Psychiatric emergencies: Pathology review

2,148views

test

00:00 / 00:00

Psychiatric emergencies: Pathology review

Watch later

Watch later

Serotonin and norepinephrine reuptake inhibitors
Monoamine oxidase inhibitors
Typical antipsychotics
Atypical antipsychotics
Lithium
Nonbenzodiazepine anticonvulsants
Anticonvulsants and anxiolytics: Barbiturates
Anticonvulsants and anxiolytics: Benzodiazepines
Psychomotor stimulants
Mood disorders: Clinical
Anxiety disorders: Clinical
Eating disorders: Clinical
Obsessive compulsive disorders: Clinical
Personality disorders: Clinical
Sleep disorders: Clinical
Substance misuse and addiction: Clinical
Somatic symptom disorders: Clinical
Sexual dysfunctions: Clinical
Opioid agonists, mixed agonist-antagonists and partial agonists
Opioid antagonists
Schizophrenia spectrum disorders: Clinical
Dissociative disorders: Clinical
Trauma- and stressor-related disorders: Clinical
Disruptive, impulse-control and conduct disorders: Clinical
Paraphilic disorders: Clinical
Toxidromes: Clinical
Medication overdoses and toxicities: Pathology review
Drug misuse, intoxication and withdrawal: Hallucinogens: Pathology review
Psychiatric emergencies: Pathology review
Potter sequence
Hyperphosphatemia
Hypophosphatemia
Hypernatremia
Hyponatremia
Hypermagnesemia
Hypomagnesemia
Hyperkalemia
Hypokalemia
Hypercalcemia
Hypocalcemia
Renal tubular acidosis
Minimal change disease
Diabetic nephropathy
Focal segmental glomerulosclerosis (NORD)
Amyloidosis
Membranous nephropathy
Lupus nephritis
Poststreptococcal glomerulonephritis
Rapidly progressive glomerulonephritis
IgA nephropathy (NORD)
Alport syndrome
Kidney stones
Hydronephrosis
Acute pyelonephritis
Chronic pyelonephritis
Prerenal azotemia
Renal azotemia
Acute tubular necrosis
Postrenal azotemia
Renal papillary necrosis
Renal cortical necrosis
Chronic kidney disease
Polycystic kidney disease
Multicystic dysplastic kidney
Medullary cystic kidney disease
Medullary sponge kidney
Renal artery stenosis
Renal cell carcinoma
Angiomyolipoma
Nephroblastoma (Wilms tumor)
WAGR syndrome
Beckwith-Wiedemann syndrome
Posterior urethral valves
Hypospadias and epispadias
Vesicoureteral reflux
Bladder exstrophy
Urinary incontinence
Neurogenic bladder
Lower urinary tract infection
Transitional cell carcinoma
Non-urothelial bladder cancers
Congenital renal disorders: Pathology review
Renal tubular defects: Pathology review
Renal tubular acidosis: Pathology review
Acid-base disturbances: Pathology review
Electrolyte disturbances: Pathology review
Renal failure: Pathology review
Nephrotic syndromes: Pathology review
Nephritic syndromes: Pathology review
Urinary incontinence: Pathology review
Urinary tract infections: Pathology review
Kidney stones: Pathology review
Renal and urinary tract masses: Pathology review
Renal system anatomy and physiology
Hydration
Body fluid compartments
Movement of water between body compartments
Renal clearance
Glomerular filtration
TF/Px ratio and TF/Pinulin
Measuring renal plasma flow and renal blood flow
Regulation of renal blood flow
Tubular reabsorption and secretion
Tubular secretion of PAH
Tubular reabsorption of glucose
Urea recycling
Tubular reabsorption and secretion of weak acids and bases
Proximal convoluted tubule
Loop of Henle
Distal convoluted tubule
Renin-angiotensin-aldosterone system
Sodium homeostasis
Potassium homeostasis
Phosphate, calcium and magnesium homeostasis
Osmoregulation
Antidiuretic hormone
Kidney countercurrent multiplication
Free water clearance
Vitamin D
Erythropoietin
Physiologic pH and buffers
Buffering and Henderson-Hasselbalch equation
The role of the kidney in acid-base balance
Acid-base map and compensatory mechanisms
Respiratory acidosis
Metabolic acidosis
Plasma anion gap
Respiratory alkalosis
Metabolic alkalosis
Osmotic diuretics
Carbonic anhydrase inhibitors
Loop diuretics
Thiazide and thiazide-like diuretics
Potassium sparing diuretics
ACE inhibitors, ARBs and direct renin inhibitors
Anatomy of the heart
Anatomy of the coronary circulation
Anatomy clinical correlates: Heart
Anatomy of the superior mediastinum
Anatomy of the inferior mediastinum
Anatomy clinical correlates: Mediastinum
Development of the cardiovascular system
Fetal circulation
Cardiovascular system anatomy and physiology
Lymphatic system anatomy and physiology
Coronary circulation
Blood pressure, blood flow, and resistance
Pressures in the cardiovascular system
Laminar flow and Reynolds number
Resistance to blood flow
Compliance of blood vessels
Control of blood flow circulation
Microcirculation and Starling forces
Measuring cardiac output (Fick principle)
Stroke volume, ejection fraction, and cardiac output
Cardiac contractility
Frank-Starling relationship
Cardiac preload
Cardiac afterload
Law of Laplace
Cardiac and vascular function curves
Altering cardiac and vascular function curves
Cardiac cycle
Cardiac work
Pressure-volume loops
Changes in pressure-volume loops
Physiological changes during exercise
Cardiovascular changes during hemorrhage
Cardiovascular changes during postural change
Normal heart sounds
Abnormal heart sounds
Action potentials in myocytes
Action potentials in pacemaker cells
Excitability and refractory periods
Cardiac excitation-contraction coupling
Electrical conduction in the heart
Cardiac conduction velocity
ECG basics
ECG rate and rhythm
ECG intervals
ECG QRS transition
ECG axis
ECG normal sinus rhythm
ECG cardiac infarction and ischemia
ECG cardiac hypertrophy and enlargement
Baroreceptors
Chemoreceptors
Arterial disease
Angina pectoris
Stable angina
Unstable angina
Myocardial infarction
Prinzmetal angina
Coronary steal syndrome
Peripheral artery disease
Subclavian steal syndrome
Aneurysms
Aortic dissection
Vasculitis
Behcet's disease
Kawasaki disease
Hypertension
Hypertensive emergency
Coarctation of the aorta
Cushing syndrome
Conn syndrome
Pheochromocytoma
Hypotension
Orthostatic hypotension
Abetalipoproteinemia
Familial hypercholesterolemia
Hypertriglyceridemia
Hyperlipidemia
Chronic venous insufficiency
Thrombophlebitis
Deep vein thrombosis
Lymphedema
Lymphangioma
Shock
Vascular tumors
Human herpesvirus 8 (Kaposi sarcoma)
Angiosarcomas
Truncus arteriosus
Transposition of the great vessels
Total anomalous pulmonary venous return
Tetralogy of Fallot
Hypoplastic left heart syndrome
Patent ductus arteriosus
Ventricular septal defect
Atrial septal defect
Atrial flutter
Atrial fibrillation
Premature atrial contraction
Atrioventricular nodal reentrant tachycardia (AVNRT)
Wolff-Parkinson-White syndrome
Ventricular tachycardia
Brugada syndrome
Premature ventricular contraction
Long QT syndrome and Torsade de pointes
Ventricular fibrillation
Atrioventricular block
Bundle branch block
Pulseless electrical activity
Tricuspid valve disease
Pulmonary valve disease
Mitral valve disease
Aortic valve disease
Dilated cardiomyopathy
Restrictive cardiomyopathy
Hypertrophic cardiomyopathy
Heart failure
Cor pulmonale
Endocarditis
Myocarditis
Rheumatic heart disease
Pericarditis and pericardial effusion
Cardiac tamponade
Dressler syndrome
Cardiac tumors
Acyanotic congenital heart defects: Pathology review
Cyanotic congenital heart defects: Pathology review
Atherosclerosis and arteriosclerosis: Pathology review
Coronary artery disease: Pathology review
Peripheral artery disease: Pathology review
Valvular heart disease: Pathology review
Cardiomyopathies: Pathology review
Heart failure: Pathology review
Supraventricular arrhythmias: Pathology review
Ventricular arrhythmias: Pathology review
Heart blocks: Pathology review
Aortic dissections and aneurysms: Pathology review
Pericardial disease: Pathology review
Endocarditis: Pathology review
Hypertension: Pathology review
Shock: Pathology review
Vasculitis: Pathology review
Cardiac and vascular tumors: Pathology review
Dyslipidemias: Pathology review
Sympatholytics: Alpha-2 agonists
Adrenergic antagonists: Presynaptic
Adrenergic antagonists: Alpha blockers
Adrenergic antagonists: Beta blockers
Calcium channel blockers
cGMP mediated smooth muscle vasodilators
Class I antiarrhythmics: Sodium channel blockers
Class II antiarrhythmics: Beta blockers
Class III antiarrhythmics: Potassium channel blockers
Class IV antiarrhythmics: Calcium channel blockers and others
Lipid-lowering medications: Statins
Lipid-lowering medications: Fibrates
Miscellaneous lipid-lowering medications
Positive inotropic medications
Pulmonary embolism
Pulmonary edema
Pulmonary hypertension
Sleep apnea
Apnea of prematurity
Respiratory distress syndrome: Pathology review
Cystic fibrosis: Pathology review
Pneumonia: Pathology review
Tuberculosis: Pathology review
Deep vein thrombosis and pulmonary embolism: Pathology review
Pleural effusion, pneumothorax, hemothorax and atelectasis: Pathology review
Obstructive lung diseases: Pathology review
Restrictive lung diseases: Pathology review
Apnea, hypoventilation and pulmonary hypertension: Pathology review
Lung cancer and mesothelioma: Pathology review
Antihistamines for allergies
Bronchodilators: Beta 2-agonists and muscarinic antagonists
Bronchodilators: Leukotriene antagonists and methylxanthines
Respiratory system anatomy and physiology
Reading a chest X-ray
Lung volumes and capacities
Anatomic and physiologic dead space
Alveolar surface tension and surfactant
Compliance of lungs and chest wall
Combined pressure-volume curves for the lung and chest wall
Ventilation
Zones of pulmonary blood flow
Regulation of pulmonary blood flow
Pulmonary shunts
Ventilation-perfusion ratios and V/Q mismatch
Breathing cycle
Airflow, pressure, and resistance
Ideal (general) gas law
Boyle's law
Dalton's law
Henry's law
Graham's law
Gas exchange in the lungs, blood and tissues
Diffusion-limited and perfusion-limited gas exchange
Alveolar gas equation
Oxygen binding capacity and oxygen content
Oxygen-hemoglobin dissociation curve
Carbon dioxide transport in blood
Breathing control
Pulmonary chemoreceptors and mechanoreceptors
Pulmonary changes at high altitude and altitude sickness
Pulmonary changes during exercise
Choanal atresia
Laryngomalacia
Allergic rhinitis
Nasal polyps
Upper respiratory tract infection
Sinusitis
Laryngitis
Retropharyngeal and peritonsillar abscesses
Bacterial epiglottitis
Nasopharyngeal carcinoma
Tracheoesophageal fistula
Congenital pulmonary airway malformation
Pulmonary hypoplasia
Neonatal respiratory distress syndrome
Transient tachypnea of the newborn
Meconium aspiration syndrome
Apnea of prematurity
Sudden infant death syndrome
Acute respiratory distress syndrome
Decompression sickness
Cyanide poisoning
Methemoglobinemia
Emphysema
Chronic bronchitis
Asthma
Cystic fibrosis
Bronchiectasis
Alpha 1-antitrypsin deficiency
Restrictive lung diseases
Sarcoidosis
Idiopathic pulmonary fibrosis
Pneumonia
Croup
Bacterial tracheitis
Lung cancer
Pancoast tumor
Superior vena cava syndrome
Pneumothorax
Pleural effusion
Mesothelioma
Pulmonary embolism
Pulmonary edema
Pulmonary hypertension
Sleep apnea
Respiratory distress syndrome: Pathology review
Cystic fibrosis: Pathology review
Pneumonia: Pathology review
Tuberculosis: Pathology review
Deep vein thrombosis and pulmonary embolism: Pathology review
Pleural effusion, pneumothorax, hemothorax and atelectasis: Pathology review
Obstructive lung diseases: Pathology review
Restrictive lung diseases: Pathology review
Apnea, hypoventilation and pulmonary hypertension: Pathology review
Lung cancer and mesothelioma: Pathology review
Glucocorticoids
Protein synthesis inhibitors: Aminoglycosides
Antimetabolites: Sulfonamides and trimethoprim
Antituberculosis medications
Miscellaneous cell wall synthesis inhibitors
Protein synthesis inhibitors: Tetracyclines
Cell wall synthesis inhibitors: Penicillins
Miscellaneous protein synthesis inhibitors
Cell wall synthesis inhibitors: Cephalosporins
DNA synthesis inhibitors: Metronidazole
DNA synthesis inhibitors: Fluoroquinolones
Mechanisms of antibiotic resistance
Integrase and entry inhibitors
Nucleoside reverse transcriptase inhibitors (NRTIs)
Protease inhibitors
Hepatitis medications
Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
Neuraminidase inhibitors
Herpesvirus medications
Azoles
Echinocandins
Miscellaneous antifungal medications
Anthelmintic medications
Antimalarials
Anti-mite and louse medications
Osmotic diuretics
Carbonic anhydrase inhibitors
Loop diuretics
Thiazide and thiazide-like diuretics
Potassium sparing diuretics
ACE inhibitors, ARBs and direct renin inhibitors

Assessments

USMLE® Step 1 questions

0 / 3 complete

Questions

USMLE® Step 1 style questions USMLE

0 of 3 complete

A 55-year-old woman comes to the emergency department (ED) for evaluation of recurrent left flank pain and vomiting. She has a history of recurrent nephrolithiasis and recently noticed gross blood in her urine. Medical history is notable for obesity, hypertension, hyperlipidemia, depression, and type II diabetes mellitus. The patient has been taking ondansetron at home for nausea as well as losartan, metformin, rosuvastatin, and sertraline for her other medical conditions. On physical exam, the patient has left costovertebral angle tenderness. Blood is detected on urinalysis. The patient's symptoms are well controlled during the ED visit, and she is subsequently discharged with prescription analgesia, additional antiemetics, and urology follow-up. Three days later, the patient is brought back to the ED altered, diaphoretic, and agitated. Temperature is 39.4°C (103°F), pulse is 122/min, respirations are 20/min, and blood pressure is 184/95 mmHg. She has bilateral mydriasis and myoclonus. Which of the following medications was the most likely precipitant of this patient's clinical presentation?

Transcript

Watch video only

A 53 year old male named Noah is brought to the emergency department by his son, who found him with an empty bottle of fluoxetine in his hand. His son mentions that Noah was recently diagnosed with depressive disorder. Upon physical examination, you realize that Noah has a body temperature of 38.9 degrees Celsius, or 102.02 degrees Fahrenheit, and a blood pressure of 162 over 95 millimeters of mercury. In addition, Noah’s pupils appear dilated, and his muscles are very stiff. Finally, neurological examination reveals that Noah has overactive reflexes. Later that day, a 34 year old female named Amelia is brought to the emergency department by her husband. He explains that Amelia has a medical history of schizophrenia, and a few days back she took multiple doses of haloperidol. Upon physical examination, Amelia’s body temperature is 38.7 degrees Celsius or 101.66 degrees Fahrenheit, and her blood pressure is 170 over 100 millimeters of mercury. Similarly to Noah, Amelia has muscle stiffness, but neurological examination reveals diminished reflexes.

All right, now, both Noah and Amelia seem to have some form of psychiatric emergency, which is when a psychiatric condition becomes life-threatening and requires prompt treatment. For your exams, some high yield psychiatric emergencies include suicide attempts, serotonin syndrome, acute dystonia, neuroleptic malignant syndrome, tyramine-induced hypertensive crisis, and delirium tremens.

Now, a very relevant psychiatric emergency, not only for your exams, are suicide attempts. Suicide is when someone takes their own life intentionally. Now, many suicide attempts can be prevented by keeping an eye out for red flags or risk factors, which can be easily remembered with the memory trick SAD PERSONS. The first S here stands for sex, as suicide tends to be more common among males. Next, A stands for age, so remember that suicide is more common among young adults and the elderly. For your exams, you should know that suicide is the second leading cause of death among individuals aged 15 to 34 in the USA, behind motor vehicle crashes. D is for depressive disorder, which is a psychiatric disorder that causes a persistent feeling of sadness, associated with a loss of interest in everyday activities like hobbies. Then P stands for previous suicide attempts, which remember is the most important risk factor for suicide. E stands for excessive alcohol or substance abuse, which causes individuals to be more impulsive, taking risks they normally wouldn’t take like driving recklessly. Oftentimes, alcohol or substance abuse occur together with depression. In fact, many people who experience depression turn to alcohol or substances to temporarily numb their feelings. And vice versa, chronic alcohol or substance abuse can ultimately cause depression, creating a vicious cycle. R is for rational thinking loss in psychosis, a severe mental disorder that can impair thought and emotions, to the point where individuals lose touch with reality. The next S is for sickness, which refers to chronic nonpsychiatric diseases, like end-stage cancer, that can be very hard to deal with. O stands for organized plan, which is when the individual has a specific method for suicide in mind. What’s very important to remember is that the most common method involves firearms like guns. For that reason, it’s key to evaluate if the individual has access to firearms. Next, N stands for no social support, meaning that they have no friends or family to turn to during vulnerable times. The last S refers to stated future intent, which is when a person expresses their suicidal thoughts or intentions.

Now, even if there are no risk factors for suicide, some people may impulsively take their lives in a moment of overwhelming life stress. This could be due to the loss of a loved one, going through a financial crisis, or experiencing various social pressures. Because of that, it’s just as important to focus on protective factors that can reduce the potential for suicidal behavior. Protective factors can include helping individuals develop self-esteem and coping skills. In addition, having cultural and religious beliefs, as well as a sense of purpose in life can discourage suicide. Finally, a key protective factor is companionship and emotional support.

If you suspect that someone’s at risk for attempting suicide, the first thing you should do is evaluate how serious the threat is, and suggest that they seek for help or be hospitalized voluntarily. If they refuse to get help, and they’re an imminent threat, they should be hospitalized involuntarily.

The next high yield psychiatric emergency is serotonin syndrome. Now, serotonin, also called 5-hydroxytryptamine or 5-HT for short, is a neurotransmitter that mainly helps regulate mood and emotions. Presynaptic serotonergic neurons synthesize serotonin and store it in small vesicles. When an action potential reaches the presynaptic membrane, the vesicles fuse with the membrane and release the serotonin into the synaptic cleft. The free serotonin then binds to serotonin or 5HT receptors on the postsynaptic neuron, causing it to fire off its own action potential. The presynaptic membrane also has serotonin reuptake transporters or SERTs, which take serotonin back into the presynaptic neuron, so the postsynaptic neuron stops firing. Inside the presynaptic neuron, some of this serotonin is packed into pre-existing vesicles, waiting to be released once more, while the rest of the serotonin is broken down by mitochondrial enzymes called monoamine oxidases or MAOs for short.

Okay, now, serotonin syndrome is a potentially life-threatening condition caused by high levels of serotonin in the brain. For your tests, remember that most cases of serotonin syndrome occur in people taking psychiatric medications to treat depression, which can be classified as typical and atypical antidepressants. Typical antidepressants include medications that block serotonin reuptake transporters, such as selective serotonin reuptake inhibitors or SSRIs like fluoxetine, serotonin norepinephrine reuptake inhibitors or SNRIs like duloxetine, and tricyclic antidepressants or TCAs like amitriptyline. Typical antidepressants also include medications called monoamine oxidase inhibitors or MAOIs for short, which inhibit the breakdown of serotonin by monoamine oxidases. What’s very high yield is that serotonin syndrome is most likely to occur when MAOIs are taken in combination with another antidepressant medication! Now, some atypical antidepressants, such as vilazodone and vortioxetine, can also cause serotonin syndrome by blocking serotonin reuptake inhibitors. Another important psychiatric medication that can cause serotonin syndrome is buspirone, which is mainly used to treat anxiety disorders. What buspirone does is it binds to serotonin receptors on the postsynaptic membrane and activates them, thereby potentiating the effect of serotonin in the central nervous system.

Now, it’s important to note that serotonin syndrome can also be caused by some nonpsychiatric medications, which you can remember using the mnemonic: The LOSt MD Took MDMA - Tramadol, Linezolid, Ondansetron, St. John’s wort, Meperidine, Dextromethorphan, Triptans, and MDMA. Okay, so tramadol, meperidine, dextromethorphan, and St. John’s wort, all increase the concentration of serotonin by blocking serotonin reuptake transporters. Another medication you should think of is linezolid, which blocks monoamine oxidases and prevents them from breaking down serotonin. Next we have ondansetron, which acts as a serotonin receptor antagonist, which means that it binds and inhibits serotonin receptors on the postsynaptic membrane. As a result, serotonin can’t bind to its receptors, so it builds up throughout the central nervous system. On the flip side, triptans act as serotonin receptor agonists, so they bind and activate serotonin receptors. Finally, MDMA stimulates the presynaptic neurons to release serotonin.

Okay, to remember the most common clinical features of serotonin syndrome, think of the 3 A’s, which are autonomic effects, abnormal neuromuscular activity, and altered mental status. Autonomic effects can include gastrointestinal disturbances like diarrhea, diaphoresis or excessive sweating, mydriasis or dilated pupils, and hyperthermia or increased body temperature, as well as hypertension or elevated blood pressure, and tachycardia or increased heart rate. Abnormal neuromuscular activity may manifest as myoclonus or muscle twitching, hyperreflexia or excessive reflexes, hypertonia or increased muscle tone, tremor or involuntary shaking, and even seizures. Finally, altered mental status may present with agitation, confusion, hallucinations, or even coma.

Treatment of serotonin syndrome involves the administration of benzodiazepines and supportive care, and in severe cases administration of cyproheptadine, which can inhibit serotonin receptors.

Now, another very similar psychiatric emergency is neuroleptic malignant syndrome. Now, the exact mechanism behind neuroleptic malignant syndrome is unclear, but it seems to be associated with dopamine receptor blockade. In fact, it typically occurs in individuals taking antipsychotic medications, which remember is often used to treat schizophrenia. Most cases are caused by typical antipsychotic medications, such as haloperidol. Now, typical antipsychotics work by blocking dopamine D2 receptors, which are found in various pathways within the brain. Some high yield pathways include the mesolimbic pathway, which controls feelings of motivation, reward, and desire; the mesocortical pathway, which helps regulate emotions; and the nigrostriatal pathway, which helps control involuntary movements and coordination. Less frequently, neuroleptic malignant syndrome may be caused by atypical antipsychotics like clozapine, which can block both dopamine D2 receptors and serotonin receptors. What’s really important to note is that medications are usually not enough to develop neuroleptic malignant syndrome. In fact, there seems to be a genetic predisposition in those who have genetic variations in the gene that codes dopamine D2 receptors. And that’s a high yield fact!

Symptoms of neuroleptic malignant syndrome typically start days to weeks after starting the medications. To help you recall the most high yield symptoms, think of FEVER. F actually stands for fever or hyperthermia, and it’s one of the most characteristic symptoms of neuroleptic malignant syndrome. The first E stands for encephalopathy or brain dysfunction, which presents with an altered mental status that can range from confusion or delirium to coma. Then there’s V for vitals, which are typically unstable. This means that individuals with neuroleptic malignant syndrome may experience tachycardia, as well as a labile blood pressure that may suddenly go from normal to really high levels. Now, unstable vitals can often be associated with diaphoresis, and that’s a very high yield fact! Okay, the second E stands for enzymes, such as creatine kinase that may be elevated in blood, as well as myoglobinuria or the presence of myoglobin in urine. What’s important to note here is that these enzymes are normally found inside skeletal muscle cells, so finding them around in blood or urine typically indicates rhabdomyolysis or abnormal skeletal muscle breakdown. And what's even more important is that these enzymes can be harmful to the kidneys and often lead to acute renal failure. Finally, R stands for rigidity of muscles, which is characterized by an increased muscle tone that causes constant resistance when another person tries to move the joint of the affected individual. In a test question, this may be referred to as “lead pipe” rigidity.

Now, some of these symptoms may trick you into thinking of serotonin syndrome, so to set these two apart, remember that neuroleptic malignant syndrome tends to cause more severe hyperthermia and muscle rigidity. In addition, individuals with serotonin syndrome typically also experience mydriasis, hyperreflexia, myoclonus, and diarrhea. So be sure to keep an eye out for these clues!

Sources

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
  4. "Diagnostic and Statistical Manual of Mental Disorders" NA (1980)
  5. "Suicide prevention strategies revisited: 10-year systematic review" The Lancet Psychiatry (2016)
  6. "Psychiatric Emergencies in the Intensive Care Unit" AACN Advanced Critical Care (2015)
  7. "Neuroleptic Malignant Syndrome" American Journal of Psychiatry (2007)