UW5 Flashcards
Second generation antipsychotics
Olanzapine
Clozapine
first vs second generation Antipsychotics
2nd gen have less chance of extrapyramidal side effects but are associated with metabolic effects
weight gain
Dyslipidemia
hyperglycemia
2nd generation antipsychotics monitoring guidelines
BMI
Fasting glucose & lipids
Blood pressure
Waist circumference
Question
D. Secondary Mitral Regurgitation
This patient’s presentation with fatigue, progressive dyspnea, orthopnea, pulmonary crackles, and an S3 heart sound is consistent with decompensated heart failure. Appropriate treatment with diuretics and vasodilators resulted in symptomatic improvement and disappearance of the apical holosystolic murmur, which was most likely due to secondary (functional) mitral valve regurgitation (MR).
Whereas primary MR is caused by an intrinsic defect of the mitral valve apparatus (eg, cleft in a valve cusp, myxomatous degeneration of the chordae tendineae), secondary MR occurs due to other factors. Decompensated heart failure is a common cause of secondary MR because it leads to an increase in left ventricular end-diastolic volume (LVEDV), or preload, with dilation of the mitral valve annulus (the tissue on which the mitral valve cusps are mounted) and taut stretching of the chordae tendineae. The dilated annulus and restricted movement of the chordae tendineae can cause insufficient closure of an intrinsically normal mitral valve, resulting in MR. Systemic hypertension can also contribute to secondary MR by favoring relatively lower-resistance regurgitant flow.
Treatment with diuretics to reduce LVEDV and vasodilators to reduce blood pressure can lead to resolution of heart failure-induced MR.
(Choice A) Calcification of the mitral valve annulus may occur with aging, and can be accelerated by hypertension or advanced kidney disease. It is usually an incidental finding that does not affect mitral valve function.
(Choice B) Increased flow velocity through the aortic valve occurs with aortic valve stenosis. The resulting murmur is crescendo-decrescendo and best heard at the right second intercostal space (rather than holosystolic and best heard at the apex).
(Choice C) Chordae tendineae rupture is a potential cause of primary MR that can occur in the setting of bacterial endocarditis, connective tissue disease (eg, Marfan syndrome), or acute myocardial infarction. The resulting murmur does not resolve with diuretics and vasodilators; surgical repair is typically required.
(Choice E) Thickened and deformed mitral valve cusps can occur in rheumatic heart disease and are a potential cause of primary MR. Such a murmur does not resolve with treatment of decompensated heart failure. In addition, mitral stenosis (evidenced by an opening snap and mid-diastolic rumble) is more likely than MR to occur with rheumatic heart disease.
Educational objective:
Decompensated heart failure is a common cause of secondary (functional) mitral valve regurgitation. Increased left ventricular end-diastolic volume causes dilation of the mitral valve annulus and restricted movement of the chordae tendineae with subsequent regurgitation. Treatment with diuretics and vasodilators can improve heart failure-induced MR.
Question
C. Novobiocin Resistant
Question
D. Methylnaltrexone
Question
A. Decreased libido
pituitary adenoma
Question
A. Distribution is limited to the Extracellular fluid compartment
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E.
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Type I collagen locations
8 Listed
- Skin
- bone
- tendons
- ligaments
- dentin
- cornea
- blood vessels
- scar tissue
Type I collagen diseases
Osteogenesis imperfecta
Type II Collagen Locations
- Cartilage
- vitreous humor
- nucleus pulposus
Type III Collagen Locations
- Skin
- lungs
- intestines
- blood vessels
- bone marrow
- lymphatics
- granulation tissue
Type IV collagen Locations
Basement membrane
Type IV collagen diseases
Alport Syndrome
Type III collagen Diseases
Vascular Ehler-Danlos Syndrome (Type IV)
Type II Collagen Diseases
Skeletal dysplasias
Question
D. Organ of Corti
This patient has high-frequency hearing loss due to chronic noise exposure. Transduction of mechanical sound waves into nerve impulses occurs in the organ of Corti through the following steps:
Sound reaches the middle ear by vibrating the tympanic membrane.
The vibration is transferred to the oval window by the ossicles.
Vibration of the oval window causes vibration of the basilar membrane, which in turn causes bending of the hair cell cilia against the tectorial membrane.
Hair cell bending causes oscillating hyperpolarization and depolarization of the auditory nerve, thereby creating nerve impulses from sound.
Noise-induced hearing loss results from trauma to the stereociliated hair cells of the organ of Corti. The acoustic reflex normally dampens the effects of loud noise by causing the stapedius and tensor tympani muscles to contract, which lessens the responsiveness of the ossicles to sound. However, prolonged noise exposure can cause distortion or fracture of the stereocilia due to shearing forces against the tectorial membrane. High-frequency hearing is lost first, regardless of the frequency of the sound causing the damage.
Question
This man with a large area of localized cardiac apical wall thinning likely died of chronic Chagas cardiomyopathy. Chagas disease is caused by infection with the protozoan Trypanosoma cruzi, which is transmitted by the triatomine “kissing” bug (Reduviid family) found throughout the Americas as far north as the southern United States. Infection is rare in developed regions, but the disease is endemic throughout Central and South America where widespread open-air and thatched-roof housing exposes individuals to routine contact with the triatomine vector.
Years following initial infection, some individuals develop serious end-organ damage affecting the cardiac, gastrointestinal, and/or central nervous systems. Cardiac disease results from a chronic parasite-induced and immune-mediated myocarditis that leads to dilated cardiomyopathy (DCM). Chronic Chagas cardiomyopathy is relatively unique among DCMs in that there is characteristically localized apical wall thinning with the development of a large apical aneurysm. In addition to impairing ventricular systolic function, the aneurysm can harbor mural thrombus that may systemically embolize and cause stroke. Damage to the cardiac conduction system can also trigger ventricular arrhythmias (eg, ventricular tachycardia, ventricular fibrillation) that can lead to sudden cardiac death (the likely cause of death in this patient).
The gastrointestinal manifestations of Chagas disease result from destruction of the myenteric plexus, which can lead to progressive dilation and dysfunction of the esophagus and, less commonly, the colon
Question
D. Selective
This patient with dysuria and urethral discharge has gonococcal urethritis as indicated by the Gram stain showing gram-negative diplococci within leukocytes. Neisseria gonorrhoeae can be cultured on Thayer-Martin VCN selective medium, which contains vancomycin, colistin, nystatin, and trimethoprim. These antibiotics kill potential contaminants such as gram-positive organisms (vancomycin), gram-negative organisms other than Neisseria (colistin and trimethoprim), and fungi (nystatin).
(Choice A) Differential media help identify cultured organisms based on their metabolic and biochemical properties. Examples of differential media include the MacConkey and eosin methylene blue (EMB) agars used to culture enteric organisms. Organisms that ferment lactose will appear pink on MacConkey agar and black on EMB agar.
(Choice B) Enrichment media contain special growth factors required for some organisms. Examples include the X and V factors required by Haemophilus or the anaerobic conditions needed by Clostridium species.
(Choice C) Reducing media (eg, thioglycolate broth) remove oxygen and are used to culture anaerobic organisms.
(Choice E) A synthetic medium is any chemically-defined medium for which all of the chemical contents are known.
Educational objective:
Neisseria can be isolated by culture on selective media such as the Thayer-Martin VCN (vancomycin/colistin/nystatin) medium, which inhibits growth of contaminants such as gram-positive organisms, gram-negative organisms other than Neisseria, and fungi.
Identify cranial nerves
Question
D. Sensory right side of face and left side of body
This patient has occlusion of the right posterior inferior cerebellar artery (PICA), which arises from the vertebral artery. Occlusion of the PICA results in lateral medullary (Wallenberg) syndrome. This disorder classically results in a constellation of symptoms because of damage to specific areas:
Vertigo and nystagmus (vestibular nucleus)
Ataxia (inferior cerebellar peduncle)
Loss of pain and temperature sensation in the ipsilateral face (spinal trigeminal nucleus) and contralateral body (spinothalamic tract)
Bulbar weakness (eg, dysphagia, dysarthria) (nucleus ambiguus)
Horner syndrome (ie, miosis, ptosis, anhidrosis) may also occur in the ipsilateral eye due to damage to descending sympathetic nervous system fibers.
(Choice A) Damage to the oculomotor nerve (CN III) can lead to impaired extraocular movements with a down-and-out eye due to unopposed action of the superior oblique muscle (innervated by the trochlear nerve [CN IV]) and the lateral rectus muscle (innervated by the abducens nerve [CN VI]). When this finding (ie, down-and-out eye) is accompanied by contralateral lower facial weakness and hemiplegia, it is suggestive of midbrain infarction due to occlusion of the posterior cerebral artery (ie, Weber syndrome).
(Choice B) Hemiparesis of the arm and leg with an upper motor neuron pattern of facial weakness (ie, only involves the lower face) is the classic presentation of an internal capsule stroke. The internal capsule is supplied by the lenticulostriate arteries, which are branches of the MCA.
(Choice C) Internuclear ophthalmoplegia (ie, loss of conjugate lateral gaze) is caused by damage to the medial longitudinal fasciculus, which can occur with occlusion affecting the pontine arteries. Bilateral loss of conjugate gaze is more likely with other etiologies (eg, multiple sclerosis plaques) because bilateral ischemic injury to the same area is uncommon.
(Choice E) Homonymous hemianopia (ie, vision loss in the same half of the visual field in both eyes) with macular sparing is classically caused by occlusion of the posterior cerebral artery; the macula is spared due to collateral blood supply from the middle cerebral artery. Homonymous hemianopia without macular sparing can occur due to damage of the optic tract or optic radiation, which can occur with occlusion of several different vessels (eg, anterior choroidal, middle cerebral artery).
Educational objective:
Posterior inferior cerebellar artery occlusion causes lateral medullary (Wallenberg) syndrome. This disorder is characterized by vertigo/nystagmus, ipsilateral cerebellar signs, loss of pain/temperature sensation in the ipsilateral face and contralateral body, bulbar weakness, and ipsilateral Horner syndrome.
Wallenberg syndrome
lateral medullary syndrome
Occlusion of the PICA results in lateral medullary (Wallenberg) syndrome. This disorder classically results in a constellation of symptoms because of damage to specific areas:
Vertigo and nystagmus (vestibular nucleus)
Ataxia (inferior cerebellar peduncle)
Loss of pain and temperature sensation in the ipsilateral face (spinal trigeminal nucleus) and contralateral body (spinothalamic tract)
Bulbar weakness (eg, dysphagia, dysarthria) (nucleus ambiguus)
Question
A normal (Gaussian) distribution refers to a symmetrical, bell-shaped distribution with a fixed proportion of observations lying within a certain distance of the mean. This distance is called the standard deviation (SD) and reflects the degree of dispersion from the mean. According to the properties of this distribution, 68% of observations lie within 1 SD on either side of the mean, with half (ie, 68/2 = 34%) above and half (34%) below the mean. The remaining 32% (= 100% − 68%) lie outside 1 SD from the mean, with half (ie, 32/2 = 16%) above and the other half (16%) below 1 SD from the mean. In addition, 95% of all observations lie within 2 SDs of the mean, and 99.7% of all observations lie within 3 SDs of the mean. This is the 68-95-99.7 rule.
For men age 35-44 in this sample, the mean systolic blood pressure (SBP) is 120 mm Hg with an SD of 20 mm Hg. Therefore, subjects with SBP >140 mm Hg (to fit the proposed definition of hypertension) represent observations >1 SD above the mean. Based on the 68-95-99.7 rule, 32% of observations (= 100% − 68%) lie outside 1 SD from the mean, with half (16%) above and half (16%) below 1 SD from the mean. Therefore, 16% of men age 35-44 have SBP >140 mm Hg.
(Choices B, C, D, and E) Based on the 68-95-99.7 rule, 34% of subjects lie either 1 SD above the mean or 1 SD below the mean. In men age 35-44:
34% have SBP 100-120 mm Hg, 34% have SBP 120-140 mm Hg, and, 68% have SBP 100-140 mm Hg.
Half (50%) have SBP above the mean (ie, >120 mm Hg) and half have SBP below the mean (<120 mm Hg).
Given that 84% = 50% + 34%, this could represent the sum of those with SBP 100-120 mm Hg (34%) and those with SBP >120 mm Hg (50%): in other words, those with SBP >100 mm Hg.
Question
C. Pediculus humanus capitis
This patient has numerous nits, which are egg casings of the head louse Pediculus humanus capitis. Pediculosis capitis (ie, head lice infestation) is common in school children and adults who come into close contact with infested individuals (eg, sports teams, homeless shelters). Transmission is usually by direct contact, although transmission by fomites (eg, hats, hairbrushes) can also occur. Head lice require multiple blood meals a day and die within 2 days if separated from a host. They do not carry arthropod-borne infection, but the bite can induce a pruritic allergic reaction.
Female lice attach their nits to the hair shaft about 0.5 cm from the skin surface; nits further from the surface often represent old egg casings that have hatched and generally do not require treatment. First-line treatment includes topical pediculicides (eg, permethrin, ivermectin). Manual lice removal via wet combing is an alternate treatment for patients for whom standard pediculicides are not feasible (eg, children age <2 years, resource-poor populations).
(Choice A) Cimex lectularius (ie, bedbugs) bites present as pruritic, red papules in clusters. The females lay eggs away from the host and do not produce nits.
(Choice B) Colonization with Malassezia yeasts is associated with seborrheic dermatitis. On the scalp, this condition can produce white skin flakes in the hair (ie, dandruff). The flakes are not adherent to the hair shaft and are typically found loosely throughout the hair and on the clothing.
(Choice D) Pthirus pubis (ie, crab louse, pubic louse) is usually transmitted by sexual contact. The louse is adapted for attaching to thick hair shafts, and the nits are usually found on pubic and other thick hair (eg, eyelashes); however, scalp hair is not typically affected.
(Choice E) Sarcoptes scabiei causes scabies, which presents with pruritic papules and burrows on the interdigital and flexural skin of the extremities. The female mite lays eggs in burrows and does not form nits.
(Choice F) Trichophyton tonsurans is a dermatophyte that causes tinea capitis, which presents as a scaly, erythematous patch of hair loss. There are often small, black dots that represent broken hair shafts.
Educational objective:
Pediculus humanus capitis (ie, head lice) infestation is common in school children and adults who come into close contact with infested individuals. Transmission is usually by direct contact. The eggs (nits) are attached to the hair shaft and can be identified on inspection. First-line treatment includes topical pediculicides (eg, permethrin, ivermectin).
Question
C. Decreased IL-2 production
Question
E. muscular dystrophy
This patient has distal muscle weakness (eg, difficulty opening jar lids) with delayed muscle relaxation after contraction (myotonia), key features of myotonic dystrophy (DM).
DM is an autosomal dominant muscular dystrophy caused by a trinucleotide repeat expansion in the DMPK gene, which is then transcribed into mutant mRNA. The mutant mRNA is untranslatable and toxic to the expression of other genes, particularly those related to skeletal muscle chloride channels, resulting in myotonia. Grip myotonia is classic and characterized by impaired muscle relaxation after voluntary release of a contracted hand.
The toxic mRNA also affects T tubules, which usually facilitate synchronized release of calcium ions for organized muscle contraction, resulting in weakness due to impaired excitation-contraction coupling. Weakness classically involves the face (eg, long, narrow face with sagging) and distal skeletal muscles. This patient’s recent falls are likely due to footdrop, but quadriceps involvement can occasionally occur and may be contributing to his difficulty walking up stairs. Muscular atrophy in DM preferentially affects the type I (slow-twitch) fibers, as seen on this patient’s muscle biopsy.
Other common features of DM include cataracts, insulin resistance, and early-onset frontal balding.
(Choice A) Inflammatory myopathies (eg, dermatomyositis, polymyositis) present with symmetric proximal muscle weakness without myotonia. In addition, inflammatory cell infiltration is seen on muscle biopsy.
(Choice B) Certain ion channel myopathies can manifest with myotonia, but those that do so are associated with muscle hypertrophy (not atrophy) due to muscle overactivity. In contrast, the genetic defects causing muscular dystrophy result in progressive muscle damage that leads to atrophy of muscle fibers.
(Choice C) Mitochondrial myopathies are characterized by varying degrees of muscle weakness, typically presenting in infancy or early childhood with multisystem involvement (eg, seizures). In addition, ragged red fibers (due to bright red mitochondrial bundles) are classically seen on muscle biopsy.
(Choice D) Motor neuron disease (eg, amyotrophic lateral sclerosis) is characterized by progressive nerve degeneration, resulting in skeletal muscle weakness. Muscle wasting and a weak grip are common, but impaired muscle relaxation does not occur.
(Choice F) Myasthenia gravis, caused by postsynaptic acetylcholine receptor antibodies, is the most common neuromuscular junction disorder and presents with proximal muscle weakness. However, the weakness is fluctuating and fatigable, and hand weakness and relaxation impairment would not be expected.
Educational objective:
Myotonic dystrophy is characterized by muscle weakness and myotonia (impaired muscle relaxation) with muscle atrophy, particularly of the type I (slow-twitch) muscle fibers. Pathophysiology involves a trinucleotide repeat expansion causing mutant RNA that disrupts muscle contraction and relaxation.
Question
F. Polymyositis
This patient, a middle-aged man with progressive, symmetric proximal muscle weakness, has typical symptoms of polymyositis. The weakness may be painless or associated with diffuse myalgias. Muscle enzyme levels (eg, creatine kinase) are invariably elevated, and autoantibodies (eg, antinuclear antibodies, anti-Jo-1 antibodies) are present in most cases. Polymyositis is similar to dermatomyositis, although it lacks the typical skin findings; both may occur independently or as a paraneoplastic manifestation of an underlying malignancy.
Polymyositis is an inflammatory myopathy triggered by unknown, possibly viral, antigens. It likely represents a cell-mediated immune response against myocytes. Increased expression of major histocompatibility complex class I antigens on the sarcolemma has been demonstrated and likely leads to presentation of autoantigens to CD8+ cytotoxic cells that subsequently initiate myocyte destruction. Muscle biopsy in polymyositis reveals inflammation, patchy necrosis, and regeneration and fibrosis of muscle fibers. Infiltration of the endomysium by macrophages and CD8+ lymphocytes is typically seen.
(Choice A) Joint involvement in systemic sclerosis may cause arthralgias and contractures, but muscle weakness is not seen.
(Choices B and C) Myasthenia gravis is caused by anti-acetylcholine receptor autoantibodies and is characterized by episodic weakness that initially affects the ocular/bulbar musculature. The Eaton-Lambert myasthenic syndrome is a paraneoplastic condition causing fatigable weakness in the extremities; it is caused by autoantibodies to presynaptic calcium channels. Light microscopy of muscle biopsy specimens is normal in these conditions.
(Choice D) Polyarteritis nodosa is an uncommon systemic vasculitis that presents with intermittent episodes of abdominal pain, peripheral neuropathy, renal insufficiency, and severe hypertension. Biopsy is characterized by transmural inflammation of the arterial wall with fibrinoid necrosis.
(Choice E) Polymyalgia rheumatica (PMR) causes myalgias of the shoulder and pelvic girdle muscles, often with systemic symptoms (eg, fever, weight loss). Weakness is not typical, and PMR occurs almost exclusively in patients age >50.
Educational objective: Polymyositis causes symmetric proximal muscle weakness. Muscle biopsy reveals inflammation, necrosis, and regeneration of muscle fibers. Over-expression of major histocompatibility complex class I proteins on the sarcolemma leads to infiltration with CD8+ T lymphocytes and myocyte damage.
Question
Cytotoxic chemotherapy induces apoptosis in dividing cells by impairing mitosis or inducing DNA damage. These medications are administered at the highest tolerable dose so that maximal effect can be achieved. However, the effects are not selective; all cell lines with high turnover rates are impacted, including tumor, hair follicle, bone marrow, and gastrointestinal (GI) epithelial cells.
Damage to the bone marrow and GI lining following chemotherapy dramatically increases risk of life-threatening systemic infection due to the following:
Neutropenia: Neutrophils are normally the most prevalent leukocyte and are crucial for initiating the local and systemic response to invading bacteria and fungi. Because cytotoxic chemotherapy damages granulocyte precursors, patients often develop neutropenia 10-14 days after treatment. Risk of infection increases with the duration and severity of neutropenia.
Mucositis: The gastrointestinal epithelium has abundant blood flow and a high turnover rate, which makes it particularly susceptible to damage from chemotherapy. Patients frequently develop oral and gastrointestinal ulcers (mucositis), which create a portal of entry for commensal bacteria to translocate from the lumen to surrounding tissue. Because the neutrophil response is usually concurrently impaired, the bacteria are frequently able to establish a nidus of infection and spread through the vasculature.
Therefore, to reduce the risk of serious infection, patients who receive systemic chemotherapy are often empirically treated with prophylactic antibiotics (eg, ciprofloxacin) to prevent commensal organisms from invading and with granulocyte-stimulating agents (eg, filgrastim) to increase neutrophil count.
(Choice A) In contrast to the gastrointestinal epithelium, which has a very high turnover rate, the urothelial barrier regenerates every 3-6 months. Therefore, it is minimally affected by short chemotherapy cycles.
(Choices B and D) Unlike neutrophils, which live 5-10 days, plasma cells have low turnover rates; therefore, levels of circulating immunoglobulin are typically unaffected by most chemotherapy for solid tumors (eg, breast cancer). Similarly, tissue-resident macrophages have a long life-span and are not significantly impaired by chemotherapy cycles.
Educational objective:
Cytotoxic chemotherapy nonselectively kills rapidly dividing cells, including tumor, hair follicle, bone marrow, and gastrointestinal epithelial cells. Severe infections are common due to neutropenia from myelosuppression and commensal bacterial invasion via gastrointestinal epithelial damage from mucositis.
Question
Thyroid follicular cells take up inorganic iodide (iodide trapping) against a concentration gradient using a sodium-iodide symporter. Iodide is then released into the thyroid follicular lumen, where it is oxidized to iodine radical by thyroid peroxidase. Iodine then binds to tyrosine residues (organification) in thyroglobulin to form monoiodotyrosine (MIT) and diiodotyrosine (DIT). Coupling of MIT and DIT produces triiodothyronine (T3; MIT coupled with DIT) and thyroxine (T4; two DITs coupled). The thyroid follicular cells then engulf thyroglobulin, which contains the iodinated tyrosine compounds, via pinocytosis. In the thyroid cytoplasm, T3 and T4 (collectively, thyroid hormones) are removed from the rest of the thyroglobulin and secreted from the basolateral border.
This patient with elevated T4 and suppressed TSH has primary hyperthyroidism. Methimazole and propylthiouracil are thioamide drugs used for treating hyperthyroidism. They inhibit thyroid peroxidase, the enzyme responsible for both iodine organification and coupling of iodotyrosines. Propylthiouracil also decreases the peripheral conversion of T4 to the active hormone T3, although methimazole does not have this effect (Choice D).
(Choice A) Colloid is a gelatinous material in the follicular lumen that consists mainly of thyroglobulin. The production of colloid is regulated primarily by TSH; it is not dependent on thyroid peroxidase and is not inhibited by thioamides.
(Choice C) Iodide uptake is upregulated by TSH. Perchlorate and pertechnetate are competitive inhibitors of the sodium-iodide symporter.
(Choice E) Hyperthyroidism is characterized by increased sensitivity to catecholamines due to the thyroid hormone–mediated upregulation of beta-adrenergic receptors. Beta blockers help decrease the target organ effects of thyroid hormones, and certain ones (eg, propranolol) also decrease the peripheral conversion of T4 to T3.
Educational objective:
Thioamides (eg, methimazole, propylthiouracil) decrease the formation of thyroid hormones via inhibition of thyroid peroxidase, the enzyme responsible for both iodine organification and coupling of iodotyrosines. Propylthiouracil also decreases the peripheral conversion of T4 to T3.
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A. Buprenorphine
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B. focal structural abnormality
Question
E. sympathomimetic activity
This hemodynamically unstable patient has severe bronchospasm and impending respiratory failure and requires intubation. Prior to intubation, anesthesia must be induced. Three medications are commonly used because of their rapid onset of action and short duration of effect.
Propofol: A highly lipophilic GABA agonist that may be used for long-term sedation. Disadvantages include vasodilation, which can result in hypotension and an increase in serum triglycerides and lipase.
Etomidate: A GABA agonist that has the advantage of being the most hemodynamically neutral. It does not cause changes in heart rate, blood pressure, or cardiac output. However, it inhibits cortisol synthesis, which can lead to (reversible) adrenocortical suppression. Because of this, it is often avoided in patients with septic shock, and it should not be used as maintenance of sedation after induction.
Ketamine: An N-methyl-D-aspartate (NMDA) antagonist that is similar to PCP; it preserves the respiratory drive during induction of anesthesia. In contrast to propofol and etomidate, it also provides an analgesic effect. Ketamine stimulates the release of catecholamines (ie, sympathomimetic), which can cause bronchodilation but also increase the heart rate, myocardial contractility, and cerebral blood flow, potentially putting the patient at risk for cardiovascular events or increased intracranial pressure.
In this patient with an acute asthma attack, ketamine was likely chosen because it stimulates release of catecholamines that increase sympathomimetic activity and may improve bronchospasm.
(Choice A) Propofol and etomidate are both GABA agonists, but ketamine works at the NMDA receptor.
(Choice B) Both ketamine and etomidate are much less lipophilic than propofol.
(Choice C) Both ketamine and etomidate are metabolized primarily by the liver. Propofol is also metabolized by the liver, but the effect is terminated by its redistribution rather than metabolism.
(Choice D) Neuromuscular blockade is often used to facilitate intubation. None of the three commonly used induction anesthetics cause significant neuromuscular blockade, so an additional medication (eg, succinylcholine, rocuronium) is used if needed.
Educational objective:
Ketamine can be used for anesthesia induction. The side effects of increased catecholamine release (eg, bronchodilation) are often exploited in patients with bronchospasm.
Question
This patient’s presentation of chest pain and diaphoresis along with a history of systemic atherosclerosis and type 2 diabetes mellitus is suggestive of acute coronary syndrome. ECG findings are consistent with an inferior ST elevation myocardial infarction (STEMI). Percutaneous coronary intervention (PCI) or fibrinolysis to achieve myocardial reperfusion is recommended for acute MI patients who present within 12 hours of symptom onset. PCI is preferred over fibrinolytic therapy due to lower rates of intracerebral hemorrhage (ICH) and recurrent MI; however, it may not be available at all institutions. In such cases, treatment with fibrinolytics (tenecteplase, alteplase) improves clinical outcomes in the absence of contraindications (eg, gastrointestinal bleeding, recent surgery).
Alteplase binds fibrin in the thrombus (clot) and converts entrapped plasminogen to plasmin. Plasmin hydrolyzes key bonds in the fibrin matrix causing clot lysis and restoration of coronary arterial blood flow. The most common adverse effect of fibrinolytic therapy is hemorrhage. This patient has signs of ICH, such as decreased level of consciousness, asymmetric pupils, and irregular breathing.
(Choice A) Carotid artery thrombosis can cause an ischemic stroke with fluctuating symptoms that may progress with periods of improvement. Abrupt onset of symptoms along with loss of consciousness after treatment with thrombolytics favors ICH over thrombotic stroke.
(Choice B) Aortic dissection typically presents with severe, tearing chest pain that radiates to the interscapular area. It occurs most commonly in patients with hypertension and Marfan/Ehlers-Danlos syndrome. Chest x-ray typically reveals a widened mediastinum.
(Choice C) Interventricular septum perforation results in a left-to-right shunt and symptoms of acute heart failure. It presents with chest pain, dyspnea, symptoms of cardiogenic shock, and a harsh holosystolic murmur on the left sternal border.
(Choice E) Reperfusion of ischemic myocardium may result in paradoxical cardiomyocyte dysfunction, a phenomenon known as reperfusion injury. This can occur in patients treated with PCI, thrombolytics, or coronary artery bypass grafting. Clinical manifestations include arrhythmias, myocardial stunning (prolonged but reversible contractile dysfunction), and myocyte death.
(Choice F) Opioid overdose typically presents with small, constricted pupils (miosis) and respiratory depression (respirations usually <12/min).
(Choice G) Pulmonary embolism (PE) presents with acute onset of dyspnea, pleuritic chest pain, and possibly hemoptysis. Tachycardia, hypotension, cyanosis, and loss of consciousness can occur when PE is severe.
Educational objective:
Fibrinolytic therapy for acute ST segment elevation myocardial infarction is a reasonable reperfusion technique for patients with no contraindications to thrombolysis. Fibrinolytic agents such as alteplase bind to fibrin in the thrombus (clot) and activate plasmin, which leads to thrombolysis. The most common adverse effect of thrombolysis is hemorrhage (eg, gastrointestinal, intracerebral).
