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Fa: Coexisting 2 > 7. Coex Exam 2 > Flashcards

7. Coex Exam 2 Flashcards

1
Q

T1DM is what % of all DM

A

5-10%

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2
Q

Type 1a

A

T-cell mediated
autoimmune destruction of beta cells

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3
Q

Type 1b

A

absolute insulin deficiency
not immune mediated

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4
Q

T2D

A

insensitivity of insulin in peripheral tissues
beta cell insufficiency

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5
Q

3 defects in T2D

A
  • incr rate of hepatic glu release
  • impaired basal/stimulated insulin secretion
  • insulin resistance
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6
Q

normal serum glu

A

70-100 mg/dL

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7
Q

normal Hgb A1C

A

4-6%

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8
Q

intraop glu goals

A

80-180 mg/dL

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9
Q

1 unit of insulin lowers glu

A

30 mg/dL

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10
Q

50 ml of D50 raises glu

A

100 mg/dL

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11
Q

insulin prior to surgery

A

continue basal rates
supplement with short acting boluses

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12
Q

metformin prior to surgery

A

STOP day of surgery

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13
Q

SGLT2 inhibitors prior to surgery

A

STOP 3-4 days prior

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14
Q

oral glu lowering agents prior to surgery

A

STOP day of surgery

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15
Q

periop glu monitoring in diabetic pts should occur every

A

2-4 hours

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16
Q

biguanides

A

metformin

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17
Q

biguanides indication

A

first line therapy for T2D

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18
Q

biguanide mech

A

suppress hepatic glu release
incr glu use by muscle/adiopse

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19
Q

biguanide SE

A

lactic acidosis

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20
Q

GLP1 agonists

A

semaglutide

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21
Q

GLP1 mech

A

stimulated glu-dependent insulin secretion from beta cells
slows gastric emptying
inhibits post-meal glucagon release

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22
Q

GLP1 SE

A

delayed gastric emptying
acute pancreatitis
acute renal failure/insufficiency

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23
Q

GLP1 should be held ______ before surgery

A

weekly GLP1 dose should be held 1 week prior to surgery

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24
Q

DPP4 inhibitor

A

sitagliptin

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25
Q

DPP4 inhibitor mechanism

A

DPP4 deactivated peptides

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26
Q

DPP4 SE

A

delayed gastric emptying

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27
Q

secretagogues

A

glyburide
repaglinide

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28
Q

secretagogues mech

A

incr insulin availability

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29
Q

secretagogues only work on what pts?

A

pt with beta cell function

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30
Q

secretagogues SE

A

hypoglycemia

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31
Q

SGLT2

A

canagliflozin

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32
Q

SGLT2 mech

A

decr blood glu by incr urinary glu excretionS

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33
Q

SGLT2 SE

A

osmotic diuresis
hypovolemia
AKI

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34
Q

insulin indication

A

1st line treatment for T1D

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35
Q

basal insulin

A

suppress hepatic glu production

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36
Q

bolus insulin

A

controls glu peaks
given before meals

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37
Q

insulin most dangerous SE

A

hypoglycemia < 50 mg/dL

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38
Q

hypoglycemia symptoms

A

sweating
tachycardia
palpitations
pallor
fatigue
confusion
convulsions

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39
Q

treat hypoglycemia

A

25g of D50w

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40
Q

cushing’s syndrome

A

hypercortisolism

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41
Q

cushing’s syndrome is associated with

A

hypernatremia
hypokalemia
hyperglycemia
metabolic alkalosis

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42
Q

hypercortisolism: ACTH dependent

A

innappropriately high ACTH stimulate adrenal cortex to incr cortisol

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42
Q

treat ACTH depended hypercortisolism

A

transsphenoidal dissection or irradiation of the anterior pituitary

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42
Q

Cushing’s

A

pituitary tumor excessively stimulates ACTH

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43
Q

treat cushing’s

A

transphenoidal resection of microadenoma

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44
Q

ACTH independet hypercortisolism

A

excessive production of cortisol secondary to abnormal adrenocortical tissue

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45
Q

ACTH independent regulation

A

not regulated by secretion of CRH or ACTH

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46
Q

ACTH independent treatment

A

adrenalectomy

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47
Q

conn’s syndrome

A

primary hyperaldosteronism

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48
Q

conn’s is associated with

A

hypernatremia
hypokalemia
metabolic alkalosis

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49
Q

hypoaldosteronism SE

A

hyponatreamia
hyperkalemia
possible dehydration
possible metabolic acidosis

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50
Q

hyperthyroid

A

graves
toxic multinodular goiter
toxic adenoma

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51
Q

grave’s

A

autoimmune
hypersecretion of T4 and T3

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52
Q

grave’s SE

A

opthalmopathy

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53
Q

toxic multinodular goiter

A

extreme thyroid enlargement

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54
Q

toxic multinodular goiter SE

A

dysphagia
stridor

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55
Q

toxic adenoma

A

benign lesions

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56
Q

toxic adenoma pts are at an incr risk of

A

iodine deficiency

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57
Q

hyperthyroid treatment

A

PTU
beta blockers
iodine

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58
Q

hypothyroid diseases

A

hashimoto’s
primary hypothyroidism
pituitary dysfunction
myxedema coma

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59
Q

hashimotos

A

autoimmue
w/goiter enlargement

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60
Q

primary hypothyroid

A

basal TSH are elevated

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61
Q

pituitary dysfunction

A

bluted/absent responses to TRH

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62
Q

myxedema coma

A

impaired thermoregulation caused by defective hypothalamus

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63
Q

myxedema coma SE

A

delerium
hypoventilation
hypothermia
brady
hypotension
hyponatremia

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64
Q

hypothyroid treatment

A

IV L-thyroxine
or L-triiodothyonine

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65
Q

hyperparathyroid

A

benign parathyroid adenoma
results in excessive secretion of parathyroid

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66
Q

hyperparathyroid s+s

A

hypercalcemia
sk muscle weakness
decr GFR
anemia
prolonged PR
short QT
HTN
sk demineralization

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67
Q

hyperparathyroid treatment

A

saline
loop diuretics
disodium etidronate
+/- dialysis

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68
Q

hyperparathyroid surgery complications

A

hypocalcemic tetany
hyperchloremic metabolic acidosis

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69
Q

secondary hyperparathyroidism

A

compensatory response of parathyroid in disease that produce hypocalcemia

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70
Q

secondary hyperparathyroid is rare because

A

it is adaptive not autonomous

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71
Q

ectopic hyperparathyroidsm

A

secretion of parathyroid hormone by tissues other than parathyroid

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72
Q

hypoparathryoid

A

secretion of PTH is absent or deficieny
peripheral tissues are resistant to PTH

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73
Q

hypoparathyroid can be caused by

A

accidental removal of parathyroid during thyroidectomy

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74
Q

hypoparathyroid serum Ca

A

< 4.5

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75
Q

hypoparathyroid ionized ca

A

< 2

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76
Q

hypoparathyroid acute S+S

A

parestehsias
restlessness
neuromuscular irritability

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77
Q

hyperarathryoid chronic s+s

A

fatigue
sk muscle cramps
prolong QT
lethargy
cataracts

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78
Q

hypoparathyroid managemetn

A

prevent decr Ca
avoid hyperventilation

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79
Q

PTH relationship with serum ca

A

PTH is inversely proportional to serum Ca

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80
Q

PTH bone

A

bone breakdown
ca2+ release

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81
Q

PTH kidneys

A

incr ca2+ reabsorption
stimulates Vit D formation

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82
Q

PTH intestines

A

no direct effect

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83
Q

what incr ca2+ absorption in gut

A

vit D

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84
Q

what stops PTH production

A

incr serum ca2+ are negative feedback to stop PTH

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85
Q

calcitonin

A

hormone produced by thyroid that inhibits osteoclasts

decr serum ca2+ by incr bone ca2+

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86
Q

what is calcitonin indicated for

A

treating osteoporosis
treating hypercalcemic emergencies

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87
Q

Addison’s

A

autoimmune adrenal destruction
affects cortisol and aldosterone production

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88
Q

addison’s is associated with

A

hyponatremia
hyperkalemia
dehydration
met acidosis
hypoglycemia

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89
Q

secondary adrenal insufficiency

A

glucocorticoid deficiency due to decr ACTH

normal aldosterone

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90
Q

aldosterone in secondary adrenal insufficiency

A

normal

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91
Q

secondary adrenal insufficeincy SE

A

hypoglycemia

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92
Q

hypokalemia

A

< 3.5 mEq/L

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93
Q

treat hypokalemia

A

potassium chloride < 20 mEq/hr peripheral

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94
Q

hyperkalemia

A

> 5.5 mEq/L

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95
Q

treat hyperkalemia

A

CaCl
IV insulin + glucose
albuterol

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96
Q

hypocalcemia

A

< 8.8 mg/dL

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97
Q

treat hypocalcemia

A

10 mL of 10% CaGlu
10 mL of 10% CaCl

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98
Q

hypercalcemia

A

> 12 mg/dL

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99
Q

hypercalemia treat

A

fluid
parathyroidectomy
calcitonin (4 u/kg)

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100
Q

thyroid storm s+s

A

hyperpyrexia
tachycardia
hypermetabolism

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101
Q

thyroid storm treat

A

IV fluids
cooling
beta blockers
decadron
PTU
iodine

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102
Q

adrenal cortex zones

A

glomerulosa
fasciculata
reticularis

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103
Q

zona glomerulosa

A

mineralcoricoids
(aldosterone)

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104
Q

zona fasciculata

A

glucocorticoids
(cortisol)

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105
Q

zona reticularis

A

androgens

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106
Q

what produces catecholamines

A

adrenal medulla

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107
Q

pheochromocytoma

A

catecholamine-secreting tumor
typical NE

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108
Q

which drug should you give first for pheos

A

alpha blockade
- phenoxybenzamine
- prazosin

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109
Q

phenoxybenzamine

A

non-competitive a1 antag with some a2

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110
Q

when should you stop phenoxybenxamine

A

24-48 hrs prior to surgery

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111
Q

prazosin

A

competitive a1 blocker

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112
Q

prazosin advantage

A

less tachycardia

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113
Q

what should you give for BP control in HTN for pheo pts

A

nipride
cleviprex
NTG

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114
Q

when do catecholamine levels return to level in pheo post-op

A

7-10 days post-op

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115
Q

what is the most frequent cause of death in pheo pts

A

hTN post-op

116
Q

SIADH

A

incr ADH

117
Q

SIADH SE

A

hyponatremia
decr serum osm
incr urine Na+
incr urine osm

118
Q

treat SIADH

A

restrict fluids
demeclocycline
hypertonic saline (0.5 mEq/L/hr)

119
Q

diabetes insipidus

A

decr ADH

120
Q

diabetes insipidus SE

A

hypovolemia
high volume of low concentrated urine
normal-high Na+

121
Q

neurogenic DI causes

A

trauma
neurosurgery
tuymors
idipathic destruction of hypothalamus

122
Q

neurogenic DI treatment

A

DDAVP

123
Q

nephrogenic DI

A

hereditary
lithium tox
hypercalcemia
hypokalemia
CKD

124
Q

nephrogenic DI treat

A

thiazide
chloropropamide

125
Q

acromegaly

A

incr GH

126
Q

acromegaly SE

A

difficult airway
narrow glottic opening
longer mandible = longer blade
possible poor collateral flow through ulnar

127
Q

why do obese pts have incr DVT risk?

A

polycythemia
incr abdomial pressure
incr fibrinogen
incr tPA causing decr fibrinolysis
immobile

128
Q

does obesity incr risk for delayed gastric emptying?

A

no

129
Q

does obesity incr risk for GERD?

A

no

130
Q

obesity hypoventilation syndrome AKA

A

pickwikian

131
Q

obesity hypoventilation syndrome

A

obestity
daytime hypercapnia
OSA

132
Q

why do obese pts have systemic HTN?

A

hyperinsulinemia incr NE
RAAS activation

133
Q

BMI =

A

BMI = weight / (height^2)

134
Q

overweight BMI

A

25-30

135
Q

obese BMI

A

> 30

136
Q

android

A

abdominal fat

137
Q

gynoid

A

peripheral fat

138
Q

which type of fat leads to more metabolic distrubance?

A

android (abdominal fat)

139
Q

what does waist to hip ratio predict?

A

CAD
stroke
DM

140
Q

male waist-to-hip

A

< 1.0

141
Q

female waist-to-hip

A

< 0.8

142
Q

GLP-1 daily dose should be help

A

day of procedure

143
Q

GLP-1 weekly dose should be held

A

1 week prior to procedure

144
Q

options if pt did not hold GLP-1

A

consider gastric ultrasound
treat as full stomach

145
Q

which drugs have a different volume of distribution in obese pts?

A

highly lipophilic drug has incr Vd

146
Q

lipophilic drugs should be dosed based on

A

total body weight

147
Q

liophilic drug DOA

A

may be longer

148
Q

LBW =

A

1.3*IBW

149
Q

which drug may be able to treat roc-induced anaphylaxis

A

sugammadex

150
Q

does propofol cause allergic rxn in pts

A

rarely - even with soy and egg allergies

151
Q

NSAIDs can have a _____ reaction

A

psuedoallergenic reaction

152
Q

pts with what triad of symptoms are at higher risk for NSAID reaction

A

asthma
hyperpastic sinusitis
nasal polyps

153
Q

latex allergy is _______ mediated

A

IgE - mediated

154
Q

which pts are at higher risk for latex allergies

A

spina bifida
tropical fruits
healthcare workers

155
Q

what pts are more likely to react to protamine?

A

seafood allergies
diabetics w/NPH insulin
post-vasectomy pts

156
Q

protamine SE

A

direct histamine release
bronchoconstriction
pulm HTN

157
Q

which opioids have a direct histamine response

A

morphine
codeine
meperidine

158
Q

are opiate histamine responses immune mediated

A

no

159
Q

which opioid cannot degranulate mast cells

A

fentanyl

160
Q

does penicillin allergy correlated with cephalosporin allergy

A

no

161
Q

vancomycin reaction

A

non-igE mediated direct histamine release

162
Q

which local anesthetics are more likely to cause an allergic reaction

A

esters&raquo_space; amides

163
Q

what causes rxn in local anesthetics

A

ester breakdown releases PABA
or
preservatives

164
Q

which drug category is the most common allergic reaction?

A

neuromuscular blockers
- roc
- sux

165
Q

2 types of angioedema

A
  1. mast cell mediated
  2. serpin deficiency/dysfunction
166
Q

mast cell mediated angioedema mech

A

histamine release

167
Q

mast-cell mediated angioedema treatment

A

epi
antihistamines
glucocorticoids

168
Q

serpin deficiency angioedema mech

A

bradykinin incr vascular permeability

169
Q

serpin deficiency angioedema treatment

A

C1 inhibitor concentrate
bradykinin receptor antagonist

170
Q

anaphylaxis pt positioning

A

supine
elevate lower extremities

171
Q

anaphylaxis treatment

A

IV crystalloid
Epi
consider:
vasopressin
glucagon
MB
ECMO
antihistamines
corticosteroids

172
Q

anaphylaxis crystalloid dose

A

10-25 mL/kg over 20 mins

173
Q

anaphylaxis Epi IM dose

A

0.01 mg/kg

174
Q

anaphylaxis Epi IV dose

A

0.5-1 mg bolus
0.1 mcg/kg/min infusion

175
Q

anaphylactic reaction

A

igE dependent
requires previous exposure

176
Q

anaphylactoid reaction

A

IgE independent
can occur on 1st exposure

177
Q

acanthosis nigricans

A

thick dark velvet skin associated w/underlying condition

178
Q

acanthosis nigricans mechanism

A

activation of inulin-like growth factor receptors
proliferation of keratinocytes and fibroblasts

179
Q

acanthosis nigricans is associated with

A

DM
obesity
drugs
cancer

180
Q

atopic dermatitis AKA

A

eczema

181
Q

atopic dermatitis mechanism

A

type 1 hypersensitivity
IgE mediated immune response to allergen

182
Q

atopic dermatitis clinical sig

A

protect lesions
manage asthma/sinusitis
therapuetic adjustment based on treatment

183
Q

epidermolysis bullosa

A

hereditary disorder
blistering of skin and mucous membranes

184
Q

epidermolysis bullosa mechanism

A

fibrils that anchor the epidermis to dermis are damaged or absent

185
Q

epidermolysis bullosa is most common in

A

peds

186
Q

epidermolysis bullosa clinical sig

A

protect skin
pad BP cuff
remove EKG adhesive
IV suture
gentle airway management
minimize suctioning

187
Q

epidermolysis bullosa are ______ infection risk

A

high infection risk

188
Q

epidermolysis bullosa pts might need

A

stress dose of steroids

189
Q

pemphigus

A

autoimmune condistion
fluid filled lesions involving skin and mucus membranes
painful oropharynx lesions

190
Q

pemphigus mechanism

A

autoantibodies attach desmogleins in skin and membranes causing friction lesions

191
Q

pemphigus pts are typically taking

A

immunosuppressants
and/or
steroids

192
Q

scleroderma

A

autoimmune
involves the skin and other tissues or organs

193
Q

3 processes in scleroderma

A

inflammation/autoimmunity
vascular injury
fibrosis

194
Q

which disorder is associated with CREST syndrome

A

scleroderma

195
Q

CREST syndrome

A

Calcinosis
Raynauds
Esophageal hypomobility
Scleodactyly
Telangiectasia

196
Q

scleroderma pts are often a difficult

A

airway
and
IV

197
Q

scleroderma pts lung function

A

decr lung compliance
decr O2 reserve

198
Q

scleroderma pts have high risk of

A

esophageal rupture

199
Q

most common and severe form of childhood progressive myopathies

A

duchenne muscular dystrophy

200
Q

duchenne MD symptoms

A

myocardial degeneration
resp muscle weakness
pulm HTN
mitral regurge

201
Q

what drug can we not give duchenne MD pts

A

Sux - causes rhabdo and hyperkalemia

202
Q

duchenne pts are a higher risk for

A

MH
aspiration

203
Q

rheumatoid arthritis

A

long term autoimmune disorder affecting the joints
chronic inflammation

204
Q

RA pts can have

A

CV manifestations
decr neck mobility
TMJ

205
Q

RA pts may be taking

A

NSAIDS

206
Q

SLE

A

multisystem autoimmune disease
chronic inflammation

207
Q

what is produced in SLE

A

ANA

208
Q

SLE management is dependent on

A

amount of organ systems involved

209
Q

SLE pts may have

A

laryngeal nerve palsy
baseline stridor
phonation defects

210
Q

achondroplasia

A

decr rate of endochondral ossification
short tubular bones

211
Q

achondroplasia is responsible for _____% of dwarfism

A

70%

212
Q

achondroplasia tube sizing

A

based on weight not age

213
Q

achondroplasia intubation

A

midline stabilization
+/- video scope

214
Q

achondroplasia pts have difficult

A

epidurals

215
Q

prader willi

A

genetic defect on chromosom 15

216
Q

prader willi pts have decr ability to

A

decr ability to cough
= incr risk of atelectasis/pneumonia

217
Q

prader willi pts require lower doses of what drugs

A

lower doses of muscle relaxant

218
Q

can you use sux with prader willi

A

yes

219
Q

how should you dose drugs for prader willi

A

IBW

220
Q

klippel feil

A

cervical vertebral fusion syndrome
short neck w/lmited mobility

221
Q

klippel feil pts will have a difficult

A

difficult airway

222
Q

osteogeneis imperfecta

A

autosomal dominant
impairs production of type 1 collagen

223
Q

osteogenesis imperfecta treatment

A

biphosphonates

224
Q

osteogenesis imperfecta managment

A

protect bones
midline stabilization

225
Q

osteogenesis imperfecta pts should avoid what drug

A

sux

226
Q

osteogenesis imperfecta pts might have

A

mild hyperthermia not associated with MH

227
Q

most common disease affecting NMJ

A

myasthenia gravis

228
Q

myasthenia gravis treatment

A

pyridostigmine (anticholinesterase)

229
Q

MG pts have ________ sensitivity to NDMB

A

incr sensitivity to NDMB
decr dose required

230
Q

MG pts have ______ sensitivity to depolarizing MB

A

decr sensitivity to Sux
normal intubation dose is sufficient

231
Q

Myasthenic syndrome aka

A

eaton lambert

232
Q

eaton lambert

A

acquired immune mediated myopathy
IgG antibodies decr Ach release

233
Q

eaton lambert treatment

A

3, 4 DAP

234
Q

eaton lambert _______ sensitivity to NDMB

A

incr sensitivity to NDMB

235
Q

eaton lambert ________ sensitivity to deoparlizing MB

A

incr sensitivity to sux

236
Q

CPP =

A

CPP = MAP - ICP

237
Q

CPP < 50 mmHg

A

cerebral max vasodilation

238
Q

CBF is dependent on

A

CPP

239
Q

CPP > 150 mmHg

A

cerebral edema

240
Q

CBF is proportional to

A

PaCO2

241
Q

PaCO2 20 mmHg causes

A

50% decr in CBF

242
Q

when is CBF affected by PAo2

A

below 50 mmHg

243
Q

why is hypocapnia not a long term solution for intracranial HTN

A

pH eventually compensates

244
Q

incr venous pressure will

A

incr CBV
incr ICP

245
Q

HTN will ______ cerebral autoregulation

A

right shift

246
Q

head trauma will _____ cerebral autoregulation

A

widen

247
Q

intracranial tumors will ______ cerebral autoregulation

A

narrow

248
Q

normal ICP

A

< 15 mmHg

249
Q

when should you treat ICP

A

sustained incr in ICP > 20 mmHg

250
Q

methods to lower ICP

A

elevated head 30 deg above heart
hyperventialtion
CSF drain
mannitol
hypertonic saline
loop diuretics
steroids
barbituates/propofol
surgical decompression

251
Q

what EtCo2 to lower ICP

A

30-35 mmhg

252
Q

how long will hyperventilations lower ICP

A

6-12 hrs

253
Q

mannitol dose to lwoer ICP

A

0.25-0.5 g/kg over 15-30 mins

254
Q

mannitol ICP duration of action

A

6 hrs

255
Q

mannitol requires what to work

A

in tact BBB

256
Q

mannitol is CI

A

brain trauma
TBI

257
Q

furosemide ICP dosing

A

0.5-1 mg/kg

258
Q

loop diuretics are ideal for what pts

A

pts who will not tolerate incr in IV volume

259
Q

steroids for ICP are best in which pts

A

brain tumor pts

260
Q

which tumors are more likely to bleed during resection

A

metastatic brain tumor

261
Q

what capnia state for brain tumor resection

A

normocapnia
30-35 mmhg
avoid hypoventilation

262
Q

induction paralytic for brain tumor resectuion

A

non-depolarizer

263
Q

why shouldnt you use sux in brain tumor resection

A

transient incr in ICP

264
Q

which med for HTN in brain tumor resection

A

esmolol

265
Q

PEEP and ICP

A

high PEEP can change ICP

266
Q

when can you use vasodilators in brain tumor resection

A

after craniotomy and dura opening

267
Q

why is hyperglycemia bad in brain tumor pts

A

hyperglycemia can exacerbate neuronal injury

268
Q

what is a common SE of posterior fossa craniotomy

A

apnea

269
Q

what can cause this apnea?

A

hematoma formation
tension pnuemocephalis
cranial nerve injury

270
Q

which surgeries have incr risk of venous air embolism

A

any time operative site is above the level of the heart

271
Q

how much air needs to be entrained to produce symtopms

A

5 mL/kg

272
Q

the air causes a

A

RVOT preventing flow

273
Q

ways to detect VAE

A

TEE
doppler
sudden decr EtCO2
incr RA or PA pressures
sudden gasps by pt

274
Q

late signs of VAE

A

hypotension
tachycardia
cardiac
dysrythmmias

275
Q

VAE treatment

A

flood field w/fluid
aspirate through central line
BP support
hyperbaric therapy
LLD (right side up)

276
Q

VAE pt positioning

A

LLD (right side Up)

277
Q

how to treat VAE bronchospams

A

beta 2 agonists

278
Q

intracerebral hemorrhage

A

hematoma within parenchyma

279
Q

treat intracerebral hemorrhage

A

IV factor VII
surgical hematoma evac
BP management

280
Q

subarachnoid hemorrhage

A

ruptured intracranial aneurysm

281
Q

subarachnoid hemorrhage presents with

A

thunderclap headach

282
Q

subarachnoid hemorrhage pts have a high risk of

A

vasospasm

283
Q

vasospasm triad

A

HTN
hypervolemia
hemodilution

284
Q

3 goals for intracranial aneurysm surgery

A

limit risk of rupture
prevent cerebral ischemia
facilitate surgical exposurre

285
Q

GCS lowerst score

A

3

286
Q

GCS coma

A

< 8

287
Q

GCS 3-8

A

severe

288
Q

GCS 9-12

A

mod

289
Q

GCS 13-15

A

mild

290
Q

TBI treatment

A

high MAPs > 70
low ICP
normocapnia
avoid hyperventialtion

Fa: Coexisting 2 (7 decks)

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