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Pathophysiology > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Islets of Langerhans

A

Group of Endocrine cells

  • alpha- releases glucagon (18-20% of endocrine cells)
  • beta- releases insulin (73-75% of endocrine cells)
  • delta- somatostatin (4-6% of endocrine cells)
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3
Q

What stimulates insulin secretion?

A

glucose

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4
Q

What is the process for insulin secretion?

A
  • glucose enters beta cell through GLUT2 transporter by diffusion
  • glucose goes through glycolysis, turning ADP into ATP
  • ATP is the ligand for the K channel. K channel closes.
    • cell starts to depolarize with K channel closed
  • Once cell depolarizes to threshold of voltage gated calcium channel, Ca channel opens and Ca rushes in
  • Calcium causes release of insulin vesicles and the making of more insulin
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5
Q

What inhibits glucagon secretion?

A

insulin

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7
Q

When is glucagon released?

What is the target organ for glucagon?

A

when insulin levels are low

Target: liver

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8
Q

How does insulin get glucose into the cell?

A
  • insulin binds to the GPCR
  • GLUT4 transporter is recruited to the plasma membrane and facilitates glucose into the cell along with amino acids, K, Mg, and Phosphate.
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9
Q

What happens to:

insulin

glucagon

free fatty acids

blood glucose

liver glycogen

blood ketone bodies

As hours of starvation increases?

A
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10
Q

Effects of insulin

A
  • decreased appetite
  • decreased glucagon
  • increased glucose uptake by muscles and fat
  • increased glycolysis
  • increased glycogen synthesis
  • increased triglyceride synthesis
  • increased amino acid uptake
  • increased protein synthesis
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11
Q

Effects of lack of Insulin

primarily because of glucagon

A
  • increased appetite
  • increased glucagon
  • decreased glucose uptake by muscle and fat
  • increase blood glucose
  • increase gluconeogenesis
  • increased lipolysis
  • increased protein breakdown
  • increase glycogenolysis
  • Increase ketone body production
  • decrease protein synthesis
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13
Q

Type 1 Diabetes mellitus

A

Autoimmune destruction of Beta cells

about 10% of diabetes

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14
Q

Type 2 diabetes mellitus

A

Insulin resistance

about 90%

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15
Q

Mature onset diabetes of youth (MODY)

A
  • Genetic defect in insulin production or release
    • insulin will help, but not as much as oral meds that increas K channel sensitivity
  • about 2% of young diabetics
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16
Q

Gestational diabetes

A

Any diabetes identified during pregnancy

*precursor to actual diabetes

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17
Q

How does Type 1 diabetes happen?

A
  • Pancreatic Beta cells get destroyed.
    • person gets some kind of bug
    • body makes antigen
    • proteins coming off the beta cell matches antigens too closely
    • Beta cell gets attacked by immune system
    • body continues to make the beta cells, but they all get killed by the antibodies
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18
Q

gluconeogenesis

A

making glucose from non carbohydrates; lactate, glycerol, amino acids

*Important to get glucose to the brain. Everything else can survive on ketones. Happens in liver.

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19
Q

What is gestational diabetes?

When does it occur?

How does this affect the baby?

A
  • During pregnancy, hormonal changes can cause impaired insulin sensitivity
    • diagnosis cutoffs are lower than with normal DM
  • Occurs btw weeks 24 and 28 of pregnancy
  • If poorly controlled, glucose can cross the placenta, giving the baby hyperglycemia
    • these babies have a higher risk for developing HTN and cardiovascular disease
    • dangerous for mother and baby
  • mother is 2-3x more likely to get gestational diabetes in future pregnancies
20
Q

What is pre-diabetes?

A
  • aka impaired fasting glucose and/or impaired glucose tolerance
  • IFG is blood glucose level 100-125 after an overnight fast, not high enough to be considered diabetic
  • IGT is glucose level of 140-199 after 2 hour oral glucose tolerance test
  • about 40% of US adults ages 40-74 have pre-diabetes
21
Q

What are the acute complications of DM?

A
  • hypoglycemia
  • diabic ketoacidosis
  • hyperosmolar hyperglycemic nonketotic syndrome
22
Q

What are the chronic complications of DM?

A
  • Hyperglycemia and non-enzymatic glycosylation
    • advanced glycosylation end-products (AGEs)
  • Microvascular disease
    • diabetic retinopathy, nephropathy, cardiomyopathy
  • Macrovascular disease
    • CAD, stroke, PVD
  • Increased activity of polyol/sorbitol pathway (ETOH produced by glucose)
    • diabetic neuropathy
    • cataracts
    • gloucoma???
    • infection
23
Q

What are the symptoms of mild hypoglycemia?

severe hypoglycemia?

A
  • mild: <70 mg/dl
    • hunger
    • shakiness
    • paleness
    • blurry vision
    • sweating
    • anxiety
  • severe: <20 mg/dl
    • extreme tiredness
    • confusion
    • dazed appearance
    • sz
    • unconsciousness leading to coma and death
24
Q

What is DKA?

symptoms?

A
  • Life threatening hyperglycemia, can cause brain damage
  • Ketosis results from breakdown of fat and protein when cells can’t get glusose
  • symptoms
    • fruity acetone breath
    • kussmaul breathing
    • dehydration
    • N/v abdominal pain
    • altered LOC, weakness, paresthesia
    • severe hyperglycemia, electrolyte imbalance, metabolic acidosis, ketones in urine
25
Q

1 mM of glucose = _____ mg/dl

If GFR = 125 ml/min, Tmax = _____

How do you calculate how much glucose is reabsorbed?

A

18

300 mg/min

Filtered load = BS * GFR

Normal GFR = 125

*if calculated value is higher than 300, that much is not reabsorbed and will be excreted in the urine

26
Q

What causes Ketogenesis?

A
  • Very high rates of gluconeogenesis will deplete oxaloacetate and slow the entry of acetylCoA into the Krebs cycle
  • Instead, acetyl-CoA will be converted into ketone bodies for use by:
    • brain
    • heart
    • kidney
    • liver
27
Q

What are the different types of ketone bodies?

A
  • acetoacetate
  • acetone
  • B-hydroxybutyrate
28
Q

What are the major differences between HHNKS and DKA?

A
  • HHNKS is more of an osmolarity problem than an acidotic problem (pH of about 7.3)
    • due to the high glucose in the blood, raising osmolarity and pulling water out of tissues like brain
  • HHNKS:
    • very high BS
    • high osmolarity
    • normalish pH
    • only slightly elevated ketones and B-hydroybutyrate
    • elevated C-peptide
  • DKA
    • elevated glucose, but not as high as HHNKS
    • elevated osmolarity, but not as high as HHNKS
    • much more acidotic (7.12)
    • much higher B-hydroxybuterate and other ketones
    • low C-peptide and elevated anion gap
29
Q

What complications are seen with chronic diabetes?

(pic)

A

everything in pic plus autonomic neuropathy

30
Q

What is Advance glycosylation End-products (AGEs)?

A
  • When glucose binds to a protein causing crosslinking
    • this is seen normally with aging, but happens at an increased rate for diabetics
  • It is still reversible as a schiff base and an Amadori product, but then two proteins crosslink together, it is irreversible
    • causes stiff valves, arteries, wrinkles and everything else associated with aging
31
Q

What are the average BS goasl and A1C for diabetic patients?

A

BS 170

A1C under 7.0

32
Q

What are the different phases of diabetic retinopathy?

A
  • Background diabetic retinopathy (earliest phase)
    • the arteries in the retina become weakened and leak, forming small, dot-like hemorrhages
  • Proliferative diabetic retinopathy (later stage)
    • circulation problems cause areas of the retina to become oxygen-deprived/ischemic.
    • new, fragile vessels develop to improve oxygenation to the retina, but they hemorrhage easily
  • After I typed this all up I read my note that says “dont worry about different stages” so dont spend too much time memorizing this crap
33
Q

Why is an assessment of the retina useful?

A

Because if the microvasculature of the retina looks good, then most likely so does the microvasculature everywhere else, like the heart and autonomic nervous system

34
Q

What happens with diabetic nephropathy?

A
  • leakiness of glomerular capillaries causing microalbuminuria and proteinuria
  • Glomerulosclerosis and tubulointerstitial fibrosis
  • Arteriolar sclerosis
  • All this leads to renal failure, HTN and cardiovascular disease
35
Q

What causes diabetic nephropathy?

A
  • Aggregates of proteins and collagen form nodules is the glomerulus faster than macrophages can clear keep up
  • this decreases surface area and decreases GFR
  • ppl with type 1 and type 2 DM are at risk
    • greatest progression seen in pts with poor glucose control
  • Once proteinuria is noted, main treatment is BP control under 130/80
36
Q

What is the difference between peripheral neuropathy, autonomic neuropathy, and focal neuropathy?

A
  • peripheal neuropathy- causes pain or loss of feeling in extremeties
    • blisters and sores appear, become easily infected, pt doesnt notice the pain
  • Autonomic neuropathy– causes changes to digestion, bowel/bladder function, sexual response, perspiration, and can affect the heart and control blood pressure
  • Focal neuropathy- results in sudden weakness of one nerve or a group of nerves, causing muscle weakness or pain. Can happen to any nerve in the body.

Pathophysiology (26 decks)

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