Pancreas Flashcards
Pancreatic Islet Cells (Islets of Langerhans)
90% Exocrine 10% Endocrine
Insulin is produced by _______and facilitates
Produced by beta cells. Facilitates transport of glucose & K+ into cell.
Normal adult production of insulin is
40 – 50 units / Day.
Insulin is metabolized by
Liver and Kidney.
Normal fasting glucose
70 – 100 mg/dL
Diabetes
↓insulin production
↑ insulin resistance
Hyperglycemia results in abnormal
metabolic effects and tissue/organ damage
Why does Hyponatremia occurs with hyperglycemia ? It occurs as each
100 mg/dL increase in glucose = 1.6 mEq/L decrease in sodium (dilutional)
What are Some tissues can transport glucose without insulin:
Neurons, Kidney, Retina, RBCs, Vascular endothelium
Damaged results from prolonged hyperglycemia.
Diabetes Type 1a
T-cell mediated autoimmune destruction of beta cells.
Diabetes Type 1b
Not immune mediated.
10% of all cases.
IDDM
Type 1
Acute onset in children and adolescents.
Type 1
Previously “Juvenile Diabetes”.
Type 1
Etiology unknown, genetic factors may play a role.
Type 1
**Trick to remember short acting
Onset 30, peak 3, Duration 6
***Trick to remember Intermediate acting (2x)
Onset 1 peak 6 duration 12
***Trick to remember long acting (2x interm)
ONset 2, peak 12, Duration 24
_____________ before hyperglycemia
occurs.
80-90% beta cell function lost before hyperglycemia
occurs.
Type 1 Presentation is often
severe and sudden: Hyperglycemia occurs over days to weeks.
Type I with Signs/Symptoms:
Fatigue Weight loss Polyuria Polydipsia Blurred vision Volume depletion Random Glucose >200 HbA1c >7%
Type 1 DM 2 most important signs and symptos
Random Glucose >200
HbA1c >7%
Type 2 DM Immune?
Not immune mediated.
Type 2 DM results form
Results from insulin deficiency with receptor defect
90% of all cases.
Type II DM
Affects older age group.
Type II DM
Subtle presentation (4 – 7 yrs. before dx)
Type II DM
What are the 3 defects with NIDDM
3 defects:
↓ insulin
↑ hepatic glucose release
↑ insulin resistance
Non–insulin-dependent
Type 2
Oral hypoglycemic medications may be used.
Type 2
Type 2 DM caused by
Caused by decreased production of insulin
and/or increased resistance by body cells to
insulin
Commonly associated with obesity
Type 2
In type 2 “Beta cell burnout” –
compensatory hyperinsulinemia to maintain normoglycemia. Increasing incidence in teens and young
adults
Type 2 Component of Metabolic Syndrome
(aka insulin-resistance syndrome):
Metabolic syndrome At least 3 of the following:
Fasting glucose >110 mg/dL Abdominal obesity (waist >40 m / 35 f) Trigycerides => 150 mg/dL HDL < 40 (m) / 50 (f) BP => 130/85
***DM diagnostic Criteria
DM Diagnostic Criteria
• Fasting glucose > 100 mg/dL
∞ 101 – 125 = “impaired fasting glucose”
∞ 126+ = “clinical diabetes”
OR
∞ 2 hr. glucose >200 during glucose tolerance test
OR
∞ Random glucose >200 with symptoms of polyuria,
polydispsia, unexplained weight loss
∞ HbA1c > 6.5%
∞ Urine glucose poor indicator since renal glucose
threshold not reached until conc. >180 mg/dL
**Oral Hypoglycemics classes
Sulfonyureas
Biguaides
Thiazolidinediones
Alpha-Glucosidase inhibitors
***Sulfonyureas
Sulfonyureas (glimepiride)
↑ insulin secretion
**Biguanides
Biguanides (metformin)
↓ hepatic glucose release (& ↑ insulin sensitivity
***Thiazolidinediones (
rosiglitazone, pioglitazone)
↑ insulin sensitivity
***α-glucosidase inhibitors
(acarbose, miglitol)
↓ GI glucose absorption
Insulin and Hypoglycemia
Hypoglycemia: most frequent and dangerous complication of insulin therapy.
Adrenergic Warning Symptoms:
HTN tachycardia diaphoresis palpitations, restlessness, pallor, lacrimation
Neuroglycopenic Warning Symptoms:
Fatigue, confusion, HA, somnolence, convulsions, coma
Repetitive episodes result in Hypoglycemia
Unawareness (secondary to autonomic sympathectomy)
***Acute Complications of DM
- HYPOGLYCEMIA
* DKA (Diabetic Ketoacidosis) •HHS (Hyperglycemic Hyperosmotic Syndrome)
Hypoglycemia glucose level
Glucose < 60
3 causes of hypoglycemia
Caused by medication, alcohol, exercise
***Hypoglycemia symptoms
Tachycardia Palpitations Diaphoresis Tremors Pallor
If hypoglycemia not corrected
If uncorrected, Neuroglycopenia occurs
***Signs and symptoms of Hypoglycemia Neuroglycopenia
HA Dizziness Irritability Fatigue Poor judgment Confusion Visual changes Hunger Seizures Coma
**Hypoglycemia Treatment:
- Conscious pt. – 20g glucose (tablets or gel)
* Unconscious pt. – 0.5 g/kg IV or glucagon 0.5 to 1 mg IV, IM, or SC
DKA Occurs more commonly in
Type 1
***DKA is associated with
Profound insulin deficiency = ↑ lipolysis and
gluconeogenesis
***Pathophysiology : In DKA, Gluconeogenesis =>
↑ production of production of ketones ketones, permits strong organic acids to circulate freely. Bicarbonate buffering does not correct it. Metabolic acidosis develops.
***DKA Precipitated by
by infection or acute illness:(CVA, MI, acute pancreatitis)
***Symptoms: VADANK
Vomiting Abdominal pain Dehydration Acetone odor on breath Neurologic changes/stupor Kussmaul respirations
***DKA Labs:
glucose > 250 mg/dL pH < 7.3 Bicarb < 18 Osmolarity < 320 Hyponatremia Presence of anion gap Presence of serum & urine ketones
Electrolyte deficits of K+ and Phos. can
lead to
diaphragmatic dysfunction and impaired myocardial contractility
DKA Treatment:
Large amounts of saline
Effective doses of insulin
Electrolytes
During DKA treatment Fluid and Na+ levels should be
monitored closely to avoid development of cerebral edema during correction
***HHS
Hyperglycemic Hyperosmolar Syndrome
“HHNKS”
hyperosmolar hyperglycemic nonketotic syndrome
HHS Characterized by:
↑ ↑ hyperglycemia
↑ ↑ hyperosmolarity
↑ ↑ Dehydration (more severe than in DKA)
In HHS , it Occurs more commonly in
Type 2 (60+ yrs) evolves over days-wks with ↑↑↑ glucosuric diuresis
In HHS No ketosis why?
ketosis - insulin levels are still high enough to
preclude lipolysis/ketosis.
Precipitated by dehydration and acute illness
***HHS Symptoms/Presentation:
Polyuria Polydipsia Hypovolemia Hypotension Tachycardia Organ hypoperfusion Neurologic changes/stupor/coma
***HHS Labs:
Glucose >600 Near-normal pH & Bicarb. Osmolarity >320 Vascular occlusions may occur (secondary to mesenteric artery thrombosis)
HHS Treatment:
Large amounts of saline
Effective doses of insulin
Electrolytes
In HHS treatment, If renal blood flow and GFR are not restored,
hyperglycemia will persist. (Normally perfused kidney will not permit extreme hyperglycemia)
***Chronic Complications of DM
Vascular Disease (CAD, PAD, PVD) Nephropathy Retinopathy Neuropathy Immune suppression Glycosylated Hb & Collagen
Chronic Complications: Vascular Macrovascular
Cardiovascular
Cerebrovascular
Peripheral vascular disease
**Chronic Complications: Vascular Microvascular
Nephropathy
Retinopathy
Macrovascular Complications
Poorly controlled pts develop Dyslipidemia:
↑ Triglycerides
↑ LDL
↓ HDL
Macrovascular complications Leads to
Atherosclerosis with increased tendency for thrombosis resulting in: Cardiovascular (CAD) HTN Angina MI CHF
Cerebrovascular (PAD)
CVA
Oxidative Stress from
↑ ROS (reactive oxygen Species) also plays a
roll in vessel damag
Macrovascular Complications PVD (arterial & venous)
May result in ulcers on lower extremities with: Slow healing Frequent infections Gangrene Amputation
Microvascular Complications
- Nephropathy
- Glomerulosclerosis develops with thickening of basement membrane over several years.
- Proteinuria (albuminuria) is earliest lab manifestation; w/ HTN and peripheral edema.
- Pt.s progress to renal failure within 3 – 5 yrs
Microvascular Complications Diabetic Retinopathy Caused by:
Occlusions Microaneurysms Hemorrhages Exudates Abnormal vessels Fibrous tissue
Cotton wool spots
Diabetic retinopathy
Cataracts and hyperglycemia
Hyperglycemia also accelerates lens
degeneration leading to formation of
cataracts
**Neuropathy
↓ Sensory and motor) nerve conduction
Distal symmetrical polyneuropathy most common
**In Neurpopathy Polyol Pathway (Sorbitol Pathway) causes
neuroedema
Neuropathy Deficits appear in
toes and feet, then progress proximally
***Neuropathy Results in loss of:
Light touch Pain proprioception Temperature Muscle weakness Paresthesias Neuropathic pain
Neuropathy
Ulcers develop secondary to________results in
loss of sensation
•Impaired circulation (PVD)
•Autonomic dysfunction
• Charcot’s joint
Neuropathy Signs of autonomic neuropathy:
LELIG
Lack of orthostatic changes in HR Early satiety Lack of sweating Impotence Gastroparesis (carries ↑ risk of aspiration perioperatively)
Immune Suppression ; Infections
Common and often more severe in diabetics
Infections in feet and legs caused by vascular and neurological impairment
Fungal infections common
• Caused by
Candida • In vagina and/or oral cavity Urinary tract infections Dental caries Gingivitis and periodontitis
**Glycosylation
A process that normally involves reversible
attachment of glucose to proteins, lipids and nucleic acids
**Glycosylation With persistent
hyperglycemia, glucose becomes irreversibly bound to collagen, decreasing elasticity.
***Glycosulation Can cause
“Stiff Joint Syndrome” which may affect cervical mobility leading to difficult intubation.
**Insulinoma is a
Insulin-secreting tumor of beta cells.
Insulinoma Manifest as
fasting hypoglycemia.
10% are malignant.
**Insulinoma associated
Profound hypoglycemia can occur with manipulation of tumor during surgical excision.
Insulinoma: Signs of hypoglycemia
- (HTN, tachycardia, diaphoresis) may be masked during anesthesia.
- Preop mgmt. is w/ Diazoxide, inhibits insulin release.
- Glucose should be included in IV fluids administered intra-op.
Anesthesia Considerations – pre-op
Evaluation
Pre-op evaluation should emphasize cardiovascular, renal, neurologic and musculoskeletal joint mobility.
Anesthetic consideration: Labs should include
full electrolyte, urea and creatinine screen, CBC w/ diff, CXR, ECG.
Beta Blockers and ACEI
Beta blockers recommended if CAD present.
ACE inhibitors for HTN if renal disease present.
Autonomic neuropathy predisposes pt. to peri-op.
dysrhythmias and intra-op. hypotension, gastroparesis with possible aspiration.
Anesthetics considerations
Morning dose of insulin should be held.
IV with D5 ½ NS @100ml/hr. should be started pre-op
When to delay surgery
If glucose >270, delay surgery until corrected
If glucose >400, postpone nonemergent surgery
Anesthesia Considerations – intra-op
Aggressive
glycemic control necessary to minimize
hyperglycemia and avoid hypoglycemia.
Anesthesia Considerations – intra-op glucose
Intra-op serum glucose s/b 120 – 180 mg/dL.
Typically, one Unit of insulin lowers glucose
25 mg/dL
Post-op hypoglycemia may be masked by
anesthetics, sedatives, analgesics, Beta-blockers, sympatholytics and autonomic neuropathy
Hypoglycemia Treatment:
50 mL of 50% dextrose (D50).
Increases glucose 100 mg/dL.
