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Endocrine Flashcards

1
Q

Insulin dosing the the evening before and AM of surgery

oral hypoglycemic agents?

A

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

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2
Q

Physiolgical effects of DM head to toe.

A

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

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3
Q

Complications from TURP (transurethral resection of prostate

A

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

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4
Q

What is TURP syndrome , sx, tx

How much fluid abs, and what determines how much?

A
  • 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

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5
Q

What level of spinal for TURP and why?

why do neuraxial

A

T10 allows detection of bladder perforation

early detection of TURP syndrome, bladder perforation, MI

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6
Q

Ideal TURP solution (Nite)

solutions used

A
  1. nonhemolytic/ isotonic: hypotonic solutions result in hemolysis
  2. electrically inert: cetain solutions can interfere w electrocautery and diserpse current (NACL, water) –>burn
  3. transparent for surgical visualizaton
  4. nontoxic,, min metabolism, rapid elim-due to toxicity with significant absorption
  5. cheap-larger volume used

Currently used: ***solutions: glycine, mannitol, sorbitol, dextrose, urea (all hypoosmolar), LR

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7
Q

What level of hyponatremia does sx develop

EKG changes?

sx

A

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

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8
Q

ddx for restless pt during TURP

A

pain: spinal wearing off, MI, bladder perforation

anxiety

TURP syndrome

hypoxia hypercarbia

hypothermia

septiemia

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9
Q

How to treat coaulopathy during TURP

A

order: CBC, plt, PT/PTT, fibrinogen, Fibrin split products, D-dimer

primary fibrinolysis: fibrinogen (cryo), antifibrinolytic

DIC: supportive, blood products

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10
Q

What is diabetes

A

impairment of carbohydrate metabolism due to def of insulin or resistance to its effect.

fasting >140mg/dL or postprandial >200

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11
Q

Physiologic role of insulin?

What are the counterregulatory hormones

A

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

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12
Q

Types of Dm

A

Insulin dependent: autoimmune cause, ketone prone

NIDDM- non insulin dependent, do not usually develope ketosis

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13
Q

What is DKA and how is it dx and tx

vs NKHC (non ketotic hyperosmolar coma)

A

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

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14
Q

How long does regular and NPH insulin take to work, peak, duration?

A

Regular 1hr, 2-3 hr, 6-8 hr

NPH 2hr, 10, 24

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15
Q

perioperative benefits of tights glucose control, disadvantage?

A

decreased worsening neuro outcomes under ischemic conditions, limit osmotic diuresis, impair wound healing and predisposition to infection.

-risk: hypoglyemia

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16
Q

daily cortisol production?

how much cortisol produced w surgical stress?

How does cortisol affect CV system?

A

20 mg/day; 75-150mg/day’

plays important role in catecholamine production, regulation of B receptors thus affecting cardiac contractility and vascular tone

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17
Q

steriod regimens

A
  • 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
18
Q

Risk of periop steriod supplementation

A

impaired wound healing/infection

HTN fluid retention

hypergycemia

19
Q

PHEO

signs:

dx

preop optimization

methylparatryosine use

why get a starting Hct

A
  • 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)
20
Q

signs of addisionian crisis

A

fever, AMS

dehydration, circulatory collapse

abdominal pain, N/V

hypoglycemia, acidosis, hyperkalemia, hyponatremia,

21
Q

What drug to a avoid w pheo

A
  • 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
22
Q

HTN during pheo resection: what do you do

A
  • 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

23
Q

ddx of residual HTN after pheo removal

A
  • 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

24
Q

how does exogenous steriods lead to addisonian crisis in perioperative period

normal amount/day/surgical stress

A

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

25
Q

most common pit tumor

sx

A

protacinoma

galactorrhea, amenorrhea, infertility

26
Q

signs of excessive ACTH, TSH

A

truncal obesity, adbominal striae

HTN, hyperglycemia

TSH: hyperthyroidism

27
Q

effects of acromegaly

dx

tx

A
  • GH: acromegaly: IGF-1lvels, glucose tolerance test
    • Difficult mask: large lips, tongue, tonsils, epiglottis, mandible, nose (turbinates enlarged) , glottic stenosis, recurrent larngeal nerve injury, impaired cricothyroid mobility, OSA
    • , HTN , accelerated atherscosis (CAD), cardiomegaly, CHF
    • DM, hypopit (thyroid and adrenal fxn?)
    • Peripheral neuropathy (positioning),
    • Poor collateral flow in hands-place a line elsewhere
  • bromocriptine: dopamine R agonist that inhibits secretion of GH and prolactin
  • octreotide: somatostatin analog that inhibits secretion of GH
28
Q

post op stridor after thyrpiectomy

A
  • Post extubation airway obstruction/ stridor
    • Hematoma
    • Edema
    • Post intubation croup
    • Tracheolamacia
    • laryngospasmm
    • RLN injury-partial hoarseness, complete-aphonia, aspiration risk b/l partial laryngeal obstruction (abduction of VC)
    • Hypocalcemia removal of parathyroid 1-3 days later
    • Residual paralysis (MG common in hyperthyroid pts)
29
Q

substances released by carcinoid tumor

sx

A

serotonin histamine, catechoamines, bradykinin, tachykinin, VIP, prostaglandin

flushing, diarrhea, broncospasm, abdominal pain, palpitation, HTN, hypotension, HF

30
Q

anesthetic considerations for carcinoid

A

triggers: stress, anxiety, exercise, food high in serotonin (coffee, cheese, ETOH,),

keep preop anxiety and stress low during nduction/intubatio

avoid histamine releasing medications,

avoid indirect agents: B agonist, ephediri

vigilnt during tumor manipulation

31
Q

mech lithium

signs toxicity

anesthetic considerations

A
  • Mech: reduction in the release of neurotransmitters in the CNS and PNS
  • toxicity
    • Neuro: skeletal muscle weakness, ataxia, cognitive changes, seizure
    • Cards: widened QRS, AV block, hypotension
    • GI: NVD
    • Renal: polyuria (nephrogenic DI)
  • Anesthesia considerations
    • Stop night before-no withdrawl sx
    • Evaluate for signs of toxicity
    • Avoid drugs that may contribute to toxicity: NSAID, ACE inhibitors, thiazide diuretics
    • Admin sodium containing fluids to prevent excess renal abs of lithium (hyponatremia increases reabs)
    • Monitor depth of anesthesia and NMB (can reduce anesthetic requirement and prolong depolarizing and NDNB
    • Lithium level
    • Watch EKG for lithium induced dysarthmia or AV block
32
Q

hypoglyemcia after pheo removal

A

surge of insulin sensitivity 2/2 low catecholamine levels

33
Q

signs of inadeuately treated hyperthyroidism (H&P and labs(

A
  • neuro: heat intolerance, warm sweaty skin, muscle weakness, tremor, hyperactive reflexes
  • cards: tachycardia, HTN, arrhythmia
  • gi: diarrhea
  • Lab: TSH (low), Free T4 and T3 (high)

risk hemodynamic instability arrythmia, hyperdynamic circ

34
Q

what to do if pt not euthyroid: elective vs urgent/emergent case

A
  • Not euthyroid
    • Elective cancel to achieve euthyroid state (may require time due to large stores hormone in thyroid gland (PTU, Iodide, BB, steroids)
      • 6-8 weeks thiourea:
        • PTU (decrease hormone synthesis and peripheral conversion (6-8 weeks)
        • Methimazole: decrease synthesis
      • Iodide decrease synthesis and secretion, can trigger thyrotoxicosis (treat w PTU first)-1-2 weeks to work
      • BB block sympathetic activity- treat anxiety, tremor tachycardia, heat intolerance. Prevent peripheral conversion
      • Steroids: decrease secretion and peripheral conversion, esp if concern of adrenal insufficient
      • 1-2 weeks w propranolol & iodides & 6-8 weeks with PTU
    • Urgent/emergent: consult endocrine to medically optimize and procced
      • BB
      • Steroids: decreases thyroid hormone secretion and conversion T4T3
      • Adequate hydration
35
Q

How to treat thyroid storm

A
  • Thyroid storm
    • BB to control tachycardia, benzo for anxiety
    • Steroids: reduce secretion and peripheral conversion
    • PTU-inhibit synthesis and peripheral coversion
    • sodium iodide to reduce circulating hormone
    • Acetaminophen/cooling
    • IV hydration ensure adequate intravascular volume
36
Q

MH vs NMS vs thyroid storm

A
  • All get tachycardic and hyperthermic
  • MH/NMS vs thyroid storm: met acidosis, profound hypercarbia, muscle rigidity
  • NMS vs MH:
    • NMS slower progression
    • Nondepolarizing agents lead to flaccid paralysis inNMS not MH
  • Tx unclear cause
    • MH vs NMS: dantrolene help tx both syndromes
      • Intubate nontriggering agent and non depolarizing relaxant (observe if muscle rigidity gone)
      • Hyperventilate
      • Cool pt
      • Consider bromocriptine (dopamine agonist used in NMS)
37
Q

Carcinoid triad

dx

caricinoid syndrome

A

Flushing diarrhea, cardiac involvement (TR PS-serotonin induced fiborsis), broncoconstrition

urine 5-HIAA: hydroxyindoleacetic acid (breakdown product of serotonin), chromogranin A elevated

-complex sx that occur when carcinoid tumor releases excessive amounts of hormones (serotonin, histamine, bradykinin) into systemic circulation (met to liver substances bypass portal circ or occur outside the GI tract

38
Q

preop optimization for carcinoid syndrome

A

-somtaostatin analog-octreotide to decrease serotonin secretion, optimize fluid status

anxiolytic (reduce stress induced release vasoactive substances

H1 and H2 blockers to attenuate the effect of histamine,, alpha and BB blockeer to prevent catecholamine mediated release of vasoactive sustances, steriods

succ fasculations and histamine release

serotonin antagonist for nausea-zofran

avoid sympthomimic agents and those assocated with histamine release

39
Q

anesthetic considerations for hyperthyoid goiter

A
  • Exaggerated sympathetic response to surgery: maintain adequate depth
  • avoid agents that may increase sympathetic activity: epi ephedrine, ketamine, des
  • Treat hypotension with fluids and phenylephrine
  • Hypovolemia: optimize flud
  • Mass compression: rigid broncoscope, trach Kit, ENT surgeon present, armored tube (more flexible and less subjection to compression
  • No ASA: decrease protein binding and increase free T3 T4
  • min hemodyanmic instability, arrytmias, and thyroid storm
40
Q

hyperthyroid head–>toe

A

Lab: TSH (low), Free T4 and T3 (high)

Neuro: anxiety, agitation, tremors, insomnia, muscle weakness, sweating/heat intolerance, weightloss

cards: tachycardia, HTN (increased SV and CO), arrythimia, cardiomegaly, hypovolemia

GI: dirrhea

arrythmia, hyperdynamic circ, risk hemodynamic instability

AW (15 decks)

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