DM Lecture 54 Flashcards
Microalbuminuria results due to what?
Advanced Glycation end products of protein (AGE)
Sickling crisis results in jaundice. What is a characteristic lab finding in this person? (IMCQ)
Increased serum unconjugated (indirect) bilirubin
-Prehepatic
A person has renal colic due to the passage of stones in his urine. What is a clinical scenario? (IMCQ)
- Cystinuria (defect in cysteine reabsorption
- Cysteine stones
If you don’t intake essential amino acids, you can get a negative nitrogen balance (IMCQ)
PVT TIM HALL
- Phenylalanine
- Valine
- Threonine
- Tryptophan
- Isoleucine
- Methionine
- Histidine
- Alanine
- Leucine
- Lysine
What clinical disorder is an example of Secondary diabetes?
Hemochromatosis
Type I diabetes
- Autoimmune destruction of B cells
- Marked reduction in insulin secretion (insulin is low or absent)
Type II diabetes
- Metabolic syndrome/Syndrome X
- Insulin resistance and Beta cell dysfunction/fatigue
Polyuria, Polyphagia, and Polydipsia are typically seen with what clinical finding?
Type I diabetes
Explain why there is weight loss in type 1 diabetes?
Accelerated lipolysis and muscle proteolysis (negative nitrogen balance due to increased tissue protein catabolism)
Hyperglycemia in both type I and II diabetes is due to what 2 clinical findings?
- Gluconeogenesis is activated because of low insulin
2. Decrease in number of GLUT-4 receptors bc of low insulin
What two pathways are inhibited during diabetes I or II? And why?
Glycolysis and Glycogenesis due to low insulin levels
What is a dietary recommendation for people with Type I or II diabetes?
Avoid Carbohydrate rich diets because you cannot break it down as Glycolysis and Glycogen synthesis are inactive. You already might have high Glucose because of gluconeogenesis
What may you recommend to diabetic patients?
Exercise - causes uptake of Glucose by muscle in the absence of insulin (via AMPK pathway)
Osmotic dieresis/dehydration
Can occur with patients with diabetes if you have an increasingly high amount of polyuria.
What are the acute complications of Type I and II diabetes?
Type I
-Ketoacidosis
Type II
-Hyperosmolar hyperglycemic state
What are the chronic complications of Type I and II diabetes?
Type I and II
- Microvascular
- Macrovascular
Diabetic Ketoacidosis
- Deep sighing respiration (Kussmaul breathing) –> washout of CO2
- Fruity odor/high acetone in breath due to increase in ketone bodies (spontaneous reaction)
- Increased anion gap (high 3-hydroxybutyrate- anion)
- Increased ammonium and phosphate excretion
Acetone
has to be lost in the urine or breath, it’s an end product of Ketone bodies synthesis
-Spontanenous, non-enzymatic reaction
What may cause drowsiness in diabetics?
water leaving the ECF
What are 3 cardinal clinical features of diabetic ketoacidosis?
- Hyperglycemia
- Ketosis
- Metabolic acidosis
What happens to insulin levels during an illness?
insulin requirements increase during an episode of illness due to insulin resistance due to stress
Where do gluconeogenesis, ketogenesis, and lipolysis take place?
liver, liver, and adipose tissue
What happens to Potassium during diabetes?
Hyperkalemia, but when you inject insulin Potassium goes back into the ICF and you can get Hypokalemia.
Hyperosmolar Hyperglycemic (Type II)
- Confused and lethargic
- occurs during superseding stress or infection/illness
- High plasma glucose and osmolarity (name)
What are the 3 clinical feautures of Hyperosmolar hyperglycemic state?
- Hyperglycemia
- dehydration (glucose is excreted in the urine and pulls water with it)
- hyperosmolarity
How do you tell diabetic ketoacidosis apart from hyperosmolar hyperglycemic?
Ketone bodies levels are normal in the latter, which they are high in Diabetic ketoacidosis.
Why don’t you have ketoacidosis in Type II?
You have some insulin
HbA1c levels in diabetes indicate what?
The higher the levels, the more chronic the complications of Type I and II diabetes
Microvascular Chronic complication occur where?
Eyes, retina, neurons, kidney
-entry of glucose into these tissues does not require insulin
Macrovascular Chronic complications occur where?
Atherosclerosis changes
What 4 things contribute to Microvascular complication?
-non-enzymatically bind to glucose
1) Sorbitol formation
2) AGE
3) Hexosamine pathway
4) DAG and Protein Kinase C
Advanced glycation end products (AGE) and clinical findings
- Glycation of proteins results in cross-linking of glycated proteins and altered function
- Diabetic retinopathy and microalbuminuria
- painless foot ulcers
DAG pathway
-Hyperglycemia increases DAG and PKC activation
Hexisamine pathway
- Hyperglycemia forms Fructose 6-P and Hexosamine –> can make amino sugars
- Damages basement membrane
Hypertriglyceridemia
-decreased action of LPL
High 3 hydroxybutyrate
-HSL activity
High LDL
-macrovascular complications
Higher HbA1c levels indicate:
higher complications
Microalbuminemia
early indicator for renal nephropathy
