diabetes Flashcards

0
Q
(1)
Acinar cells
1.make up what percent of the pancreas?
2. secretes what?
3. via what duct?
A
(1)
Acinar cells
1.make up what percent of the pancreas?
--The exocrine portion of the pancreas accounting for 98-
99% of the pancreas weight.
2. secretes what?
-- They are responsible for synthesizing and secreting digestive enzymes and bicarbonate into the pancreatic ducts to aid in digestion
3. via what duct?
--through sphincter of oddi
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1
Q

objectives

A
  1. define glucagon, glycogenesis, lipogenesis, gluconeogenesis, glycogenolysis, and lipolysis.
  2. explain the causes and complications of diabetes mellitus, including the metabolic/physiologic implications of the disease process.
  3. recognize the cardiovascular issue sassociated with diabetes, particularly ANS neuropathy and CHF.
  4. differentiate the types of diabetes mellitus.
  5. discuss the perioperative management of the patient with DM, including BS management.
  6. describe the symptoms of and the treatment for diabetic ketoacidosis, hyperglycemic hyperosmolar nonketotic syndrome, and hypoglycemia.
  7. discuss various anitdiabetogenic agents for the patient with type I or type II diabetes and anesthetic implications of these medications.
  8. recognize the anesthetic implications for the diabetic patient.
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2
Q

(2)
Islet’s of Langerhans:
1. what is function?
2. makes up what percent of pancreas weight?
3. what is produced?
4. what controls (innervates) islets?
5. what is the path of endocrine hormones into general circulation?

A

(2)
Islet’s of Langerhans:
1. what is function?
– endocrine portion of panceras;
2. makes up what percent of pancreas weight?
– 1-2% of the pancreas weight. There are more than 1 million islets in a pancreas.
3. what is produced?
–Produces hormones that are secreted directly into the capillary blood vessels.
4. what controls (innervates) islets?
– Innervated by adrenergic and cholinergic fibers of the autonomic nervous system.
5. what is the path of endocrine hormones into general circulation?
– Each islet has an abundant blood supply → hepatic portal vein→ general circulation.

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3
Q
(3)
define:
1. glucagon 
2. glycogenesis
3. lipogenesis
4. gluconeogenesis
5. glycogenolysis
6. lipolysis
A

(3)
define:
1. glucagon
–glucagon- secreted by alpha (A) cells; it is a hormone for glucose release (opposite of insulin).
2. glycogenesis
–glyco-genesis-formation of glycogen (for storage)from glucose
3. lipogenesis
–lipo-genesis-storage of lipids
4. gluconeogenesis
– gluco-neo-genesis-the creation of glucose from lactate, pyruvate, amino acids, and glycerol in the liver
5. glycogenolysis
–glycogen-o-lysis-the breakdown of glycogen into glucose
6. lipolysis
– lipo-lysis-the breakdown of triglycerides into fatty acids and glycerols

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4
Q

(4)

1a. what causes diabetes type 1(what chromosome)?
1b. What age is onset?
1c. what happens in terms of insulin?
1d. What will be needed.
2. what causes diabetes type 2
2b. When is onset?
2c. what happens in terms of insulin?

A

(4)

1a. what causes diabetes type 1(what chromosome)?
- -most likely autoimmune etiology (destruction of cells of islets of langerhan d/t human lymphocyte antigen (HLA) on chromosome 6)
1b. What age is onset?
- - onset usually at puberty but can be prior to 20-40 yrs old, abrupt onset
1c. what happens in terms of insulin?
- - destruction of islets decreases insulin production
1d. What will be needed.
- - lifelong insulin replacement
2a. what causes diabetes type 2
- -caused by obesity and sedintary lifestyle
2b. When is onset?
- -type 2- late onset (usually after 40 y/o)
2c. what happens in terms of insulin?
- -insulin resesitance at receptor causes decreased uptake of insulin (and thus glucose) at skeletal muscle

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5
Q

(5)
complications of diabetes (CARDIOVASCULAR):
a) what vascular issues accompany diabetes?
b) this can lead to what cardiac issues (related to coronary vessels)?
c) what can this do diabetes do to the heart itself? ___% of ___ patients are diabetics.
d) what nerve condition caused by diabetes has severe cardiac manifestations?
e) why do diabetics develop feet problems?
f) in essence how are the vascular changes caused by diabetes classified?

A

(5)
complications of diabetes (CARDIOVASCULAR):
a) what vascular issues accompany diabetes?
–increased risk of thrombotic lesions (which increase risk of: nepropathy, atherosclerosis, stroke, retinopathy & CAD (which is the leading cause of diabetic death))
b) this can lead to what cardiac issues (related to coronary vessels)?
–higher disk of myocardial ischemia, MI, silent MI, increased infarct size in MI
c) what can this do diabetes do to the heart itself? ___% of ___ patients are diabetics.
–CHF/ diabeic cardiomyopathy. 35% of CHF paients are diabetics
d) what nerve condition caused by diabetes has severe cardiac manifestations?
– ANS neuropathy (cardiac manifestations)
e) why do diabetics develop feet problems?
–diabetes causes PVD (and PAD)
f) in essence how are the vascular changes caused by diabetes classified?
–vascular changes caused by diabetes are either micro or macrovascular changes

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6
Q

(6)

  1. what does insulin do?
    2a. when is insulin production highest?
    2b. Lowest?
    2c. what about post prandial?
  2. what works against insulin (counterregulatory hormones)?
  3. how much insulin is produced per hour and per day?
  4. what type of cells does insulin come from?
A

(6)

  1. what does insulin do?
    - - insulin causes the storage of glucose, fats and amino acids until needed;
    - -insulin is a hormone of growth (anabolic)
    - -favors lipogenesis and inhibits lipolysis
    2a. when is insulin production highest?
    - - Insulin levels are highest in AM (0800)
    2b. Lowest?
    - -lowest between 12 & 4 pm
    2c. what about post prandial?
    - -insulin is highest 30-60 mintes after a meal(post prandial)
  2. what works against insulin (counterregulatory hormones)?
    - -counterregulatory hormones: glucagon, cortisol, growth hormone and epinephrine
  3. how much insulin is produced per hour and per day?
    - -insulin release: 1 unit for hour; increases 5-6 units after a meal for a total of 60 units daily.
  4. what type of cells does insulin come from?
    - - beta cells of langrahan
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7
Q

(7)

  1. what blood pressure medications should be used with diabetics?
  2. what medications are USUALLY avoided (but are used more frequently)?
  3. why?
A

(7)
1. what blood pressure medications should be used with diabetics?
–ACE inhibitors are usually used with diabetics
2. what medications are USUALLY avoided (but are used more frequently)?
–beta blockers had been avoided for a long time
3. why?
d/t blocking the s/s of hypoglycemia (tachycardia) and the fact that it may block beta cell function causing an alteration in glucose and lipid metabolism (blocks insulin causing increased blood glucose)

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8
Q

(8)

  1. define diabetes?
  2. what happens to cause diabetes (in the body)?
  3. how many types of diabetes are there and what are they?
A

(8)
1. define diabetes?
–a disease of glucose dysregulation and carbohydrate intolerance, associated with acute and long term, predictable systemic consequences which may significantly affet morbidity and mortality
2. what happens to cause diabetes (in the body)?
–a)when insulin production is low or absent
OR
b)the tissues become resistant to normal levels of insulin
OR
c) both decreased insulin production with increased resistance
3. how many types of diabetes are there and what are they?
–4 types-
-type 1 (insulin dependent)
-type 2 (non insulin dependent)
-gestational (during pregnancy)
-situational (d/t conditions such as pancreatitis, acromegaly, cystic fibrosis, pheochromocytosis, steroids)

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9
Q

(9)

  1. how many americans have diabetes?
  2. how many type 1 (%)?
  3. how many type 2 (%)?
A

(9)

  1. how many americans have diabetes?
    - - 20 million
  2. how many type 1 (%)?
    - - 5-10%
  3. how many type 2 (%)?
    - -90% of diabetics are type 2 (50% of them don’t even know they have it)
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10
Q

(10)

  1. what is diabetic cardiomyopathy?
  2. what happens to the ventricles?
  3. is it eccentric or concentric?
  4. what is the goal of anesthesia of a patient with diabetic cardiomyopathy?
  5. when does diabetic cardiomyopathy develop?
A

(10)

  1. what is diabetic cardiomyopathy?
    - -a form of heart failure (similar to alcoholic cardiomyopathy) that occurs independent of CAD, HTN or valvular disease; caused by hyperglycemia
  2. what happens to the ventricles?
    - -progressive ventricular relaxation causing DD (DIASTOLIC DYSFUNCTION) (d/t high filling pressures from stiffness of ventricles) –systolic function is preserved–dilated cardiomyopathy like alcohol related cardiomyopathy
  3. is it eccentric or concentric?
    - -diabetic cardiomyopathy is eccentric (in which the heart grows outward in size and the volume is enlarged-but it cannot contract as well).
  4. what is the goal of anesthesia of a patient with diabetic cardiomyopathy?
    - -goal of anesthesia is to prevent and treat hypertension (lower SVR allows for better ventricle emptying).
  5. when does diabetic cardiomyopathy develop?
    - - diabetic cardiomyopathy occurs 4-5 years after diagnosis
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11
Q

(11)
Complications of diabetes (AIRWAY):
1. what condition would cause a type 1 diabetic to be intubated with a glidescope?
1b. what test tests for this condition?
2. what condition would make intubating a type 2 diabetic difficult?
3. what condition should you consider when intubating a diabetic; and what should be done?

A

(11)
Complications of diabetes (AIRWAY):
1. what condition would cause a type 1 diabetic to be intubated with a glidescope?
–1/3 of type 1 diabetics are difficult to intubate d/t glycosylation of tissue proteins leading to stiff joint syndrome; especially atlanto-occipital joint (the joint between atlas of neck and occiput)
1b. what test tests for this condition?
–prayer sign
2. what condition would make intubating a type 2 diabetic difficult?
– obesity in type 2 diabetics makes intubation challenging
3. what condition should you consider when intubating a diabetic; and what should be done?
–gastroparesis in diabetics makes them an aspiration risk; give aspiration prophylaxis and consider RSI or awake intubation.

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12
Q

(12)

  1. what are microvascular changes?
  2. what are macrovascular changes?
  3. which type of diabetic (type 1 or 2) gets which type?
A

(12)

  1. what are microvascular changes?
    - - microvascular changes affect the retina and kidney
  2. what are macrovascular changes?
    - - macrovascular changes affect the coronary and peripheral vasculature
  3. which type of diabetic (type 1 or 2) gets which type?
    - -type 1= microvascular; type 2=macrovascular (1 is smaller than 2; 1=micro & 2=macro)
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13
Q

(13)

  1. what are the side effects of diabetes (vascular)
  2. and integument
A

(13)

  1. what are the side effects of diabetes (vascular)
    - -PVD (circulatory insuffeciency to feet and legs)
  2. and integument.
    - -delayed wound healing
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14
Q
(14)
diabetics have how many "x" more of a chance of developing these?
1. atherosclerosis:
2. CVA
3. MI:
4. PVD:
5. CHF (male & female)
A
(14)
diabetics have how many "x" more of a chance of developing these?
1. atherosclerosis:
-- atherosclerosis: 2.5x
2. CVA
--CVA: 2x
3. MI:
-- MI: 2-10x
4. PVD:
-- PVD: 5-10x
5. CHF (male & female)
-- CHF: male=2x; female=5x
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15
Q

(15)

what are the neurological s/e of diabetes?

A

(15)
what are the neurological s/e of diabetes?
-ANS neuropathy

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18
Q

(16)

  1. ANS neuropathy is diagnosed how?
  2. what are the symptoms seen with this test?
A

(16)

  1. ANS neuropathy is diagnosed how?
    - - diagnosed by abnormal CV results to reflex tests
  2. what are the symptoms seen with this test?
    - - symptoms seen:
    a) orthostatic hypotension
    b) resting tachycardia at fixed rate
    c) absent beat to beat variability
    d) excercise intolerance
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19
Q

(17)

  1. what are GU alterations with diabetes?
  2. what medications (for HTN) slow the progression of diabetic nephropathy
  3. what does that medicine cause regarding blood pressure
    3b. what medication wont work?
  4. what does the renal disease make the diabetic patient prone to?
A

(17)

  1. what are GU alterations with diabetes?
    - -a) acute renal failure
    - -b) end stage renal disease (ESRD)
    - –type 1: 30%
    - –type 2: 4-20%
  2. what medications (for HTN) slow the progression of diabetic nephropathy
    - -ace inhibitors
  3. what does that medicine cause regarding blood pressure
    - - causes hypotension
    3b. what medication wont work?
    - -ephedrine
  4. what does the renal disease make the diabetic patient prone to?
    - - volume overload, hyperkalemia, longer half life of drugs (insulin and NDMR (aminosteroids))
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20
Q

(18)
what are the GI and GU effects of diabetic ANS neuropathy?
1. GI:
2. GU:

A

(18)
what are the GI and GU effects of diabetic ANS neuropathy?
1. GI:
–GI: gastroparesis leading to N?V, abdominal distention, noctournal diarrhea, early satiety
2. GU:
– GU: impotence, bladder infection,

21
Q

(19)

what are 5 initial s/s of diabetes type 1?

A

(19)
what are 5 initial s/s of diabetes type 1?
1. glucocosuria: after glucose > 180-200, kidneys can no longer absorb glucose
2. polyuria: excess glucose acts as an osmotic diuretic (causes extracellular dehydration and electrolyte depletion)
3. polydipsia: d/t hypovolemia
4. weight loss
5. (not mentioned) polyphagia- always hungry dt “starvation in a sea of plenty” (inability to utilize nutrients leads to cellular starvation)

22
Q

(20)

what are initial symptoms of diabetes type 2?

A

(20)
what are initial symptoms of diabetes type 2?
–any of the type 1 symptoms i.e….
1. glucocosuria: after glucose > 180-200, kidneys can no longer absorb glucose
2. polyuria: excess glucose acts as an osmotic diuretic (causes extracellular dehydration and electrolyte depletion)
3. polydipsia: d/t hypovolemia
4. weight loss
5. (not mentioned) polyphagia- always hungry dt “starvation in a sea of plenty” (inability to utilize nutrients leads to cellular starvation)
–as well as…
6. infections (bladder, skin, gums with slow wound healing)
7. blurred vision
8. numbness
9. tingling of extremities

23
Q

(21)

what happens with the nutrients with diabetes (including metabolism, by products and the body’s reaction)?

A

(21)
what happens with the nutrients with diabetes (including metabolism, by products and the body’s reaction)?
1. there is a shift from carbohydrate to fat metabolism, using free fatty acids (FFAs) for fuel
2. FFAs are converted by the liver into ketone bodies i.e.
–aceto-acetic acid
–B-hydroxy-butyric acid
–acetone
3. acetone is a volitile acid and is excreted (in some part) by the lungs (acetone breath)
4. protein is also catabolized for fuel (leading to weight loss)
5. polyphagia d/t loss of protein

24
Q
(22)
insulin types and duration:
1. rapid acting:
2. short acting:
3. intermediate acting:
4. long acting:
A

(22)
insulin types and duration:
1. rapid acting: Lispro, Aspart (novalog):
2. short acting: regular (novalin)
3. intermediate acting: NPH, Lente
4. long acting: Ultralente, Glargine (Lantus)

25
Q
(23)
Insulin:
rapid acting: Lispro, Aspart (novalog): 
onset:
peak:
duration:
A
(23)
Insulin:
rapid acting: Lispro, Aspart (novalog): 
onset: 15-30 min
peak: 30-90 min
duration: 3-4 hrs
26
Q
(24)
Insulin:
short acting: regular (novalin)
onset:
peak:
duration:
A
(24)
Insulin
short acting: regular (novalin)
onset: 30-60 min
peak: 2-4 hrs
duration: 6-10 hrs
27
Q
(25)
Insulin:
intermediate acting: NPH, Lente
onset:
peak:
duration:
A
(25)
intermediate acting: NPH, Lente
onset: 1-4 hrs
peak: 4-12 hrs
duration: 12-24 hrs
28
Q
(26)
Insulin:
long acting:
1.  Ultralente, 
onset:
peak:
duration:
2. Glargine (Lantus)
onset:
peak:
duration:
A
(26)
Insulin
long acting:
1.  Ultralente, 
onset: 1-2 hrs
peak: 8-20 hrs
duration: 24-30 hrs
2. Glargine (Lantus)
onset:1 hr
peak: 3-20 hrs
duration: 24 hrs
29
Q

(27)
ANS neuropathy:
1. what defect (caused by diabetes) causes it?
2. what happens to these patients under anesthesia?
3. what medications may not work?

A

(27)
ANS neuropathy:
1. what defect (caused by diabetes) causes it?
– predominance of sympathetic nervous system activity (increased HR, BP)
2. what happens to these patients under anesthesia?
a) blood pressure lability (d/t inability of normal ANS responses (vasoconstriction and tachycardia) to compensate for vasodilation caused by anesthesia
b) hypothermia
c) may have sudden decrease in HR which is refractory to atropine
(must treat with epinephrine)
d) may not respond to beta blockers
e) sudden death syndrome d/t shortened QT
3. what medications may not work?
–atropine (for bradycardia); propanolol, (?? Vasopressin, (im just wonderin))

30
Q

(28)

  1. what is diabetic ANS (autonomic nervous system) neuropathy?
  2. how often does it occur in diabetics?
A

(28)

  1. what is diabetic ANS (autonomic nervous system) neuropathy?
    - - manifests as alterations in the CV, GI & GU systems
  2. how often does it occur in diabetics?
    - -20-40% of type 1 diabetics
31
Q

(29)

  1. what is DKA?
    1b. what is the mortality?
  2. in which diabetes does it most occur?
  3. symptoms of diabetic ketoacidosis:
  4. treatment (surgical preparation) for diabetic ketoacidosis:
A

(29)

  1. what is DKA?
    - - a medical emergency triggere by a hyperglycemic event (illness, infection, gangrene, steroids) in which the patent is dehydrated with elevated glucose and acidosis d/t ketone bodies (from fat metabolism)
    1b. what is the mortality?
    - - mortality is 5-10%
  2. in which diabetes does it most occur?
    - -occurs mostly in type 1 diabetic
  3. symptoms of diabetic ketoacidosis:
    - a)hyperglycemia >250
    - b)volume depletion (down 3-8 L)
    - c)tachycardia, metabolic acidosis (pH320 mOsm/kg)
    - f) n/v
    - g)abdominal pain
    - h) lethargy
    - i) acetone breath
    - j) kussmal respirations (deep/labored breathing)
  4. treatment (surgical preparation) for diabetic ketoacidosis:
    - a) restrore intravascuar volume
    - b) decrease blood glucose
    - c) decrease stress hormone levels
    - d) correct ketosis and acidosis
    - e) correct electrolyte imbalance
32
Q

(30)

  1. what is HHNK?
  2. what type diabetic is it most common in?
  3. symptoms of hyperglycemic hyperosmolar nonketotic syndrome
  4. treatment for hyperglycemic hyperosmolar nonketotic syndrome
A

(30)

  1. what is HHNK?
    - -a hyerosmolar state triggered by a hyperglycemic event; the patient has enough insulin to prevent lypolysis and ketone formation (thus no acidosis), however they do not have enough insulin to prevent hyperglycemia; in other words DKA without the KA.
  2. what type diabetic is it most common in?
    - - occurs more in type 2
  3. symptoms of hyperglycemic hyperosmolar nonketotic syndrome
    - a) hyperglycemia >600 mg/dL
    - b) hyperosmolar blood (>350 mOsm/L)
    - c) normal pH
    - d) osmotic diuresis
    - e) hypovolemia
    - f) CNS depression
    - g) electrolyte imbalance (hypokalemia d/t osmotic diuresis)
    - h) dehydration (down 7 liters)
  4. treatment for hyperglycemic hyperosmolar nonketotic syndrome
    - a) same as DKA
    - b) fluid replacement
    - c) correct hyperglycemia,
    - d) correct electrolyte imbalance
33
Q

(31)

  1. what is hypoglycemia?
    1b. what level = hypoglycemia (mg/dL)?
    1c. What does a glucose level <55 cause?
  2. symptoms of hypoglycemia in awake patient:
  3. treatment for hypoglycemia:
A

(31)

  1. what is hypoglycemia?
    - -excess insulin relative to carb intake;
    1b. what level = hypoglycemia (mg/dL)?
    - -glucose levels of 40-50 mg/dL.
    1c. What does a glucose level 100 via dextrose (oral or IV)
34
Q

(32)

how much does 1 mL of D50 increase your glucose if you weigh 70 kg?

A

(32)
how much does 1 mL of D50 increase your glucose if you weigh 70 kg?
–every 1 ml of D50% will increase your blood glucose by 2 mg/dL (if you weigh 70 kg).

35
Q

(33)

how much does 1 unit of insulin lower your glucose if you weigh 70 kg?

A

(33)
how much does 1 unit of insulin lower your glucose if you weigh 70 kg?
–each unit of insulin lowers your glucose 40-50 (50) mg/dL if you weigh 70 kg

36
Q

(34)
treatment of DKA:
1. What is the fluid calculation /kg?
1b. how much IV fluid in the first hour?
2. start D5 gtt when glucose reaches what level?
3. what are the common electrolyte abnormalities?

A

(34)
treatment of DKA:
1. What is the fluid calculation /kg?
–10-20 ml/kg of 0.9%;
1b. how much IV fluid in the first hour?
–1-2 L in the first hour, then 250-500 mL/hr
2. start D5 gtt when glucose reaches what level?
–start D50 once glucose reaches 250mg/dL or less.
3. what are the common electrolyte abnormalities?
–decreased K+,(potassium usually increases with acidosis, but potassium is decreased here d/t polyuria)
– Mg+,
– Phosphate

37
Q

(35)
antidiabetic agents:
what are the 5 types?

A
(35)
antidiabetic agents:
what are the 5 types?
1.sulfonyl-ureas
2. meglit-imides
3. biguan-ides
4. thia-zoli-dine-diones
5. "_"glucoside-ase
38
Q
(36)
summary of complications of diabetes:
1. CNS
2. CV
3. GI
4. GU
5. Misc.
A

(36)

  1. CNS- strokes, peripheral neuropathy, autonomic neuropathy
  2. CV- hypertension, coronary artery disease, cardiomyopathy, retinopathy, cardiac autonomic neuropathy
  3. GI- gastroparesis, nocturnal diarrhea
  4. GU- nephropathy, chronic renal failure
  5. Misc.-infections, DVT, protamine reactions, stiff joint syndrome
39
Q
(37)
oral antidiabetic agents: sulfonylureas:
1. name them:
2. mechanism of axn:
3. side effects:
4. contraindications:
A

(37)
oral antidiabetic agents: sulfonylureas:
1. name them: glyburide (diabeta), chlorpropamide (diabinase)
2. mechanism of axn: stimulates release of insulin
3. side effects: hypoglycemia, nausea, gi discomfort
4. contraindications: hepatic or renal impairment

40
Q
(38)
oral antidiabetic agents: meglitimides:
1. name them:
2. mechanism of axn:
3. side effects:
4. contraindications:
A

(38)
oral antidiabetic agents: meglimitides:
1. name them: repaglinide (gluconorm)
2. mechanism of axn: stimulates release of endogenous insulin (rapid acting with better post prandial glucose control)
3. side effects: hypoglycemia (but less frequent than with sulfonylureas)
4. contraindications: hypersensitivity, DKA

41
Q
(39)
oral antidiabetic agents: biguinides:
1. name them:
2. mechanism of axn:
3. side effects:
4. contraindications:
A

(39)
oral antidiabetic agents: biguinides:
1. name them: metformin (glucophage)
2. mechanism of axn: reduce gluconeogenesis, increase glucose utilization `
3. side effects: lactic acidosis, anorexia, nausea, diarrhea, gi discomfort
4. contraindications: hepatic or renal impairment, alcoholism, advenced age

42
Q
(40)
oral antidiabetic agents: thiazolidinediones:
1. name them:
2. mechanism of axn:
3. side effects:
4. contraindications:
A

(40)
oral antidiabetic agents: thiazolidinediones:
1. name them: rostiglitazone (avandia), pyoglitazone (actos)
2. mechanism of axn: increase peripheral sensitivity to insulin, reduce gluconeogenesis
3. side effects: increased triglycerides, weight gain, hepatotoxicity, anemia
4. contraindications: liver disease, CHF

43
Q
(41)
oral antidiabetic agents: _ glucosidases:
1. name them:
2. mechanism of axn:
3. side effects:
4. contraindications:
A

(41)
oral antidiabetic agents:_ glucosidase :
1. name them: acarbose (prandase)
2. mechanism of axn: decreases the absorption of carbs (thus preventing post prandial increase in glucose)
3. side effects: flatulence, abdominal cramps, diarrhea
4. contraindications: hypersensitivity, DKA, IBD

44
Q

(42)

  1. what are the 3 main anesthetic goals for diabetics?
  2. anesthetic implications for diabetics is… in essence…
A

(42)

  1. what are the 3 main anesthetic goals for diabetics?
    - - risk stratification (identify associated end organ disease)
    - - initiate appropriate interventions
    - - limitation or treatment of metabolic, cv and renal complications
  2. anesthetic implications for diabetics is… in essence.
    - - in essence, the goal is to mimic normal metabolism as closely as possible by avoiding hypoglycemia, excessive hyperglycemia, ketoacidosis and electrolyte issues.
45
Q
(43)
pre operative assessment of diabetic:
1. what history are we looking for?
2. what is the patient at risk for?
3. at what blood glucose should an elective surgery be postponed?
4. what meds should be given?
A

(43)
pre operative assessment of diabetic:
1. what history are we looking for?
– CAD, HTN, PVD, need ECG, renal damage, diabetic autonomic neuropathy, GERD
2. what is the patient at risk for?
– labile bp (d/t volume depletion), MI
3. at what blood glucose should an elective surgery be postponed?
– >300-400, postpone elective surgery
4. what meds should be given?
– reglan 10 mg (per 70 kg) 30 min before surgery

46
Q

(44)
the day before surgery and the day of surgery:
1a. By how much should REGULAR sq insulin be reduced?
1b. By how much should LONG ACTING insulin be reduced?
2. how much should insulin pump be reduced?
3. how many days should oral antidiabetics be held?

A

(44)
the day before surgery and the day of surgery:
1a. By how much should regular sq insulin be reduced?
– regular: take only the night before, hold on am of surgery
1b. By how much should long acting insulin be reduced?
– long acting: reduce by 20% the night before or 50% the day of
2. how much should insulin pump be reduced?
– insulin pump: reduce basal rate by 20% at midnight before surgery
3. how many days should oral antidiabetics be held?
– oral antidiabetics: stop evening before procedure

47
Q

Fasting Glucose of___ equates to diabetes?

A

> 126