Chest Videos Pt 2 Flashcards
Miosis vs. mydriasis
Drugs that cause miosis
Drugs that cause mydriasis
Concept between alkalinizing urine
(a) Used to enhance removal of which two drugs?
Alkalinize urine by giving bolus followed by infusion of sodium bicarbonate. Goal is urine pH > 7.5-8 without getting serum pH > 7.55-7.6
Purpose- urinary ion trapping, basically shift acid to ion form that is less easily reabsorbed in the renal tubule => enhance secretion out in urine
(a) Aspirin (salicylates) and phenobarbital toxicity
Fomepizole vs. flumazenil
Fomepizole = inhibits alcohol dehydrogenase, for toxic alcohols
Flumazenil = benzo receptor blocker, for acute benzo OD (be careful, contraindicated in chronic benzo use b/c high risk of seizures and arrhythmia
Antidotes for
(a) Ethanol overdose
(b) Benzo overdose
Antidote
(a) Ethanol OD = fomepizole = competitive inhibitor of alcohol dehydrogenase => ethanol not broken down in to the toxic acids
(b) Benzo OD = flumazenil = GABA receptor blocker
Explain why ethanol was historically used in mgmt of methanol toxicity
Alcohol dehydrogenase (common enzyme used by the toxic alcohols) has much higher affinity for ethanol- so reduce production of toxic byproducts by keeping it busy (competitively inhibiting) with ethanol
Clinical settings to suspect cyanide toxicity
House fire, high-dose nitroprusside drip
Management of cyanide toxicity
Cyanokit- sodium thiosulfate, hydroxycobalamin (vitamin B12)
Explain two clinical features that may help differentiate beta-blocker from calcium-channel blocker toxicity
Presence of AMS supports beta-blocker toxicity, possibly due to CCB protective effects on the CNS
Presence of hyperglycemia suggests CCB toxicity due to inhibition of Ca-mediated insulin release from the pancreas
Features differentiating nifedipine vs. diltiazem overdose
Non-dihydropyridine CCBs are cardiac selective = diltiazem, verapamil- see mostly negative inotropy and chronotropy => hypotension and bradycardia
vs.
Dihydropyridine CCBs cause peripheral vasodilation (nifedipine, amlodipine)- see hypotension but with compensatory tachycardiac
Treatments for beta blocker and CCB toxicity
BB and CCB toxicity
-glucagon (non-Ca channel dependent inotrope but increasing intracellular cAMP)
- high dose insulin adn glucose (unclear mechanism)
- IV calcium to overcome inhibition
- pressors
- lipid emulsion: thought to sequester/inactivate drug or maybe myocardial energy supply
Mechanism of glucagon in beta-blocker toxicity
Glucagon increases intracellular cAMP in a non-calcium channel dependent way => is an inotrope independent of CCB/BB receptors
Indication(s) for glucagon in toxicology (overdoses)
Glucagon indicated in both BB and CCB overdoses b/c increases intracellular cAMP => acts as inotrope independent of calcium channels
Why is flumazenil so rarely used?
Contraindicated in chronic benzo use b/c of the high risk of seizures and arrhythmias- typically suspect chronic use in an overdose
If suspecting opiate dose but needing crazy high doses of naloxone, what should you suspect?
Suspect a synthetic opiate like fentanyl or carfentanil (elephant tranq)
3 most common bugs for bacterial meningitis
- 70% strep pneumo even with vaccines, tons of serotypes
- 12% Neisseria
- 7% group B strep
- H. influenza
Explain antimicrobial choice for empiric coverage of bacterial meningitis
Vanc (for double coverage of strep pneumo in case cephalosporin resistant, not for MRSA) + 3rd gen cephalosporin (CTX, cefotaxime, ceftazidime)
then
+ampicillin (for listeria coverage) if immunocompromised, over age 50, or pregnant
+acyclovir given such high morbidity/mortality of HSV encephalitis
When to add ampicillin for empiric meningitis coverage
Immunocompromised, age over 50, pregnant
Unique features of West Nile Enchephalitis
Eye symptoms (uveitis, retinitis) and acute flaccid paralysis similar to Guillain-Barre
So immunocompromised pt presents with AMS, acute asymmetric paralysis- consider West Nile encephalitis
West nile virus vs. guillain-barre syndrome
(a) Type of weakness
(b) CSF profile
Both can cause acute flaccid paralysis
West nile
(a) Asymmetric, proximal paralysis with eye symptoms more common
(b) CSF pleiocytosis (elevated WBC count), elevated protein
Guillain-Barre
(a) Symmetric, ascending paralysis
(b) CSF without pleiocytosis, yes elevated protein
CSF findings
(a) Opening pressure in viral infection
(b) What cause has the highest cell count?
(c) When to expect low glucose
CSF findings
(a) Opening pressure elevated in bacterial, fungal but typically normal in viral infections
(b) Bacterial typically has the highest cell count, moderately elevated in viral and TB
(c) Low glucose in bacterial and Tb, glucose normal in viral
CSF profile factors to differentiate bacterial from viral meningitis
Bacterial- high opening pressure, highest WBC count, low glucose, neutrophilic differential
Viral- normal opening pressure, elevated but not as high WBC count with lymphocytic predominance, normal CSF glucose
Typical cause of septic thrombophlebitis of the jugular vein
Fusobacterium
Toxic shock from what organism is associated with tampons or other packing
(a) Treatment
Staph TSS from tampons/packing (ex: wound or nasal packing)
(a) Tx = staph coverage for nafcillin or vanc + clinda for toxin
Toxic shock from what organism is more typically
(a) Post-partum
(b) Associated with nasal packing
(c) Higher mortality
(d) More associated with bacteremia
(e) requires surgical debridement
Staph vs. Strep toxic shock
(a) post-partum- strep
nasal packing, tampons, wound packing = staph
higher mortality (30-80%!), incidence of bactermia, and need for surgical debridement with strep
How does treatment for staph and strep toxic shock differ?
Both want gram negative coverage + clinda for toxin
For strep toxic shock (post-partum, higher mortality): typically requires surgical debridement of extensive tissue necrosis, also some evidence of benefit of IVIG to boost passive immunity
Botulism paralysis mimics what other syndrome?
Myasethenia gravis- eye/bulbar symptoms (diplopia, ptosis), descending flaccid weakness/paralysis
3-pronged treatment for wound botulism
- botulism antitoxic from the CDC
- wound debridement
- PCN
Differentiate CNS findings in
(a) Myxedema coma
(b) Thyroid storm
CNS
(a) Myxedema coma- everything slower, CNS depression, hyporeflexia
(b) Thyroid storm- everything amped up- hyperpyrexia, psychosis/agitation, tremors
Most common cause of Addison’s disease
(a) Other less common causes
Addison’s disease = primary adrenal insufficiency
80% from autoimmune destruction of adrenal gland
-also seen in hemorrhage, infection (tb, histo), meds
Utility of AM cortisol in diagnosis of adrenal insufficiency
Helpful at the extremes, under 3 is diagnostic for AI (no further testing needed) and over 15 rules out AI
Then between 3-15 use ACTH stim test to see if adrenal glands respond
Why dexamethasone is a helpful initial treatment for presumed adrenal insufficiency
Doesn’t suppress ACTH production so can still test cortisol and ACTH levels
Key management pearl for pre-operative care of pt with pheochromocytoma
Never give unopposed beta-blockade, always make sure alpha blocade (to expand contracted invascular space) is done first
Use alpha blocker (terazosin or more classically phenoxybenzamine) to vasodilate before giving any beta
Beta without alpha- blockade of vasodilator peripheral effects without alpha blockade can cause acute worsening and rise of BP
So pre-operatively: at least 7 days give alpha blocker (classically phenoxybenzamine), then about 2 days before also start beta-blocker
Location of majority of blunt injuries of the thoracic aorta
Aortic isthmus- just distal to the L subclavian artery
-most common site of thoracic aortic injury during blunt trauma (MVA)
-possibly b/c it is loosely tethered relative to fixed descending thoracic aorta
Bladder pressure cutoff for
(a) Intraabdoinal hypertension
(b) Decompressive laparotomy
Bladder pressure
(a) Over 12 and end-expiration considered IAH (intraabdominal hypertension)
(b) Over 20-25- decompressive laparotomy
2 mechanisms by which abdominal compartment syndrome causes issues
- reduced venous return to the heart
- reduced abdominal perfusion pressure => gut ischemia3
3 main clinical features of acute graft vs host disease following
Graft vs host occurs after allogenic hematopoietic cell transplantation when immune cells from non-identical donor (graft) recognize transplant recipient (host) as foreign => initiating immune reaction
- Skin- diffuse rash typically involving palms/soles
- Liver- high direct bili
- GI symptoms- N/V/diarrhea
ex: 18F 18 days s/p allogenic hematopoietic stem cell transplant with diarrhea, abd pain, erythematous rash on hands and trunk, now with scleral icterus
Which local anesthetic carries highest risk of cardiotoxicity if injected intravascularly?
All local anethetics have the potential to cause local anesthetic systemic toxicity (LAST), but bupivocaine (for local nerve blocks) carry highest risk of cardiac toxicity
LAST = local anesthetic systemic toxicity
Pt gets reginal peripheral nerve bock with bupovacaine and 5 mins later becomes hypotensive, tachy, and siezes
(a) Most likely cause
(b) Mgmt
(a) Local anesthetic systemic toxicity- CNS and CV manifestations
(b) Mgmt- Lipid emulsion
Guillain Barre vs. Myasthenia Gravis
(a) Mechanism of defect
(b) Timeline
(c) Type of weakness
GBS
(a) demyelinating and axonal forms
(b) Days to weeks, esp after diarrheal illness
(c) Ascending symmetrical paralysis with sensory abnormalities, autonomic findings, and areflexia
vs.
MG
(a) ACh-receptor autoantibodies
(b) Weeks to months, progressive but can be fluctuating
(c) Weakness with repetitive action, starts oculobulbar progresses peripherally
Buzzwords for type of neuromuscular weakness
(a) Cranial nerve weakness developing over days
(b) Tongue fasciculations
(c) Ascending
(d) Descending
Weakness
(a) Cranial nerve weakness- Miller-Fischer variant of Guillain Barre, associated with GD1a antibodies
(b) Tongue fasciculations = ALS
(c) Ascending- GBS, ALS
(d) Descending- botulism
What other type of neuromuscular weakness does botulism typically mirror and why?
(a) How to differentiate
Differentiate (a) botulism from myasthenia gravis by wound infection, contaminated food, or IVDU
Botulism and MG both have oculobulbar symptoms (diplopia, dysphagia, dry mouth)
Guillain Barre
(a) Diagnostic test
(b) First line tx
GBS- demyelinating
(a) Elevated protein in CSF, nerve conduction studies
(b) IVIG or PLEX (not steroids!!)
Myasthenia Gravis
(a) Diagnostic test
(b) First line tx
ACh-receptor autoantibodies
(a) ACHR, MuSK antibodies. Repetitive nerve stimulation
(b) Pyridostigmine, PLEX or IVIG, + steroids
Differentiate first line treatment for guillain-barre and myasthenia gravis
GBS (demyelinating syndrome)- PLEX or IVIG, NOT steroids
vs.
MG (anti-AChR)- PLEX or IVIG + steroids + pyridostigmine (AChE inhibitor) to help with symptoms
Mechanism of injury in TBI
Diffuse axonal injury at the grey-white cortical interface from axonal sheer
How to grade TBI
TBI graded by duration of LOC, GCS (<10 should get seizure prophylaxis), and imaging findings
Seizure prophylaxis in TBI patients?
(a) Who to give it to
(b) What to give
TBI patients with moderate to severe injury (basically if anything on imaging or GCS < 10) should get seizure ppx with either keppra or phenytoin x7 days
When to call NSGY for patient with SDH
Subdural hemorrhage- >10mm in greatest diameter or >5mm midline shift- should get craniectomy
When to use steroids to reduce ICP
Tumorgenic edema only
(not for any bleeds, strokes, TBI)
Normal
(a) ICP
(b) CPP
Normal
(a) ICP upper limit of normal is 15
(b) CPP (MAP - ICP) of 50-70
Goal pCO2 when hyperventilating to temporarily reduce ICP
pCO2 goal 35-40, pCO2 < 30 associated with harm (hypoxia from too much vasoconstriction seen <20)
CO2 cutoffs for positive apnea test
Abort for hypoxia (use 100% oxygen and preoxygenate), want to see if hypercapnia triggers breath)- positive if no breath triggered with pCO2 > 60 or more than 20mHg rise from baseline
