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N552 Patho > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What does the Glut4 transporter do?

A

It is on the plasma membrane and transports glucose into the cell so we can make ATP and store glycogen
Glucose coming into the cell helps lead to protein synthesis

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2
Q

Insulin is good for ____kalemia

A

HYPER

Insulin makes the cell suck up glucose, then it has more ATP to run NaK pump, more K comes into the cell

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3
Q

Effects of insulin on: appetite, glucagon, glucose uptake by muscle/fat, glycolysis, glycogen synthesis, fat synthesis, amino acid uptake, protein synthesis

A

Dec appetite, dec glucagon
Inc glucose uptake, glycolysis, glycogen synthesis, fat synthesis
Inc amino acid uptake, protein synthesis

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4
Q

Effects of lack of insulin (mediated by glucagon) on: appetite, glucagon, glucose uptake by muscle/fat, BG, gluconeogenesis, lipolysis, protein breakdown, glycogenolysis, ketone body production, protein synthesis

A 
Inc appetite, glucagon
Dec glucose uptake by muscle/fat
Inc BG
Inc gluconeogenesis, lipolysis, protein breakdown, glycogenolysis, ketone body production (ketoacidosis)
Dec protein synthesis
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5
Q

Pancreas releases ___ when stimulated by high BG

Pancreas releases ____ when stimulated by low BG

A

Insulin when BG is high
Glucagon when BG is low (signals the liver to do gluconeogenesis)
They have an effect on the liver, fat, and muscle

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6
Q

What functions does the pancreas have?

A

Digestive, endocrine, and exocrine functions

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7
Q

In the pancreatic islet of Langerhans, alpha cells produce ____, and beta cells produce ____

A

Alpha cells produce glucagon (inhibited by insulin, not affected by glucose)
Beta cells produce insulin (stimulated by glucose)

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8
Q

In a normal person, when BG is high, they have ___ insulin and ____ glucagon (high/low)
In DM type 1, when BG is high, they have ___ insulin and ___ glucagon

A

Normal insulin high, glucagon is low

DM1 insulin low, glucagon high

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9
Q

Glucose uptake by the ___ transporter leads to cell depolarization, calcium influx, exocytotic release of insulin from the beta cell. How does it do this??

A

GLUT2
Glucose comes in, generates lots of ATP, an ATP-ligand-gated K channel closes so K is stuck in the cell, depolarizing the cell, leading Ca to come in, letting the cell do what it does best, release insulin

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10
Q

After fasting for 12 hours what happens to your level of… Insulin? BG? Glucagon? Liver glycogen? Free fatty acids? Blood ketone bodies?

A

Insulin and BG go down
Glucagon goes up
Free fatty acids and blood ketone bodies up
Liver glycogen down

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11
Q

What is maturity-onset diabetes of youth (MODY) and what is the best treatment?

A

Genetic defect in insulin production/release
Looks like DM type 1, often misdiagnosed and they get treated with insulin, but the better treatment is oral agents given in type 2 DM

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12
Q

What endocrine disorders can cause DM?

A

Cushings, acromegaly, pheochromocytoma

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13
Q

Why does someone get type 1 DM?

A

Type IV hypersensitivity disease in which the immune system kills pancreatic beta cells
Effects males and females equally, symptoms show up around puberty

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14
Q

Why does someone get type 2 DM?

A

Fat and muscle cells fill up and can’t take anymore glucose, insulin amount doesn’t matter in this case
When beta cells are full of glucose it is damaging (glucotoxicity) and insulin production goes down, the progression takes over 10 years

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15
Q

Does type 1 or 2 have ketoacidosis? HLA-D linked? Insulitis in islet cells?

A

Type 1 has ketoacidosis, is HLA-D linked, and has insulitis

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16
Q

Gestational diabetes is most likely caused by what?

A

Chorionic somatomammotropin

Presents during pregnancy, resolves after birth, increased risk of type 2 DM and subsequent gestational DM.

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17
Q

Clinical diagnosis of DM: fasting glucose level of over _____ (normal is 100) or plasma glucose over _____ after 2 hours of a OGTT (oral glucose tolerance test)

A

Fasting over 126

Or over 200 after 2 hours of OGTT

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18
Q

Clinical diagnosis of gestational DM: fasting blood glucose over _____, 1-hour of ___, 2-hour of ____, 3-hour of _____

A 
Fasting of 95
1 hour of 180
2 hour of 155
3 hour of 140
Glucose levels are lower in pregnancy
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19
Q

What effect does gestational diabetes have on the baby?

A

The baby gets extra glucose so it puts on extra weight

20
Q

Gestational diabetes usually occurs between which weeks of pregnancy? Once you’ve had it, what are your chances in getting it in your next pregnancy

A

24-28 weeks

2/3 chance in getting it again in the next pregnancy

21
Q

Poorly controlled gestational DM can give the baby what?

A

Hyperglycemia

Glucose crosses the placenta

22
Q

Babies from moms with gestational DM have higher risk for developing

A

HTN

CV disease

23
Q

What is pre-diabetes?

A

Impaired fasting glucose: 100-125
Impaired glucose tolerance
Completely reversible, walking after a meal helps
40% of US adults have this

24
Q

Acute complications of DM

A

Hypoglycemia
DKA
HHNK

25
Q

S/S of hypoglycemia, mild vs. severe?

A

BG under 70
Mild: hunger, shaky, pale, blurred vision, sweating, anxiety
Severe: extreme tiredness, confusion, dazed, seizures, unconscious, coma, death

26
Q

What does ketosis in DKA result from?

A

Breakdown of fat and protein for energy when glucose is not available
This can happen to normal people that starve themselves, but normal people don’t become acidotic

27
Q

DKA causes?

A

Untreated/undiagnosed DM (usually IDDM), non-compliance to meds, infection, illness

28
Q

DKA s/s

A

Fruity acetone breath
Kussmaul’s breathing (deep, rapid, gasping)
Dehydration
N/V, abd pain, ketones in urine
Altered LOC, weakness, paresthesia
Severe hyperglycemia, electrolyte imbalance, metabolic acidosis

29
Q

Glut2 vs Glut4?

A

Glut2 is for insulin release
Glut4 is for glycogen storage, transports glucose into cells so glucose can take up CO2 to make ATP to be stored as glycogen

30
Q

HHNK- Hyperosmolar hyperglycemic nonketotic syndrome- what is it?

A

Hyperosmolar: blood osmolarity is high. It will suck water our of cells, especially brain, leading to coma and death. Will see in type II. Glucose is the high osmolarity. Non ketotic.
Glucose sticks to protein and causes it not to work properly (nonenzymaticly)

31
Q

How do we calculate glucose load?

A

GFR x blood glucose

Then subtract Tmax from the total to see how much (if any) is reabsorbed

32
Q

Ketogenesis? (using acetyl-CoA)

A

Ketogenesis generates ketone bodies from acetyl-CoA, releasing coA to do beta-oxidation

33
Q

How do ketone bodies slow entry of acetyl-CoA to the Krebs cycle? Why is this important?

A

Depletion of oxaloacetate via high rates of gluconeogenesis slows the entry of acetyl-CoA to the Krebs cycle. This happens so the brain, heart, kidney, and liver can use the ketone bodies for fuel.

34
Q

HHNK vs DKA: who has the higher glucose? Who’s pH is very acidotic?

A

Higher glucose: HHNK 900 (vs. DKA 600)

pH: DKA 7.12 (vs. HHNK 7.3)

35
Q

HHNK vs DKA: who has higher B-hydroxybutyrate? Higher C-peptide? Anion gap?

A

B-hydroxybutrate: DKA 9 (vs. HHNK 1)- both high
C-peptide: HHNK inc, DKA dec (shows how much insulin a pt produced recently, type 1 doesn’t make insulin)
Anion gap: DKA elevated (17) - shows ketoacids

36
Q

Chronic DM complications

A

Microvascular: retinopathy, nephropathy, neuropathy, cardiomyopathy
Macrovascular: CAD, stroke, PAD
Other: infection, cataracts, glaucoma

37
Q

What are Advance glycosylation end-products (AGEs)?

A

When a glucose and protein get together and cross-link, its bad bc they don’t do what they are supposed to do anymore, creating Schiff base, amadori product, and AGEs. These are anything from heart disease to wrinkles. Increases with age.

38
Q

Why does AGE advance with age?

A

With age, we get more brittle collagen, traps LDL, leads to lipid oxidation
RAGE (AGE-receptors)destroys AGE with monocytes, but if happens too much, RAGE destroys other things

39
Q

Chemical properties of AGEs?

A

Cross-link polypeptides of same protein (collagen)
Trap non-glycosylated proteins (LDL)
Confer resistance to proteolytic digestion
Induce lipid oxidation
Inactivate nitric oxide
Bind nucleic acids

40
Q

RAGE on monocytes/mesencymal cells induce what?

A 
Monocyte emigration
Cytokine and growth factor secretion
Inc vascular permeability
Procoagulant activity
Enhanced cellular proliferation
Enhanced ECM production
41
Q

How does HbA1C work (glycosylated hemoglobin)?

A

…

42
Q

Diabetic retinopathy?

A

DM is the leading cause of irreversible blindness
DM (more type 1 than type 2) are more at risk for cataracts, glaucoma, and retina damage, these can all lead to blindness (retina damage #1 cause)

43
Q

Diabetic nephropathy causes what issues?

A

Leaky glomerular capillaries cause microalbuminuria-proteinuria, glomerulosclerosis, tubulointerstitial fibrosis, arteriolar sclerosis (hardened wall, narrowed lumen), renal failure, hypertension, CV disease

44
Q

What tx is most effective in diabetic nephropathy in controlling HTN?

A

ACEI

ARBs

45
Q

Diabetic neuropathy caused by what?

A

Blisters and sores may appear on numb areas of food because pressure/injury goes unnoticed, without prompt treatment, infection spreads and may need amputation

46
Q

What can autonomic neuropathy cause?

A

Changes in digestion, bowel/bladder function, sexual response, perspiration, heart/BP control

47
Q

Prevention of type 2 DM?

A

Exercise: muscle takes up glucose independent of insulin, a single bout of exercise increases insulin sensitivity for 48-72h
Diet: losing weight increases insulin sensitivity, omega-3 FA dec incidence and complications of DM2

N552 Patho (13 decks)

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