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UBP Pearls > Misc 3 > Flashcards

Misc 3 Flashcards

1
Q

Brief pathophys and systemic manifestations of RA?

A
  • vasculitis develops 2/2 deposition of immune complexes –> systemic stuff
  • cardiac: effusion, pericarditis, myocarditis, aortitis, MI, diastolic dysfxn, pulm HTN, dysrhythmias
  • pulm: effusions, fibrosis, ILD
  • peripheral neuropathy, liver/kidney dysfxn, anemia
  • intubation: cervical spine, TMJ, cricoarytenoid issues
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2
Q

Med tx of RA?

A
  • NSAIDs
  • disease modifying antirheumatics (methotrexate, sulfasalazine, azathioprine)…slow dz progression
  • corticosteroids
  • goals: analgesia, dec infl, immunosuppression, inducing remission
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3
Q

Anesthetic considerations for NSAIDs?

A

Gastric ulcers, renal insufficiency, platelet dysfxn

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4
Q

What is “b/l eye irritation w/gritty sensation when blinking” pathognomonic for?

A
  • keratoconjunctivitis (impaired lacrimal gland fxn –> inadequate tear formation)
  • manifestation of Sjogren syndrome (a condition a/w/ rheumatoid arthritis)
  • inc risk for periop corneal abrasion
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5
Q

Why can pts w/pituitary adenoma be taking octreotide, bromocriptine?

A

Used for hormone secreting (functional) adenomas:

  • octreotide acts thru 4 mechanisms to dec abnl GH secretion (to treat acromegaly): 1) supresses GH secretion from pit gland/adenomas 2) dec GH binding to hepatocytes 3) inhibits hepatic IFG-1 prod, 4) controls tumor growth
  • octreotide can also help if have a TSH secreting adenoma: can suppress TSH secretion in > 90% of cases
  • bromocriptine tx acromegaly (GH) and pituitary prolactinomas (it’s a dopamine agonist, binding to R inhibits prolactin & GH synth and secretion). Prolactin secretion causes dec level of estrogen, testosterone –> amenorrhea, galactorrhea, infertility
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6
Q

Types of fxnl pituitary adenomas?

A
  • prolactinoma: too much prolactin –> dec estrogen/T –> amenorrhea, galactorrhea, infertility
  • ACTH: Cushing’s dz –> truncal obesity, HTN, hyperglycemia
  • GH: acromegaly –> HTN, insulin resistance, osteoporosis, skeletal/soft-tissue overgrowth
  • TSH: hyperthyroidism (rare)
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7
Q

What are the 6 tropic hormones secreted by the ant pituitary? Post pit?

A
  • ACTH
  • prolactin
  • GH
  • TSH
  • FSH
  • LH
  • ADH
  • oxytocin
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8
Q

Some features of acromegaly?

A
  • skeletal and soft tissue overgrowth (body, hands, feet, but specific to anesthesia: prognathism, lips, tongue, epiglottis, VCs)
  • RLN paralysis (stretching 2/2 surrounding structures overgrowth)
  • peripheral neuropathy
  • osteoarthritis
  • CM, CHF, HTN, OSA
  • DM
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9
Q

“Negatives” to using any of the types of neuromonitoring, like VEPs

A
  • VEPs are extremely sensitive to inhalational and iv agents –> hard to do consistent monitoring. So use low conc of volatile + narcs
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10
Q

How would you intubate a patient w/acromegaly?

A
  • awake fiberoptic intubation
  • d/t subglottic stenosis, large protruding mandible, large tongue, hoarse voice suggesting acromegalic involvement of the larynx
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11
Q

What will you hear on a precordial doppler if has a VAE? What to do?

A
  • sporadic roaring sounds, or millwheel sound
  • flood field w/saline
  • d/c any nitrous
  • aspirate thru central line
  • direct jugular venous compression to inc venous pressure at surgical site
  • CV support
  • tx any bronchospasm (can be a reflex w/entry of air into pulm artery)
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12
Q

What can you do to try to help blunt symp induced HTN or tachycardia upon extubation?

A

Give lido
- can also do this if you want to prevent coughing (for many reasons, but one could be that they had to repair a CSF leak and you don’t want it to re-open. However, I would actually suggest a remi wake up instead in this case)

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13
Q

How long should you monitor a patient with OSA and apnea in PACU?

A
  • until their SpO2 remains >90% during sleep
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14
Q

Describe how to place an IO line?

A
  • 1-2 cm below, 1cm medial to tibial tuberosity
  • slight caudal angulation to avoid epiphyseal plate
  • advance needle until felt a pop/reduced resistance
  • confirm w/aspiration of bone marrow
  • ensure that fluids flowed freely through line w/o signs of extravasation
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15
Q

Complications a/w/ IO access?

A
  • compartment syndrome 2/2 extravasation
  • muscle necrosis 2/2 extrav of caustic/hypertonic meds (bicarb, CaCl, dopamine)
  • osteomyelitis
  • bacteremia
  • cellulits
  • growth plate injury if pediatric pt
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16
Q

How does preE predispose pt to DIC?

What is DIC?

A
  • extensive vascular damage
  • pathological activation of coag cascade a/w/ variety of conditions (burn, head trauma, preE). Formation of small clots in bv’s throughout body –> consumption of coag factors, thrombocyto, hemolytic anemia, diffuse bleeding, thromboembolic phenomena
  • inc PT/PTT, dec fibrinogen, dec pltlt, inc DDimer
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17
Q

How to tx DIC?

A
  • tx any hypovol, hypoTN, hypoxemia, acidosis which can exacerbate DIC
  • admin cryo, FFP, pltlts, pRBCs PRN (cryo not always needed but good if fibrinogen <50)
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18
Q

What is TRALI?

A
  • not fully understood pathophys: transmission of donor leuk ABs activates neutrophils on pulm vasc endothelium –> endothel damage, capillary leakage, ALI
  • noncardiogenic pulm edema that occurs w/in 1-6 hrs s/p transfusion of any blood product, but more after FFP and platelets
  • clinically indistinguishable from ARDS, but much lower mortality
  • dx criteria: acute hypoxemia, pulm edema w/in 6 hrs of transfusion, absence of cardiac failure/fluid overload
  • tx: supportive, will recover w/in 96 hrs (diuretics and steroids not beneficial)
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19
Q

Tx for cardiogenic pulm edema?

A
  • tx geared towards dec pulm capillary P
  • diuretic to correct fluid overload
  • possibly blood products to ensure adequate Hct (low Hct –> dec viscosity and inc blood flow thru pulm circuit)
  • if vent dysfxn, consider inotrope/afterload reducing agent (dobutamine/milrinone)
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20
Q

1/2 life of IV vs IM narcan?

A
  • IV: 30-60 min
  • IM: 90m - 6hr
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21
Q

What is pseudotumor cerebri? S/s? Tx?

A
  • aka benign intracranial HTN, or IIH (idiopathic intracranial HTN)
  • a/w/ normal CSF prod, nl sensorium, absence of mass lesion
  • usually in obese childbearing-age women, but can be in kids too
  • s/s: HAs, visual stuff, papilledema
  • tx: acetazolamide/lasix (dec CSF prod), CSs to dec ICP if severe sxs, serial LPs, VP shunt
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22
Q

What do you do (access wise) after obtaining an IO line?

A
  • obtain more definitive access via surgical cut-down (e.g. to the femoral or saphenous vein)
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23
Q

What are the 4 areas of the abdomen that the FAST exam examines? (Names)

A
  • pericardium: subxiphoid
  • hepatorenal recess: RUQ
  • perisplenic space: LUQ
  • retrovesical pouch: superior to pubic symphysis
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24
Q

How is abdominal compartment syndrome diagnosed?

A
  • early signs: dyspnea, dec UOP, abd pain and distention
  • dx: abd CT, intra-abd P (indirectly measured via NGT in stomach or foley in bladder to get intravesicular P)
  • triad of inc intra-abd P, abd distention, and end-organ dysfxn (renal, cardiac, hepatic, etc) strongly suggest the dx
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25
Q

How does RhoGAM work?

A

It’s given to pregnant people who are Rh-negative and carrying an Rh-positive fetus to prevent their immune system from making antibodies that attack the fetus’s Rh-positive red blood cells. This can help prevent complications like anemia, jaundice, fetal brain damage, and stillbirth.
RhoGAM works by “fooling” the mother’s immune system into thinking it has already produced a response, which reduces the body’s attempt to produce active antibodies. This is known as passive antibody immunosuppression

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26
Q

Can you give a male patient Rh+ blood if the blood bank is trying to preserve inventory of Rh- blood?

A
  • Yes technically
  • Sometimes need to save Rh- for women of childbearing age bc danger of them developing Rh disease if they are sensitized before pregnancy)
  • Exposing Rh- male to Rh+ pRBC can still result in delayed txn rxn w/subsequent Rh+ transfusions, though
  • So, should give RhoGAM w/in 72 yrs and recommend checking for any anti-D ABs prior to any subsequent Rh+ txns
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27
Q

Does FFP need to be ABO typed?

A
  • yes, should be compatible w/recipient’s RBCs to prevent hemolysis
  • if pt’s blood type is unknown, should transfuse w/donor AB blood since the plasma won’t have any anti-A or anti-B isoagglutinins
  • FFP doesn’t contain any RBCs, so Rh matching unnecessary
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28
Q

What is propofol infusion syndrome? Time frame of acquiring it? Who usually gets it? Tx?

A
  • usually in kids and critically ill adult pts being infused w/high doses (like 4-5mg/kg/hr) anywhere from 6hrs - 48hrs
  • causes refractory brady w/met acidosis, rhabdo, hyperK, fatty liver, renal failure, CM
  • ends in CV collapse refractory to resus
  • tx: supportive, d/c prop gtt. Mortality rate 80%!!
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29
Q

Difference between narcotic abuse, addiction, and dependence?

A
  • abuse: use of substance detremental to individual or society
  • addiction: compulsive use of drug w/loss of control + irrepressible craving
  • dependence: physiological state of adaptation to specific psychoactive substance characterized by w/d sxs during abstinance)
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30
Q

What are the systemic effects of cirrhosis?

A
  • pulm: intrapulm AV shunts (I think this is what’s eval for w/”bubble study” for hepatopulm syndrome), dec FRC if ascites, pleural effusions, attenuation of HPV
  • cerebral: accumulation of ammonia + other toxins –> HE
  • hepatic: leads to thrombocytopenia + clotting factor deficiencies –> coagulopathy
  • CV: dec peripheral vasc R, inc CO, CM
  • metabolic effects: dilutional hypoNa, hypoK, hypoglycemia, hypoalbuminemia
  • misc: portal HTN, esophageal varicies, delayed gastric emptying, ascites, hepatorenal syndrome
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31
Q

Within what time period should PMs and AICDs be interrogated preop?

A
  • PM: w/in the past year
  • AICD: w/in past 6 mo
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32
Q

What is the equation for BMI? Rough classifications?

A

kg/m^2
Nl: 18.5-25
Overweight: 25-30
Obese I, II, III: 30-35, 35-40, 40-50
Superobese: >50

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33
Q

Types of liposuction and their risks?

A
  • tumescent: large volumes of dilute lido + epi injx into subQ, usually remove <3L fat. Most common
  • semitumescent: larger amounts of fat removed, higher risk of fluid overload, pulm edema, LAST, fat emboli
  • laser + ultrasonic energy techniques: newer, low complication rate, local/MAC
34
Q

Particular complications for liposuction procedure?

A
  • periop fluid overload
  • pulm edema
  • LAST
  • systemic epi uptake
  • cardiac arrhythmias
  • PE
35
Q

What would you do if 13yo’s mom refused consent for blood transfusion for child?

A
  • I’m legally obligated to provide life saving care to this minor (parents can’t make decisions that result in grossly inappropriate under or overtx of minors)
  • would reassure that I would do everything possible to respect wishes and avoid blood tx (see what she would accept, like albumin), but ultimately, if the parent still did not consent to the possibility of blood product, I would need to obtain a court order authorizing the admin of them. This is regardless of the minor agreeing with the parent etc
36
Q

Possible tx for post-herpetic neuralgia?

A
  • gaba or pregaba
  • opioids
  • nortriptyline
  • tramadol
  • for allodynia: topical lido patch, capsaicin
  • if all of this fails: PNB (PVB), symp n blocks (stellate ganglion, lumbar symp), neuraxial blockade, spinal cord stim
37
Q

How could someone become unconscious and apneic s/p retrobulbar block? Other possible complications?

A
  • LA spread through optic n sheath –> CNS –> GA and apnea
  • direct trauma to optic nerve
  • retrobulbar hemorrhage
  • inc intraocular pressure 2/2 transient globe compression
  • globe perforation
  • stim of oculocardiac reflex
  • intravasc/intraneural injx
38
Q

What is carcinoid syndrome?

A
  • complex of s/s when carcinoid tumor releases excessive hormones like histamine, kallikrein, serotonin into systemic circulation
  • If tumor in GI tract (most common), lack sxs bc enter portal system and inactivated in liver. But, if tumor in head/neck, lungs, breast, or mets to liver –> bypass portal circ –> sxs (cutaneous flushing, bronchoconstriction, diarrhea, R sided heart dz, hypoTN, HTN
39
Q

How to dx carcinoid syndrome?

A
  • 24h urine levels of 5 HIAA, a metabolic product of serotonin
  • PET/CT/MRI often used to localize 1* and metastatic lesions
  • elevated level of chromogranin A (glycoprotein secreted by carcinoid tumors) also c/w/ disease
40
Q

How to dec risk of carcinoid crisis preop?

A
  • give somatostatin analogue (octreotide) to dec tumor secretion of serotonin …optimally given at least 2d (up to 2w) prior to surgery and continued periop
  • optimize fluid status (can be very depleted if N/V/D/bowel obstruction)
  • give anxiolytic and alpha/beta blockers (prevent stress release of and effects of vasoactive substances from tumor)
  • H1/H2 blockers (attenuate effects of histamine release)
  • steroids (inhibit kallikrein cascade)
41
Q

How to deal with “PCN” allergies periop?

A
  • would feel comfy administering (assuming not anaphylaxis before)
  • <10% of pts who report an allergy have true allergy, and most of these nonimmunological (V/D/rash)
  • studies stating high X reactivity between PCN and cephalosporins flawed, true % is ~0.5% for 1st gens, near zero for 2nd and 3rd
  • still want to avoid if anaphylaxis to PCN
42
Q

Explain rationale for using/not using cricoid pressure for RSI?

A
  • would consider it may serve to dec risk of aspiration. However:
  • insufficient evidence to prove it’s actually useful
  • radiological studies have shown >90% of the time, esophagus displaced laterally instead
  • cric P dec LES tone
  • proper amount of force –> inc intubation difficulty (if this is the case, remove the P!)
  • most practitioners apply insufficient or excessive force
  • remove the force if pt begins to vomit! Can cause esophageal rupture
43
Q

How to explain why using nitrous due to c/f gas expansion?

A
  • nitrous diffuses into gas-filled cavities 34x faster than air diffuses out (air is primarily nitroGEN), leading to expansion of the cavity
  • e.g. in SBO: amount of air in bowel is greatly increased in this setting, use of nitrous –> significantly inc intraluminal pressures –> bowel ischemia and necrosis
44
Q

What to do when suddnely have HD instability, wheezing during a case w/carcinoid pt?

A
  • ask surgeon to stop manipulation of tumor
  • deflate pneumoperitoneum
  • 100% FiO2, hand ventilate, check all other monitors for inc/dec CO2, arrhythmias, etc
  • PE for hives vs flushing (anaphylaxis vs carcinoid crisis)
  • auscultate lungs for tPTX vs bronchospasm
  • look at CVP for hypovol vs RHF
  • fluid bolus, phenylephrine, octreotide bolus, benadryl. If nothing else worked, epi, vaso. Hopefully wouldn’t need epi unless nothing else worked d/t possible exacerbation or carcinoid crisis
45
Q

Changes to the CVP waveform in TR?

A

Remember “Acxvy” - sounds like anchovy or a Utah baby name hehe

46
Q

3 instances where ppx abx could be considered after aspiration event?

A
  • pt demonstrates bacterial infx based on cx and sensitivity testing
  • high likelihood of gram - or anaerobic organisms (like in an SBO)
  • pt’s clinical course fails to improve or worsens after 2-3 days
47
Q

What does a “line isolation” monitor alarm mean?

A
  • potential flow of current from the isolated power supply to the ground is at unacceptable level - places the pt at risk for micro shock
  • likely 2/2 too many pieces plugged into circuit (faulty alarm) vs fault piece of equipment (true alarm) in which case it needs to be removed
48
Q

Anesthetic concerns a/w/ autonomic neuropathy?

A
  • aspiration
  • hypoTN! (2/2 impaired peripheral vasoconstriction and baroR fxn
  • silent ischemia
  • intraop hypothermia
  • impaired ventilatory response to hypoxia/hypercapnia
49
Q

In what circumstance would you induce therapeutic hypothermia post-ROSC?

A
  • if the pt remained unable to respond meaningfully to verbal commands after treating any precipitating causes and optimizing ventilation/oxygenation/cardiopulm fxn
  • believed to provide protection for the brain and other organs
  • there are specific indictations if it was an in vs out of hospital arrests (don’t worry about memorizing)
50
Q

What is the ankle-brachial index (ABI)?

A
  • noninvasive doppler measurement of the ankle + brachial systolic pressures
  • assess presence and severity of PAD
  • nl = 1.0, claudication at <0.9, pain at rest <0.4, and ulceration/gangrene at <0.2
51
Q

Risk factors for contrast-induced nephropathy (CIN)?

A
  • already has CKD, DM, HTN, hypovol
  • age, CHF, kidney transplant
  • other random things, unimportant
52
Q

What are the 3 different adverse reactions that can happen with protamine admin?

A

1) histamine release w/rapid admin (should give over 5-10 mins)
2) anaphylaxis
3) protamine-induced catastrophic pulm HTN w/subsequent HF (dose-dependent, and less likely in vascular cases where low dose of protamine required for reversal (unlike in CPB)

53
Q

Consideration for penetrating eye injury irt type of anesthetic administered?

A
  • can potentially be performed with retrobulbar block (regional), but there is an inc risk of extrusion of intraocular contents 2/2 pressure generated by injection of LA, instrumentation of orbit, bleeding, squeezing of eyelids 2/2 pain of injx
  • should consult w/opthalmic surgeon
54
Q

What are a few things to remember about Li toxicity?

A
  • cognitive changes, seizures
  • widened QRS, AV block, hypoTN
55
Q

What to remember re: patients who are inadequately treated for their hyperthyroidism perioperatively?

A
  • they’re often hypovolemic –> inc risk of periop hypoTN (esp at induction)
  • compounded by need to ensure deep plane of anesthesia in order to avoid symp response to laryngoscopy and surgical stimulation
56
Q

Why should you care more about free T3/T4 vs total?

A
  • thyroid hormone binding influences these concentrations
  • principle binding protein (TBG) doesn’t stay constant; inc w/acute liver dz, pregnancy, OCPs, etc. and dec w/chronic liver dz, elevated glucocorticoids etc
57
Q

Things you can do to optimize hyperthyroid pt for urgent surgery (can’t delay)?

A
  • consult endocrinologist
  • continue PTU
  • give BB (propanolol is best bc it also dec conversion of T4 –> T3)
  • give glucocorticoid (decadron/hydrocort) to dec thyroid hormone secretion and peripheral conversion
  • give iodide (but wait until PTU has created euthyroid state first. However, if in thyroid storm, iodide should be given w/i 1 hr of giving PTU)
  • ensure adequate hydration, correct lytes, small dose of BDZ to relieve anxiety
  • prepare to tx HD instability, arrhythmias, thyroid storm
58
Q

Pt 3 hrs after thryoidectomy has stridor, restlessness, perioral tingling…ddx?

A
  • hypoCa: 2/2 inadvertent surgical removal of parathyroid glands. Usually 24-96hrs postop, but can start 1 hr postop
  • cervical hematoma formation
  • aspiration, post-intubation croup
  • residual NM blockade (MG - inc incidence in hyperthyroid pts)
  • RLN injury
  • hypoglycemia, hypoxia, hypercapnia
59
Q

Mech of NMS, sxs, and how to tx?

A
  • DA R blockade. Usually from antipsychotic meds (olanzapine, etc)
  • tachycardia, tachypnea, AMS, ANS dysfxn (altered BP), acidosis, fever
  • meds that increase amount of DA! Like bromocriptine, amantadine (these are Parkinsons drugs too) Or dantrolene, which dec muscular rigidity, fever, and CK levels
60
Q

Strategy for glu control perioperatively?

A
  • dec nighttime subQ dose to 2/3 night before
  • hold short-acting agents morning of
  • check glu upon arrival, then q1-2hrs
  • if insulin pump, dec overnight gtt to 2/3, then continue basal rate or separate insulin gtt at same rate
  • if mod/major surgery: same as above, but also start continuous/concurrent/and separate gtts of insulin and glu (D51/2NS + KCl)
61
Q

Complications a/w/ TURP? How to help prevent?

A
  • TURP syndrome: fluid overload (all solutions are hypotonic, so body absorbs it. Distilled water would be worst d/t this), hypoNa, HTN/brady/AMS. Laser ablation (L-TURP) has decreased risk of syndrome, but complications a/w/absorptions of large volumes of irrigation solution may still occur
  • Also hypothermia, bladder perf, hemorrhage, hemolysis, DIC, hyperglycinemia –> circ dep, enceph, seizures, transient blindness (if glycine), hyperammonemia (glycine), hyperglycemia (if sorbitol)
  • try to limit resection time to <1hr, don’t suspend irrigation bag >30cm above OR table, tx hypoTN w/vasopressors (bc dec venous P –> promote fluid absorption thru hydrostatic P)
62
Q

What dermatome level would you like to achieve anesthesia at for TURP?

A

T10 optimally
- above T9 –> would mask pain a/w/ bladder or prostatic capsule perf
- hyperbaric bupi good choice (90-120m duration)

63
Q

What to do if suspect bladder perf during TURP?

A
  • must r/o MI since presents similarly (shoulder pain, agitation, HTN, brady, diaphoretic, nausea)
  • then ask surgeon if any dec return of irrigation solution from bladder, finish procedure quickly, ID and assess if any bladder perf, and consider suprapubic cystostomy (cath) - worse outcomes if this is delayed >2hrs
64
Q

What would fade on TOF indicate if only received sux at beginning of case?

A
  • residual nondepol blockade (if was given inadvertently or whatnot)
  • phase II blockade from depol NMB, which could happen if:
    1) excessive dose given (7-10mg/kg), prolonged gtt
    2) abnl metabolism of sux (atypical pseudocholinesterase –> much larger dose of sux reaching NMJ –> phase II block)
65
Q

What are the different dibucaine number cutoffs for normal, hetero, and homozygous atypical pseudocholinesterase?

A
  • 80% nl
  • 40-60% hetero
  • 20% homo (would need 4-8 hrs to washout)
66
Q

Possible causes of postop vision issues?

A
  • if glycine irrigation for TURP, toxicity (transient, 24h)
  • ant/post ischemic optic neuropathy
  • cortical blindness
  • acute glaucoma
  • retinal ischemia
  • hemorrhagic retinopathy (rough emergence)
  • corneal abrasian, chemical injury, laser injury, etc
67
Q

Why is postop septicemia a/w/ TURP?

A

Movement of g+/g- bacteria –> systemic circulation thru surgically disrupted prostatic venous sinuses (prostate usually colonized w/bacteria)
- hydrostatic P during irrigated further facilitates entry into systemic circ

  • ppx abx won’t prevent systemic transmission, but can make bloodstream hostile to bacteria –> dec progression to septicemia. Also dec risk of UTI w/postop foley
68
Q

What’s your cutoff for delaying case for hyperK in a pt with CRF?

A

5.5 (mildly elevated 5.0-5.5 usually tolerated well bc chronic in nature for these pts)
- if mild, just monitor levels and EKG closely periop, be prepared to tx arrhythmias, check resp fxn closely prior to extubation (high K can interfere w/resp drive)

69
Q

With current preservation techniques, how long is cold-ischemia time for kidneys?

A

48hrs!

70
Q

HD prior to kidney tx - thoughts?

A
  • should be dialyzed w/in 24hrs of tx
  • if s/s of volume overload, should dialyze since at risk for CHF/pulm edema –> possible EOD and adversely effecting graft fxn
  • however, pts receiving tx immediately following HD often hypovolemic! –> intra-op hypoTN –> EOD and ATN, poor graft fxn
  • so, if hypervolemic, can dialyze, then admin non-K-containing IVF PRN (LR contains K, use w/caution)
71
Q

What kind of pRBCs to transfuse during kidney tx?

A

CMV- pRBCs

72
Q

What drugs and when to administer during a kidney tx?

A
  • heparin prior to clamping iliac vessels (prevent clotting)
  • prior to revasc, CCB often injected into arterial circ of graft to prevent vasospasm
  • mannitol/lasix after reperfusion to induce urine formation and dec risk of ATN
  • mannitol also acts as free radical scavenger
  • ATP (anti-thymocyte, rabbit Ig) and hydrocort given for anti-rejection
73
Q

WHy might a pt become acutely hyperKalemic s/p perfusion of new transplanted kidney during transplant?

A
  • washout of K containing preservative solution
74
Q

Mechanisms by which uremia contributes to thrombocytopenia? Tx?

A

Main two:
1) dec formation and release of vWF
2) uremia-induced anemia, which contributes to dec viscosity –> dec in platelet interaction

  • DDAVP to inc release of vWF
  • EPO, to help correct anemia
  • cryo, which contains vWF
  • platelets
  • HD to remove uremic acid (fastest, most effective)
75
Q

What 3 things are incorporated into the MELD score?

A
  • Cr
  • bili
  • INR
76
Q

S/s of hepatopulm syndrome?

A
  • platypnea, orthodeoxia (arterial deoxygenation in upright position)
  • fatigue, hypoxia (PaO2 < 70 on RA)
  • digital clubbing, spider angiomata

Defined by triad of:
- liver dz
- dec oxygenation
- intrapulm vascular dilation (dx w/ contrast echo/perfusion lung scanning/pulm angiography)

  • It’s an indication for liver tx!
77
Q

How to determine if elevated Cr is d/t HRS in pt w/liver dz?

A
  • eval response to fluid challenge (1.5L); if improves, consistent w/prerenal
  • review meds to see if any nephrotoxic drugs/contrast
  • check labs (UNa, UOsm, U:Plasma Cr, Usediment); if granular casts or UNa >10, c/w/ ATN
  • there are official major/minor criteria, but the ones listed above would be adequate
78
Q

Pathophys of HRS?

A
  • splanchnic arterial vasodilation (d/t inc prostacyclin, NO a/w/liver dz) –> dec in “effective” blood vol –> compensatory RAS activation –> renal vasoconstriction (but insufficient to counteract the vasodil –> persistent dilation of splanchnic circ + dec perfusion of kidneys –> HRS
  • type I worse than type II, definitive tx = liver tx
  • however, medical tx w/albumin, midodrine, octreotide can greatly improve kidney fxn in some and serve as bridge
79
Q

Why do pts become hyperK during anhepatic phase of liver tx?

A
  • 2/2 acidemia that occurs during this phase (interrupted liver metabolism)
  • dec UOP 2/2 HRS
  • dec hepatic uptake of K+ ions
  • high K levels of stored blood
  • washout of K containing preservative solution into systemic circ
80
Q

What is thought to cause reperfusion syndrome in neohepatic phase of liver txs?

A
  • excessive K load
  • release of vasoactive substances and acid metabolites from LE or graft
  • deleterious effects of cold blood from graft on the heart
  • release of cytokines
  • factors that exacerbate: metabolic acidosis, hypovol, hypothermia, hypoCa, hyperK
  • so, you’ll want to give bicarb, Ca (to counter effects of K on heart), and inotropes/pressors to correct hypoTN to dec incidence of this syndrome!
81
Q

Therapeutic level of digoxin? S/s of toxicity?

A
  • 0.5 - 2.0
  • EKG changes, arrhythmias, fatigue/confusion, N/V, visual disturbances
  • during an anesthetic, avoid factors that would potentiate toxicity: hypoK, hypoMg, hyperCa

UBP Pearls (9 decks)

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