Diabetes mellitus Types 1 and 2 Flashcards
Diabetic ketoacidosis:
treatment (3)
- fluids (b/c of osmotic diuresis)
- insulin
- replace electrolytes lost from diuresis (esp K+)
Diabetic ketoacidosis:
-describe mechanisms (2 main mechanisms)
Coma/shock is result of 2 main pathways:
- Ketone production
Lack of insulin results in increased glucagon. Glucagon stimulates lipolysis, resulting in liver conversion of free fatty acids to ketones. Ketones are important to supply the brain with energy in starvation state, but they cause acidosis.
- severe hyperglycemia
- lack of insulin results in severe hyperglycemia, leading to osmotic diuresis and severe dehydration. This increases concentration of ketones.
In general, why are pts with T2DM overweight, and pts with untreated T1DM underweight?
In T1DM, lack of insulin induces increased glucagon release. Glucagon stimulates lipolysis, proteolysis for gluconeogenesis.
In T2DM, there is still some insulin. This insulin keeps glucagon levels low (neg feedback), preventing glucagon’s chronic body wasting effects.
Insulin overdose symptoms:
- mild
- moderate
- severe
hypoglycemia stimulates sympathetic response:
- shakiness, headaches, dizziness, sweating, tachycardia
- confusion, slurred speech, poor coordination
- seizure, coma
Your pt has HTN and diabetes
Is it safe to prescribe a beta blocker for his HTN?
With caution.
Dangerous because beta blockers remove the adrenergic warning signs of hypoglycemia (tachycardia, sweating, etc)
Names of Ketone bodies in DKA (2)
- beta hydroxybutyric acid
- acetoacetate
What levels to diagnose pre-diabetes:
- A1C
- fasting glucose
- glucose tolerance test, 2 hours
- 5.7-6.4%
- 100-125
- 140-199
“pre-diabetes” is a somewhat vague diagnosis, compared to actual diabetes
How does obesity cause type 2 diabetes mellitus?
Obesity induces a pro-inflammatory state that leads to insulin resistance.
Details:
-Adipocyte hypertrophy activates inflammatory cells (macrophages, T cells, etc), which increase production of cytokines (TNF, IL6, IL1, etc), which cause insulin resistance.
T2DM:
- risk for what acute crisis?
- mech
Hyperosmolar non-ketotic coma (DKA is in T1DM)
- high glucose (>500) leads to life-threatening diuresis with hypotension and coma
- ketones are absent b/c the small amount of insulin in T2DM counteracts glucagon’s lipolytic effect (which is also why T2DM remain fat and T1DM are skinny)
How does diabetes cause peripheral neuropathy, retinopathy, and cataracts?
(explained well by pathoma)
Osmotic damage to cells.
Certain cells allow free entry of glucose and contain Aldose reductase. Aldose reductase converts glucose to sorbitol, which leads to osmotic cellular damage.
These cells are:
- schwann cells–peripheral nerve damage
- retinal blood vessel pericytes–retinopathy
- Lens–cataracts
Gestational diabetes
-mechanism
Fetus steals mom’s glucose:
During pregnancy, the placenta secretes hormones which cause insulin resistance in the mother–this way nutrients can be directed to the fetus.
This can unmask a woman’s existing predisposition to insulin resistance, causing gestational diabetes.
Insulin overdose treatment:
- mild hypoglycemia
- moderate
- severe
- juice, candy
- frosting, sugar-gel
- glucagon injections
List Diabetes mellitus long term complications:
- microvascular (3)
- macrovascular (2)
microvascular:
- retinopathy
- nephropathy
- neuropathy
macrovascular:
- coronary artery disease
- peripheral vascular disease
T1DM:
-mech/etiology of disease
- autoimmune
- Environmental damage (eg infection) to islet cells induces immune system to recognize beta islet cells as foreign. Immune system mounts a CD8 response to attack beta cells.
- Type 4 hypersensitivity reaction
How does diabetes cause macrovascular and microvascular damage?
non-enzymatic glycosylation (NEG)
-glucose deposits on vessel walls, causing damage that leads to atherosclerosis (big/med vessel) and hyaline arteriolosclerosis (small vessels)
T1DM
-etiology
Autotimmune beta-cell destruction by T cells
Pt presents to ED with DKA
-classic clinical presentation
- breathing heavily (Kussmaul respiration to breathe out acid)
- fruity breath (caused by acetone ketone bodies)
- dehydrated
- mental confusion
Basic progression of type 2 diabetes, from -20 years to +20 years
(Dr Raff’s “most important slide”)
- Insulin resistance develops many years before T2DM
- Beta cells compensate by increasing insulin secretion.
- Eventually, beta cells poop out and can’t keep up with increasing insulin resistance. This is onset of T2DM– insulin secretion decreases, and serum glucose increases
- eventually, there is a “point of no return”
How are these electrolytes affected in untreated T1DM:
- Na+
- K+
- HCO3
- PO4
- hyponatremia–osmotic dilution of plasma
- hyperkalemia–insulin’s effect is to push K inside cells. However, there is net LOSS of total K+ because of osmotic diuresis
- low HCO3– acid from ketoacidosis is breathed out as CO2
- low PO4–osmotic diuresis
What 2 types of foods are worst for diabetics and why?
- sugar:
sugar/simple carbs are absorbed too fast for insulin’s effect.
- Fat
- fat absorbed too slowly, so insulin’s duration has ended before fat is complete absorbed.
So, pizza is bad for diabetics.
What levels required for diagnosis of diabetes mellitus:
- A1C
- fasting glucose
- oral glucose tolerance test, 2 hours
- random glucose
You need only 1 of these to dx DM
- >6.5%
- >126
- >200
- >200
Diabetes mellitus:
-why is there poor wound healing?
Result of diminished blood supply, caused by glycosylation damage of vessels.
T2DM
-2 main physiologic defects
- insulin resistance
- impaired suppression of glucose production
- impaired glucose uptake - inadequate insulin secretion
Diabetes mellitus short-term complications
(5)
- electrolyte abnormalities, hyperosmolar hyperglyemic state (from osmotic diuresis)
- fatigue
- poor wound healing (impaired blood supply)
- impaired immune defense (hyperglycemia effect)
- DKA (lack of insulin leads to glucagon-stimulated lipolysis and ketone formation)
