Medicine and Anesthesia Flashcards
Which of the following is considered a biological marker seen in malignant hyperthermia?
A. Creatine phosphatase
B. Acetyl cholinesterase
C. Acetyl phosphatase
D. Creatine Kinase
D. Creatine Kinase
In malignant hyperthermia (MH), a serious pharmacogenetic disorder often triggered by certain anesthetic agents (like halothane or succinylcholine), creatine kinase (CK) levels are elevated due to muscle cell damage. Elevated CK is a significant biomarker seen in malignant hyperthermia and reflects muscle breakdown (rhabdomyolysis), which is a key feature of the condition
The earliest sign of impending malignant hyperthermia is:
A. elevated core temperature.
B. increased end tidal CO2.
C. skeletal muscle rigidity.
D. tachycardia.
D. Increased end tidal CO2
Early signs: hypercapnia, tachycardia, muscle rigidity
Later signs: ECG changes secondary to hyperkalemia, rhabdomyolysis (elevated plasma
creatine kinase and urine myoglobin—dark urine), and hyperthermia.
Most common causes of death are hyperkalemia and coagulopathy from hyperthermia
Which of the following is contraindicated in management of cardiac arrhythmias during a malignant hyperthermia episode?
A. Procainamide
B. Cardizem
C. Regular insulin and D50
D. Sodium bicarbonate
B. Cardezim
Cardizem (diltiazem) is a calcium channel blocker and is contraindicated in the management of arrhythmias during a malignant hyperthermia (MH) episode because it can exacerbate the already compromised calcium homeostasis in muscle cells. In MH, excessive calcium is released within the muscle cells due to the hypermetabolic state, contributing to the muscle rigidity and hyperthermia. Adding a calcium channel blocker like Cardizem could worsen the situation by further disturbing calcium balance, potentially leading to cardiovascular collapse.
Other Options:
A. Procainamide: This is a Class 1a antiarrhythmic drug used to manage arrhythmias. It is not contraindicated in the treatment of arrhythmias during MH. However, it should be used cautiously, considering the underlying metabolic and acid-base disturbances.
C. Regular insulin and D50: This is commonly used in cases of hyperkalemia associated with malignant hyperthermia or other conditions leading to muscle breakdown. Insulin facilitates the movement of potassium into cells, while D50 (glucose) prevents hypoglycemia. This combination is appropriate in managing hyperkalemia.
D. Sodium bicarbonate: This is used to correct metabolic acidosis that may develop during an MH crisis. It is generally indicated for acidosis in MH and helps correct the disturbed acid-base balance.
Which of the following patients exhibits a contraindications to BMP2 use in bone grafting?
A. 23 y/o female with HIV
B. 25 y/o cleft lip pt
C. 35 y/o DM2
D. 55 y/o with cancer
D. 55 y/o with cancer
BMP-2 is a growth factor that promotes bone formation by stimulating osteoblast differentiation and bone matrix production. However, it is also a potent stimulator of cell proliferation, which could promote the growth of existing cancer cells or contribute to tumorigenesis in tissues.
In reconstructing a mandibular defect using rh-BMP, one must depend on the chemical process of:
A. osteocompetence
B. osteoconduction
C. osteogenesis
D. osteoinduction
D. Osteoinduction
Osteoinduction refers to the process by which BMPs (Bone Morphogenetic Proteins) stimulate undifferentiated mesenchymal cells to differentiate into osteoblasts (bone-forming cells), thereby inducing new bone formation. rh-BMPs such as BMP-2 or BMP-7 are potent inducers of osteogenesis (bone formation), and their use in bone defects promotes the formation of new bone tissue, which is the basis of reconstructing the mandibular defect.
Other Terms:
(A) Osteocompetence: This refers to the ability of a tissue or scaffold to support the process of bone formation, but it is not the primary process induced by BMP.
(B) Osteoconduction: This is the process by which bone grows along a scaffold or surface, providing a framework for new bone tissue to grow. It is important for bone healing but does not directly induce bone formation like BMP.
(C) Osteogenesis: This refers to the actual formation of new bone by osteoblasts. Osteoinduction leads to osteogenesis, but osteogenesis itself is not the process directly activated by BMPs; BMPs induce osteogenesis.
What is the first course of action for patients strongly suspected or documented to have a deep
vein thrombosis (DVT)?
A. Warfarin
B. Thrombectomy
C. Heparin
D. Streptokinase
C. Heparin
For patients strongly suspected or documented to have a deep vein thrombosis (DVT), the first course of action typically involves anticoagulation therapy to prevent further clot formation and complications such as pulmonary embolism (PE).
Heparin is the initial treatment of choice for DVT. It is an anticoagulant that works by inhibiting thrombin and other clotting factors, thereby preventing the clot from growing and reducing the risk of complications.
Other Options:
A. Warfarin: Warfarin is an oral anticoagulant that is used for long-term anticoagulation in patients with DVT but is not used as the initial treatment because it has a delayed onset of action. It is often used after heparin to maintain anticoagulation once the patient is stable.
B. Thrombectomy: This is a surgical procedure to remove the clot and is not typically the first-line treatment for DVT. It is reserved for severe cases, such as when there is a significant risk of pulmonary embolism or if the DVT is not responding to anticoagulation therapy.
D. Streptokinase: Streptokinase is a fibrinolytic agent used in some cases of acute myocardial infarction or pulmonary embolism, but it is not routinely used for DVT because of its higher risk of bleeding and limited evidence for its benefit in DVT.
A 64 year-old female is now two days postoperative from a iliac crest graft harvest for a mandibular defect reconstruction. She continues to have dyspnea at rest since emergence from anesthesia. Her B-type natriuretic peptide (BNP) assay is elevated. This may indicate that the patient is suffering from:
A. pulmonary embolism.
B. chronic obstructive pulmonary disease.
C. metabolic acidosis.
D. congestive heart failure.
D. Congestive Heart Failure
BNP is B-type natriuretic peptide which is released from the ventricles of the heart. Elevated levels of BNP indicates heart strain from congestive heart failure.
Which antihypertensive medication should be held pre operatively?
A. Calcium channel blocker
B. ACE Inhibitor
C. Angiotensin Receptor Blocker
D. Beta blocker
B. ACE Inhibitor
ACE inhibitors should generally be held preoperatively due to the risk of hypotension, renal complications, and hyperkalemia
Other options:
A. Calcium Channel Blocker: These are usually not contraindicated before surgery and may be continued, as they primarily control blood pressure through vasodilation and do not typically cause the same degree of perioperative complications as ACE inhibitors.
C. Angiotensin Receptor Blocker (ARB): Like ACE inhibitors, ARBs can also lower blood pressure, but holding them preoperatively is not always required unless the patient has a high risk of hypotension. In general, the decision is individualized, but they are sometimes continued up to the time of surgery.
D. Beta Blocker: Beta blockers should not be routinely held preoperatively, especially in patients with cardiovascular disease or hypertension. In fact, they are often continued to prevent perioperative cardiovascular events such as tachycardia or arrhythmias.
A patient presents with tachycardia and low systemic vascular resistance. What type of shock do they likely have?
A. distributive
B. hypovolemic
C. cardiogenic
D. obstructive
A. Distributive
Distributive shock is characterized by low systemic vascular resistance (SVR) due to widespread vasodilation and impaired vascular tone. This leads to reduced effective circulating blood volume, which can cause the body to compensate with tachycardia (increased heart rate) to try to maintain cardiac output and tissue perfusion.
Common Causes of Distributive Shock:
Septic shock: Caused by severe infection and release of inflammatory mediators that cause vasodilation.
Anaphylactic shock: An acute allergic reaction leading to massive vasodilation and increased vascular permeability.
Neurogenic shock: Caused by damage to the central nervous system (e.g., spinal cord injury), leading to loss of sympathetic tone and widespread vasodilation.
Other Options:
B. Hypovolemic shock: Typically associated with low blood volume (due to bleeding, dehydration, etc.), which leads to increased systemic vascular resistance (not low) as the body tries to compensate for the fluid loss. Tachycardia is also present, but the hallmark is low blood volume, not low SVR.
C. Cardiogenic shock: Caused by heart failure or severe cardiac dysfunction, leading to low cardiac output and increased SVR (as the body tries to compensate for poor perfusion). Tachycardia may be present, but SVR is typically elevated due to the body’s attempt to maintain blood pressure.
D. Obstructive shock: Caused by a physical obstruction (e.g., pulmonary embolism, cardiac tamponade), which leads to impaired cardiac output. This condition usually results in increased SVR, not low SVR.
Which of the following will not lead to serotonin syndrome?
A. Selegeline
B. Amitriptyline
C. Lexapro
D. Cyproheptadine
D. Cyproheptadine
Serotonin syndrome is a potentially life-threatening condition caused by excessive serotonin activity in the central nervous system, typically due to the use of certain medications, particularly those that increase serotonin levels or enhance its effects. Cyproheptadine is an antihistamine and serotonin antagonist. It works by blocking serotonin receptors, specifically the 5-HT2A receptor, and can be used as a treatment for serotonin syndrome. Cyproheptadine actually works to counteract serotonin syndrome and does not cause it.
Other options:
Selegiline is a monoamine oxidase inhibitor (MAOI) that inhibits the breakdown of serotonin, which can increase serotonin levels in the brain. This can lead to serotonin syndrome, especially if combined with other serotonergic drugs. Therefore, selegiline can contribute to serotonin syndrome.
Amitriptyline is a tricyclic antidepressant (TCA) that has serotonergic effects and can increase serotonin levels. Like other TCAs, it can lead to serotonin syndrome, especially when combined with other serotonergic medications. So, amitriptyline can contribute to serotonin syndrome.
Lexapro (escitalopram) is a selective serotonin reuptake inhibitor (SSRI), which works by increasing serotonin levels in the brain. SSRIs like Lexapro are commonly associated with serotonin syndrome, especially when taken in combination with other drugs that also increase serotonin. Therefore, Lexapro can cause serotonin syndrome.
A patient with diastolic heart failure will likely exhibit which of the following signs?
A. Preserved ejection fraction
B. S3 gallop on auscultation
C. Left ventricular hypertrophy
D. Reduced filling pressures
Diastolic heart failure, also known as heart failure with preserved ejection fraction (HFpEF), occurs when the heart’s ventricles are unable to relax and fill properly during diastole due to stiffness or thickening of the heart muscle. Despite impaired filling, the heart’s ability to contract and pump blood out (ejection fraction) is preserved, which distinguishes it from systolic heart failure (HFrEF), where the ejection fraction is reduced. In HFpEF, the ejection fraction remains normal (typically greater than 50%), despite the impaired filling of the ventricles. The problem lies in the ventricle’s inability to fill properly, not in its ability to contract and pump blood out.
Other options:
An S3 gallop is more often associated with systolic heart failure (HFrEF), especially when there is volume overload or a dilated left ventricle. In diastolic heart failure, an S4 gallop is more commonly heard due to the stiffness of the left ventricle and impaired filling.
Left ventricular hypertrophy (LVH) is indeed common in diastolic heart failure, particularly due to chronic hypertension or other conditions that increase afterload. While LVH is associated with diastolic dysfunction, it is not the primary characteristic being asked about in this question, which focuses on the key feature of diastolic heart failure (preserved ejection fraction).
In diastolic heart failure, filling pressures (such as left atrial pressure and pulmonary capillary wedge pressure) are typically elevated due to the stiff and non-compliant ventricle that resists proper filling. Therefore, reduced filling pressures would not be expected.
A 43-year-old alcoholic male has acute onset confusion and amnesia and is brought to the ER for further evaluation. His toxicology screen is negative. His head CT shows some focal demyelination and gliosis of the thalamus, cerebellum and periaqueductal grey matter, without evidence of intracranial mass or bleeding. Further careful physical examination reveals bilateral lateral rectus palsy. What is his most likely diagnosis?
A. Korsakoff syndrome
B. Wernicke’s encephalopathy
C. Parkinson’s disease
D. Diffuse axonal injury
B. Wernicke’s encephalopathy
The patient’s presentation of acute onset confusion, amnesia, focal demyelination and gliosis in the thalamus, cerebellum, and periaqueductal grey matter, along with bilateral lateral rectus palsy, is most consistent with Wernicke’s encephalopathy (WE), which is a neurological emergency associated with thiamine deficiency, commonly seen in alcoholics. The triad of findings is confusion (Acute onset), ataxia, and ocular abnormalities
Other options:
Korsakoff syndrome is a chronic condition resulting from long-term thiamine deficiency and often follows Wernicke’s encephalopathy. It is characterized by severe memory impairment (especially anterograde amnesia) and confabulation. However, it does not typically present acutely or with focal neurological findings such as lateral rectus palsy or demyelination seen in this patient.
Parkinson’s disease typically presents with resting tremor, bradykinesia, rigidity, and postural instability. It is a chronic neurodegenerative disorder and is not characterized by acute confusion or demyelination. The presence of lateral rectus palsy is not typical in Parkinson’s disease.
Diffuse axonal injury typically results from trauma (e.g., motor vehicle accidents), leading to widespread axonal damage and brain swelling. The symptoms are usually related to coma, global brain dysfunction, and severe neurological deficits. There is typically no focal demyelination or specific cranial nerve involvement like in this case.
The diagnosis of mitral valve prolapse is associated with which of the following?
A. Early systolic murmur
B. Von Willebrand’s syndrome
C. Murmur accentuated by respiration
D. Patent ductus arteriosus (PDA)
B. Von Willebrand’s Syndrome
Mitral valve prolapse (MVP) is a condition in which the mitral valve leaflets prolapse into the left atrium during systole, often causing a systolic murmur and potentially a mid-systolic click. The diagnosis of MVP is often associated with various conditions, one of which is Von Willebrand’s disease.
MVP is commonly seen in patients with von Willebrand’s disease, a genetic bleeding disorder caused by a deficiency of von Willebrand factor, which plays a role in platelet adhesion and blood clotting. There is an increased association between MVP and von Willebrand’s disease, possibly due to connective tissue abnormalities affecting both the mitral valve and platelet function.
Why the other options are less likely:
MVP typically presents with a mid-systolic click and a late systolic murmur that results from mitral regurgitation (if present). The murmur is usually not early in systole, making this answer incorrect.
The murmur of MVP is usually not significantly affected by respiration. Murmurs that are accentuated by respiration are more commonly associated with conditions like right-sided heart murmurs (e.g., tricuspid regurgitation) or pulmonary stenosis, not MVP.
PDA is a congenital condition where the ductus arteriosus fails to close after birth. While both MVP and PDA are cardiac conditions, they are not typically associated. The murmur of a PDA is continuous and machine-like, which is different from the murmur of MVP, which is systolic.
Infusion of which of the following can increase vWF release by four times?
A. Platelets
B. Fresh Frozen Plasma
C. Factor 8
D. DDAVP
D. DDAVP
DDAVP (Desmopressin, 1-deamino-8-D-arginine vasopressin) is a synthetic analog of vasopressin, which can increase the release of von Willebrand factor (vWF) from the endothelial cells, particularly in patients with von Willebrand disease (vWD) or other bleeding disorders. DDAVP stimulates the endothelial cells to release stored vWF and factor VIII into the circulation, significantly increasing vWF levels.
DDAVP can increase vWF release by up to four times, which can help improve clotting in patients with bleeding disorders like von Willebrand disease or mild hemophilia A.
Why the other options are less likely:
Platelets themselves do not directly increase the release of vWF from endothelial cells. While platelets are involved in hemostasis and platelet aggregation, they do not play a role in stimulating the release of vWF into the bloodstream.
Fresh Frozen Plasma (FFP) contains clotting factors, including vWF and factor VIII, but it does not specifically stimulate the release of vWF from endothelial cells. It provides supplemental clotting factors but does not boost the body’s own vWF production or release.
Factor VIII is important in the clotting cascade and is often deficient in hemophilia A, but it does not directly affect the release of von Willebrand factor. Factor VIII is part of the vWF complex in circulation, and while it is necessary for proper function of vWF, it does not stimulate vWF release from endothelial cells.
Which of the following is often seen during respiratory acidosis?
A. Decreased pCO2
B. Hyperkalemia
C. Hypocalcemia
D. Decreased [H+]
B. Hyperkalemia
Respiratory acidosis occurs when there is an accumulation of carbon dioxide (CO2) in the body, leading to an increase in H+ ions and a decrease in pH (making the blood more acidic). This is typically caused by impaired ventilation or respiratory failure, leading to CO2 retention.
In response to the increased hydrogen ions in respiratory acidosis, the body attempts to compensate through various mechanisms, one of which involves changes in potassium (K+) levels.
Hyperkalemia occurs because, during acidosis, hydrogen ions (H+) move into cells in exchange for potassium ions (K+). This process leads to an increase in potassium concentration in the extracellular fluid, causing hyperkalemia.
Why the other options are less likely:
In respiratory acidosis, pCO2 is increased, not decreased, because CO2 is not being adequately removed from the body due to impaired ventilation.
Hypocalcemia is not typically associated with respiratory acidosis. Instead, respiratory acidosis may lead to a slight increase in ionized calcium concentration due to the effects of acidosis on protein binding. In contrast, metabolic acidosis can lead to hypocalcemia by increasing the ionized calcium fraction.
In respiratory acidosis, [H+] (hydrogen ion concentration) is increased, not decreased. The increase in H+ is the primary cause of the acidosis.
Which of the following is the cause of peptic ulcers in patient’s taking NSAIDs?
A. COX-2 Inhibition
B. Inhibition of prostaglandin synthesis
C. Increase in arachidonic acid metabolism
D. Decreased gastric motility
B. Inhibition of prostaglandin synthesis
Prostaglandins play a key role in protecting the gastric mucosa by stimulating the production of mucus, bicarbonate, and promoting blood flow to the stomach lining, all of which help prevent ulcer formation.
NSAIDs inhibit cyclooxygenase (COX) enzymes, particularly COX-1, which is involved in the synthesis of prostaglandins that protect the gastric mucosa. This inhibition reduces the protective effects of prostaglandins, leading to a higher risk of gastric injury, including peptic ulcers.
How much of the sleep cycle is used for REM?
A. 15%
B. 25%
C. 35%
D. 50%
B. 25%
Rapid Eye Movement (REM) sleep typically accounts for about 20-25% of the total sleep cycle in a healthy adult. During REM sleep, the brain is highly active, and most vivid dreaming occurs. REM sleep is essential for memory consolidation and overall cognitive functioning.
REM sleep is when obstructive apnea occurs.
Which medication would you use to treat wolff-parkinson-white syndrome?
A. Adenosine
B. Dopamine
C. Procainamide
D. Amlodipine
C. Procainamide
Procainamide is an antiarrhythmic medication that works by inhibiting the electrical conduction through the accessory pathway (bundle of Kent) seen in WPW. It is first-line therapy in the acute management of WPW-associated tachyarrhythmias, especially if the patient is hemodynamically stable.
Other options:
Adenosine is commonly used to treat reentrant arrhythmias like AV nodal reentrant tachycardia (AVNRT), but it is not recommended in WPW syndrome with atrioventricular (AV) reentrant tachycardia (AVRT), as it can potentially accelerate the conduction through the accessory pathway and worsen the arrhythmia.
Dopamine is a sympathomimetic used to treat conditions like shock and bradycardia. It does not address the underlying electrical problem in WPW syndrome.
Amlodipine is a calcium channel blocker used primarily to treat hypertension and angina. It is not effective for treating the arrhythmias associated with WPW syndrome.
What role do the following interventions play in ACLS:
Lidocaine
Amiodarone
Epinephrine
Cardioversion
Adenosine
Atropine
- Lidocaine:
Role: Antiarrhythmic
Indication: Lidocaine is used in the treatment of ventricular arrhythmias such as ventricular tachycardia (VT) and ventricular fibrillation (VF), especially when amiodarone is not available.
Mechanism: It works by inhibiting sodium channels, which slows depolarization and stabilizes the cardiac cell membrane, preventing abnormal electrical conduction. - Amiodarone:
Role: Antiarrhythmic
Indication: Amiodarone is used in the treatment of life-threatening arrhythmias, particularly ventricular fibrillation (VF) and ventricular tachycardia (VT). It is often used when defibrillation is unsuccessful or as part of the post-resuscitation care.
Mechanism: Amiodarone has multiple mechanisms of action, including blocking potassium channels, which helps prolong the action potential and stabilize the heart’s electrical activity. - Epinephrine (Epi):
Role: Vasopressor/Adrenergic stimulant
Indication: Epinephrine is used in cardiac arrest (both VF and pulseless VT), asystole, and pulseless electrical activity (PEA). It is given during resuscitation efforts to improve perfusion to vital organs, particularly the heart and brain.
Mechanism: Epinephrine is a potent alpha-adrenergic agonist that causes vasoconstriction, increasing systemic vascular resistance and blood pressure, and a beta-adrenergic agonist that can increase myocardial contractility and heart rate. - Cardioversion:
Role: Electrical therapy
Indication: Cardioversion is used to treat unstable tachyarrhythmias, such as atrial fibrillation, atrial flutter, and ventricular tachycardia (with a pulse). It involves the synchronized delivery of electrical shocks to restore normal sinus rhythm.
Mechanism: By delivering an electrical shock at a specific point in the cardiac cycle (synchronized with the QRS complex), cardioversion disrupts the abnormal electrical circuit and restores a normal rhythm. - Adenosine:
Role: Antiarrhythmic
Indication: Adenosine is used to treat supraventricular tachycardia (SVT), including paroxysmal SVT and AV nodal reentrant tachycardia (AVNRT). It is also used diagnostically to help identify the rhythm if there is a question about the arrhythmia type.
Mechanism: Adenosine works by slowing down the conduction through the AV node, interrupting the reentrant pathway and potentially terminating the arrhythmia. It has a very short half-life, and the effect is typically brief. - Atropine:
Role: Anticholinergic
Indication: Atropine is used to treat bradycardia (slow heart rate) in cases where the heart rate is causing hypoperfusion or symptoms. It can be used in symptomatic bradycardia (e.g., caused by AV block or sinus node dysfunction).
Mechanism: Atropine blocks the vagus nerve’s effects on the heart, increasing heart rate by preventing acetylcholine from binding to its receptors and blocking parasympathetic tone.
Summary of Indications:
Lidocaine and Amiodarone: Used for ventricular arrhythmias (VF/VT).
Epinephrine: Used for cardiac arrest (VF, VT, PEA, asystole) to improve perfusion.
Cardioversion: Used for unstable supraventricular and ventricular tachyarrhythmias with a pulse.
Adenosine: Used for supraventricular tachycardia (SVT), particularly AVNRT.
Atropine: Used for bradycardia (symptomatic or causing hemodynamic instability).
Which of the following statements regarding temporal arteritis is true?
A. Predilection for adolescent females (older females)
B. Rarely causes severe headaches
C. Associated with masticatory muscle pain during chewing
D. Unresponsive to corticosteroid therapy
C. Associated with masticatory muscle pain during chewing
Masticatory muscle pain during chewing (also known as jaw claudication) is a classic symptom of temporal arteritis. The inflammation of the temporal artery can lead to insufficient blood supply to the muscles involved in chewing, causing pain or discomfort during mastication.
Temporal arteritis typically affects older individuals (50s), is associated with severe headaches, and is responsive to corticosteroid therapy.
What lab values are needed prior to administration of phenytoin?
CBC to evaluate for megaloblastic anemia because phenytoin can disrupt folate metabolism.
What lab values are needed prior to depakote administration?
Liver Function Tests are needed prior to administration of depakote (valproic acid) because Valproate is metabolized in the liver, and hepatotoxicity is a known side effect, particularly during the first 6 months of treatment. It can cause elevations in liver enzymes (AST, ALT), which may progress to liver failure in rare cases.
Which of the following is used to treat bradycardia in pediatric patients?
A. epinephrine
B. atropine
C. dopamine
D. adenosine
B. atropine
In pediatric patients, bradycardia (a heart rate that is too slow) is often treated with atropine, especially if the child is symptomatic (e.g., hypotension, shock, or poor perfusion). Atropine works by blocking the effects of the vagus nerve on the heart, leading to increased heart rate.
Why the other options are less appropriate:
While epinephrine is used in pediatric resuscitation (particularly in cases of cardiac arrest), it is not the first-line treatment for simple bradycardia. Epinephrine is typically used for more severe scenarios like asystole or pulseless electrical activity (PEA).
Dopamine is another option in the management of bradycardia, particularly if atropine is ineffective. It may be used as a second-line drug, but it is not the first choice for treatment of pediatric bradycardia.
Adenosine is used to treat supraventricular tachycardia (SVT), not bradycardia. It works by temporarily blocking conduction through the AV node, helping to reset the heart’s rhythm.
Which of the following is not used to treat hyperkalemia?
A. Insulin with glucose
B. Calcium
C. Spironolactone
D. Hemodialysis
C. Spironolactone
Spironolactone is a potassium sparing diuretic, so administration will exacerbate hyperkalemia.
Insulin helps shift potassium from the bloodstream into cells, lowering serum potassium levels. Glucose is given simultaneously to prevent hypoglycemia.
Calcium gluconate or calcium chloride can stabilize the cardiac membrane, helping to prevent arrhythmias associated with severe hyperkalemia. It does not lower potassium levels directly but can be life-saving in acute situations.
Hemodialysis is a definitive treatment for severe hyperkalemia that is not responsive to other interventions. It removes excess potassium from the bloodstream directly.
Which of the following is used to treat angioedema?
A. ACE Inhibitors
B. Bradykinin
C. Danazol
D. Benadryl
C. Danazol
Danazol is a synthetic androgenic steroid that is used in the treatment of hereditary angioedema (HAE), a condition often associated with bradykinin-mediated swelling. It works by increasing the levels of C1 esterase inhibitor (C1-INH), which helps regulate the complement system and prevents the excessive production of bradykinin, the mediator responsible for the swelling in angioedema.
Why the other options are incorrect:
ACE inhibitors are known to cause angioedema, especially in the face, lips, and airway, due to their effect on bradykinin metabolism. They are not used to treat angioedema but rather can trigger it in some individuals.
Bradykinin is the substance that causes the swelling in angioedema, so it is not used as a treatment. Instead, treatments aim to reduce its effects.
While Benadryl (diphenhydramine) is an antihistamine used for histamine-mediated allergic reactions (like hives), it is not effective for bradykinin-mediated angioedema. Angioedema that is not histamine-related (like in hereditary angioedema) requires other treatments like Danazol or C1-INH concentrates.
Which of the following is contraindicated in myasthenia gravis?
A. immunoglobulin therapy
B. cholinesterase inhibitor
C. corticosteroids
B. cholinesterase inhibitor
Myasthenia gravis (MG) is an autoimmune neuromuscular disorder that leads to weakness of voluntary muscles. The condition is caused by autoantibodies that block or destroy the acetylcholine receptors at the neuromuscular junction, impairing neuromuscular transmission.
Cholinesterase inhibitors (such as neostigmine or pyridostigmine) are used to increase acetylcholine at the neuromuscular junction by inhibiting the enzyme acetylcholinesterase, which breaks down acetylcholine.
In myasthenia gravis, excessive acetylcholine can worsen the condition and lead to cholinergic crisis, which can result in increased muscle weakness, respiratory failure, and other complications.
Therefore, cholinesterase inhibitors are typically not used in patients with myasthenia gravis unless under careful monitoring, as they can worsen symptoms if not carefully dosed.
Immunoglobulin therapy: Immunoglobulin (IVIg) therapy is often used in the treatment of severe exacerbations of myasthenia gravis. It works by modulating the immune system and reducing the circulating autoantibodies that attack acetylcholine receptors.
Corticosteroids: Corticosteroids, such as prednisone, are commonly used to treat myasthenia gravis because they reduce inflammation and autoimmune activity. They can help to decrease the production of autoantibodies against acetylcholine receptors and improve symptoms.
What are the reversible causes of pulseless electrical activity?
In the context of pulseless electrical activity (PEA), the H’s and T’s are a mnemonic used to remember the reversible causes of PEA. These are conditions that can lead to PEA and, if treated, may restore a normal rhythm and pulse. Here are the H’s and T’s:
H’s:
Hypovolemia – Low blood volume (e.g., from hemorrhage, dehydration) leading to insufficient perfusion.
Hypoxia – Lack of oxygen in the blood, which impairs cellular function and tissue oxygenation.
Hydrogen ion (acidosis) – Increased acidity in the blood, often from metabolic acidosis or respiratory acidosis, which can impair cardiac function.
Hypo-/Hyperkalemia – Abnormal potassium levels, with either low potassium or high potassium affecting the heart’s electrical system.
Hypothermia – Low body temperature that can reduce cellular function and lead to arrhythmias.
T’s:
Toxins – Drug overdose or toxicity, such as from opioids, sedatives, or other substances, that can depress the cardiovascular system.
Tamponade (cardiac) – Fluid accumulation in the pericardial sac, which compresses the heart and impairs its ability to pump effectively.
Tension pneumothorax – A life-threatening condition where air accumulates in the pleural space, compressing the lungs and heart, leading to a decreased venous return and cardiac output.
Thrombosis (pulmonary or coronary) – A blood clot in the lungs (pulmonary embolism) or coronary arteries (myocardial infarction) that obstructs blood flow and can cause PEA.
Management:
To treat PEA effectively, you would consider addressing these underlying conditions. For example:
Hypovolemia may be treated with fluid resuscitation.
Hypoxia requires oxygen administration or ventilation.
Acidosis may require bicarbonate or other treatments.
Electrolyte imbalances may need correction with appropriate IV medications (e.g., potassium).
Toxins may need antidotes (e.g., naloxone for opioids).
Tamponade and tension pneumothorax may require surgical intervention (e.g., pericardiocentesis, needle decompression).
Thrombosis may require anticoagulation or thrombolytic therapy, depending on the source.
