PHARM ANESTHESIA INFECTION Flashcards
nitroprusside complication and treatment
The patient is exhibiting symptoms of cyanide toxicity secondary to the nitroprusside medication. These patients can have weakness and confusion and develop pulmonary edema. Thiocyanate (choice C) levels can be checked to ensure the patient does not have a toxic level of cyanide.
Antidotes for cyanide toxicity include amyl nitrite (choice A), sodium nitrite, and sodium thiosulfate.
Bottom Line: The treatment for cyanide toxicity is amyl nitrite.
Propofol
metabolism
hepatic metabolism by conjugation to glucuronide and sulfate
excreted by the kidneys in this water soluble form.
Propofol has an antiemetic effect at low doses possibly by acting on GABA receptors which causes decreased serotonin levels in the area postrema.
Propofol DECREASES intracranial pressure (ICP) in patients with normal or elevated ICP (choice D) while maintaining normal cerebral CO2 reactivity and autoregulation. Propofol also DECREASES intraocular pressure by 30- 40%.
Propofol infusion syndrome is rare and potentially lethal
Clinical features include refractory bradycardia, asystole, metabolic acidosis, rhabdomyolysis, hyperlipidemia, cardiomyopathy, skeletal myopathy, and enlarged liver.
A 48-year-old male presents to the emergency department with complaints of shortness of breath and dyspnea on exertion. A chest x-ray shows a small calcified lesion in the right upper lobe that is new from previous films. The patient reports that he was recently on a hiking trip in Ohio prior to the onset of his symptoms.
The patient is presenting with a Histoplasmosis infection.
Ohio and Mississippi river valleys and are identified on chest x-rays as calcified lesions.
Tx of histoplasmosis
self limiting
do not require any further intervention if the patient’s condition is uncomplicated.
These patients can have bulky mediastinal nodes that can cause compressive symptoms. (and still no tx?)
Bottom Line: The majority of infections with Histoplasmosis are self-limiting and do not warrant treatment.
Steps in Rapid Sequence Intubation:
- Preoxygenation - Administration of 100% oxygen for 3 minutes of normal, tidal volume breathing in a normal, healthy adult establishes an adequate oxygen reservoir to permit 8 minutes of apnea before oxygen desaturation to less than 90% occurs.
- Pretreatment - Patients with significant cardiovascular disease (e.g., ischemic coronary disease) who are being intubated in the ED may benefit from the administration of the synthetic opioid, fentanyl, in a dose of 3 !g/kg to mitigate the release of catecholamines in response to airway manipulation.
- Paralysis with induction - In this phase, a potent sedative agent (Etomidate) is administered by rapid IV push in a dose capable of rapidly producing unconsciousness. This is immediately followed by rapid administration of an intubating dose of an NMBA, usually succinylcholine.
It is usual to wait 45 seconds from the time the succinylcholine is given to allow sufficient paralysis to occur.
- Positioning - The patient should be positioned for intubation as consciousness is lost. Usually, positioning involves head extension, often with flexion of the neck on the body, but there is evidence that simple extension of the head alone, or extension of both the head and neck (the extension-extension position) are equivalent or superior.
Sellick’s maneuver (application of firm backward-directed pressure over the cricoid cartilage) has long been recommended to minimize the risk of passive regurgitation and, hence, aspiration.
- Tube placement and confirmation of placement – End-tidal CO2 detector
Bottom Line: The order for rapid sequence intubation is preoxygenation, pretreatment with fentanyl as needed for cardiovascular disease, paralysis with a potent sedative agent, succinylcholine for paralysis, positioning and tube placement.
Succinylcholine is degraded by
plasma pseudocholinesterase and has a very short half-life.
Succinylcholine is a DEpolarizing neuromuscular blocking agent.
Patients with renal or hepatic dysfunction may have a prolonged response to what non-depolarizing paralytic
vecuronium,
because it is cleared by both the kidney and liver.
pancuronium is eliminated by
both the kidney and liver
and
requires dose adjustments in the setting of renal or hepatic dysfunction.
Cisatracurium elimination is by
elimination is by ester hydrolysis and Hoffman elimination.
and both liver and kidney get “poly” cyst
an isomer of atracurium,
with fewer tendencies to induce release of histamine.
Rocuronium onset
rapid onset of action
and
intermediate duration of action,
which makes it useful for short procedures, and is eliminated by the liver.
Patients with absolute indications for an IVC filter
have thromboembolic disease with a contraindication to anticoagulation or a complication or failure of anticoagulation.
thrombolysis is indicated for
treatment of
acute myocardial infarction,
acute ischemic stroke,
most cases of massive pulmonary embolism.
CAREFUL- “acute” is 24h catheter therapy
Currently approved fibrinolytic agents and their mechanisms
streptokinase, acylated plasminogen streptokinase activator complex (anistreplase),
urokinase, recombinant tissue-type plasminogen activator (rt-PA) (Alteplase; Activase),
and
two recombinant derivatives of rt-PA, tenecteplase (TNKase) and reteplase (Retaplase). All of these agents act by converting the proenzyme, plasminogen, to plasmin, the active enzyme
Heparin acts as
an anticoagulant by
activating antithrombin III a
nd accelerating the rate at which antithrombin inhibits enzymes involved in blood coagulation, particularly thrombin and factor Xa
Mycobacterium avium complex (MAC)
Mycobacterium avium
and
Mycobacterium intracellulare.
aerobic, non-spore forming, and non-motile bacilli.
These organisms produce pulmonary disease in patients with normal immune function
and may lead to
disseminated disease in patients with immunodeficiency.
Disseminated MAC is diagnosed with positive cultures from blood or other normally sterile sites including bone marrow, liver, and spleen (choice A). Blood cultures are the best test for disseminated infection. Sending two separate blood samples will achieve a diagnosis in 99% of cases of disseminated MAC. In cases of early disease, bone marrow biopsy with culture may be the most sensitive test.
MAC cultured from lymph nodes may indicate local disease alone (choice B).
Sputum cultures, bronchial washings, and stool samples can test positive for MAC and represent colonization or local disease (choice C, D and E). Positive cultures from more than one of these sites indicates disseminated disease.
Bottom Line: Disseminated MAC infection occurs in immunocompromised patients. Diagnosis is confirmed with positive cultures from blood, bone marrow, spleen, or liver.
Cilostazol
(pletal)
FDA approved treatment for intermittent claudication.
phosphodiesterase III inhibitor - increases cyclic adenosine monophosphate (cAMP).
nhibition of smooth muscle cell contraction and platelet aggregation.
Pentoxyfiline
FDA approved treatments
for claudication.
is another treatment for claudication.
It increases blood cell flexibility but its exact mechanism is unknown
Statins mechanism
HMG CoA reductase inhibitors
ASA mechanism
inhibitors of cyclooxygenase
and have effects on platelets.
Clopidogrel mechanism
(plavix)
antiplatelet agent that irreversibly inhibits an adenosine diphosphate (ADP)
chemoreceptor on platelet cell membranes
Lymphangitis In individuals with normal immunity, the most common organism is
Streptococcus pyogenes
can gain entry to lymphatic channels through a distal skin breach or disruption from local trauma or dermatophyte infection.
Lymphangitis can also occur in the setting of Staphylococcus aureus infection.
In immunocompromised patients, gram-negative organisms (choice D) are also important causes of lymphangitis following lower limb cellulitis.
Hydrofluoric acid binds what electrolyte and what is result
binds calcium
causing life threatening hypocalcemia
possible cardiac arrest.
The antidote of hydrofluoric burns is
copious irrigation
intra-ARTERIAL calcium gluconate infusion
symptomatic managment is calcium gluconate gel that may be soothing,but does not treat the hypocalcemia.
Because of the potential cardiac side effects, the patient should be monitored in an ICU setting.
signs of local anesthetics an overdose or inadvertent intravascular injection list early to late
numbness or tingling of the tongue or lips
metallic taste,
light-headedness,
tinnitus
or
visual disturbances.
---- progress to slurred speech disorientation, SEIZURE! ---
Cardiovascular widened PR interval, widened QRS sinus tachycardia. cardiovascular collapse
The primary treatments of local anesthetic toxicity are oxygen and airway support. If a seizure does not terminate spontaneously, a benzodiazepine (e.g., midazolam) or thiopental
Ketamine contraindications and indications
Cerebral HTN
Intra ocular pressure
Heart failure
direct and indirect stimulator of the sympathetic nervous system.
This results in increased myocardial oxygen consumption and elevated intracranial pressures.
Ketamine is often used for sedation in a combative and mentally retarded patient
Ketamine assists in bronchodilation and can be a useful endobronchial agent in thoracic surgery
Ketamine is used in patients with a congenital intracardiac shunt
Atropine
treatment of bradycardia, excess salivary secretion, anticholinesterase poison, and to decrease the effects of anticholinesterases for neuromuscular blocker reversal.
rapid onset
half-life of 2-3 hours.
The mechanism of action is competitive inhibition of acetylcholine at muscarinic receptors.
It functionally reverses parasympathetic effects.
Neostigmine is used for
symptomatic control of myasthenia gravis
reversal of nondepolarizing muscle relaxants.
Ogolvies
inhibition of acetylcholinesterases which prolonges acetylcholine’s actions at motor endplates.
Succinylcholine mechanism of action
depolarization of motor endplates which causes paralysis.
depolarizing neuromuscular blocker used for rapid sequence intubation.
One of the major protective IG for the intestinal tract
IgA
Action of IgA in gut
binds antigens at the mucosal surface.
inhibits the adherence of bacteria to epithelial cells
prevents their colonization and multiplication.
neutralizes bacterial TOXINS
neutralizes VIRAL activity
blocks the absorption of antigens from the gut
NOT cell mediated
IgA also does not cause the destruction (just neutralize / block) of infectious organisms or antigens, which sharply contrasts to the role of other immunoglobulins.
Major role and fxn of IgG
associated with complement fixation, opsonization, fixation to macrophages, and membrane transport.
most abundant immunoglobulin class in the serum.
Minimum alveolar concentration (MAC)
defined as the alveolar concentration of an inhaled anesthetic required to prevent movement in 50% of patients in response to noxious stimuli
reflects concentrations of the drug in other well perfused organs after equilibrium such as the brain and heart.
