1c) – 5
False elevation of HbA1c:
• Splenectomy
• Alcohol
• Iron deficiency: less iron bind with haem groups and hence more hb can be glycated
• Steroids use, surgery, illness, stressful periods
Falsely lowered HbAc:
• Blood transfusion
• Recovery fcute Blood loss
• Chronic blood loss
• Hemolytic anemia: HS, elliptocytosis, AIHA, MAHA
• Chronic renal failure: Dialysis or due to the prolonged problem of anaemia
Questions to ask
• What is your diagnosis?
• When was it diagnosed?
• How is it being controlled?
o On insulin? What medications?
• Are you taking your sugar levels regularly? What are the readings? (4 times a day is
best)
• What complications? Eye: cataracts, glaucoma, macular degeneration and hence
driving? Renal: dialysis? Peripheral neuropathy: tingling, shooting burning pain,
amputations? Autonomic: gastroparesis, postural hypotension, erectile dysfunction?
o Peripheral: use pin prick and test pulses
• Podiatry/optometry review?
• Hypoglycaemic episode (BSL <3.2)? How often? Do you get it? What happens
o Neuroglycopenic symptom: light headedness, irritabile, altered conscious
state
o Adrenergic effect: Tachycardia, sweating, tremors
• Any diabetes educator?
Epidemiology
• Usually <30 yo
• More common in caucasians
• Account for 5-10%
• Less genetic concordance
Aetiology
• Autoimmune caused by autoimmune antibodies (islet cell Ab up to 60-85%, often
against glutamic acid decarboxylase and insulin Ab up to 60%)
• Just to note: after initial presentation, honeymoon period often occurs where glycemic
control is achieved with little or no insulin as residula cells are still abel to produce
insulin
, • Disease results from some level of genetic predisposition and an environmental
trigger
Risk Factors:
• Personal or family history of autoimmune conditions: Hashimoto thyroiditis, graves,
coeliac disease
• Family history (less so)
o If father has T1DM: kids have 5% risk of T1DM
o If mother has T1DM: kids have 1% risk of T1DM
Pathophysiology
• Synergistic effects of genetic, immune, environmental factor causing B cells
destruction
• Autoimmune process triggered by environment (e.g virus, bovine milk protein,
urea compound)
• Pancreatic cells infiltrated with lymphocytes causing destruction
• 80-90% of islet B cells destroyed before DM signs appear
• HLA-DR3/DR4 in >90% of patients (confers about 50% of genetic susceptibility)
• In DKA, ketones are produced because sugars remain in blood vessels and are
not intracellular for cells to use. As such, fat metabolism takes over and
produces Acetyl CoA units. Usually these acetyl CoA will be burnt for energy
and removed. However, in DKA, oxaloacetate will be used up for
gluconeogenesis in the liver and no longer available to combine with acetyl
CoA and as a result, acetyl CoA forms Acetoacetate and B-hydroxybutyrate
(ketone bodies). Ketotic breath will be acetone
• Symptoms of abdo pain, feeling unwell are all due to the ketone bodies within
the body as well as the stress response from a sudden release of cortisol to
activate the sympathetic nervous system
Clinical Presentation
• Inspection: polyuria, polydipsia, weight loss (may not be apparent in obese),
Abnormal endocrine facies (cushing/acromegaly), Bronze pigmentation
(haemachromatosis), LOC (comatose in hyperosmolar hyperglycemic state, vitiligo
(also seen in Grave disease, addison’s, hashimoto thyroiditis and T1DM, loss of
skin pigments)
• Peripheral neuropathy
• Sometimes polyphagia due to sugar not being metabolized
• Lower limb: Charcot’s knees, Ulcers, non-healing wounds, cellulitis, fungal infections,
absensce of hair, atrophy of legs, necrobiosis lipoidica diabeticorum, Peripheral
neuropathy
• Upper Limb: candida infection in fingers Autonomic neuropathy (postural
hypotension), diabetic cheiroarthropathy: cutaneous condition characterized by
thickened skin and limited mobility and lead to flexion contractures
• Eye: cataract, rubeosis iridis, Argyll Robertson pupil, absent light reflex,
proliferative/non-proliferative changes
• Face: otitis externa and oral candidiasis
• When severely high sugars, you get DKA. The ketones has to be >0.6 for it to be
considered DKA: N/V, Kussmaul breathing (deep labored brethig pattern), abdominal
pain, warm dry skin, sweet-smelling breath
• Hypoglycemia: hunger, stomachache, wobbly feeling, pallor, cold sweat, tremor,
pounding heartbeat, tachycardia
• DKA: fatigue, nausea, vomiting, abdominal pain (due to gastric dilation and
ileus), kussmaul breathing, confusion
o Hyperglycemia, keotsis acidosis (pH<7.3, HCO3<15)
o Beware fluids, low K+, low BGL and cerebral edema
• In absence of adequate of insuin
o Polyuria, polydipsia
• Alterative fuel souce:
o Lipolysis causing ketosis
