HYPOGIYCAEMIA

HYPERGLYCAEMIA
The Pancreas and Its Functions

• The pancreas is an organ located in the abdomen. It plays an essential role

in converting the food we eat into fuel for the body's cells. The pancreas
has two main functions: an exocrine function that helps in digestion and
an endocrine function that regulates blood sugar.
• Endocrine Function:
The endocrine component of the pancreas consists of islet cells (islets of
Langerhans) that create and release important hormones directly into the
bloodstream. Two of the main pancreatic hormones are insulin, which acts
to lower blood sugar, and glucagon, which acts to raise blood sugar.
Maintaining proper blood sugar levels is crucial to the functioning of key
organs including the brain, liver, and kidneys.
 .
  Complications of Diabetes Mellitus 

Acute Chronic
Hypoglycaemia Neiropathy

Dibetic ketoacidosis Nephropathy

Hyperosmolar
Retinopathy
hyperglycaemic state

Vsculopathy

Stive joint syndrome

INTRODUCTION GLUCOSE
HOMEOSTASIS
• Two major hormones regulating glucose homeostasis are insulin (beta
cells) and glucagon (alpha cells). They work together to promote
homeostasis of energy and metabolism of carbohydrates and fats.
There are also other regulating hormones, such as somatostatin,
epinephrine and cortisol.
High blood glucose stimulates insulin release from pancreas stimulates
glucose uptake from blood into skeletal muscles and fat, stimulates
glycogen formation in liver, inhibits release of glucagon
INTRODUCTION H Y P O G LYC E M I A
• Definition Hypoglycaemia is defined by either one of the following two
conditions:
• a) Low plasma glucose level (<4.0 mmol/L).
• b) Development of autonomic or neuroglycopenic symptoms in patients treated
with insulin or OADs which are reversed by caloric intake. Plasma glucose <3.0
mmol/L (OXFORD HANDBOOK) Blood glucose <3.5 mmol/L (DAVIDSON)
• Can mimic any neurological presentation including coma, seizure, acute
confusion or isolated hemiparesis.
• “Always exclude hypoglycemia in any patient with coma, altered behavior,
neurological symptoms or signs.” – OXFORD HANDBOOK OF ACCIDENT AND
EMERGENCY MEDICINE, 2ND EDITION
• The diagnosis of hypoglycemia is not based on an absolute
blood glucose level; it requires fulfillment of the Whipple
triad:
• I) Signs and symptoms consistent with hypoglycemia
• 2) Associated low glucose level
• 3) Relief of symptoms with supplemental glucose
• People with diabetes should
become concerned about the
possibility of hypoglycemia at a
self-monitored blood glucose
(SMBG) level ≤70 mg/dL (3.9
mmol/L).  This cut-off value has
been debated, with some
favoring a value of <63 mg/dL
(3.5 mmol/L).
• The brain relies almost
exclusively on glucose
So …
Adequate uptake of glucose
from the plasma is essential for
normal brain function and survival
Luckily …
Very effective physiological and
behavioral mechanisms normally
prevent or rapidly correct
hypoglycemia
Classifications of Hypoglycemia
• In diabetes mellitus the hypoglycemia is classified as :
1) Severe hypoglycemia
2) Documented symptomatic hypoglycemia
3) Probable symptomatic hypoglycemia
4) Asymptomatic hypoglycemia(or hypoglycemic Unawareness)
5) Relative hypoglycemia •
• Without diabetes mellitus the hypoglycemia is classified as:
1) reactive(sometimes called "postprandial")
2) and nonreactive(sometimes called "fasting").
• Severe hypoglycemia: which requires the assistance of another
person to administer a carbohydrate (preferably glucose
sublingually or intravenously) or subcutaneous glucagon
• Documented symptomatic hypoglycemia : which occurs when a
patient feels typical hyperadrenergic hypoglycemic symptoms and
verifies the blood glucose level is less than 70 mg/dL (3.9
mmol/L) before self treating with 15 grams of a carbohydrate
• Probable symptomatic hypoglycemia : Typical hypoglycemia
symptoms not accompanied by plasma glucose determination but
likely caused by plasma glucose ≤70 mg/dL (≤3.9 mmol/L)
• Asymptomatic hypoglycemia (or hypoglycemic
unawareness): in which a patient does not develop typical
hyperadrenergic symptoms but has a measured plasma glucose
level of less than 70 mg/dL (3.9mmol/L).  this situation
occurs most often in type 1 diabetes in patients striving for
excellent glycemic control (hemoglobin A1c value <7.0%)
who have chronic, frequent episodes of hypoglycemia.
• The body's ability to recognize hypoglycemia and secrete
counterregulatory hormones in response to hypoglycemia
deteriorates and leaves these patients vulnerable to further
episodes of severe hypoglycemia.
• In diabetic patients, if severe neuropathy is present, the
autonomic response (epinephrine) to hypoglycemia is not
activated. This leads to neuroglycopenic symptoms.
Symtoms
• Hyper-adrenergic
Plasma Glucose < 70 mg/ dL (3.9 mmol/L)
Diaphoresis (Sweating)
Tachycardia (Rapid heartbeat )/Palpitation Anxiety Tremor
/Shaking Tachypnea Vomiting Dizziness Hunger

• Neuro-glycopenic
Plasma Glucose < 50 mg/dL (2.8 mmol/L)
Slurred speech Cognitive impairment Inattention and confusion
Focal neurologic deficits Seizures Behavioral/ Irritability/ Sudden moodiness
Change in personality Lack of coordination
Severe and prolonged hypoglycemia LOC/Coma Irreversible brain injury
Hyperosmolar hyperglycemic state (HHS)
• is a complication of diabetes mellitus (predominantly type 2) in which
high blood sugars cause severe dehydration, increases in osmolarity
(relative concentration of solute) and a high risk of complications,
coma and death.
• Older names for HHS were hyperosmolar nonketotic coma (HONC),
hyperosmolar hyperglycemic nonketotic coma, etc…
Name changed to HHS in order to present the alterations in the mental
status that occur without coma. Coma is found in fewer than 20% of
patients with HHS
 Pathophysiology
 there is enough insulin to prevent acidosis and formation of ketone
bodies at the cellular level, but there is not enough insulin to facilitate
transportation of all the glucose into the cells.
 : glucose molecules accumulate in the blood stream,
causing serum hyper osmolality with resultant osmotic
diuresis and simultaneous loss of electrolytes, most
notably potassium, sodium, and phosphate.
• Patients may lose up
to 25% of their total
body water. Fluids are
pulled from individual
body cells by
increasing serum
hyper osmolality and
extracellular fluid
loss, causing
intracellular
dehydration and body
cell shrinkage.
Symptoms of HHC
• The patient with HHC has severe hyperglycemia and azotemia without
ketoacidosis. The intravascular volume is contracted, and the patient shows
signs and symptoms of hypovolemia and severe dehydration.
• Both diffuse and focal central nervous system deficits may occur.
• These may include hallucinations, aphasia, nystagmus, hemianopsia,
hemiplegia, hemi sensory deficits, and focal or grand mal seizures. Coma
may ensue
•  As extracellular volume decreases……. blood viscosity increases, causing
slowing of blood flow Thromboemboli are common (increased blood
viscosity, enhanced platelet aggregation and adhesiveness, and possibly
patient’s immobility).
• Cardiac workload is increased and may lead to MI(myocardial
infarction)
• Renal blood flow is decreased, potentially resulting in renal
impairment or failure.
• Stroke may result from thromboemboli or decreased cerebral
perfusion.
• Mortality rate of HHS ranges from 10%-50%, which is higher than that
of DKA (1.2%-9%).
• The cardinal symptoms of polyuria and polydipsia are noted first but
may be ignored by older persons or their families.
 DIABETIC KETOACIDOSIS (DKA)
• A state of absolute or relative insulin deficiency aggravated by
ensuing hyperglycemia, dehydration, and acidosis-producing
derangements in intermediary metabolism, including production of
serum acetone.
• Can occur in both Type I Diabetes and Type II Diabetes – In type II
diabetics with insulin deficiency/dependence
• The presenting symptom for ~ 25% of Type I Diabetics.
•  Diabetic KetoAcidosis (DKA) 1. 160,000 Admissions to private
hospitals/year 2. Cost = over 1 billion $ annually 3. 65% = <19 years
old 4. Main cause of death in children with diabetes (approximately
85%) 5. Cerebral edema in 69%
• Why do ketones develop?
No carbohydrate intake • fasting • gastroenteritis • Atkins diet,
neonates fed high-fat milk Prolonged exercise, pregnancy Lack of insulin
activity • onset of diabetes (insufficient secretion) • interruption of
insulin delivery in established pt Increase in insulin resistance •
infection, illness, surgery, stress Alcohol, salicylate ingestion, inborn
metabolic errors
•  Causes of DKA/HHS
Stressful precipitating event that results in increased
catecholamines, cortisol, glucagon. – Infection (pneumonia, UTI) –
Alcohol, drugs – Stroke – Myocardial Infarction – Pancreatitis – Trauma
– Medications (steroids, thiazide diuretics) – Non-compliance with
insulin