Diabetes Mellitus

• Chronic disease
• Multisystem--affects every body system

1. No insulin produced

2. Not enough/unable to use

Insulin

Produced in Beta cells of the Islets of Langerhans in the pancreas. 

Basal Rate

• Steady production of insulin
• constant 

Bolus

• ↑ production and release r/t ↑ blood glucose 

Counter Regulation of Insulin

• Glucagon
• Epinephrine
• Growth Hormone
• Cortisol

↑ BG levels by liver

↑ Production & Output

↑ Movement into cells

Function of Insulin

• Transport glucose to cells (lock & key)
• promotes storage of glucose in liver & muscles
• ↓ gluconeogenesis (inhibits)
•  enhances/promotes fat storage (adipose)
• ↑ protein synthesis

Type 1 Diabetes

• No insulin production
• autoimmune, Beta Cells destroyed by T-cells
• genetics (biggest factor)

Type 1 Diabetes

s/s

• polydipsia
• poluria
• polyphagia
• wt loss
• fatigue 

Type 1 Diabetes

Tx

Insulin

If no insulin given:

• hyperglycemia
• unable for cells to use sugar
• DKA
• coma
• death

Type 2 Diabetes

• insulin resistance
• Not enough insulin produced for individuals needs 

Pre-diabetes

• Most people in pre-diabetic state do not know
• Can be prediabetic for up to 10 years without seeing consequences

Type 2 Diabetes

s/s

gradual onset:

• polydipsia
• polyphagia
• polyuria
• May or May Not cause wt loss

Type 2 Diabetes

Risk Factors

• onesity
• diet
• HTN
• sedentary
• genetics
• ethnicity
• age
• stress
• endocrine disorder (HYPERthyroidism)
• pregnancy
• baby >9lbs, higher risk 

Resistance...

Tissue not responding to insulin

↓

decreased or NO insulin entering cells

↓

hyperglycemia

↓

pancreas increses insulin production

(hyperinsulin)

↓

Increased insulin

Increased glucose storage in liver r/t liver thinking there is too much insulin

↓

too much sugar

toomuch insulin

pancreas eventually wears out

Other diseases/conditions

that may lead to DM

If caught early, treatment of cause may take away the symptoms or even cresolve the DM

• Cushings
• Hyperthyroidism
• pancreatitis
• hemochromotosis (too much iron in blood)
• steroid use
• anti-psychotics--long term use
• anti-seizure meds
• thiazides

Dx DM

• A1C    ≥6.5%   (the last 90-120 days of glucose on Hgb)
• Fasting Glucose ≥ 126 mg/dL
• 2 hours post pradial ≥ 200mg/dL (after meal)

 ^the above must be repeated, cannot go by single test

• Classic s/s with random glucose >200
• look at s/s % Hx (fam, comorbidities, risks, etc.) 

Tx Type 1

• Insulin

Tx Type 2

• Insulin
• diet/lifestyle change
• oral meds

DM

Tx goal

• ↓ s/s
• promote wellbeing
• prevent complications

Insulin

• Used to be from pigs
• NOW-genetically engineered from bacteria--E.coli

• Typically given subQ
• inhaled
• IV
• continuous pump

Somogyi Effect

• Rebound effectin which insulin overdose induces hypoglycemia
• Usually occurs during sleep hours

Counterregulatory hormones are released:

• stims lypolysis
• gluconeogenesis
• glycogenolysis

This inturn produces hyperglycemia and Ketosis

Somogyi Effect

s/s

• HA apon arousal  (< NOT THAT KIND OF AROUSAl, c'mom guys ;)
• Night sweats
• nightmares

Somogyi Effect

what to do?

• check BG between 2-4am for hypoglycemia
• ↓ noc insulin if needed

Dawn Effect

• Hyperglycemia present on awakening to to release of counterregulatory hormones in the predawn hours
• Counterregulatory hormoned may include epinephring, nor-epi, growth hormone, or cortisol.

• Dawn effect tends to occur more often or be more severe in adolescence when GH is at its peak

Dawn Effect

dx/tx?

• BG checks between 2-4am
• <60
• if hypoglycemic, a change in dosage or timing may be necessary

• Careful assessment is required to document the Somogyi and Dawn Phenom. bc tx for each is different.