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CCP > Genitourinary/Toxicology > Flashcards

Genitourinary/Toxicology Flashcards

1
Q

How do you confirm contrast induced renal failure?

A
  • 25% increase in serum creatinine from baseline
  • Temporal relationship to contrast (<72hrs ago)
  • No other cause
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2
Q

Outliers of AKI:

A
  • It can be linked to strep throat. As much as 6-14 days post pharyngitis, patients can develop HTN and edema.
  • Build up of urea makes you itchy.
  • Can cause pericardial effusions
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3
Q

Treatment for testicular torsion….

A
  • A hell of a lot of analgesia.
  • Twisting them back into place (opening a book)
  • Ensure a negative Phren’s test (lifting the teste to take pressure off of the epididymis), fever, gradual onset in order to differentiate from epididymitis/orchid is.
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4
Q

Treatment for hyperkalemia:

A
  • Membrane stability (CaCl2)
  • Shift K+ (Beta agonists, sodium bicarbonate, insulin with glucose)
  • Eliminate (Lasix, dialysis, kayexalate)
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5
Q

Calculate the osmolar gap:

A

Subtract the calculated osmolarity from the laboratory osmolarity.

Calculated osmolarity = 2(Na+) + glucose + BUN + EtOH(1.25)

*An osmolarity gap >10 indicates you have a toxic alcohol that the laboratory machine can’t read.

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6
Q

Name the four types of alcohol, their metabolites and if they’re toxic or not.

A

Isopropyl alcohol -> acetone (no, but still not good)
Ethanol -> acetaldehyde -> acetate (no)
Methanol -> formaldehyde -> formate acid (yes)
Ethylene glycol -> glycoldehyde -> glycolic/oxalic acid (yes)

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7
Q

What is the treatment of methanol and ethylene glycol intoxication?

A

Fompizole ($1000/shot)
Vodka, or any other EtOH (seriously!)
Cofactors (thiamine, folic acid, magnesium)
Sodium Bicarbonate

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8
Q

Key features of methanol intoxication:

A
  • AGMA
  • Osmolar gap >10
  • Blindness
  • Negative AKI/Calcium oxalate stones
  • Treat with EtOH
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9
Q

Key features of ethylene glycol intoxication:

A
  • AGMA
  • Osmolar gap > 10
  • AKI with calcium oxalate stones
  • Negative for blindness
  • Treat with EtOH
  • Binds to calcium and can cause hypocalcemia and heart failure
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10
Q

Key features of Isopropyl Alcohol intoxication:

A
  • No metabolic acidosis
  • Positive Osmolar gap
  • May cause gradual AKI/lung damage
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11
Q

Progression of ASA intoxication:

A
  • ASA triggers medulla and causes tachypnea (resp. alk.)
  • ASA (acid) causes a metabolic acidosis
  • Vomiting causes a metabolic alkalosis
  • Respiratory fatigue causes respiratory acidosis
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12
Q

Relationship between osmolar gap and anion gap for methanol and ethylene glycol toxicity

A

The alcohols causing the osmolar gap will get turned into acids. As the osmolar gap decreases over time, the anion gap will increase.

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13
Q

What is the major bacteria involved in UTIs?

A

-75% of UTIs are caused by gram-negative bacteria, most often E. Coli.

If you suspect UTI, check for leukocytes and nitrites in urine dip.

Tx with 2g ceftrixone, cipro or piptaz if you need a “bomb.”

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14
Q

GOLDMARK

A

G - Glycols (ethylene glycol, propylene glycol)
O - Oxoproline (acetaminophen ingestion)
L - L Lactate
D - D Lactate (short bowel, propylene glycol)
M - Methanol
A - ASA
R - Renal failure
K - Ketoacidosis (DKA, starvation, alcoholism)

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15
Q

Uremia can lead to fluid shifting and pericardial effusions. What is one thing you must consider before intubating a patient with a tamponade?

A

They are very preload dependant and PPV can quickly turn them into a PEA.

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16
Q

What’s a double gap acidosis?

A

Both anion gap and osmolar gap

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17
Q

DDx for Cl- sensitive Metabolic Alkalosis

A

NG suction
Vomitting
Diuretics (Cl- pissed out, HCO3- retained instead)
Massive blood transfusion

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18
Q

DDx for non-anion gap metabolic acidosis aka hyperchloremic acidosis

A

GI (diarrhea, pancreatic fistula)
Renal (RTA I, II, IV)
Too much N/S

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19
Q

DDx for AGMA (KULT)

A

Ketones (starvation, DKA, alcoholism)
Uraemia
Lactate (L and D lactate)
Toxins (ASA, methanol, ethylene glycol, toluene)

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20
Q

What circumstances must exist to diagnose a Hyperchloremic acidosis?

A

Urine pH > 5.5
Plasma HCO3- < 15
Anion Gap 8-12

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21
Q

What is the tipping point for intubating a metabolic acidosis?

A

When there is a superimposed respiratory acidosis as well.

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22
Q

What three features drive the pH?

A 
CO2 production (basilar metabolism)
Albumin (liver function, protein intake)
Strong Ion Difference (Na+, Cl-)
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23
Q

DDx for respiratory alkalosis

A
  • Head injury
  • CVA
  • Salicylic toxicity
  • PE
  • Early pneumonia
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24
Q

Broad considerations for dealing with a suspected toxicological overdose:

A
  • Decontaminate/PPE
  • Don’t assume it’s just an OD. Check for bleeds/infections/labs
  • 95% of work is supportive care
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25
Q

Key features of serotonin syndrome:

A
  • Altered LOC
  • Tremor, hyper-reflexia, clonus, rigidity, nystagmus
  • Autonomic instability
  • QTc prolongation

-Doesn’t have to be from an SSRI (TCA, sympathomimetic, cough syrup, tramadol, merpedine, LSD, etc…)

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26
Q

Is phenytoin an appropriate agent for treating toxicology related seizures?

A

No. Treat with benzos/barbs/propofol/Mg++ instead.

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27
Q

What is an LD50/TD50, the ED50 and the therapeutic index?

A

LD50/ED50: The dose required to kill/toxic to 50% of patients
ED50: The effective dose for 50% of patients

The therapeutic index is calculated by dividing the ED50 from the LD50. The larger the TI, the safer the drug. Ie, if the the LD50 is 100 and the ED50 is 1, you got a lot of wiggle room!

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28
Q

How do some drugs switch from first order kinetics to zero order kinetics?

A

In overdose situations, if all of the metabolic enzymes get saturated, the drug must be eliminated more slowly by the renal system in a zero order fashion. ASA is an example of one drug that does this.

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29
Q

How is N-acetyl-para-aminophel (APAP) metabolized and eliminated?

A

It is metabolized by four different pathways in the liver. One of these pathways produces a toxic metabolite (NAPQI) that is metabolized by glutathione. If glutathione is used up, NAPQI will destroy hepatocytes. If the kidneys survive this process, that’s where APAP metabolites are eliminated… If…

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30
Q

How do you treat APAP ingestion?

A

N-acetylcysteine (NAC).

It must be given in first 8 hours following ingestion in order to preserve the liver. Patients are often asymptomatic up to two days following ingestion, but AST levels will rise after 8 hours and APAP detectable in serum after 4 hours. Use Rumack-Matthews line to guide Tx.

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31
Q

Can the liver regenerate following an APAP intoxication?

A

Yes, it will fully regenerate. The body might be fucked from the encephalopathy/coagulopathy/cerebral edema/ARDS/sepsis that the transient liver failure caused, though.

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32
Q

What common preparations can salicylitic acid be found in?

A
  • ASA
  • Oil of Wintergreen
  • Tiger Balm
  • Ben Gay
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33
Q

What are some system effects of salicylate poisoning?

A
  • Acts on medulla and causes respiratory alkalosis
  • Interferes with cellular metabolism and renal elimination of H+ and causes AGMA
  • Stimulates vomiting which leads to metabolic alkalosis
  • Pulmonary edema, cerebral edema and hypokalemia.
  • Patient’s become obtruded/tired which leads to respiratory acidosis
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34
Q

How is respiratory alkalosis actually a benefit to ASA toxicity?

A

A higher pH keeps the salicylate acid neutralized so it can’t cross the BBB barrier. If the body’s pH goes down, ASA can cross the BBB and cause CNS dysfunction and cerebral edema.

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35
Q

Treatment considerations for Salicylate toxicity

A
  • IV fluids to treat fluid loss (hypervent, hyperthermia, vomit).
  • Correct hypoK+ since you won’t be able to alkalinize the urine otherwise. Use PO and/or high dose IV (150mL/hr of 40mEq).
  • NaHCO3 to alkalinize urine and keep pH high (target pH 7.5).
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36
Q

When making a sodium bicarbonate infusion, what do you use?

A
  • Draw out 150cc of D5W from a 1L bag
  • Put 3 amps of NaHCO3 in to replace it
  • Standard infusion rate = 250mL/hr

-If you mix it in NaCl, it can create a hypertonic solution from all the sodium.

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37
Q

What are the three causes of toxicological bradycardia?

A
  • Beta Blocker OD
  • Calcium Channel Blocker OD
  • Digoxin OD (Digoxin can cause all sorts OD dysrhythmias)
38
Q

Key features of Beta Blocker overdose?

A
  • Hypoglycemia
  • Sinus bradycardia
  • Hypotension
  • Wide QRS/Prolonged QTc
  • Respiratory depression
39
Q

Beta blocker overdose management:

A
  • Fluids to correct hypotension
  • 1 to 2g of CaCl2, or 3 to 6g of calcium glucose (keep iCal < 2)
  • 3 to 5g of glucagon
  • Sugar -> Insulin/more sugar
  • Epi infusion
  • Be prepared to treat for hypoK+!
40
Q

When administering glucagon, what’s one thing you have to be really prepared for?

A

Lots of vomit!

Give empirical antiemetics if you’re on your game but we wary of prolonged QT if giving odansetron. Gravol or Maxeran instead.

41
Q

If treating with insulin/glucose, will you develop a hypo or hyperkalemia?

A

Hypokalemia.

When treating a beta blocker overdose, insulin is effective since it utilizes a different pathway, but it will shift K+ into the cell. Be prepared to keep the K+ at least at 3.0.

42
Q

What are two key differences between Beta blocker overdose and calcium channel blocker overdose?

A

Beta blocker OD causes hypoglycemia while CCB OD causes hyperglycaemia.

You can use glucagon to treat beta blocker OD, but do not use it for CCB OD.

43
Q

What dysrhythmias is pathognomonic for digoxin overdose?

A

Digoxin toxicity can cause all sorts of brady/tachydysrhythmias but biventricular tachycardia is it’s very own.

44
Q

Which electrolyte must you closely monitor in the setting of digoxin overdose?

A

Potassium

K+ levels of 5.5mmol are 100% lethal, but if treatment starts below 5.0mmol, then there is a 100% survival rate.

*Also, don’t admin calcium to digoxin toxicity = stone heart

45
Q

What seven different receptors do TCAs have effect?

A
  • Alpha antagonism -> hypotension, tachycardia
  • Na+ channel blockade -> wide QRS
  • NE/serotonin reuptake blockade -> antidepressant
  • Muscarinic blockade -> anticholinergic effects/seizures,tachycardia
  • Histamine blockade -> sedation
  • K+ blockade -> Prolonged QTc
  • Indirect GABA blockade -> seizures
46
Q

Typical features of TCA OD:

A
  • Hypotension and tachycardia
  • Sedation
  • Seizures
  • ECG findings (wide QRS, long QTc, R’ in aVR)
  • Anticholinergic effects (dry, mydriasis, flushed, hot)
47
Q

Can an ECG be used to determine the severity of TCA toxicity?

A

Yes. The key features of TCA OD are very specific. Also, the wider the QRS, the more likely the patient is to have seizures and go into VF/VT. Be very concerned if QRS > 160ms.

48
Q

Treatment for TCA OD:

A
  • Normal saline boluses
  • NaHCO3 (if QRS > 100ms). Don’t let pH > 7.55. IF you still need to overcome Na+ blockade, give HTS 3%.
  • Benzos for any seizure activity. Not Phenytoin!!
49
Q

Treatment for serotonin syndrome:

A
  • Cool patient. Paralyze if you have to

- Treat long QTc with Mg++

50
Q

Fomepizol costs about $1000/shot. What’s it’s benefit as opposed to just giving the toxic alcohol patient booze?

A

Booze is an LOC depressant and, therefore, requires ICU monitoring. Each day in the ICU costs thousands of dollars.

51
Q

If requesting fomepizol, does it come from the pharmacy?

A

No. It’s often found in the poison kit and sometimes needs to be unlocked by poison control center.

52
Q

Parent metabolites aren’t dangerous in alcohol metabolism. What can be used to stop the breakdown into harmful toxins?

A

IV alcohol and fomepizol “use up” the enzymes that break down methanol and ethylene glycol into toxins. They make much less harmful acetate while the toxic alcohols are excreted via the kidneys in their unmetabolized form.

Thiamine can also be used in the case of ethylene glycol.

53
Q

How long post EtOH ingestion is an alcoholic most at risk for seizures?

A

24-72 hours

54
Q

Treatment for cocaine intoxication:

A

IV crystalloids
Benzos, benzos, benzos!
NaHCO3- to overcome Na+ blockade
Phentolamine to lower HTN (not Beta blockers!)

55
Q

Pulmonary irritants (chlorine gas, ammonia) can be split into highly and poorly soluble agents. What’s the difference?

A

Highly soluble agents interact quickly and tend to cause symptoms in the upper respiratory tract while poorly soluble agents penetrate deeper into the lung tissue and cause delayed reactions.

56
Q

Treatment for chlorine gas inhalation:

A

Aerosolized sodium bicarbonate.

Beta agonists.

57
Q

Patient is pulled from a house fire. What are two key exposures and how do you treat them?

A

Cyanide and carbon monoxide.

  • Treat with hydroxocobalamin for CN
  • Treat with FiO2 1.0 and hyperbaric treatment for CO
58
Q

How does hydroxocobalamin work?

A

It binds to cyanide to form cyanocobalamin (vit B12) and is then excreted in the urine harmlessly (except in makes your pee look like Kool-Aid).

Treat with 5g IV over 15 min. It can cause hypertension.qw

59
Q

Indications for hydroxocobalamin:

A

Pt must be suspected of being in an enclosed fire with one of the following:

  • DLOC
  • Hypotension
  • Lactate > 8
60
Q

How does increasing the FiO2 help with carbon monoxide poisoning?

A

The presence of high levels of oxygen decreases the duration of COHb:

  • Room air: 5 hours
  • 100% O2: 1 hour
  • Hyperbaric: 0.5 hour
61
Q

Patient populations specifically at risk for complications from CO poisoning:

A
  • Fetuses
  • Children
  • Really old people
  • Any patient with cardio-respiratory insufficiency
62
Q

Indications for hyperbaric “dive” following CO exposure:

A
  • DLOC
  • CVS instability
  • COHb > 40% in asymptomatic patients
  • COHb > 15% in pregnant patients
63
Q

Why are fatal tachydysrhythmias a complication of paint/gas/glue “huffing” or “bagging?”

A

The hydrocarbons hypersensitize myocardial receptors to catecholamines. Even a small surge of intrinsic catecholamines (like running) can cause the heart to fuck up.

64
Q

Examples of organophosphates:

A
  • Sarin Gas
  • VX Gas
  • Pestecides
  • Fertilizers
65
Q

How do organophosphates (OPs) fuck you up?

A

OPs bind to acetylcholinesterase (ACh-ase) so that it can’t break down ACh and it stays in nicotinic, muscarinic, and neuromuscular synaptic clefts for longer.

66
Q

Effects of OPs at muscarinic sites:

A
  • Bad Bs (bronchospasm, bronchorrhea, bradycardia)

- SLUDGE (salivation, lacrimation, urinary incontinence, diarrhea, GI cramps, emesis)

67
Q

Effects of OPs at nicotinic sites:

A
  • Hypertension
  • Tachycardia
  • Mydriasis
68
Q

Effects of OPs at neuromuscular junctions:

A
  • Fasiculations

- Respiratory muscle paralysis

69
Q

What happens when an organophosphate ages?

A

Each OP “ages” at a different rate. Once it ages, it can no longer be reversed and it stays bound to ACH-ase. Call Poison Control to establish the aging time of the agent you’re dealing with.

70
Q

In what manners can OPs be introduced to the body?

A
  • Inhaled, dermal contact, oral contact, ocular contact or parenteral. Decontamination and PPE are extremely important!
  • Treat dermal exposure with soap, water and mild bleach. Don’t wear latex gloves since OPs will absorb through.
71
Q

Treatment for organophosphate poisoning:

A
  • Atropine 3mg q. 2 min. Each dose should be double your last dose. Some patients require 200-500mg doses. Keep giving atropine until SLUDGE “drys up.”
  • Administer 2-PAM. It helps generate more ACh-ase and prevent OPs from binding to it.
72
Q

What’s worse? A exposure to an acid, or an exposure to an alkali?

A

Alkalis are worse. Acids will form an eschar layer and prevent further tissue damage. Alkalis just keep on burning through tissue (liquid necrosis).

73
Q

Costophrenic angle tenderness indicates what?

A

Pyelonephritis

74
Q

Where do creatinine and BUN come from?

A

BUN is associated with protein metabolism (diet, hemolysis, muscle) while creatinine is associated with muscle breakdown (seizures, exercise, starvation)

75
Q

Describe fraction of excreted sodium:

A

If the kidneys are working well, sodium is excreted in the urine. If there is 1-2% Na, then consider intra-renal failure. Greater than 2% and suspect that the kidneys have totally loss their ability to concentrate urine.

76
Q

Indications for dialysis:

A 
A - Acidemia
E - Electrolytes
I - Ingestion of toxins
O - Fluid overload
U - Uremia
77
Q

Three conditions where benzodiazepines won’t stop seizures:

A
  • Eclampsia (Tx Mg++)
  • Hyponatremia (Tx HTS)
  • Isoniazid (tuberculosis Rx) overdose (Tx Pyridoxal)
78
Q

Treatment for HRS:

A

Vasopressin. It constricts the efferent arterioles and improves GFR.

79
Q

How do you measure a delta-delta gap?

A

[calculated AG - expected AG (10)] - [Expected HCO3 (24) - measured HCO3]

80
Q

What does a measured delta-delta ratio < 1.0 likely mean and will bicarbonate administration be effective?

A

It means there is more serum HCO3 being used up that the anion gap suggests. This is likely due to a HAGMA combined with a NAGMA (diarrhea, RTA, NS bolus). Administration of NaHCO3 will likely be beneficial.

81
Q

What does a delta-delta ratio of 1.0-20 suggest.

A

It likely means that it is a pure HAGMA. The amount of bicarbonate being used up is directly related to the acids in the anion gap.
*A pure lactic acidemia usually has a delta-delta of 1.6

82
Q

What does a delta-delta of > 2.0 indicate?

A

There is a metabolic acidosis that is pulling the bicarbonate down, but also a metabolic alkalosis contributing to driving it back up. Consider a vomiting patient or too much OG suctioning; citrate from transfusions; contraction alkalosis from fluid loss or a patient that had a high bicarbonate level to begin with such as a COPDer.
*Administration of NaHCO3 in these patients will likely be ineffective or worsen the intracellular acidemia,

83
Q

What electrolytes commonly build up in the setting of AKI?

A

Mg++, PO4-, K+

84
Q

When you give Ca++, what electrolyte goes down?

A

Phosphate binds to the added Ca++ and levels go down. Be cautious replacing Ca++ when PO4 is also low.

85
Q

Why must you correct Mg++ before you try to correct K+?

A

Mg++ acts as a co-factor for Na+/K+ exchange pumps.

86
Q

Tests you can order to help differentiate your AGMA

A
  • Extended lytes (to determine if it’s true anion gap)
  • Lactate
  • Hydroxybutyrate (ketones)/urinary ketones
  • ASA
  • APAP
  • CO
  • Osmolar gap
87
Q

What are some medications that can increase lactate?

A
  • Propofol
  • Metformin
  • Beta agonists (salbutamol, epinephrine…)
  • Salicylates
  • Nitroprusside
88
Q

Alright, your patient’s pH is fucked up! Like, really bad lactic acidosis! They’re sedated on propofol and extremely acidotic. What can you do?

A

Swap out their propofol (which increases lactate) infusion for a ketamine infusion.

*Maybe try thiamine for malnourished/GI disorder patients???
(thiamine is an essential co-factor for the enzyme pyruvate dehydrogenase that allows oxidation of pyruvate to acetyl CoA

89
Q

Is Bicarb good for lactic or uremic acidosis?

A

Uremic only. It can reduce the need for dialysis. Lactate acidosis requires you fix the source of the lactate production and bicarb can harm lactic acidosis patients.

90
Q

This one’s a doozy… How do you treat hyponatremia?

A
  1. Is there a neurological emergency? If so, give up to 2 x 100-150cc of HTS3% over 5-10 minutes.
  2. Defend intravascular volume, determine volume status.
    - If hypovolemic and unstable, give 250cc Ringer’s Lactate.
    - If hypovolemic and stable, don’t do anything
    - If euvolemic, prevent worsening
    - If hypervolemic, treat with lasix and hold all water and sodium.
  3. Prevent worsening hyponatremia
    - Saline lock IV and make patient NPO even if they look dry.
  4. Prevent rapid correction by monitoring urine osmolarity q. 1h.
    - Insert a foley
    - If U/O > 100mL/hr, send for urine osmolarity testing
    - If osmolarity is < 100, give 1mcg of DDAVP
  5. Identify the cause
91
Q

Winter’s Formula

A

To assess respiratory compensation in a metabolic acidosis patient.

Expected PaCO2 = (1.5 x measured HCO3) + 8 (+/- 2)

92
Q

Why is normal saline so bad?

A
  • pH of 5.5
  • Chloride pushes out bicarbonate to maintain electro-neutrality. This worsens acidemia.
  • Hyperchloremia causes renal vessel constriction and reduces GFR. Many patients that get too much N/S go on to requiring dialysis due to AKI.

CCP (18 decks)

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