6.2 DM badness

Question 1

What is lipolysis? Why does it occur?

Answer 1

When insulin is low, or in profound starvation, the body will break down fats.
triglycerides= fatty acids + glycerol
The body turns glycerol into glucose and fatty acids into ketones.

Question 2

What is the pH for ketoacidosis?

Answer 2

<7.3

Question 3

Sx of DKA?

Answer 3

N/V
Fruity odor to breath, sweat
Dehydration, hyperventilation
CNS–> confusion, disorientation, lethargy, coma

Question 4

What are the symptoms of HHS?

Answer 4

glucose >600
glucosuria, polyuria, anorexia, weight loss, weakness, visual disturbances, poor turgor, tachycardia, confusion

profound dehydration, abdominal distension, seizure, lethargy, coma

Question 5

In HHS what is the patients volume status? Why?

Answer 5

insufficient water intake causes hypovolemia (low blood volume), hyperosmolarity, metabolic acidosis

Question 6

In HHS why hydrate then insulin?

Answer 6

Risk of worsening hypotension–> hypovolemic shock

Question 7

What causes DMI?

Answer 7

immune mediated: T-cell destruction of pancreatic Beta cells
genetic causes
rate of Beta cell destruction is variable
susceptible to other autoimmune disorders

Question 8

What are the classic signs of DMI?

Answer 8

classic signs: polyuria, polydipsia, polyphagia
other signs: visual disturbances, fatigue, weakness, malaise, inability to concentrate, history of candida infection genital tract

Question 9

What causes DMII?

Answer 9

insulin resistance by body cells (mechanisms unknown) causes pancreas to over-work
pancreas may or may not be exhausted – insulin levels insufficient
linked to genetics, obesity, age, lack of physical activity
linked to Metabolic Syndrome: hyperinsulinism, dyslipidemia, hypertension, glucose intolerance

Question 10

What are the classic signs of DMII?

Answer 10

polyuria, polydipsia, polyphagia

Question 11

How can DM lead to atherosclerosis?

Answer 11

High sugar surrounding cells, high blood osmolarity damages cells, including endothelial cells (damage de to osmotic gradient, more)

Question 12

What is the polyol pathway in DM?

Answer 12

enzyme aldose reductase converts glucose into polyol sorbitol, enters endothelial cells as sorbitol –> endothelial cell damage, oxidative damage during enzyme reaction

Question 13

What is the advanced glycation end-product theory of DM?

Answer 13

glucose attaches to proteins on endothelial cell membranes –> alters protein function, gene expression, increase permeability, increases coagulation, releases growth factors, inflammatory cytokines

Question 14

What is the protein kinase C theory of DM?

Answer 14

intracellular signaling molecule activation –> cell permeability, activation of vascular endothelial cell growth factor (VEGF), endothelin, vasoconstriction, coagulation, inflammatory cytokines, oxidative stress

Question 15

What is peripheral neuropathy in DM?

Answer 15

hyperglycemia damages endoneurial arterioles, demyelination, axonal degeneration
sensory neuropathy: sensory loss, burning pain in lower limb that progresses proximally
motor neuropathy: weakness can also present in lower limbs
autonomic neuropathy: sympathetic and parasympathetic dysfunction can cause a wide range of organ symptoms, alter organ responses to other illnesses

Question 16

What are symptoms of ANS neuropathy in DM?

Answer 16

postural hypotension, tachyardia, gastoparesis (nausea, bloating, vomiting, satiety, anorexia, alternating diarrhea/constipation), incontinence, erectile dysfunction, heat intolerance, dry skin

Question 17

Why does DM lead to increased infections?

Answer 17

hyperglycemia damages white blood cells, including T-Cells and phagocytes
less able to fight infection
colonization of microorganisms

Question 18

What kinds of infections are common with DM?

Answer 18

skin and soft tissue infections, esp. staphylococcus aureus
candida (yeast) infections in genital tract, skinfolds
tuberculosis
fungal infection
pneumonia
urinary tract infection

Question 19

What are foot complications with DM?

Answer 19

Susceptibility to infection, poor vascularization can lead to poor wound healing, combined with poor sensation and circulation  Foot complications
Commonly associated with Diabetes:
foot ulcer
gangrene
osteomyelitis (bone infection)

Question 20

What causes retinopathy in DM?

Answer 20

Retinal arteries are fragile, susceptible to endothelium damage, inflammation, occlusion retinal ischemia
progressive, cumulative
“cotton wool spots” areas of damage can be seen on the retina
proliferation of new blood vessels, causes “floaters”, can lead to retinal detachment
can cause blindness

Question 21

What is diabetic nephropathy?

Answer 21

injury to glomeruli, capillaries within the nephron, microscopic structures within the kidney
hyperpermeability of glomerular capillaries causes loss of blood serum albumin proteins in the urine – proteinuria
atherosclerosis of glomerular basement membrane causes glomerular hypertension, renin secretion
increases systemic hypertension, worsens diabetic retinopathy, other complications