Endocrine Flashcards
Insulin dosing the the evening before and AM of surgery
oral hypoglycemic agents?
1/2 am dose NPH or regular insulin
work by releasing endogenous insulin, half life 24 hrs, continue until day bf surgery, check glucose levels

Physiolgical effects of DM head to toe.
Neuro: peripheral neuropathy, retiniopathy
Cards: autonomic neuropathy: silent MI, resting tachycardia, lack HR varibility w respirations, orthostasis, insensitivity to atropine and propranolol, lack HR response to hypovolemia, impaired vasoconstriction (susceptible to hypothermia), lack sweating, impotence
CAD, HTN, cardiomyopathy, PVD, MI
Resp: difficult intubation stiff join syndrome (TMJ, AO, cervical spine-prayer sign)
GI: gastroparesis (early satiety)
renal: nephropathy
endocrine: hyper/hypoglycemia, DKA, NKHC
Heme: impaired phagocytosis
Complications from TURP (transurethral resection of prostate
TURP sundrome: hyervolemia, cerebal edema, hyponatremia
hypothermia
septicemia-release of bacteria from prostate (surgically disrupted venous sinuses). abx will not prevent systemic transmission (hard to penetrate prostate gland) but may reduce progression to septicemia.
bleeding
coagulopathy (DIC from release of thromboplastins, prrimary fibrinolysis from release urokinase from metastatic prostate.
bladder perforation (N/diaphoresis, hypotension/HTN, bradycardia, abdominal/shoulder pain)
hyperglycinemia-transient blindness, cardiac depression
hyperammonia-degredation glycine, delayed arousal
hyperglycemia (excess sorbitol or dextrose broken down into glucose)
position injury: common peroneal, sciatic, femoral, LFCN
What is TURP syndrome , sx, tx
How much fluid abs, and what determines how much?
- constellation of sx and signs from excess absorption on irrigation fluid (hypervolemia and hyponatremia)
- sx:
H/A, restlessness, agitation/confusion, AMS, seizures
signs: decrease return of irrigation solution from bladder
dyspnea,
arrythmias, hypotension
tx: terminate surgery, lasix
seziure: hypertonic saline no faster than 100cc/hr; midaz, diazpam, phenytoin
- depends on size of gland, height of irrigation fluid, length of procedure
What level of spinal for TURP and why?
why do neuraxial
T10 allows detection of bladder perforation
early detection of TURP syndrome, bladder perforation, MI
Ideal TURP solution (Nite)
solutions used
- nonhemolytic/ isotonic: hypotonic solutions result in hemolysis
- electrically inert: cetain solutions can interfere w electrocautery and diserpse current (NACL, water) –>burn
- transparent for surgical visualizaton
- nontoxic,, min metabolism, rapid elim-due to toxicity with significant absorption
- cheap-larger volume used
Currently used: ***solutions: glycine, mannitol, sorbitol, dextrose, urea (all hypoosmolar), LR
What level of hyponatremia does sx develop
EKG changes?
sx
110-120meq/L AMS, cerebal edema,
100meq/L LOC and seizures
widened QRS, PVC, impaired contractility
sx: lethargy, H/A, confusion, irritable, restless, , muscle weakkness, anorexia, N/V
ddx for restless pt during TURP
pain: spinal wearing off, MI, bladder perforation
anxiety
TURP syndrome
hypoxia hypercarbia
hypothermia
septiemia
How to treat coaulopathy during TURP
order: CBC, plt, PT/PTT, fibrinogen, Fibrin split products, D-dimer
primary fibrinolysis: fibrinogen (cryo), antifibrinolytic
DIC: supportive, blood products
What is diabetes
impairment of carbohydrate metabolism due to def of insulin or resistance to its effect.
fasting >140mg/dL or postprandial >200
Physiologic role of insulin?
What are the counterregulatory hormones
Glucose: stimulates glucose entry into cells, increases glycogensis
Fat: increases synthesis and storage of TG, inhibits lipolysis
protein: increases protein synthesis
- GH, glucagon, epi, cortisol: catabolic-glucogenolysis, lipolysis, gluconeogensis
Types of Dm
Insulin dependent: autoimmune cause, ketone prone
NIDDM- non insulin dependent, do not usually develope ketosis
What is DKA and how is it dx and tx
vs NKHC (non ketotic hyperosmolar coma)
DKA: life threatening result of insulin def-
hyperglycemia, ketosis, osmotic diuresis, dehdration, anion gap met acidosis (12+-4)
tx: hydration, insulin ggt, D5W when glucose at 250 (reduce 75-100mg/dL too fast can result in cerebral edema), potassium phosphate & mag when UOP resumes, bicarb if pH<7.0 myocardial depression or not responding to treatment
(hydrate, tx glucose, and electrolytes), watch for cerebral edema
NKHC
enough insulin to prevent ketosis but not enough to prevent hyperglycemia and dehydration
glucose>1000mg/dL, no ketosis, less metabolic acidosis, more hyperosmolarity
How long does regular and NPH insulin take to work, peak, duration?
Regular 1hr, 2-3 hr, 6-8 hr
NPH 2hr, 10, 24
perioperative benefits of tights glucose control, disadvantage?
decreased worsening neuro outcomes under ischemic conditions, limit osmotic diuresis, impair wound healing and predisposition to infection.
-risk: hypoglyemia
daily cortisol production?
how much cortisol produced w surgical stress?
How does cortisol affect CV system?
20 mg/day; 75-150mg/day’
plays important role in catecholamine production, regulation of B receptors thus affecting cardiac contractility and vascular tone
steriod regimens
- 100mg preop, followed by 100mg q8h on day of surgery
- minor: 25mg
moderate: 75mg preop, 50mg intraop, 20mg q8h on first day, return to normal dose on day 2
severe: 100mg preop, 50mg intrap, 25mg q8 hr for 2 days, return to normal day 3
Risk of periop steriod supplementation
impaired wound healing/infection
HTN fluid retention
hypergycemia
PHEO
signs:
dx
preop optimization
methylparatryosine use
why get a starting Hct
- HTN, palpitations, H/A sweating, pallor, flushing, n/V, orthostatic hypotension (2/2 excessive catecholamine secretion, stroke, CHF, sugar intolerance, RF
- based on presence of metabolites of excessive catecholamines: measurement of free metanephrine in plasma and urine, clonidine supression test (does not lower catecholamine level in pheo
- alpha blockage (phenoxybenzamine) unclear how lonr prior abour 10-14 days (stabilize BP and normalize intravascular volume-elevated Hct suggest intravascular depletion), some stop 1-2 days before to avoid hypotension w removal of tumor BB if HR>120-
- alpha methyl trysosine inhibits rate limiting enzyme in cathecholamine synthesis pathway. limited to pts w metastatic dz or requiring long term therapy (surgery contraindicated)
signs of addisionian crisis
fever, AMS
dehydration, circulatory collapse
abdominal pain, N/V
hypoglycemia, acidosis, hyperkalemia, hyponatremia,
What drug to a avoid w pheo
- succ: fasciulations stimulate catecholamine release, glucagone
- histamine releasing drugs: morphine, meperidine
- drugs that increase sympathetic activty: atropine, pancuronium, ketamine, ephedrine (exacerbate hypertension and arrythmia
- dopamine blocking agents: metochlorpromide, droperidol, haldol (similar structure to droperidol), compazine
HTN during pheo resection: what do you do
- alert surgeon and ask them to cease manipulation
- ensure adewuate, O/V normocapnia, SR, and dept of anesthesia
- if HTN persisted treat w: SNP, NO, esmolol, labetolol
magnesium (inhibits catecholamine release from adrenal medulla and peripheral nerve terminals
nicardipine-selective action on arterial reistance w no drop in prelload desireable for pts w cardiac dz
try to use short acting drugs as hypotension often results w tumor ligation
ddx of residual HTN after pheo removal
- residual pheo
- plasma catecholamines can remain elevated for days resulting in sustained hypertension in 50% (less concencerning if its sustained (vs paroxsymal) and less severe than before removal)
essential HTN
how does exogenous steriods lead to addisonian crisis in perioperative period
normal amount/day/surgical stress
exogenous steriods lead to suppression of HPA axis resulting in inability of adrenals to produce adequate amount of cortisol under stress
affects B recpetor responsiveness, vascular tone and permeability
20mg/day 100mg/day