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Concepts 3 > Obesity + DM (Lea) > Flashcards

Obesity + DM (Lea) Flashcards

1
Q

What is obesity?

A

Obesity is a disorder of energy balance
Defined as 20% or more above ideal weight
Measured by Body Mass Index (BMI)
“A complex, multifactorial disease”
Weight (kg)/ (m)2 = BMI

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2
Q

BMI Classification

A
  • Underweight <18.5
  • Normal 18.5-24.9
  • Overweight 25-29.9
  • Obese I 30-34.9
  • Obese II 35-39.9
  • Obese III (Morbid) > 40
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3
Q

Children and body weight class

A

Weight class Percentile
Overweight 85-94th
Obese 95-98th
Severely Obese 99th

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4
Q

Ideal Body Weight

A

Men IBW (kg) = height (cm)- 100
Women IBW (kg) = height (cm)-105

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5
Q

Android vs. Gynecoid

A

Android: associated with increase risk of ischemic heart disease, hypertension, dyslipidemia and death
Gynecoid: associated with joint disease and varicose veins
Apples (android) or pears (gynecoid)

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6
Q

Metabolic Syndrome

A

Cardiovascular risk is 50-60% higher than in the general population
Requires at least three of the following:
Large waist >40” men >35” women
Triglycerides > 150 mg/dl
High Density Lipoprotein <40 m < 50 w
BP > 135/80
Fasting BS > 100mg/dl

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7
Q

Respiratory Effects of Obesity

A

Causes a restrictive ventilatory defect
Lungs are compressed lung volumes and compliance is reduced
Increase in pulmonary blood flow also reduces compliance
Lung inflation is inhibited by chest fat that compresses the ribcage and prevents outward expansion
Abdominal fat shifts the diaphragm towards the head

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8
Q

FRC is inversely proportional to ____

A

BMI

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9
Q

GA causes the FRC to decrease by ___

A

50% in the obese patient compared to 20% in non obese

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10
Q

Increase O2 consumption and decrease FRC leads to ______.

A

rapid desaturation

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11
Q

Restrictive Lung pattern causes

A

Decreased Lung Compliance
Increased O2 consumption and CO2 production
Increased weight in the chest increased work of breathing results in a rapid shallow breathing pattern
A high CO2 in an obese patient signals impeding respiratory failure

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12
Q

Obesity and Lung Volumes

A

Decreased FRC
Decreased vital capacity and TLC
Decreased Expiratory reserve volume
Normal residual volume

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13
Q

Optimal tidal volume for the obese patient

A

6-8 ml/kg of Ideal Body Weight
Lungs do NOT grow in proportion to body mass
Increase RR to maintain PaCO2

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14
Q

Strategies to optimize anesthesia for obese patients

A
  • Increased O2 consumption and Decreased FRC = rapid desaturation
  • Pre Oxygenated with 100% until end tidal O2 > 90 %
  • Head Elevated Laryngoscopy Position (HELP) Aligns the oral pharyngeal and laryngeal axes
    A horizontal line drawn for the sternal notch to the external auditory meatus
  • Reverse Trendelenburg relieves the pressure on the chest and improves the FRC
  • Utilize on induction and extubation
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15
Q

How do we prevent Atelectasis?

A

Keep FiO2 < 80% Prevent absorption atelectasis
Recruitment maneuver (Valsalva) 40 cmH2O for 10 sec, may decrease BP and HR
PEEP 5-15 cmH2O

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16
Q

Postop Hypoxemia is highest risk for ___
How can we prevent it?

A

Highest risk in OSA patients
Minimize risk by:
CPAP or BiPAP after extubation esp if used at home
Elevate HOB 30 degrees
Early ambulation
Control surgical pain (non-opioid and regional to minimize resp depression)

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17
Q

Morbid obesity and aspiration…what’s the deal?

A

Obesity alone does not mandate RSI
RSI should be made on other individual risk factors of GERD and DM

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18
Q

Cardiovascular effects of Obesity

A

Two Key Changes
Expansion of intravascular volume
High cardiac output

HR is usually unchanged, SV and CO increase

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19
Q

Common EKG Changes seen with obesity

A
  • Low voltage EKG (increased distance b/t heart and leads)
  • Left axis deviation (stomach pushes heart to the left)
  • Right axis deviation (RV hypertrophy from OSA and volume overload)
  • QT prolongation (Inc. risk of sudden death)
  • Dysrhythmias (fatty infiltration of conduction system)
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20
Q

general definition of volume of distribution

A

The volume of distribution is a proportionality factor that relates the amount of drug in the body to the concentration of drug measured in a biological fluid. That’s it … a proportionality factor … nothing more.

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21
Q

volume of distribution in obese pts (lipophilic vs hydrophilic)

A
  • The Vd of lipophilic drugs is increased due to a larger fat mass
  • The Vd of hydrophilic drugs is increased due to a larger muscle mass and blood volume and increases some because of large plasma volume
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22
Q

Vd in obese patients and rate of absorption

A
  • Increased blood volume; requires a larger loading dose to achieve a given plasma concentration
  • Increased CO; faster drug delivery to the vessel rich group
  • Altered plasma protein binding; alters the free fraction available
  • Lipid solubility of the drug; large fat mass increases the Vd of lipophilic drugs
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23
Q

Drug Dosing in the Obese patient

A

IBW may under dose due to large Vd
TBW may over dose because fat is less vascular and greater percentage will go to vessel rich group
Lean Body Weight solves the issue

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24
Q

Lean Body Weight

A

LBW is IBW plus extra for increased muscle mass
LBW = IBW X 1.3

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25
Q

Dose a Propofol bolus based on ___

A

AdjBW

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26
Q

Dose a Propofol maintenance infusion based on ___

A

AdjBW

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27
Q

Dose Etomidate based on ____

A

AdjBW

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28
Q

Dose Thiopental based on ___

A

AdjBW

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29
Q

Dose Benzodiazepine boluses based on ___

A

TBW

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30
Q

Dose benzodiazepine infusions based on ____

A

AdjBW

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31
Q

Dose dexmedetomidine based on ___

A

TBW

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32
Q

Dose synthetic opioids (fentanyl, remifentanil) based on ____

A

TBW

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33
Q

Dose morphine based on ___

A

IBW

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34
Q

Dose hydromorphone based on ____

A

IBW

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35
Q

Dose steroidal NMBAs based on ____

A

IBW

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36
Q

Dose Succinylcholine based on ____

A

TBW

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37
Q

Nitrous Oxide (what’s the MAC and Blood-Gas Partition Coefficient)

A

MAC = 104%
Blood-Gas Coefficient = 0.47

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38
Q

Desflurane (what’s the MAC and Blood-Gas Partition Coefficient)

A

MAC = 6%
Blood-Gas Coefficient = 0.45

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39
Q

Sevoflurane (what’s the MAC and Blood-Gas Partition Coefficient)

A

MAC = 2%
Blood-Gas Coefficient = 0.65

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40
Q

Enflurane (what’s the MAC and Blood-Gas Partition Coefficient)

A

MAC = 1.7%
Blood-Gas Coefficient = 1.8

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41
Q

Isoflurane (what’s the MAC and Blood-Gas Partition Coefficient)

A

MAC = 1.4%
Blood-Gas Coefficient = 1.4

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42
Q

Halothane (what’s the MAC and Blood-Gas Partition Coefficient)

A

MAC = 0.75%
Blood-Gas Coefficient = 2.3

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43
Q

PEARLS for Volatile Agents in Obese Pts

A

Volatile agents are lipophilic. Agents with low blood gas solubility coefficients should be used.
MAC is unchanged by obesity

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44
Q

Propofol dosing

A

Loading dose based on LBW and maintenance based on TBW

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44
Q

Succ dosing

A

Intubating dose based on TBW. This is due to increased blood volume (increased Vd) and increased pseudo cholinesterase activity (increased clearence)

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45
Q

Non depolarizing neuromuscular drugs dosing

A

Roc and Vec are dosed on LBW
Cisatracurium and atracurium and probably TBW

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46
Q

Remi dosing

A

ALWAYS LBW

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47
Q

Midazolam dosing

A

Midazolam administered on TBW but will cause prolonged elimination and duration

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48
Q

Epidural Local Anesthetics

A

Engorgement of epidural veins and increase in epidural fat content will cause a greater spread of local anesthetics in the epidural space
Reduce the dose to 75%

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49
Q

OSA pathophysiology

A

Review: Pharyngeal muscles maintain airway patency
Tensor Palatine—opens the nasopharynx
Genioglossus—opens the oropharynx
Hyoid Muscle—opens the hypopharynx
Fat accumulation in the pharynx causes the internal diameter to narrow, decreases airflow and increase airway collapse

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50
Q

OSA

A

Defined as cessation of airflow for at least 10 seconds with five or more unsuccessful efforts to breathe and a greater than 4% reduction in SaO2
Hypoapnea is defined as 50% reduction in airflow for 10 seconds, 15 or more times per hour, and is linked to snoring and decreased SaO2

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51
Q

OSA and obesity

A

OSA is directly linked to obesity
Increases with BMI > 30 kg/m2, abdominal fat distribution and large neck circumference
- men > 17in
- women > 16in
OSA is an independent risk factor for development of HTN, CV disease, morbidity and death

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52
Q

Apnea/hypoapnea Index (AHI)

A

Polysomnography is the definitive test for OSA, and allows for the calculation of the AHI
AHI = # of episodes of apnea/hypoapnea divided by hours of sleep

Mild 5-15
Moderate 15-30
Severe > 30

53
Q

STOP - BANG

A

Snoring
Tiredness
Observed Apnea
Pressure (HTN)
BMI > 35 kg/m2
Age >50
Neck circumference > 40 cm (15.74in)
Gender (male)

High risk > 3 Low risk <3

54
Q

Obesity Hypoventilation Syndrome

A
  • OHS is a long term result of OSA
  • Medulla fails to respond to hypercarbia
  • OHS classically includes apnea during sleep without respiratory effort
  • Pickwickian syndrome is the old term
  • Signs; obesity, daytime hyper somnolence, hypoxemia, hypercarbia, resp. acidosis, comp metabolic alkalosis, polycythemia and pulmonary HTN
55
Q

Types of bariatric surgery

A

Gastric bypass surgery
Roux-en-Y (open or laparoscopic)
Biliopancreatic diversion bypass
Gastric banding (open or laparoscopic)
Gastric sleeve surgery

56
Q

Types of malabsorption procedures

A
  1. Biliopancreatic diversion bypass
  2. Jejuno-ileal bypass
  3. Duodenal Switch

Gastric reduction and removal of portion of small intestine limits nutrient absorption.
Vitamin K, B12, iron and folate depletion

57
Q

Restriction surgerys

A
  1. Gastric Band
  2. Gastric Sleeve

Limits the quantity of food that can be consumed.
Least invasive.
Gastric hormone secretion reduced.
Small intestine intact

58
Q

Combo malabsorption + restricton

A

Roux-en Y gastric bypass

Combination of malabsorption and restriction
Yields the best weight loss and comorbidity reduction
Risk nutrient deficiency

59
Q

Anastomotic Leak

A

2% incidence
Patients should not receive ketorolac
Most common signs:
- Tachycardia (72%)
- Fever (63%)
- Abdominal Pain (54%)
- Other signs shoulder pain, pelvic pain, substernal pressure, dyspnea, hypotension, oliguria, increased thirst, restlessness, hiccups

60
Q

Carcinoid Syndrome

A
  • Associated with secretions of vasoactive substances from enterochromaffin cells usually in the GI tract
  • When liver function is normal carcinoid hormones are cleared, with liver dysfunction sign and symptoms occur
  • Symptoms can occur if tumors are located in the lungs and bypass the liver and enter the circulation
61
Q

Carcinoid Hormones

A
  1. HISTAMINE
  2. KININS AND KALLIKRENS
  3. SEROTONIN
62
Q

Histamine systemic effects

A

Bronchoconstriction
Vasodilatation
Hypotension
Flushing of head and neck

63
Q

Kinins and Kallikrens systemic effects

A

Bronchoconstriction
Vasodilatation
Hypotension
Flushing of head and neck
Inc. histamine release from mast cells

64
Q

Serotonin systemic effects

A

Bronchoconstriction
Vasodilatation
Hypotension
Supra ventricular tachydysrhythmias
Inc. GI motility, diarrhea, abdominal pain

65
Q

Drugs to avoid with carcinoid syndrome

A
  • Histamine releasing drugs: MS meperidine, atracurium, thiopental, and succinylcholine
  • Succinylcholine induced fasciculation causes hormone release from tumor cells
  • Exogenous catecholamines can precipitate hormone release
  • Sympathomimetic agents ephedrine and ketamine
66
Q

drugs to give with carcinoid syndrome

A
  • Somatostatin (octreotide or lanreotide) inhibit release of vasoactive substances from carcinoid tumors
  • Antihistamines (H1 and H2) diphenhydramine and ranitidine or cimetidine
  • 5HT3 antagonist (ondansentron)
  • Steroids
  • Phenylephrine or vasopressin for hypotension
67
Q

carcinoid crisis

A

Life threatening response in patients with carcinoid syndrome
S/S include:
- Inc. HR
- hypertension or hypotension
- intense flushing (#1)
- abdominal pain
- diarrhea (#2)

68
Q

Pancreas

A

Endocrine & Exocrine Organ
Anatomy
15 cm in length
Weighs 60-140 grams
Anatomic relationship
Duodenum
Ampulla of Vater
Common bile duct
Superior mesenteric artery
Portal vein
Spleen
Transverse colon
Left lobe of the liver

69
Q

pancreas photo

A
70
Q

Pancreatic Cells

A

Composed of two tissue types:
1st. Acinar Cells
- Make up 98% of the glands weight and secrete digestive fluids into duodenum (exocrine function)

2nd. Islets of Langerhans
- Make up 2% of glands weight and compose of alpha,beta, delta, and pancreatic peptide (PP) cells (endocrine function)

71
Q

Islets of Langerhans

A
  1. PP cells secrete pancreatic polypeptide whichinhibits exocrine secretions
  2. Delta cells secrete somatostatin which restrains the ratein which nutrients are absorbed (10%)
  3. Alpha cellssecrete glucagon which raises bloodsugar (25%)
  4. Beta cells secrete insulin and amylin. Insulin regulates fat and carbohydrate metabolism and causes the cell to take up glucose (70%)
72
Q

Pancreatic polypeptide (PP)

A

Inhibits pancreatic exocrine secretion, gallbladder contraction, gastric acid secretion, and gastric motility

73
Q

Somatostatin

A
  • Growth-hormone-inhibiting-hormone
  • Released by the delta cells
  • Inhibits insulin and glucagon
  • Inhibits splenic blood flow, gastric motility and gallbladder contraction
74
Q

Glucagon

A
  • A catabolic hormone that promotes energy release from adipose and the liver
  • A physiologic antagonist to insulin
  • Released between meals (BG < 90 mg/dL), glucagon concentration increases to maintain fuel production
  • Exogenous glucagon administration
  • Increases myocardial contraction, HR, and AV conduction
  • Useful in BB overdose, CHF, Low CO after MI, relaxing sphincter during ERCP, and hypoglcemia
  • Side effect N/V
75
Q

Insulin

A
  • An anabolic hormone that promotes energy storage
  • Elimination ½ life of 7 minutes
  • Increases glucose permeability in skeletal muscle, liver, and fat
  • Converts carbohydrates to glycogen in the liver and skeletal muscle
  • Converts excess carbohydrates to fat
  • Promote cellular uptake of amino acids, potassium, magnesium and phosphate
76
Q

Normal insulin secretion

A

1 unit per hour into portal circulation

After a meal insulin increases 5-10 fold

Total is 40u per day

77
Q

factors that influence insulin release

A
78
Q

Type 1 DM

A

5 – 10% of people with diabetes have Type 1
And absolute deficiency in insulin
Entirely dependent on exogenous insulin
Insulin dependent diabetics
Autoimmune destruction of the beta cells of the pancreatic islets

79
Q

Type 2 DM

A

90% of people with diabetes have Type 2
Impaired insulin secretion peripheral insulin resistance and excess hepatic glucose production
Relative to BG, an insulin deficiency exists
May be complicated by nonketotic hyperosmolar, hyperglycemic state
Treatment includes hypoglycemic agent, exercise and diet therapy
Insulin-treated diabetics

80
Q

Chronic complications from DM

A

Microvascular:
- Retinopathy
- Neuropathy
- Nephropathy

Macrovascular:
- Coronary artery disease
- Peripheral vascular disease
- Cerebrovascular disease

Other:
- Infections
- Cataracts
- Stiff Joint Syndrome
- Glaucoma
- Poor wound healing

81
Q

Rapid-acting Insulin*

A

Onset: 5 to 15 minutes
Peak: 45-75 minutes
Duration: 2 to 4 hours
Lispro (Humalog) Aspart (Novolog) Glulisine (Apidra)

82
Q

Short-acting insulin*

A

Onset: 30 min
Peak: 2 - 4 hours
DOA: 6 - 8 hours
Regular (Human Regular) (Novulin Regular)

83
Q

Intermediate-acting insulin

A

Onset: 2 hours
Peak: 4-12 hours
DOA: 18-28 hours
NPH (Humulin NPH) (Novolin NPH)

84
Q

Long acting insulin

A

Glargine (Lantus)
Onset: 1.5 hour
Peak: NONE
DOA: 20-24 hours

Detemir:
Onset: 2 hours
Peak: 5-9 hr
DOA: 6 - 24 hours

85
Q

Long acting insulin

A

Glargine (Lantus)
Onset: 1.5 hour
Peak: NONE
DOA: 20-24 hours

Detemir:
Onset: 2 hours
Peak: 5-9 hr
DOA: 6 - 24 hours

86
Q

Ultra-long acting insulin

A

Degludec
Onset: 2 hours
Peak: none
DOA: 40+ hours

87
Q

Risks of insulin therapy

A

Hypoglycemia
Allergic Reaction
Lipodystrophy
Insulin Resistance
Drug Interactions

88
Q

hypoglycemia

A

High risk if exogenous insulin given during fasting
Under GA sign and symptoms are masked SNS stimulation increases HR, BP and the presence of diaphoresis
Possible cause of delayed emergence
Brain requires glucose: confusion, seizures coma, brain damage and death
Treat with D50 50-100ml or glucagon

89
Q

allergic reaction

A

More common when animal derived products were used
Chronic NPH use (or fish allergy) may sensitize to protamine
Use caution with large doses

90
Q

risks w/ insulin

A
  • Lipodystrophy: Fat accumulation at injection site
  • Resistance: When dose exceeds 100u/day antibodies develop to the cell receptor
  • Drug Interactions: Drugs that counter the hypoglycemic effects of insulin: Epinephrine, glucagon, estrogen, and adrenocorticotropic hormone or enhance the hypoglycemic effect

Drug Interactions:
- Drugs that counter the hypoglycemic effects of insulin: Epinephrine, glucagon, estrogen, and adrenocorticotropic hormone
- Drugs that enhance the hypoglycemic effect: MAO inhibitors, salicylates, and tetracycline

91
Q

Oral Hypoglycemic Med List

A

Biguanides
Sulfonyureas
Meglitinides
Thiazolidinediones
Alpha-Glucosidase Inhibitors
Glucagon-like Peptide-1 receptor Agonist
Dipeptidyl-Peptidase-4 Inhibitors
Amylin Agonist

92
Q

Biguanides

A

Metformin

Inhibits gluconeogenesis and glycogenolysis in the liver and decreases peripheral insulin resistance.

Does not cause hypoglycemia

Risk of lactic acidosis, increases with renal and liver disease

Discontinue 48 hrs. before surgery

93
Q

Biguanides

A

Metformin

Inhibits gluconeogenesis and glycogenolysis in the liver and decreases peripheral insulin resistance.

Does not cause hypoglycemia

Risk of lactic acidosis, increases with renal and liver disease

Discontinue 48 hrs. before surgery

94
Q

Sulfonylureas

A

Glyburide, Glipizide, Glimepride
Stimulate insulin secretion from pancreatic beta cells
Avoid if sulfa allergy
Sulfonylureas usually the initial choice for treatment of type II diabetes
Hypoglycemia most common side effect
Closes K (ATP) channels, inhibits myocardial preconditioning, increases morbidity in high risk patients

95
Q

Meglitinides

A

Repaglinide, Nateglinide
Stimulate insulin secretion from pancreatic beta cells
Risk of hypoglycemia

96
Q

Thiazolidinediones

A

Rosiglitazone and Pioglitazone

Decrease peripheral insulin resistance and increase hepatic glucose utilization

Does not cause hypoglycemia

Contraindicated in liver failure, expand ECF causes edema and increase risk of CHF

97
Q

Thiazolidinediones

A

Rosiglitazone and Pioglitazone

Decrease peripheral insulin resistance and increase hepatic glucose utilization

Does not cause hypoglycemia

Contraindicated in liver failure, expand ECF causes edema and increase risk of CHF

98
Q

Alpha Glucosidase Inhibitors

A

Acarbose and Migitol

Active in the small intestine and result in a delay in glucose absorption. Should be given before a meal.

Does not cause hypoglycemia

98
Q

Alpha Glucosidase Inhibitors

A

Acarbose and Migitol

Active in the small intestine and result in a delay in glucose absorption. Should be given before a meal.

Does not cause hypoglycemia

99
Q

Glucagon-like Peptide Receptor Agonist

A

Exenatide,Liraglutide
Increases insulin release from beta cells decreases glucagon release from alpha cells and prolongs gastric emptying
Risk of hypoglycemia

100
Q

Dipeptidyl-Peptiddase-4 Inhibitors

A

Meds end in suffix-liptin
Increases insulin release
Decreases glucagon release
Risk of hypoglycemia

101
Q

Amylin Agonist

A

Pramlintide
Inhibits glucagon release from alpha cells and reduces gastric emptying
Risk of hypoglycemia when used with insulin, may cause nausea and vomiting

102
Q

DM Tx goals

A

Fasting and pre-prandial plasma glucose 70-130 mg/dl
Peak post prandial <180 mg/dl
Glycosylated Hemoglobin (HbA1c) < 7%

103
Q

DM Deficiency of Insulin Activity

A

Decreased insulin secretion
Decreased response to insulin by target tissue
Increase in the counterregulatory hormones that oppose the effects of insulin
- Resistin
- Adiponectin
Primary cause of Type 1 DM
- T lymphocytic mediated destruction of beta cells of pancreatic islet

104
Q

DM 1 vs. 2 chart*

A
105
Q

Ketone formation graphic

A
106
Q

Diabetic Ketoacidosis

A

Lack of effective insulin
- Initial manifestation of DM
- Treatment errors
- Critical illnesses (MI, trauma, burns….)
- Infections
Increased serum glucose
- Increased hepatic glucose output & Decreased glucose uptake
Clinical hallmarks
- Metabolic acidosis - Dehydration - Electrolyte abnormalities

107
Q

Diabetic ketoacidosis - pathophys

A

Pathophysiology
Osmotic diuresis and a hyperosmolar state
Ketosis and acidosis
Low insulin levels = markedly increased glucagon levels - unchecked lipolysis = fatty acids are converted to ketone bodies
Acetoacetate and beta hydroxybutyrate cause metabolic acidosis

108
Q

Diabetic Ketoacidosis S&S

A

Polyuria
Polydipsia
Anorexia/Nausea/vomiting
Abdominal pain
Weakness & myalgias
Headache
Hypothermia
Kussmaul’s respirations
- Metabolic acidosis
- pH < 7.0 and/or [HCO3-] < 12 mEq/L
Acetone breath
Intravascular volume depletion
Hypo-reflexia
Altered mental status

109
Q

DKA labs initally

A

Glucose (300-800 mg/dl)
Ketones
HCO3- (0-15 mEq/L)
pH (6.80-7.30)
Na+ (total body depletion)
K+ (total body depletion)
Creatinine/BUN (slightly elevated BUN, Cr false increase)
Hemoconcentration
Leukocytosis
Hyperuricemia
Elevated lactate

110
Q

DKA Caveats

A

Diagnosis of DKA cannot be made without the presence of ketones
Glucose concentration is not a good index of the severity of metabolic derangement
Initially give NS to restore intravascular volume regardless of Na+ or K+ values
Phosphaturia accompanies all forms of metabolic acidosis

111
Q

DKA Tx

A

Replete volume
Treat hyperglycemia
Correct hyperosmolality
Reverse ketonemia
Reverse acidemia
Correct K+ depletion

112
Q

DKA fluid resusitation

A

Fluid resuscitation
NS 2-3 liters over first 2 hours
Thereafter - 1/2NS at high flow rates
Avoid LR
When BS approaches 250 mg/dl add D5W
Discontinue IV fluids when diet is tolerated and anion gap acidosis resolved

113
Q

DKA and K+

A

Profoundly depleted regardless of initial K+
Serum K+  by 0.6 mEq/L for ea 0.1  in pH below 7.40
20-30 mEq/hr is initiated
Observe for adequate UOP
Hypokalemia
- Rehydration
- Insulin therapy
- Correction of acidosis

114
Q

DKA & insulin replacement

A

IV bolus of regular insulin at 0.1u/kg
Regular insulin IV infusion at 0.1u/kg/hour
SC regular insulin 2 hours prior to discontinuation of insulin infusion
NaHCO3 - cardiovascular instability or altered mental status with pH < 7.0

115
Q

DKA & insulin replacement

A

IV bolus of regular insulin at 0.1u/kg
Regular insulin IV infusion at 0.1u/kg/hour
SC regular insulin 2 hours prior to discontinuation of insulin infusion
NaHCO3 - cardiovascular instability or altered mental status with pH < 7.0

116
Q

DKA complications

A

5% mortality
Infection
Arterial thrombosis
Shock
Lactic acidosis
Hyperchloremic acidosis
Cerebral edema
- H/A, papilledema & altered mental status
Hypokalemia
Hypophosphatemia (potassium phosphate)

117
Q

Hyperglycemic Hyperoslmar State (HHS)

A

Severe hyperglycemia > 800 mg/dl
Severe hyperosmolality > 350 mOsm/L
Profound intravascular volume depletion
- More severe than DKA
- 10-20% of total body wt.
Absence of ketoacidosis
Impaired renal function
Mental status changes

Patient profile:
- Elderly
- Mild, type II diabetes
- Symptomatic polyuria
- Loss of ability to ingest or retain fluids as a result of illness, drugs or injury

118
Q

DKA vs. HHS chart

A
119
Q

Preop considerations

A

Metabolic Aberrations
End – Organ complications
Peripheral neuropathies & Stiff joints
Renal disease
ANS dysfunction – delayed gastric emptying
BG – ketones – electrolytes – BUN – creatinine – UA - ECG

120
Q

DM autonomic neuropathy

A

Painless myocardial ischemia
Orthostatic hypotension
Lack of heart rate variability (fixed tachycardia)
Reduced HR response to atropine and beta blockers
Neurogenic bladder
Lack of sweating
Impotence
Gastroparesis

121
Q

DM & airway

A

Glycosylation of joints– stiff joint syndrome with reduced ROM of AO joints
The prayer sigh suggests joint glycosylation and increases the risk of difficult intubation

122
Q

Prayer Sign

A

A + prayer sign can be elicited on exam w/ the patient unable to approximate the palmar surfaces of the phalangeal joints while pressing their hands together.

demonstrates a cervical spine immobility and the potential for difficult intubation

123
Q

flowchart for DM

A
124
Q

prep and monitoring flow chart

A
125
Q

choose anesthetic technique

A
126
Q

Dose Ketamine based on _______

A

AdjBW

127
Q

Dose Lidocaine bolus and infusion based on _____

A

AdjBW

128
Q

Dose steroidal neurmoscular blocking agents based on _____

A

Depends. If you do IBW, you’ll get adequate intubating conditions and faster recovery but shorter duration. If you use TBW, you’ll get faster onset but longer duration. (well fucking DUH is this answer for real)

129
Q

Dose succinylcholine based on ___

A

TBW

130
Q

Dose reversal agents like Sugammadex and Neostigmine based on ___

A

AdjBW

Concepts 3 (12 decks)

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