7. Coex Exam 2 Flashcards
T1DM is what % of all DM
5-10%
Type 1a
T-cell mediated
autoimmune destruction of beta cells
Type 1b
absolute insulin deficiency
not immune mediated
T2D
insensitivity of insulin in peripheral tissues
beta cell insufficiency
3 defects in T2D
- incr rate of hepatic glu release
- impaired basal/stimulated insulin secretion
- insulin resistance
normal serum glu
70-100 mg/dL
normal Hgb A1C
4-6%
intraop glu goals
80-180 mg/dL
1 unit of insulin lowers glu
30 mg/dL
50 ml of D50 raises glu
100 mg/dL
insulin prior to surgery
continue basal rates
supplement with short acting boluses
metformin prior to surgery
STOP day of surgery
SGLT2 inhibitors prior to surgery
STOP 3-4 days prior
oral glu lowering agents prior to surgery
STOP day of surgery
periop glu monitoring in diabetic pts should occur every
2-4 hours
biguanides
metformin
biguanides indication
first line therapy for T2D
biguanide mech
suppress hepatic glu release
incr glu use by muscle/adiopse
biguanide SE
lactic acidosis
GLP1 agonists
semaglutide
GLP1 mech
stimulated glu-dependent insulin secretion from beta cells
slows gastric emptying
inhibits post-meal glucagon release
GLP1 SE
delayed gastric emptying
acute pancreatitis
acute renal failure/insufficiency
GLP1 should be held ______ before surgery
weekly GLP1 dose should be held 1 week prior to surgery
DPP4 inhibitor
sitagliptin
DPP4 inhibitor mechanism
DPP4 deactivated peptides
DPP4 SE
delayed gastric emptying
secretagogues
glyburide
repaglinide
secretagogues mech
incr insulin availability
secretagogues only work on what pts?
pt with beta cell function
secretagogues SE
hypoglycemia
SGLT2
canagliflozin
SGLT2 mech
decr blood glu by incr urinary glu excretionS
SGLT2 SE
osmotic diuresis
hypovolemia
AKI
insulin indication
1st line treatment for T1D
basal insulin
suppress hepatic glu production
bolus insulin
controls glu peaks
given before meals
insulin most dangerous SE
hypoglycemia < 50 mg/dL
hypoglycemia symptoms
sweating
tachycardia
palpitations
pallor
fatigue
confusion
convulsions
treat hypoglycemia
25g of D50w
cushing’s syndrome
hypercortisolism
cushing’s syndrome is associated with
hypernatremia
hypokalemia
hyperglycemia
metabolic alkalosis
hypercortisolism: ACTH dependent
innappropriately high ACTH stimulate adrenal cortex to incr cortisol
treat ACTH depended hypercortisolism
transsphenoidal dissection or irradiation of the anterior pituitary
Cushing’s
pituitary tumor excessively stimulates ACTH
treat cushing’s
transphenoidal resection of microadenoma
ACTH independet hypercortisolism
excessive production of cortisol secondary to abnormal adrenocortical tissue
ACTH independent regulation
not regulated by secretion of CRH or ACTH
ACTH independent treatment
adrenalectomy
conn’s syndrome
primary hyperaldosteronism
conn’s is associated with
hypernatremia
hypokalemia
metabolic alkalosis
hypoaldosteronism SE
hyponatreamia
hyperkalemia
possible dehydration
possible metabolic acidosis
hyperthyroid
graves
toxic multinodular goiter
toxic adenoma
grave’s
autoimmune
hypersecretion of T4 and T3
grave’s SE
opthalmopathy
toxic multinodular goiter
extreme thyroid enlargement
toxic multinodular goiter SE
dysphagia
stridor
toxic adenoma
benign lesions
toxic adenoma pts are at an incr risk of
iodine deficiency
hyperthyroid treatment
PTU
beta blockers
iodine
hypothyroid diseases
hashimoto’s
primary hypothyroidism
pituitary dysfunction
myxedema coma
hashimotos
autoimmue
w/goiter enlargement
primary hypothyroid
basal TSH are elevated
pituitary dysfunction
bluted/absent responses to TRH
myxedema coma
impaired thermoregulation caused by defective hypothalamus
myxedema coma SE
delerium
hypoventilation
hypothermia
brady
hypotension
hyponatremia
hypothyroid treatment
IV L-thyroxine
or L-triiodothyonine
hyperparathyroid
benign parathyroid adenoma
results in excessive secretion of parathyroid
hyperparathyroid s+s
hypercalcemia
sk muscle weakness
decr GFR
anemia
prolonged PR
short QT
HTN
sk demineralization
hyperparathyroid treatment
saline
loop diuretics
disodium etidronate
+/- dialysis
hyperparathyroid surgery complications
hypocalcemic tetany
hyperchloremic metabolic acidosis
secondary hyperparathyroidism
compensatory response of parathyroid in disease that produce hypocalcemia
secondary hyperparathyroid is rare because
it is adaptive not autonomous
ectopic hyperparathyroidsm
secretion of parathyroid hormone by tissues other than parathyroid
hypoparathryoid
secretion of PTH is absent or deficieny
peripheral tissues are resistant to PTH
hypoparathyroid can be caused by
accidental removal of parathyroid during thyroidectomy
hypoparathyroid serum Ca
< 4.5
hypoparathyroid ionized ca
< 2
hypoparathyroid acute S+S
parestehsias
restlessness
neuromuscular irritability
hyperarathryoid chronic s+s
fatigue
sk muscle cramps
prolong QT
lethargy
cataracts
hypoparathyroid managemetn
prevent decr Ca
avoid hyperventilation
PTH relationship with serum ca
PTH is inversely proportional to serum Ca
PTH bone
bone breakdown
ca2+ release
PTH kidneys
incr ca2+ reabsorption
stimulates Vit D formation
PTH intestines
no direct effect
what incr ca2+ absorption in gut
vit D
what stops PTH production
incr serum ca2+ are negative feedback to stop PTH
calcitonin
hormone produced by thyroid that inhibits osteoclasts
decr serum ca2+ by incr bone ca2+
what is calcitonin indicated for
treating osteoporosis
treating hypercalcemic emergencies
Addison’s
autoimmune adrenal destruction
affects cortisol and aldosterone production
addison’s is associated with
hyponatremia
hyperkalemia
dehydration
met acidosis
hypoglycemia
secondary adrenal insufficiency
glucocorticoid deficiency due to decr ACTH
normal aldosterone
aldosterone in secondary adrenal insufficiency
normal
secondary adrenal insufficeincy SE
hypoglycemia
hypokalemia
< 3.5 mEq/L
treat hypokalemia
potassium chloride < 20 mEq/hr peripheral
hyperkalemia
> 5.5 mEq/L
treat hyperkalemia
CaCl
IV insulin + glucose
albuterol
hypocalcemia
< 8.8 mg/dL
treat hypocalcemia
10 mL of 10% CaGlu
10 mL of 10% CaCl
hypercalcemia
> 12 mg/dL
hypercalemia treat
fluid
parathyroidectomy
calcitonin (4 u/kg)
thyroid storm s+s
hyperpyrexia
tachycardia
hypermetabolism
thyroid storm treat
IV fluids
cooling
beta blockers
decadron
PTU
iodine
adrenal cortex zones
glomerulosa
fasciculata
reticularis
zona glomerulosa
mineralcoricoids
(aldosterone)
zona fasciculata
glucocorticoids
(cortisol)
zona reticularis
androgens
what produces catecholamines
adrenal medulla
pheochromocytoma
catecholamine-secreting tumor
typical NE
which drug should you give first for pheos
alpha blockade
- phenoxybenzamine
- prazosin
phenoxybenzamine
non-competitive a1 antag with some a2
when should you stop phenoxybenxamine
24-48 hrs prior to surgery
prazosin
competitive a1 blocker
prazosin advantage
less tachycardia
what should you give for BP control in HTN for pheo pts
nipride
cleviprex
NTG
when do catecholamine levels return to level in pheo post-op
7-10 days post-op
what is the most frequent cause of death in pheo pts
hTN post-op
SIADH
incr ADH
SIADH SE
hyponatremia
decr serum osm
incr urine Na+
incr urine osm
treat SIADH
restrict fluids
demeclocycline
hypertonic saline (0.5 mEq/L/hr)
diabetes insipidus
decr ADH
diabetes insipidus SE
hypovolemia
high volume of low concentrated urine
normal-high Na+
neurogenic DI causes
trauma
neurosurgery
tuymors
idipathic destruction of hypothalamus
neurogenic DI treatment
DDAVP
nephrogenic DI
hereditary
lithium tox
hypercalcemia
hypokalemia
CKD
nephrogenic DI treat
thiazide
chloropropamide
acromegaly
incr GH
acromegaly SE
difficult airway
narrow glottic opening
longer mandible = longer blade
possible poor collateral flow through ulnar
why do obese pts have incr DVT risk?
polycythemia
incr abdomial pressure
incr fibrinogen
incr tPA causing decr fibrinolysis
immobile
does obesity incr risk for delayed gastric emptying?
no
does obesity incr risk for GERD?
no
obesity hypoventilation syndrome AKA
pickwikian
obesity hypoventilation syndrome
obestity
daytime hypercapnia
OSA
why do obese pts have systemic HTN?
hyperinsulinemia incr NE
RAAS activation
BMI =
BMI = weight / (height^2)
overweight BMI
25-30
obese BMI
> 30
android
abdominal fat
gynoid
peripheral fat
which type of fat leads to more metabolic distrubance?
android (abdominal fat)
what does waist to hip ratio predict?
CAD
stroke
DM
male waist-to-hip
< 1.0
female waist-to-hip
< 0.8
GLP-1 daily dose should be help
day of procedure
GLP-1 weekly dose should be held
1 week prior to procedure
options if pt did not hold GLP-1
consider gastric ultrasound
treat as full stomach
which drugs have a different volume of distribution in obese pts?
highly lipophilic drug has incr Vd
lipophilic drugs should be dosed based on
total body weight
liophilic drug DOA
may be longer
LBW =
1.3*IBW
which drug may be able to treat roc-induced anaphylaxis
sugammadex
does propofol cause allergic rxn in pts
rarely - even with soy and egg allergies
NSAIDs can have a _____ reaction
psuedoallergenic reaction
pts with what triad of symptoms are at higher risk for NSAID reaction
asthma
hyperpastic sinusitis
nasal polyps
latex allergy is _______ mediated
IgE - mediated
which pts are at higher risk for latex allergies
spina bifida
tropical fruits
healthcare workers
what pts are more likely to react to protamine?
seafood allergies
diabetics w/NPH insulin
post-vasectomy pts
protamine SE
direct histamine release
bronchoconstriction
pulm HTN
which opioids have a direct histamine response
morphine
codeine
meperidine
are opiate histamine responses immune mediated
no
which opioid cannot degranulate mast cells
fentanyl
does penicillin allergy correlated with cephalosporin allergy
no
vancomycin reaction
non-igE mediated direct histamine release
which local anesthetics are more likely to cause an allergic reaction
esters»_space; amides
what causes rxn in local anesthetics
ester breakdown releases PABA
or
preservatives
which drug category is the most common allergic reaction?
neuromuscular blockers
- roc
- sux
2 types of angioedema
- mast cell mediated
- serpin deficiency/dysfunction
mast cell mediated angioedema mech
histamine release
mast-cell mediated angioedema treatment
epi
antihistamines
glucocorticoids
serpin deficiency angioedema mech
bradykinin incr vascular permeability
serpin deficiency angioedema treatment
C1 inhibitor concentrate
bradykinin receptor antagonist
anaphylaxis pt positioning
supine
elevate lower extremities
anaphylaxis treatment
IV crystalloid
Epi
consider:
vasopressin
glucagon
MB
ECMO
antihistamines
corticosteroids
anaphylaxis crystalloid dose
10-25 mL/kg over 20 mins
anaphylaxis Epi IM dose
0.01 mg/kg
anaphylaxis Epi IV dose
0.5-1 mg bolus
0.1 mcg/kg/min infusion
anaphylactic reaction
igE dependent
requires previous exposure
anaphylactoid reaction
IgE independent
can occur on 1st exposure
acanthosis nigricans
thick dark velvet skin associated w/underlying condition
acanthosis nigricans mechanism
activation of inulin-like growth factor receptors
proliferation of keratinocytes and fibroblasts
acanthosis nigricans is associated with
DM
obesity
drugs
cancer
atopic dermatitis AKA
eczema
atopic dermatitis mechanism
type 1 hypersensitivity
IgE mediated immune response to allergen
atopic dermatitis clinical sig
protect lesions
manage asthma/sinusitis
therapuetic adjustment based on treatment
epidermolysis bullosa
hereditary disorder
blistering of skin and mucous membranes
epidermolysis bullosa mechanism
fibrils that anchor the epidermis to dermis are damaged or absent
epidermolysis bullosa is most common in
peds
epidermolysis bullosa clinical sig
protect skin
pad BP cuff
remove EKG adhesive
IV suture
gentle airway management
minimize suctioning
epidermolysis bullosa are ______ infection risk
high infection risk
epidermolysis bullosa pts might need
stress dose of steroids
pemphigus
autoimmune condistion
fluid filled lesions involving skin and mucus membranes
painful oropharynx lesions
pemphigus mechanism
autoantibodies attach desmogleins in skin and membranes causing friction lesions
pemphigus pts are typically taking
immunosuppressants
and/or
steroids
scleroderma
autoimmune
involves the skin and other tissues or organs
3 processes in scleroderma
inflammation/autoimmunity
vascular injury
fibrosis
which disorder is associated with CREST syndrome
scleroderma
CREST syndrome
Calcinosis
Raynauds
Esophageal hypomobility
Scleodactyly
Telangiectasia
scleroderma pts are often a difficult
airway
and
IV
scleroderma pts lung function
decr lung compliance
decr O2 reserve
scleroderma pts have high risk of
esophageal rupture
most common and severe form of childhood progressive myopathies
duchenne muscular dystrophy
duchenne MD symptoms
myocardial degeneration
resp muscle weakness
pulm HTN
mitral regurge
what drug can we not give duchenne MD pts
Sux - causes rhabdo and hyperkalemia
duchenne pts are a higher risk for
MH
aspiration
rheumatoid arthritis
long term autoimmune disorder affecting the joints
chronic inflammation
RA pts can have
CV manifestations
decr neck mobility
TMJ
RA pts may be taking
NSAIDS
SLE
multisystem autoimmune disease
chronic inflammation
what is produced in SLE
ANA
SLE management is dependent on
amount of organ systems involved
SLE pts may have
laryngeal nerve palsy
baseline stridor
phonation defects
achondroplasia
decr rate of endochondral ossification
short tubular bones
achondroplasia is responsible for _____% of dwarfism
70%
achondroplasia tube sizing
based on weight not age
achondroplasia intubation
midline stabilization
+/- video scope
achondroplasia pts have difficult
epidurals
prader willi
genetic defect on chromosom 15
prader willi pts have decr ability to
decr ability to cough
= incr risk of atelectasis/pneumonia
prader willi pts require lower doses of what drugs
lower doses of muscle relaxant
can you use sux with prader willi
yes
how should you dose drugs for prader willi
IBW
klippel feil
cervical vertebral fusion syndrome
short neck w/lmited mobility
klippel feil pts will have a difficult
difficult airway
osteogeneis imperfecta
autosomal dominant
impairs production of type 1 collagen
osteogenesis imperfecta treatment
biphosphonates
osteogenesis imperfecta managment
protect bones
midline stabilization
osteogenesis imperfecta pts should avoid what drug
sux
osteogenesis imperfecta pts might have
mild hyperthermia not associated with MH
most common disease affecting NMJ
myasthenia gravis
myasthenia gravis treatment
pyridostigmine (anticholinesterase)
MG pts have ________ sensitivity to NDMB
incr sensitivity to NDMB
decr dose required
MG pts have ______ sensitivity to depolarizing MB
decr sensitivity to Sux
normal intubation dose is sufficient
Myasthenic syndrome aka
eaton lambert
eaton lambert
acquired immune mediated myopathy
IgG antibodies decr Ach release
eaton lambert treatment
3, 4 DAP
eaton lambert _______ sensitivity to NDMB
incr sensitivity to NDMB
eaton lambert ________ sensitivity to deoparlizing MB
incr sensitivity to sux
CPP =
CPP = MAP - ICP
CPP < 50 mmHg
cerebral max vasodilation
CBF is dependent on
CPP
CPP > 150 mmHg
cerebral edema
CBF is proportional to
PaCO2
PaCO2 20 mmHg causes
50% decr in CBF
when is CBF affected by PAo2
below 50 mmHg
why is hypocapnia not a long term solution for intracranial HTN
pH eventually compensates
incr venous pressure will
incr CBV
incr ICP
HTN will ______ cerebral autoregulation
right shift
head trauma will _____ cerebral autoregulation
widen
intracranial tumors will ______ cerebral autoregulation
narrow
normal ICP
< 15 mmHg
when should you treat ICP
sustained incr in ICP > 20 mmHg
methods to lower ICP
elevated head 30 deg above heart
hyperventialtion
CSF drain
mannitol
hypertonic saline
loop diuretics
steroids
barbituates/propofol
surgical decompression
what EtCo2 to lower ICP
30-35 mmhg
how long will hyperventilations lower ICP
6-12 hrs
mannitol dose to lwoer ICP
0.25-0.5 g/kg over 15-30 mins
mannitol ICP duration of action
6 hrs
mannitol requires what to work
in tact BBB
mannitol is CI
brain trauma
TBI
furosemide ICP dosing
0.5-1 mg/kg
loop diuretics are ideal for what pts
pts who will not tolerate incr in IV volume
steroids for ICP are best in which pts
brain tumor pts
which tumors are more likely to bleed during resection
metastatic brain tumor
what capnia state for brain tumor resection
normocapnia
30-35 mmhg
avoid hypoventilation
induction paralytic for brain tumor resectuion
non-depolarizer
why shouldnt you use sux in brain tumor resection
transient incr in ICP
which med for HTN in brain tumor resection
esmolol
PEEP and ICP
high PEEP can change ICP
when can you use vasodilators in brain tumor resection
after craniotomy and dura opening
why is hyperglycemia bad in brain tumor pts
hyperglycemia can exacerbate neuronal injury
what is a common SE of posterior fossa craniotomy
apnea
what can cause this apnea?
hematoma formation
tension pnuemocephalis
cranial nerve injury
which surgeries have incr risk of venous air embolism
any time operative site is above the level of the heart
how much air needs to be entrained to produce symtopms
5 mL/kg
the air causes a
RVOT preventing flow
ways to detect VAE
TEE
doppler
sudden decr EtCO2
incr RA or PA pressures
sudden gasps by pt
late signs of VAE
hypotension
tachycardia
cardiac
dysrythmmias
VAE treatment
flood field w/fluid
aspirate through central line
BP support
hyperbaric therapy
LLD (right side up)
VAE pt positioning
LLD (right side Up)
how to treat VAE bronchospams
beta 2 agonists
intracerebral hemorrhage
hematoma within parenchyma
treat intracerebral hemorrhage
IV factor VII
surgical hematoma evac
BP management
subarachnoid hemorrhage
ruptured intracranial aneurysm
subarachnoid hemorrhage presents with
thunderclap headach
subarachnoid hemorrhage pts have a high risk of
vasospasm
vasospasm triad
HTN
hypervolemia
hemodilution
3 goals for intracranial aneurysm surgery
limit risk of rupture
prevent cerebral ischemia
facilitate surgical exposurre
GCS lowerst score
3
GCS coma
< 8
GCS 3-8
severe
GCS 9-12
mod
GCS 13-15
mild
TBI treatment
high MAPs > 70
low ICP
normocapnia
avoid hyperventialtion
