Misc 3 Flashcards
Brief pathophys and systemic manifestations of RA?
- 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
Med tx of RA?
- NSAIDs
- disease modifying antirheumatics (methotrexate, sulfasalazine, azathioprine)…slow dz progression
- corticosteroids
- goals: analgesia, dec infl, immunosuppression, inducing remission
Anesthetic considerations for NSAIDs?
Gastric ulcers, renal insufficiency, platelet dysfxn
What is “b/l eye irritation w/gritty sensation when blinking” pathognomonic for?
- keratoconjunctivitis (impaired lacrimal gland fxn –> inadequate tear formation)
- manifestation of Sjogren syndrome (a condition a/w/ rheumatoid arthritis)
- inc risk for periop corneal abrasion
Why can pts w/pituitary adenoma be taking octreotide, bromocriptine?
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
Types of fxnl pituitary adenomas?
- 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)
What are the 6 tropic hormones secreted by the ant pituitary? Post pit?
- ACTH
- prolactin
- GH
- TSH
- FSH
- LH
- ADH
- oxytocin
Some features of acromegaly?
- 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
“Negatives” to using any of the types of neuromonitoring, like VEPs
- VEPs are extremely sensitive to inhalational and iv agents –> hard to do consistent monitoring. So use low conc of volatile + narcs
How would you intubate a patient w/acromegaly?
- awake fiberoptic intubation
- d/t subglottic stenosis, large protruding mandible, large tongue, hoarse voice suggesting acromegalic involvement of the larynx
What will you hear on a precordial doppler if has a VAE? What to do?
- 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)
What can you do to try to help blunt symp induced HTN or tachycardia upon extubation?
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)
How long should you monitor a patient with OSA and apnea in PACU?
- until their SpO2 remains >90% during sleep
Describe how to place an IO line?
- 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
Complications a/w/ IO access?
- 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
How does preE predispose pt to DIC?
What is DIC?
- 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
How to tx DIC?
- 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)
What is TRALI?
- 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)
Tx for cardiogenic pulm edema?
- 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)
1/2 life of IV vs IM narcan?
- IV: 30-60 min
- IM: 90m - 6hr
What is pseudotumor cerebri? S/s? Tx?
- 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
What do you do (access wise) after obtaining an IO line?
- obtain more definitive access via surgical cut-down (e.g. to the femoral or saphenous vein)
What are the 4 areas of the abdomen that the FAST exam examines? (Names)
- pericardium: subxiphoid
- hepatorenal recess: RUQ
- perisplenic space: LUQ
- retrovesical pouch: superior to pubic symphysis
How is abdominal compartment syndrome diagnosed?
- 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