Diabetes Flashcards
Glycolosis
Glucose -> ATP - happens in the cell
Glycogenesis
Glucose -> glycogen (storage) - happens in muscles and liver
Glycogenolysis
Glycogen -> glucose
Gluconeogenesis
amino acids -> glucose
Lipolysis
triglycerides (adipose tissue) -> free fatty acids
Lipogenesis
free fatty acids -> triglycerides, OR glucose -> triglycerides
Catabolism + main hormone
large molecules break down into smaller molecules, glucagon
Anabolism + main hormone
small molecules build into large molecules, insulin
Insulin lowers blood glucose through
glycolysis and glycogenesis
Glucagon increases blood glucose through
gluconeogenesis and glycogenolysis
Why does liver disease impact glucose regulation
Because glycogenesis, gluconeogenesis, and glycogenolysis happens in the liver
How does alcohol affect blood sugar?
When the liver has to process alcohol it takes precedence over other processes like gluconeogenesis and glycogenolysis that raise blood glucose, meaning blood sugar can fall dangerously
The body processes alcohol the same way it does fat
3 things to remember about insulin
- Insulin is a peptide hormone, binds to the cell membrane and needs a receptor. When it binds there is a quick reaction.
- Insulin inhibits glucagon. Insulin is much stronger than glucagon.
- Insulin chases potassium into cells
What types of cells need insulin to absorb glucose?
Fat cells and muscle cells
Agents that raise blood glucose
Glucagon
Cortisol (gluconeogenesis)
Catecholamines (glycogenolysis)
Growth hormone (antagonizes insulin)
Estrogen
Somatostatin (shuts off insulin when there’s too much of it)
Progesterone
Agents that lower blood glucose
Insulin
Somatostatin (shuts off glucagon when there’s too much of it)
Incretins (sense the level of glucose of the chyme in the duadenum and sends message to pancreas to release insulin)
What causes Type 1 diabetes
destruction of beta cells in pancreas
3 P’s
Polyphagia, polydipsia, polyuria
What two things cause hyperkalemia in hyperglycemia?
K+ can’t follow glucose into cells
Ketone bodies made by the liver increases H+, causing more H+ to be excreted in urine and more K+ being retained
What causes weight loss and increased FFA in type 1?
Lipolysis d/t tissues not receiving any glucose
What causes the liver to start making ketones?
When free fatty acids are released quickly due to no insulin mitigating glucagon, the liver can’t handle it and starts making ketones
Osmotic diuresis
When there is an increase in urine glucose, urine output is going to increase because glucose draws water to it
What causes hypokalemia in Type 1?
Increased urine output d/t osmotic diuresis
What causes acute renal failure in Type 1?
Increased urine output causing ECF deficit and decreased perfusion to the kidneys
Why is obesity often a precursor to Type 2?
Fat tissue is very resistant to insulin, even though it needs it
post-receptor defect
the high level of glucose in the blood starts corroding the insulin receptors on muscle and fat tissue
how are beta cells in pancreas affected in type 2?
As hyperglycemia continues, often it leads to injury of the beta cells in the pancreas, they get exhausted trying to put out insulin that the tissues can’t use
Why does DKA not happen usually in type 2?
Usually enough glucose is able to enter tissues to prevent ketoacidosis (not in all cases), especially in early stages
HHS: hyperglycemic hyperosmolar state
Dehydration, hyperglycemia, and hypokalemia
Because acidosis and thereby unresponsiveness is usually prevented in Type 2, blood glucose can reach incredibly high levels without symptoms getting severe enough for the person to seek care
7 Metabolic syndrome characteristics
Abdominal obesity (dominant)
Bad cholesterol
HTN
Elevated fasting glucose (dominant)
Prothrombotic state
Proinflammatory state
Vascular disease
What are people w metabolic syndrome at higher risk for?
CAD
Type 2 DM
CVA/stroke
PVD
What causes gestational diabetes
Placental hormones and weight gain of pregnancy causes insulin resistance in tissues
Risk factors of gestational diabetes
Obesity, >40yo, family hx of type 2 DM, HTN, ethnicity of higher risk to Type 2, hx baby weighing >9 lbs, hx previous GDM
Why is blood glucose usually normal in a person with gestational DM?
their blood glucose usually remains normal because the fetus uses the extra glucose to grow
maternal complications of DM
Hydramnios
Pre-eclampsia & eclampsia
Hyperglycemia
DKA
Infections
Fetal/newborn complications of DM
Congenital abnormalities
Birth defects, still birth, miscarriage
Macrosomia
IUGR (small baby)
Neonatal hypoglycemia
Infant respiratory distress syndrome
Risk for obesity and Type 2 DM in future
Treatment for gestational DM
Insulin, not oral agents, lifestyle changes
Other causes of diabetes
- Pancreas injury/disease
- Adrenal cortex disease or administration of glucocorticoids
- Renal failure: kidneys fail to metabolize glucagon so it builds up in the blood
- Growth hormone disturbance
- Genetic diseases, e.g. down syndrome
Most common reasons of hypoglycemia
- Insulin/oral agent overdose
- Omitting food intake
- Overexertion w/o compensatory carbs
- Vomiting
- Alcohol
- Extensive liver disease
- Pancreatic, adrenal, liver disease
s/s of hypoglycemia
- Adrenergic: shaky, tremor, irritable, tachycardia, palpitations, hunger, diaphoretic, pallor, paresthesia
- Neuroglycopenic: HA, confusion, slurred speech, irrational, visual problems, lethargy, decr. LOC, coma, death
causes of acute hyperglycemia
Diabetes, stress hyperglycemia, medically induced,
Dawn phenomenon, somogyi effect
Somogyi effect
Someone with low blood sugar has a strong reaction to reverse it, causing hyperglycemia
s/s of acute hyperglycemia
- Nausea, malaise, fatigue
- 3 P’s
- Blurred vision
- Hyponatremia (osmotic diuresis)
- Infections: skin, UTI, vagina, candida
(microbes love glucose)- DKA and HHS
How does chronic hyperglycemia cause other disease processes
Changes come from vascular, capillary and neurologic damage
How can hyperglycemia affect endothelium of blood vessels
Endothelium in blood vessels get damaged, leading to plaque build up: Atherosclerosis -> CAD, HTN, MI, CVA, PVD
diabetic nephropathy
Glomerular basement membrane thickens and hardens
Glomerulosclerosis -> hyperfiltration -> glomerular damage -> glomerular capillaries blocked -> capillaries start to leak -> proteins leak into urine -> damage continues -> GFR drops -> renal failure
HTN adds to risk
diabetic retinopathy
Retinal capillaries develop small aneurysms and hemorrhages
Capillary neovascularization, prone to hemorrhage
“Floaters” develop later in disease
Treatment: laser photocoagulation
21% of people with diabetes type 2 have this
charcot deformity
Charcot deformity: lost arch d/t nerve and vessel damage
