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Pathophysiology 1 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Glycolosis

A

Glucose -> ATP - happens in the cell

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2
Q

Glycogenesis

A

Glucose -> glycogen (storage) - happens in muscles and liver

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3
Q

Glycogenolysis

A

Glycogen -> glucose

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4
Q

Gluconeogenesis

A

amino acids -> glucose

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5
Q

Lipolysis

A

triglycerides (adipose tissue) -> free fatty acids

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6
Q

Lipogenesis

A

free fatty acids -> triglycerides, OR glucose -> triglycerides

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7
Q

Catabolism + main hormone

A

large molecules break down into smaller molecules, glucagon

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8
Q

Anabolism + main hormone

A

small molecules build into large molecules, insulin

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9
Q

Insulin lowers blood glucose through

A

glycolysis and glycogenesis

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10
Q

Glucagon increases blood glucose through

A

gluconeogenesis and glycogenolysis

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11
Q

Why does liver disease impact glucose regulation

A

Because glycogenesis, gluconeogenesis, and glycogenolysis happens in the liver

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12
Q

How does alcohol affect blood sugar?

A

When the liver has to process alcohol it takes precedence over other processes like gluconeogenesis and glycogenolysis that raise blood glucose, meaning blood sugar can fall dangerously
The body processes alcohol the same way it does fat

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13
Q

3 things to remember about insulin

A
  1. Insulin is a peptide hormone, binds to the cell membrane and needs a receptor. When it binds there is a quick reaction.
    1. Insulin inhibits glucagon. Insulin is much stronger than glucagon.
  2. Insulin chases potassium into cells
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14
Q

What types of cells need insulin to absorb glucose?

A

Fat cells and muscle cells

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15
Q

Agents that raise blood glucose

A

Glucagon
Cortisol (gluconeogenesis)
Catecholamines (glycogenolysis)
Growth hormone (antagonizes insulin)
Estrogen
Somatostatin (shuts off insulin when there’s too much of it)
Progesterone

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16
Q

Agents that lower blood glucose

A

Insulin
Somatostatin (shuts off glucagon when there’s too much of it)
Incretins (sense the level of glucose of the chyme in the duadenum and sends message to pancreas to release insulin)

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17
Q

What causes Type 1 diabetes

A

destruction of beta cells in pancreas

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18
Q

3 P’s

A

Polyphagia, polydipsia, polyuria

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19
Q

What two things cause hyperkalemia in hyperglycemia?

A

K+ can’t follow glucose into cells
Ketone bodies made by the liver increases H+, causing more H+ to be excreted in urine and more K+ being retained

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20
Q

What causes weight loss and increased FFA in type 1?

A

Lipolysis d/t tissues not receiving any glucose

21
Q

What causes the liver to start making ketones?

A

When free fatty acids are released quickly due to no insulin mitigating glucagon, the liver can’t handle it and starts making ketones

22
Q

Osmotic diuresis

A

When there is an increase in urine glucose, urine output is going to increase because glucose draws water to it

23
Q

What causes hypokalemia in Type 1?

A

Increased urine output d/t osmotic diuresis

24
Q

What causes acute renal failure in Type 1?

A

Increased urine output causing ECF deficit and decreased perfusion to the kidneys

25
Q

Why is obesity often a precursor to Type 2?

A

Fat tissue is very resistant to insulin, even though it needs it

26
Q

post-receptor defect

A

the high level of glucose in the blood starts corroding the insulin receptors on muscle and fat tissue

27
Q

how are beta cells in pancreas affected in type 2?

A

As hyperglycemia continues, often it leads to injury of the beta cells in the pancreas, they get exhausted trying to put out insulin that the tissues can’t use

28
Q

Why does DKA not happen usually in type 2?

A

Usually enough glucose is able to enter tissues to prevent ketoacidosis (not in all cases), especially in early stages

29
Q

HHS: hyperglycemic hyperosmolar state

A

Dehydration, hyperglycemia, and hypokalemia
Because acidosis and thereby unresponsiveness is usually prevented in Type 2, blood glucose can reach incredibly high levels without symptoms getting severe enough for the person to seek care

30
Q

7 Metabolic syndrome characteristics

A

Abdominal obesity (dominant)
Bad cholesterol
HTN
Elevated fasting glucose (dominant)
Prothrombotic state
Proinflammatory state
Vascular disease

31
Q

What are people w metabolic syndrome at higher risk for?

A

CAD
Type 2 DM
CVA/stroke
PVD

32
Q

What causes gestational diabetes

A

Placental hormones and weight gain of pregnancy causes insulin resistance in tissues

33
Q

Risk factors of gestational diabetes

A

Obesity, >40yo, family hx of type 2 DM, HTN, ethnicity of higher risk to Type 2, hx baby weighing >9 lbs, hx previous GDM

34
Q

Why is blood glucose usually normal in a person with gestational DM?

A

their blood glucose usually remains normal because the fetus uses the extra glucose to grow

35
Q

maternal complications of DM

A

Hydramnios
Pre-eclampsia & eclampsia
Hyperglycemia
DKA
Infections

36
Q

Fetal/newborn complications of DM

A

Congenital abnormalities
Birth defects, still birth, miscarriage
Macrosomia
IUGR (small baby)
Neonatal hypoglycemia
Infant respiratory distress syndrome
Risk for obesity and Type 2 DM in future

37
Q

Treatment for gestational DM

A

Insulin, not oral agents, lifestyle changes

38
Q

Other causes of diabetes

A
  • Pancreas injury/disease
    • Adrenal cortex disease or administration of glucocorticoids
    • Renal failure: kidneys fail to metabolize glucagon so it builds up in the blood
    • Growth hormone disturbance
  • Genetic diseases, e.g. down syndrome
39
Q

Most common reasons of hypoglycemia

A
  • Insulin/oral agent overdose
  • Omitting food intake
  • Overexertion w/o compensatory carbs
  • Vomiting
  • Alcohol
  • Extensive liver disease
  • Pancreatic, adrenal, liver disease
40
Q

s/s of hypoglycemia

A
  • Adrenergic: shaky, tremor, irritable, tachycardia, palpitations, hunger, diaphoretic, pallor, paresthesia
  • Neuroglycopenic: HA, confusion, slurred speech, irrational, visual problems, lethargy, decr. LOC, coma, death
41
Q

causes of acute hyperglycemia

A

Diabetes, stress hyperglycemia, medically induced,
Dawn phenomenon, somogyi effect

42
Q

Somogyi effect

A

Someone with low blood sugar has a strong reaction to reverse it, causing hyperglycemia

43
Q

s/s of acute hyperglycemia

A
  • Nausea, malaise, fatigue
    • 3 P’s
    • Blurred vision
    • Hyponatremia (osmotic diuresis)
    • Infections: skin, UTI, vagina, candida
      (microbes love glucose)
      • DKA and HHS
44
Q

How does chronic hyperglycemia cause other disease processes

A

Changes come from vascular, capillary and neurologic damage

45
Q

How can hyperglycemia affect endothelium of blood vessels

A

Endothelium in blood vessels get damaged, leading to plaque build up: Atherosclerosis -> CAD, HTN, MI, CVA, PVD

46
Q

diabetic nephropathy

A

Glomerular basement membrane thickens and hardens
Glomerulosclerosis -> hyperfiltration -> glomerular damage -> glomerular capillaries blocked -> capillaries start to leak -> proteins leak into urine -> damage continues -> GFR drops -> renal failure

HTN adds to risk

47
Q

diabetic retinopathy

A

Retinal capillaries develop small aneurysms and hemorrhages
Capillary neovascularization, prone to hemorrhage
“Floaters” develop later in disease
Treatment: laser photocoagulation
21% of people with diabetes type 2 have this

48
Q

charcot deformity

A

Charcot deformity: lost arch d/t nerve and vessel damage

Pathophysiology 1 (5 decks)

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