DM Lecture 54 Flashcards

1
Q

Microalbuminuria results due to what?

A

Advanced Glycation end products of protein (AGE)

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2
Q

Sickling crisis results in jaundice. What is a characteristic lab finding in this person? (IMCQ)

A

Increased serum unconjugated (indirect) bilirubin

-Prehepatic

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3
Q

A person has renal colic due to the passage of stones in his urine. What is a clinical scenario? (IMCQ)

A
  • Cystinuria (defect in cysteine reabsorption

- Cysteine stones

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4
Q

If you don’t intake essential amino acids, you can get a negative nitrogen balance (IMCQ)

A

PVT TIM HALL

  • Phenylalanine
  • Valine
  • Threonine
  • Tryptophan
  • Isoleucine
  • Methionine
  • Histidine
  • Alanine
  • Leucine
  • Lysine
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5
Q

What clinical disorder is an example of Secondary diabetes?

A

Hemochromatosis

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6
Q

Type I diabetes

A
  • Autoimmune destruction of B cells

- Marked reduction in insulin secretion (insulin is low or absent)

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7
Q

Type II diabetes

A
  • Metabolic syndrome/Syndrome X

- Insulin resistance and Beta cell dysfunction/fatigue

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8
Q

Polyuria, Polyphagia, and Polydipsia are typically seen with what clinical finding?

A

Type I diabetes

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9
Q

Explain why there is weight loss in type 1 diabetes?

A

Accelerated lipolysis and muscle proteolysis (negative nitrogen balance due to increased tissue protein catabolism)

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10
Q

Hyperglycemia in both type I and II diabetes is due to what 2 clinical findings?

A
  1. Gluconeogenesis is activated because of low insulin

2. Decrease in number of GLUT-4 receptors bc of low insulin

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11
Q

What two pathways are inhibited during diabetes I or II? And why?

A

Glycolysis and Glycogenesis due to low insulin levels

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12
Q

What is a dietary recommendation for people with Type I or II diabetes?

A

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

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13
Q

What may you recommend to diabetic patients?

A

Exercise - causes uptake of Glucose by muscle in the absence of insulin (via AMPK pathway)

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14
Q

Osmotic dieresis/dehydration

A

Can occur with patients with diabetes if you have an increasingly high amount of polyuria.

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15
Q

What are the acute complications of Type I and II diabetes?

A

Type I
-Ketoacidosis
Type II
-Hyperosmolar hyperglycemic state

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16
Q

What are the chronic complications of Type I and II diabetes?

A

Type I and II

  • Microvascular
  • Macrovascular
17
Q

Diabetic Ketoacidosis

A
  • 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
18
Q

Acetone

A

has to be lost in the urine or breath, it’s an end product of Ketone bodies synthesis

-Spontanenous, non-enzymatic reaction

19
Q

What may cause drowsiness in diabetics?

A

water leaving the ECF

20
Q

What are 3 cardinal clinical features of diabetic ketoacidosis?

A
  1. Hyperglycemia
  2. Ketosis
  3. Metabolic acidosis
21
Q

What happens to insulin levels during an illness?

A

insulin requirements increase during an episode of illness due to insulin resistance due to stress

22
Q

Where do gluconeogenesis, ketogenesis, and lipolysis take place?

A

liver, liver, and adipose tissue

23
Q

What happens to Potassium during diabetes?

A

Hyperkalemia, but when you inject insulin Potassium goes back into the ICF and you can get Hypokalemia.

24
Q

Hyperosmolar Hyperglycemic (Type II)

A
  • Confused and lethargic
  • occurs during superseding stress or infection/illness
  • High plasma glucose and osmolarity (name)
25
Q

What are the 3 clinical feautures of Hyperosmolar hyperglycemic state?

A
  1. Hyperglycemia
  2. dehydration (glucose is excreted in the urine and pulls water with it)
  3. hyperosmolarity
26
Q

How do you tell diabetic ketoacidosis apart from hyperosmolar hyperglycemic?

A

Ketone bodies levels are normal in the latter, which they are high in Diabetic ketoacidosis.

27
Q

Why don’t you have ketoacidosis in Type II?

A

You have some insulin

28
Q

HbA1c levels in diabetes indicate what?

A

The higher the levels, the more chronic the complications of Type I and II diabetes

29
Q

Microvascular Chronic complication occur where?

A

Eyes, retina, neurons, kidney

-entry of glucose into these tissues does not require insulin

30
Q

Macrovascular Chronic complications occur where?

A

Atherosclerosis changes

31
Q

What 4 things contribute to Microvascular complication?

-non-enzymatically bind to glucose

A

1) Sorbitol formation
2) AGE
3) Hexosamine pathway
4) DAG and Protein Kinase C

32
Q

Advanced glycation end products (AGE) and clinical findings

A
  • Glycation of proteins results in cross-linking of glycated proteins and altered function
  • Diabetic retinopathy and microalbuminuria
  • painless foot ulcers
33
Q

DAG pathway

A

-Hyperglycemia increases DAG and PKC activation

34
Q

Hexisamine pathway

A
  • Hyperglycemia forms Fructose 6-P and Hexosamine –> can make amino sugars
  • Damages basement membrane
35
Q

Hypertriglyceridemia

A

-decreased action of LPL

36
Q

High 3 hydroxybutyrate

A

-HSL activity

37
Q

High LDL

A

-macrovascular complications

38
Q

Higher HbA1c levels indicate:

A

higher complications

39
Q

Microalbuminemia

A

early indicator for renal nephropathy