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CM Critical Care Boards > Chest Videos Pt 2 > Flashcards

Chest Videos Pt 2 Flashcards

1
Q

Miosis vs. mydriasis

A
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2
Q

Drugs that cause miosis

A
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3
Q

Drugs that cause mydriasis

A
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4
Q

Concept between alkalinizing urine

(a) Used to enhance removal of which two drugs?

A

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

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5
Q

Fomepizole vs. flumazenil

A

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

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6
Q

Antidotes for

(a) Ethanol overdose
(b) Benzo overdose

A

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

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7
Q

Explain why ethanol was historically used in mgmt of methanol toxicity

A

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

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8
Q

Clinical settings to suspect cyanide toxicity

A

House fire, high-dose nitroprusside drip

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9
Q

Management of cyanide toxicity

A

Cyanokit- sodium thiosulfate, hydroxycobalamin (vitamin B12)

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10
Q

Explain two clinical features that may help differentiate beta-blocker from calcium-channel blocker toxicity

A

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

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11
Q

Features differentiating nifedipine vs. diltiazem overdose

A

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

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12
Q

Treatments for beta blocker and CCB toxicity

A

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

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13
Q

Mechanism of glucagon in beta-blocker toxicity

A

Glucagon increases intracellular cAMP in a non-calcium channel dependent way => is an inotrope independent of CCB/BB receptors

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14
Q

Indication(s) for glucagon in toxicology (overdoses)

A

Glucagon indicated in both BB and CCB overdoses b/c increases intracellular cAMP => acts as inotrope independent of calcium channels

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15
Q

Why is flumazenil so rarely used?

A

Contraindicated in chronic benzo use b/c of the high risk of seizures and arrhythmias- typically suspect chronic use in an overdose

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16
Q

If suspecting opiate dose but needing crazy high doses of naloxone, what should you suspect?

A

Suspect a synthetic opiate like fentanyl or carfentanil (elephant tranq)

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17
Q

3 most common bugs for bacterial meningitis

A
  1. 70% strep pneumo even with vaccines, tons of serotypes
  2. 12% Neisseria
  3. 7% group B strep
  4. H. influenza
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18
Q

Explain antimicrobial choice for empiric coverage of bacterial meningitis

A

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

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19
Q

When to add ampicillin for empiric meningitis coverage

A

Immunocompromised, age over 50, pregnant

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20
Q

Unique features of West Nile Enchephalitis

A

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

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21
Q

West nile virus vs. guillain-barre syndrome

(a) Type of weakness
(b) CSF profile

A

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

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22
Q

CSF findings

(a) Opening pressure in viral infection
(b) What cause has the highest cell count?
(c) When to expect low glucose

A

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

23
Q

CSF profile factors to differentiate bacterial from viral meningitis

A

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

24
Q

Typical cause of septic thrombophlebitis of the jugular vein

A

Fusobacterium

25
Q

Toxic shock from what organism is associated with tampons or other packing

(a) Treatment

A

Staph TSS from tampons/packing (ex: wound or nasal packing)

(a) Tx = staph coverage for nafcillin or vanc + clinda for toxin

26
Q

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

A

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

27
Q

How does treatment for staph and strep toxic shock differ?

A

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

28
Q

Botulism paralysis mimics what other syndrome?

A

Myasethenia gravis- eye/bulbar symptoms (diplopia, ptosis), descending flaccid weakness/paralysis

29
Q

3-pronged treatment for wound botulism

A
  1. botulism antitoxic from the CDC
  2. wound debridement
  3. PCN
30
Q

Differentiate CNS findings in

(a) Myxedema coma
(b) Thyroid storm

A

CNS

(a) Myxedema coma- everything slower, CNS depression, hyporeflexia
(b) Thyroid storm- everything amped up- hyperpyrexia, psychosis/agitation, tremors

31
Q

Most common cause of Addison’s disease

(a) Other less common causes

A

Addison’s disease = primary adrenal insufficiency

80% from autoimmune destruction of adrenal gland
-also seen in hemorrhage, infection (tb, histo), meds

32
Q

Utility of AM cortisol in diagnosis of adrenal insufficiency

A

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

33
Q

Why dexamethasone is a helpful initial treatment for presumed adrenal insufficiency

A

Doesn’t suppress ACTH production so can still test cortisol and ACTH levels

34
Q

Key management pearl for pre-operative care of pt with pheochromocytoma

A

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

35
Q

Location of majority of blunt injuries of the thoracic aorta

A

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

36
Q

Bladder pressure cutoff for

(a) Intraabdoinal hypertension
(b) Decompressive laparotomy

A

Bladder pressure

(a) Over 12 and end-expiration considered IAH (intraabdominal hypertension)
(b) Over 20-25- decompressive laparotomy

37
Q

2 mechanisms by which abdominal compartment syndrome causes issues

A
  1. reduced venous return to the heart
  2. reduced abdominal perfusion pressure => gut ischemia3
38
Q

3 main clinical features of acute graft vs host disease following

A

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

  1. Skin- diffuse rash typically involving palms/soles
  2. Liver- high direct bili
  3. 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

39
Q

Which local anesthetic carries highest risk of cardiotoxicity if injected intravascularly?

A

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

40
Q

Pt gets reginal peripheral nerve bock with bupovacaine and 5 mins later becomes hypotensive, tachy, and siezes

(a) Most likely cause
(b) Mgmt

A

(a) Local anesthetic systemic toxicity- CNS and CV manifestations

(b) Mgmt- Lipid emulsion

41
Q

Guillain Barre vs. Myasthenia Gravis

(a) Mechanism of defect
(b) Timeline
(c) Type of weakness

A

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

42
Q

Buzzwords for type of neuromuscular weakness

(a) Cranial nerve weakness developing over days
(b) Tongue fasciculations
(c) Ascending
(d) Descending

A

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

43
Q

What other type of neuromuscular weakness does botulism typically mirror and why?

(a) How to differentiate

A

Differentiate (a) botulism from myasthenia gravis by wound infection, contaminated food, or IVDU

Botulism and MG both have oculobulbar symptoms (diplopia, dysphagia, dry mouth)

44
Q

Guillain Barre

(a) Diagnostic test
(b) First line tx

A

GBS- demyelinating

(a) Elevated protein in CSF, nerve conduction studies
(b) IVIG or PLEX (not steroids!!)

45
Q

Myasthenia Gravis

(a) Diagnostic test
(b) First line tx

A

ACh-receptor autoantibodies

(a) ACHR, MuSK antibodies. Repetitive nerve stimulation
(b) Pyridostigmine, PLEX or IVIG, + steroids

46
Q

Differentiate first line treatment for guillain-barre and myasthenia gravis

A

GBS (demyelinating syndrome)- PLEX or IVIG, NOT steroids

vs.

MG (anti-AChR)- PLEX or IVIG + steroids + pyridostigmine (AChE inhibitor) to help with symptoms

47
Q

Mechanism of injury in TBI

A

Diffuse axonal injury at the grey-white cortical interface from axonal sheer

48
Q

How to grade TBI

A

TBI graded by duration of LOC, GCS (<10 should get seizure prophylaxis), and imaging findings

49
Q

Seizure prophylaxis in TBI patients?

(a) Who to give it to
(b) What to give

A

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

50
Q

When to call NSGY for patient with SDH

A

Subdural hemorrhage- >10mm in greatest diameter or >5mm midline shift- should get craniectomy

51
Q

When to use steroids to reduce ICP

A

Tumorgenic edema only

(not for any bleeds, strokes, TBI)

52
Q

Normal

(a) ICP
(b) CPP

A

Normal

(a) ICP upper limit of normal is 15
(b) CPP (MAP - ICP) of 50-70

53
Q

Goal pCO2 when hyperventilating to temporarily reduce ICP

A

pCO2 goal 35-40, pCO2 < 30 associated with harm (hypoxia from too much vasoconstriction seen <20)

54
Q

CO2 cutoffs for positive apnea test

A

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

CM Critical Care Boards (5 decks)

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