LABORATORY DIAGNOSIS OF DIABETES MELLITUS & OTHER DISORDERS OF CARBOHYDRATE METABOLISM
Lectured by: Socorro Cruz-Yañez MD, FPSP
HORMONE REGULATION
1. Insulin – secreted by particularly the beta cells in the islet
of Langerhans; hypoglycemic agent; the most important
hormone that regulates glucose metabolism
2. Glucagon - secreted by alpha cells in the islet cells of
Langerhans; antagonist of insulin; hyperglycemic effect
3. Somatostatin – secreted by delta cells , gastric mucosa and
intestine; increases glucose levels
4. Epinephrine – increases glucose levels
5. Growth Hormone
6. Cortisol – also increases blood glucose
7. Thyroxine
Insulin effects
 Induces synthesis of glycogen (storage form of glucose in
the liver)
 Induces glycolysis (splitting of glucose)
 induces synthesis of fatty acids and their esterification
 induces synthesis of proteins
 decreases glycogenolysis and gluconeogenesis (formation
of glucose from other sources)
 reduce oxidation of fatty acids and lipolysis
 overall effect: reducing blood glucose level
Insulin and its antagonists
 Glucagon – increases glycogen breakdown (into
disaccharides/monosaccharides), gluconeogenesis (from
protein and fat) and glycolysis blockade in liver
 Adrenaline, noradrenaline (secreted by adrenal medullary
cells) – induces glycogen breakdown and gluconeogenesis
in muscles, lactate  glucose in liver
 Growth hormone (anabolic hormone), lipolysis,
proteosynthesis
 Glucocorticoids – gluconeogenesis, block of
proteosynthesis
 Thyroid hormones and estrogens
**All of these hormones have hyperglycemic effect.
In physiological conditions synergism (counter-regulation)
METABOLISM of Glucose
 Ingested as glucose polymers of starch & glycogen 
digested in the lumen of the gut  oligosaccharides 
broken down into monosaccharides (simplest sugars [e.g.
glucose, lactose, galactose])  absorbed readily in the
intestinal epithelium  carried through the PORTAL VEIN
into the liver  stored into a more complex sugar
(glycogen) through glycogenesis
 When the blood glucose becomes low, glycogen is broken
down into simpler sugars.
**Laboratory plays an important part in the diagnosis and
management of diabetic patients
EXAMINATION METHODS
GLUCOSE MEASUREMENTS
 By colorimetric method (chemical reaction of the glucose
and its bounded either by oxidation-reduction or by
oxidation method and the level of intensity on the
spectrum is transmitted in the light and it is INdirectly
proportional to the concentration) *verbatim ‘to.. magulo
explanation nya..
TYPE OF SPECIMEN:
 Venous blood is the specimen choice
it is the reference standard of the normal values
of blood sugar
So if you see your normal values (e.g. 80-100
mg/dL), this will tell you that the source of
reference values comes from the venous blood
specimen(NOT arterial/capillary).
 Whole blood (anticoagulated)
used in home monitoring device
10-15% lower compared to serum glucose levels
so it is important to standardize your test (make
sure the procedure used is serum examination)
From the notes of Co-Neil Relato and Kathrina Virtusio
Brought to you by the Super Cool Non-Nerdy, Ortigas Study Club (SCNNOSC) of the UERMMMCI College of Medicine and friends.
When blood coagulates, the top portion is the
serum.
Majority of the specimen reference values in the
lab are related to serum blood sugar
 Capillary blood (by pinprick method)
higher levels than venous blood by 2-3 mg/dl or
1.1-1.7 mmol/L (SI unit) so make sure you do
NOT use the reference values for venous blood
used in infants and difficult venipuncture (i.e. in
severe burns, shock)
GLUCOSE MEASUREMENTS
 Serum is appropriate specimen
 Serum portion is the one tested for blood glucose
concentration
 Put blood in tube with red top [NO anticoagulant]);
separate serum from the red blood cell components within
30 minutes after extraction to prevent glycolysis (glycolysis
results spurious decrease in blood sugar; RBCs uses up the
glucose if you let it stand too long)
At room temp, whole blood specimen is
metabolized at approx. 7 mg/dl/h  7 mg/dl
decrease in glucose levels per hour
E.g. In a hypoglycemic patient with blood glucose
of 50 mg/dL and you let the specimen stand for 3
hours, the results will read around 20+ mg/dl
(parang falsely low).
o
 At 4 C, glucose loss is approx. 2 mg/dl/h.
 Na fluoride (a preservative which prevents glycolysis) and
refrigeration can prevent deterioration (2-4 oC retards
glycolysis)
 Bacterial contamination, sepsis, and leukocytosis can
increase glycolysis (bacteria use up glucose)
GLUCOSE METHODS
1. Chemical methods: (o-toluidine [ortho-toluidine] method)
 Less sensitive and less specific because it uses
the reducing property of glucose in its chemical
reaction
 Lack specificity (galactose, maltose , sucrose,
lactose, and fructose also react with this
method)
 Therefore, the level of glucose concentration in
this method is higher with reference to the
normal values because other sugars are also
present.
 Requires 1-2 mL of specimen (does NOT do well
with capillary pinprick method)
2. Enzymatic methods
 Most popular procedures for determining
plasma glucose because of :
superiority over chemical method
High specificity (only detects glucose;
reflects the true glucose level)
Easy to test
Rapidity of assay
Small sample quantity (2 uL or 0.2 mL)
Ease of automation
Can be used for Point of Care ( POC )
testing particularly glucose oxidase
 variants
Glucose oxidase
Hexokinase – most superior
Glucose dehydrogenase
Reference Interval
 Fasting glucose (normal) : 3.9 - 6.11 mmol/l (80-100 mg/dl
using the enzymatic method)
 100-120 mg/dl if using the chemical method because it is
NOT the true glucose level that is measured in this method
 fasting is defined as no calorie intake for at least 8 hours to
as much as 12-14 hours; beyond 12 is NOT acceptable due
to overfasting
Page 1 of 6
 DISORDERS OF CARBOHYDRATE (CHO) METABOLISM LABORATORY CRITERIA FOR DIAGNOSIS OF DM
1. Hyperglycemia – raised plasma glucose
2. Hypoglycemia – decreased plasma glucose
3. Normal or lowered plasma glucose but still with problems
of glucose metabolism

DIABETES MELLITUS
 Chronic metabolic disorder associated with increase blood
sugar level secondary to reduced insulin or impaired
insulin utilization
 Part of metabolic syndrome (patients with hyperuricemia,
hyperlipidemia, etc.)
 Associated with cerebrovascular accidents, angiopathy,
microvascular/cardiovascular (ischemic heart disease)
disease, retinopathies, neuropathy (sensorimotor), and
the more dreaded renal complication (diabetic nepropathy
 chronic renal insufficiency/renal failure); accelerated
atherosclerosis and hypertension
**random plasma glucose (aka random blood sugar [RBS]); fasting plasma
glucose (fasting blood sugar [FBS]); post-load glucose (post-prandial glucose
Etiologic Classification of Diabetes Mellitus [PPG]); OGTT (oral glucose challenge test [OGCT])
Type 1 (juvenile type) **OGTT: glucose is dissolved in 1 glass of water (to be consumed in
 Beta cell destruction usually leading to absolute insulin 5 minutes) determine glucose level after 2 hours (blood glucose
deficiency should normally go down after 2 hours)  if >200, possible
 Immune-mediated, idiopathic diabetes.
 Diabetic ketoacidosis (DKA) common **The above criteria should be confirmed by repeat testing on a
Type 2 different day. The 3-hour OGTT is NOT recommended for routine
 May range from predominantly insulin resistance clinical use.
(peripheral resistance particularly the muscle) with relative
insulin deficiency to a predominantly secretory defect with
insulin resistance
 DKA NOT common
Gestational DM (GDM)
Other Specific Types
 Genetic defects of beta cell function
 Genetic defects in insulin action
 Diseases of the exocrine pancreas
 Endocrinopathies*
 Drug or chemical-induced*
 Infections
 Uncommon forms of immune-mediated diabetes
*usual causes
** impaired fasting glucose (IFG); impaired glucose tolerance (IGT)
** Patients with IFG and IGT are NOT immediately labeled as
diabetic; this only signifies that they are at risk for developing
diabetes in the future.
**OGTT/OGCT: 75 g glucose for non-pregnant and 100 g glucose for
pregnant  check glucose level after 30 minutes, 1 hour, 2 hours,
and 3 hours

Laboratory Dx of DM
 RBS, FBS
 Post prandial blood sugar/ OGTT
 Glycosylated Hb – monitors efficacy of treatment
 Ketone – to detect DKA
 Urine glucose – home monitoring tool (self-test)
 Other tests to monitor DM complication
Renal function test: creatinine, Creatinine
clearance, BUN
Urine albumin, microalbuminemia: to check for
impending diabetic nepropathy
Lipid profile
Renal infection screen (urinalysis): DM patients
prone to renal infection

Random blood sugar

DIAGNOSTIC CRITERIA
1. History (history alone or on lab results alone do NOT suffice; it
should be symptoms plus lab result [*see next table])
 Symptoms : hunger, thirst, weight loss
 Triad: polydipsia, polyuria, polyphagia
 Blood sugar level taken at any time of the day
 Values = 45- 130mg/dL or 2.5 to 7.2 mmol/L
 Upper limit of 180 mg/dL or 10.0 mmol/L for > 65 year-
old healthy patient is acceptable
Fasting Blood Sugar
 Blood sugar level taken after overnight fast (at least 8 hrs
or 12-14 hrs recommended; you can actually have FBS in
the afternoon as long as you have a minimum of 8 hours
fast)
 Plasma specimen collected after 12 – 14 hour fast

From the notes of Co-Neil Relato and Kathrina Virtusio Page 2 of 6

Brought to you by the Super Cool Non-Nerdy, Ortigas Study Club (SCNNOSC) of the UERMMMCI College of Medicine and friends.
  Overnight fasting glucose concentration between 50 and ** normal (blue line): This is a typical behavior of an OGTT of a non-
110 mg/dl ( 2.8 – 6.2 mmol/l ) – accepted normal value pregnant patient (75 g). When you give the glucose challenge, it
 Diabetes mellitus can be dx by: maximally increases after 30 minutes to 170-180 and normalizes to
glucose level >140 mg/dl (7.8mmol/L ) or fasting levels at the 2nd hour and 3rd hour.
consistently elevated glucose on 2 separate ** IGT (pink line): slightly elevated glucose at the fasting level,
occasions (e.g. after a month) higher than normal level at 30 minutes (about 200), and does NOT
return to normal limits at the 2nd and 3rd hour (still at 160-180).
2-hour Postprandial Plasma glucose or Post-oral glucose test ** Diabetic (yellow): elevated glucose at fasting (140), 250 or >300
 Simplest loading test after 30 minutes, and also does NOT normalize in the 2nd/3rd hour.
 Measurement of plasma glucose concentration 2 hrs after
the px consumes a load containing 100g of carbohydrate
(either in a sachet or the px is given a meal [i.e. 1 full cup
of rice, 2 eggs, banana, fish or meat, or 2-4 slices of
bread])
 Screening test in diagnosing GDM
 Abnormal: Venous plasma level > 200mg/dl (11.1 mmol/L);
<120 mg /dl – normal
 Between 120 & 200 mmol/dl – equivocal (need to do
further blood testing with OGCT [subject patient to serial
blood sugar monitoring at different time interval])

OGTT
 Clinical significance: used as a reflex testing for impaired 2-
hour post-prandial test
 gold standard or confirmatory test in diagnosing patients
with GDM
 Patient preparation : * Ma’am did not discuss the details of this table.
diet of > 150 gm CHO for 3 days **In many laboratories, urine sample is collected at the same time
NO alcohol, unrestricted activity for 3 days as the plasma samples (OGTT).
NOT done after acute illness, surgery, emotional  Advantage – correlation between any glycosuria and the
stress, trauma, pregnancy, inactivity due to corresponding plasma glucose levels
chronic illness, hospitalization  Disadvantage – cost; another stress for the patient (4 urine
10 – 12 hrs fasting samples are also required together with 4 extractions of
AVOID oral diuretics, contraceptives phenytoin blood)
because they have hyperglycemic effect
 Loading dose : Impaired Glucose Tolerance
Must be consumed within 5 min  Higher than normal plasma glucose but lower than the
 Adults = 75 gms diagnostic values for DM
 Children = 1.75 gms / kg BW  Precursor for Type II DM (may have preclinical DM)
 Pregnant = 100 gms  Only about 25% develop into type II and rest go back to
After drinking, instruct patient to sit down and normal depending on the person’s lifestyle
rest or NOT walk around too much.  Patients are more susceptible to macrovascular diseases
 Draw blood (i.e. atherosclerosis)
after an 8-hour fast; after extracting the FBS (1st  Similar risk factors as DM II
blood extraction), give the glucose load.
nd
Extract another blood specimen at 30 (2 blood OGTT Clinical use
rd th
extraction), 60 (3 ), and 120 minutes (4 ) post  Reflex testing for px with borderline FBS (110-140 gm/dl):
glucose challenge means that if the FBS is within this range, the next step in
Intrusive to the patient due to 4 blood the algorithm is OGTT.
extractions  Adjunct to diagnose IGT and IFG (as a confirmatory test)
 Gold standard for dx of gestational DM
OGTT Criteria
Plasma Glucose Plasma Glucose OGTT is NOT indicated in:
( mmol/L ) ( mmol/L )  Persistent fasting hyperglycemia (> 140 mg/dl )
0 min 120 min  Persistent fasting normoglycemia(< 110 mg/dl )
Non-diabetic <6.1 <7.8  Px with s/sx of DM with FBS > 200 mg/dl (this is already a
Impaired Glucose 6.1-6.9 >7.8-11.1 diagnosis of DM so you do NOT need to confirm it with
Tolerance OGTT)
Diabetic >7 >11.1  Secondary DM
 Evaluation of reactive hypoglycemia
 dx of DM in children (because the reference values are
that of the adults)
GLUCOSE LEVEL
NORMAL Ancillary Tests
Urine Tests (Dipstick Method)
300
GLUCOSE

 Principle: There is a renal threshold for glucose in the renal

200 tubules (blood glucose 180 mg/dl). If this value is
IMPAIRED exceeded, glucose spills off into the urine.
100
TOLERANCE  Diagnostic reagent: glucose oxidase (enzymatic reagent)
0 impregnated in a strip  checks for enzyme reduction of
0 0.5 1 2 3 the glucose
DIABETIC  URINE "GLUCOSE"
DAYS lacks sensitivity = positivity in disease
poor specificity = negativity in health
** I think the abscissa should be hours and NOT days.

From the notes of Co-Neil Relato and Kathrina Virtusio Page 3 of 6

Brought to you by the Super Cool Non-Nerdy, Ortigas Study Club (SCNNOSC) of the UERMMMCI College of Medicine and friends.
  Problems
renal threshold variable 6 to 15 mg/dL therefore
lacks sensitivity and has poor specificity
interferences : Clinitest / Glucose oxidase strips
if urine test is positive, a confirmatory blood test
is NEEDED; do NOT presume that if the result in
the dipstick is 1+, then the blood sugar is 180.
This is due to the variability in renal threshold
Glycosylated proteins
 Glycosylated haemoglobin (HbA1c)
to monitor blood sugar levels for an extended
period of time
to monitor patient compliance to treatment
regimen
to monitor adequacy of blood glucose control
stable; most important
a form of fetal hemoglobin
HbA1c – LGI reference range 4.6-6.5%; 6%
indicates good control and level >8% indicates
action is needed
glucose canNOT be dissociated from hemoglobin
so HbA1c indicates cumulative glucose exposure
for the preceeding 2-3 months (3 months being
the life expectancy of a normal RBC)
Glucose binds continuously and IRreversibly with
Hb during life span of RBC (120 days)
Disadvantage: affected by altered red cell
survival (canNOT be used in
hemoglobinopathies, thalassemia, haemolytic
dse because of shortened RBC survival)
If with good diabetic control, test HbA1c q6
months; if poor control, test quarterly.
 Fructosamine
mirrors glycosylation of all serum proteins
indicates previous 2-3 weeks glycaemic exposure
used pregnancy/children in some sites
 Glycosylated albumin
indicates previous several days glycaemic
exposure
not commonly used
Glycosylated HB (HbA1c)
 Indicates average plasma glucose level for 6 to 12 weeks
 Clinical use :
monitor diabetic px compliance
 a lot of patients cheat blood glucose by
dieting for a week before they are
tested; a px canNOT cheat HbA1c
levels
index of diabetic control (direct relationship of
poor control and increased complication)
predicts development and progression of
microvascular complication
 Dietary preparation not required
 N: 4 – 8 % (*Ma’am said 4-6%)
 Can estimate the mean daily glucose level
mean daily carbohydrate (CHO) level in mg/dl =
10 x (HbA1c value + 4)
 Interpretation :
Increased levels implies poor diabetic control
when FBS is < 110 mg/dl, HbA1c is normal in 96%
of cases
when FBS is 110-125 mg/dl, HbA1c is normal in
80% of cases
when FBS is > 126 mg/dl, HbA1c is normal in
>60% of cases
HbA1c in known diabetics
 < 7 % indicates good diabetic control
 10 % indicates fair diabetic control
 13 – 20 % indicates poor diabetic control
From the notes of Co-Neil Relato and Kathrina Virtusio
Brought to you by the Super Cool Non-Nerdy, Ortigas Study Club (SCNNOSC) of the UERMMMCI College of Medicine and friends.
Increased HbA1c levels in:
 Presence of HbF (fetal hemoglobin)
 Chronic renal failure
 Post splenectomy
 Iron deficiency anemia
 Hypertriglycerenemia
 Alcohol, lead and opiate toxicity
 Salicylate treatment
Decreased HbA1c levels in:
 Shortened RBC life span particularly in hemolytic anemias
 Following transfusion
 Pregnancy
 Ingestion of large amounts of Vit C/E
 Hemoglobinopathies
Recommendations of the International Expert Committee
For the diagnosis of diabetes:
 The HbA1c is an accurate, precise measure of chronic
glycaemic levels and correlates well with the risk of
diabetes complications
 It has several advantages over laboratory measures of
glucose
 DM is diagnosed when HbA1c is ≥6.5 %. Diagnosis should
be confirmed with a repeat HbA1c test. Confirmation is
not required in symptomatic subjects with plasma glucose
levels >200 mg/dl (>11.1 mmol/l)
 If HbA1c testing is not possible, previously recommended
diagnostic methods (e.g., FBG or 2hPPG, with
confirmation) are acceptable
 HbA1c testing is indicated in children in whom diabetes is
suspected but the classic symptoms and a casual plasma
glucose >200 mg/dl (>11.1 mmol/l) are not found
Clinical implications
 HbA1c for diabetes diagnosis offers greater convenience
and accuracy than glucose measurements and correlates
well with
long-term complications
 HbA1c may be too expensive for routine use in some parts
of world
 HbA1c may be influenced by haemoglobin traits and
precluded for people with conditions that affect red cell
turnover (haemolytic anaemia, chronic malaria)
 HbA1c not ‘gold standard’ for diabetes diagnosis, as no
single assay can define the relationship between glucose
and vascular complications
**Micral Test: to test for microalbuminuria; to detect for the
presence of early renal nephropathy
Page 4 of 6
POC (Point of Care) testing for glucose
 Portable, can be used for home testing, physician’s offices Other lab tests for CHO disorders: ketone testing
or bedside KETONE TESTING
 Uses a refractometer (about the size of a Blackberry)  The ketone bodies
 Uses capillary whole blood beta-hydroxybutyric acid
 Skin is pricked and blood is put in strip impregnated with acetoacetic acid
glucose oxidase. The strip is then put into the acetone which are products of fatty degradation
refractometer for reading (diagnostic substance of choice)
 Principle: glucose oxidase enzymatic method  Used in dx of DKA in type I DM
 approximately 10-15% lower glucose readings than  DKA
venous sample a serious and potentially fatal hyperglycemic
 Used for immediately monitoring blood glucose levels condition  conversion of excess glucose into
 should NEVER be used to diagnose DM or hypoglycemic ketone bodies
disorders; it is only used to monitor blood glucose S/Sx: nausea, vomiting, abdominal pain,
particularly in patients with DKA and hypoglycemic electrolyte disturbances, mental obtundation,
disorders ocular disturbances, seizures, and severe
dehydration
Home glucose monitoring Can go into coma
 Require a drop of whole blood obtained by fingerstick to
be applied to a reagent test strip
 After incubation of color development, test is read by
reflectance photometer
 Strips usually use a a glucose oxidase enzymatic method
embedded in the strip

GESTATIONAL DIABETES
st
**Screening test is 2-hour postprandial glucose test (1 step). When
the result is abnormal, do reflex confirmatory testing (OGTT).

* Ma’am did not discuss the details of this table.

Renal testing in DM

* Ma’am did not discuss the details of this table.

*Non-diabetic renal disease is suspected when there is absence of
diabetic retinopathy in a person with renal disease, there are urinary
abnormalities such as haematuria or casts, or when there is renal
disease without microalbuminuria or proteinuria.

Tests for Diabetic renal disease:

 Urinary albumin:creatinine ratio (ACR)
 Serum creatinine
 Estimated Glomerular Filtration Rate (eGFR) – reduced
GFR means there is significant nephron mass loss
 Urinalysis , micral test
 Note : These tests are performed on px suspected with
renal complication or if there is proteinuria or
microalbuminuria
 These tests are repeated annually in px with DM
**I don’t know what values are to be followed. Hindi nya rin na-mention
Albumin : creatinine ratio
which one. Pick one nalang. Halos pareho lang naman… hehehe
 provides an estimate of daily urinary albumin excretion.
 Microalbuminuria cannot be detected on a conventional
urinary protein dip stick.

From the notes of Co-Neil Relato and Kathrina Virtusio Page 5 of 6

Brought to you by the Super Cool Non-Nerdy, Ortigas Study Club (SCNNOSC) of the UERMMMCI College of Medicine and friends.
  Microalbuminuria is urinary albumin excretion between 30  Non-beta cell tumors (can present with non-resolving
and 300 mg/day; above 300mg/day represents hypoglycemia)
proteinuria. • Mesenchymal: Fibrosarcoma, mesothelioma,
 ACR is best measured in the laboratory using a first rhabdomyosarcoma, leiomyosarcoma,
morning urine sample where possible when the patient is liposarcoma, lymphosarcoma,
well. hemangiopericytoma
 An abnormal initial test requires confirmation by testing • Carcinomas: Hepatomas, adrenocortical tumors,
on two further occasions. If at least one of these tests is hypernephroma, Wilms' tumor
positive microalbuminuria has been confirmed. • Neurological and neuroendocrine tumors:
Pheochromocytoma, carcinoid tumor,
Complications of DM: neurofibroma
 CVS, renal, micro-angiopathy, retinopathy, neural • Hematologic: Leukemias, lymphoma, myeloma
Other tests:
 Lipid profile: at least annually if stable; if unstable, q3-4 INSULINOMA
months until levels become stable and 6-12 months  Beta islet cell tumor
thereafter.  Caused by excess and inappropriate secretion of insulin by
**It is important that management should be individualised B cell tumors
 Triad
Parameter Optimal Value Hypoglycemic attacks precipitated by fasting
Total cholesterol < 4 mmol/L Plasma glucose <45 mg/dl/2.5 mmol/L during
LDL cholesterol < 2.5 mmol/L attack
HDL cholesterol > 1 mmol/L Relief of symptoms by glucose administration
TC:HDL ratio < 4.5  Lab dx
Triglycerides < 1.7 mmol/L FBS
HbA1C < 7 mmol/L Insulin assay by RIA (radioimmunoassay)

Self-Monitoring blood glucose (SMBG) HYPOGLYCEMIA (*included in the ppt but not discussed)
Clinical classification:
 People who take insulin should regularly self-monitor
• Drugs
blood glucose
Insulin, Sulfonylureas, Benzoic acid derivatives
 Makes use of a point of care device (i.e. a refractometer)
(repaglinide), Nateglinide, Alcohol, Pentamidine, Beta-
 For people with non-insulin treated type 2 diabetes testing
blockers, Quinine, Salicylates, Sulfonamides, Haloperidol,
is most useful if patients use the results to learn and alter
Propoxyphene, Para-aminobenzoic acid
behaviour, or medication.
• Hypoglycemia of infancy and childhood
 “...SMBG is most useful if patients use the results to learn,
Hyperinsulinism, transient: Erythroblastosis fetalis,
as part of an overall diabetes education package….”
Beckwith–Wiedemann syndrome, uncontrolled diabetes
(mother), Persistent: Hyperinsulinemic hypoglycemia of
Other tests
infancy, Glycogen storage diseases, Hereditary fructose
Testing of LFTs (liver function test?) is recommended for px with DM
intolerance, Galactosemia, Defects in gluconeogenesis,
 at diagnosis
Reye's syndrome, Deficiency of glucose transporters,
 at the start of antidiabetic drug therapy
Impaired ketogenesis, Carnitine deficiency, Defects in
 at any other time indicated by clinical judgement
mitochondrial function
**In patients with type 1 diabetes, intermittent checks for other
• Alimentary hypoglycemia
autoimmune conditions may be useful. This could include testing for
Post-gastric surgery
thyroid dysfunction or celiac disease.
• Idiopathic (functional) postprandial

Regulation of Blood Sugar

Cori & Cori (1947)
Signal Transduction
Decreased
Tyrosine-kinase-linked receptor

High blood sugar Insulin

Glycogen
Liver synthase

**usually you give D10W

Blood Pancreas Hormone Glycogen Glucose
HYPOGLYCEMIA Glycogen
Clinical classification: Low blood sugar Glucagon phosphorylase
 Critical illnesses (can have reactive hypoglycemia)
• Hepatic/renal/cardiac failure GTP-protein-linked receptor
• Sepsis Increased
• Malnutrition Juang RH (2004) BCbasics
 Hormonal deficiencies of
• Glucagon, epinephrine, cortisol, growth
hormone
 Endogenous hyperinsulinism
• Pancreatic beta cell disorders
• Tumor (insulinoma)
• Non-tumor (nesidioblastosis or diffuse
hyperplasia of the pancreatic islet cells)
 Autoimmune hypoglycemia
• Insulin antibodies
• Insulin receptor antibodies

From the notes of Co-Neil Relato and Kathrina Virtusio Page 6 of 6

Brought to you by the Super Cool Non-Nerdy, Ortigas Study Club (SCNNOSC) of the UERMMMCI College of Medicine and friends.