Urgencias Flashcards
1
Q
What is hypoglycemia often attributable to?
A
Insulin or other diabetes medications
Hypoglycemia can be a common side effect of diabetes treatment.
2
Q
What are C-peptide and proinsulin?
A
Byproducts of the endogenous production of insulin
They are important for assessing insulin production.
3
Q
What does elevated serum insulin with suppressed C-peptide and proinsulin levels indicate?
A
Exogenous insulin (insulin overdose)
This situation often occurs in cases of insulin overdose.
4
Q
What is associated with excess secretion of endogenously produced insulin leading to hypoglycemia?
A
Insulinoma
Insulinoma is a tumor of the pancreas that produces excess insulin.
5
Q
What levels correspond when there is excess endogenous insulin secretion leading to hypoglycemia?
A
C-peptide and proinsulin levels correspond to the level of insulin
This helps differentiate between endogenous and exogenous insulin causes.
6
Q
Fill in the blank: The cause of hypoglycemia associated with an elevated level of insulin but a suppressed level of C-peptide is an _______.
A
insulin overdose
This is a key learning point in understanding hypoglycemia.
7
Q
What effect does mannitol have on plasma osmolality?
A
Increases plasma osmolality
This increase results in osmotic shifts of water into the intravascular space.
8
Q
What is one beneficial effect of mannitol on the body?
A
Decreases cerebral edema
Mannitol is often used to reduce swelling in the brain.
9
Q
What is a potential adverse effect of mannitol?
A
Iatrogenic volume overload and pulmonary edema
These conditions can arise as a result of mannitol administration.
10
Q
What are risk factors for developing pulmonary edema when using mannitol?
A
Very high doses and low glomerular filtration rate
These factors increase the likelihood of adverse effects.
11
Q
True or False: Mannitol can lead to osmotic shifts of water into the intravascular space.
A
True
This is a key mechanism by which mannitol exerts its effects.
12
Q
Fill in the blank: Mannitol causes an increase in plasma osmolality, resulting in _______ shifts of water into the intravascular space.
A
osmotic
This term describes the process by which water moves in response to osmotic gradients.
13
Q
What is the commonality of seizures in children with febrile illnesses?
A
Common and often benign
14
Q
What severe disease indicators are present in the child described?
A
Focal neurologic deficits, encephalopathy, seizures despite benzodiazepines
15
Q
What does an analysis of the cerebrospinal fluid (CSF) reveal in this case?
A
Elevated leukocyte count and elevated protein level
16
Q
What combination of symptoms is suggestive of encephalitis?
A
Aseptic CSF profile, encephalopathy, status epilepticus
17
Q
What are potential causes of encephalitis in children?
A
Infections, inflammatory disorders, autoantibodies
18
Q
What suggests an underlying infection in the child?
A
Acute onset of symptoms and fever on presentation
19
Q
What are the most common infectious causes of encephalitis in children?
A
Herpes simplex virus (HSV) and enterovirus
20
Q
What test is most likely to yield the correct diagnosis in this patient?
A
Polymerase chain-reaction assay (PCR) for HSV and enteroviruses
21
Q
Why is testing for HSV critical in children with meningoencephalitis?
A
Prompt initiation of acyclovir improves outcomes
22
Q
Fill in the blank: The CSF profile in encephalitis typically shows _______.
A
Moderate pleocytosis, normal glucose level, moderately elevated protein
23
Q
True or False: Encephalopathy can present as irritability in children.
A
True
24
Q
What is cryoglobulinemic vasculitis characterized by?
A
Presence of cryoglobulins in the serum leading to immune complex deposition in capillaries, venules, or arterioles
25
How many types of cryoglobulinemic vasculitis are there?
Three types
26
What is Type I cryoglobulinemic vasculitis associated with?
Self-aggregating monoclonal immunoglobulins, usually secondary to B-cell or plasma-cell malignancies such as multiple myeloma or Waldenström macroglobulinemia
27
What causes Type II cryoglobulinemic vasculitis?
A mixture of polyclonal immunoglobulins and monoclonal immunoglobulins with rheumatoid factor activity, often associated with hepatitis C virus (HCV) infection
28
What diseases are associated with Type II cryoglobulinemic vasculitis besides hepatitis C?
Connective tissue diseases or lymphoma
29
What characterizes Type III cryoglobulinemic vasculitis?
Rheumatoid factor activity carried by polyclonal immunoglobulins, often due to HCV and secondary to diseases like Sjögren syndrome, systemic lupus erythematosus, and rheumatoid arthritis
30
What symptoms did the patient present with?
Malaise, headache, progressively worsening constitutional symptoms, palpable purpura, hepatomegaly, and lower-extremity edema
31
What laboratory findings are consistent with acute glomerulonephritis in this patient?
Elevated blood pressure, raised serum creatinine level, proteinuria, and hematuria
32
What are the relevant factors leading to the diagnosis of cryoglobulinemic vasculitis in this case?
Positive rheumatoid factor, hypocomplementemia, HCV infection, and a negative antinuclear antibody
33
Fill in the blank: The most likely diagnosis in a patient with purpura, renal insufficiency, an active urine sediment, and chronic hepatitis C infection is _______.
cryoglobulinemic vasculitis
34
True or False: Cryoglobulinemic vasculitis can be caused by a mixture of polyclonal and monoclonal immunoglobulins.
True
35
What is a retropharyngeal abscess?
Generally the most dangerous deep neck infection
## Footnote
It is especially concerning due to its potential complications.
36
Which age group is most commonly affected by retropharyngeal abscess?
Children < 5 years of age
37
What is the gender prevalence for retropharyngeal abscess?
♂ > ♀
38
What pathogens are commonly associated with retropharyngeal abscess?
* Streptococci (viridans streptococci, S. pneumoniae)
* Staphylococci (including MRSA)
* Haemophilus influenzae
* Oral anaerobes (peptostreptococci, Bacteroides species)
39
What are the common direct or indirect causes of retropharyngeal abscess?
* Contiguous or lymphatic spread from oral or upper respiratory tract infections
* Local penetrating pharyngeal trauma
* Spread from other deep neck infections
40
What are the clinical features of retropharyngeal abscess?
* Features of tonsillitis and trismus
* Neck asymmetry with unilateral swelling of the posterior pharyngeal wall
* Torticollis
* Anterior cervical lymphadenopathy
* Respiratory distress
41
What imaging study is preferred for diagnosing retropharyngeal abscess?
CT neck with IV contrast
42
What findings are indicative of retropharyngeal abscess on a CT scan?
* Hypodense fluid collection with ring enhancement in the retropharyngeal space
* Posterior pharynx wall with anterior displacement
* Spread of infection to other spaces
43
What is the initial screening study in patients with airway compromise for retropharyngeal abscess?
Lateral x-ray neck
44
What are some findings on a lateral x-ray neck for retropharyngeal abscess?
* Widened prevertebral space with gas or air-fluid levels
* Lordosis
* Evidence of foreign body, if present
45
What are the mainstays of therapy for retropharyngeal abscess?
* Systemic IV antibiotics
* Abscess drainage
* Supportive care
46
What should be done for patients with respiratory distress due to retropharyngeal abscess?
Prompt airway management
47
What type of antibiotics should be started for retropharyngeal abscess?
Broad-spectrum empiric antibiotics (e.g., clindamycin or ampicillin/sulbactam)
48
What is a possible complication of retropharyngeal abscess involving the airway?
Airway obstruction
49
What can happen if the infection spreads to the carotid sheath?
Internal carotid artery erosion and jugular vein thrombophlebitis (Lemierre syndrome)
50
What is a serious complication that can arise from a retropharyngeal abscess?
Descending mediastinitis
51
What should be considered to reduce inflammation in retropharyngeal abscess treatment?
Corticosteroids (e.g., dexamethasone)
52
True or False: Patients with retropharyngeal abscess should always be managed as outpatients.
False
53
Fill in the blank: The presence of _______ can help direct therapy for the causative pathogen in retropharyngeal abscess.
Microbiological studies (e.g., bacterial culture of abscess aspirate)
54
What is a retropharyngeal abscess?
Generally the most dangerous deep neck infection
## Footnote
It is especially concerning due to its potential complications.
55
Which age group is most commonly affected by retropharyngeal abscess?
Children < 5 years of age
56
What is the gender prevalence for retropharyngeal abscess?
♂ > ♀
57
What pathogens are commonly associated with retropharyngeal abscess?
* Streptococci (viridans streptococci, S. pneumoniae)
* Staphylococci (including MRSA)
* Haemophilus influenzae
* Oral anaerobes (peptostreptococci, Bacteroides species)
58
What are the common direct or indirect causes of retropharyngeal abscess?
* Contiguous or lymphatic spread from oral or upper respiratory tract infections
* Local penetrating pharyngeal trauma
* Spread from other deep neck infections
59
What are the clinical features of retropharyngeal abscess?
* Features of tonsillitis and trismus
* Neck asymmetry with unilateral swelling of the posterior pharyngeal wall
* Torticollis
* Anterior cervical lymphadenopathy
* Respiratory distress
60
What imaging study is preferred for diagnosing retropharyngeal abscess?
CT neck with IV contrast
61
What findings are indicative of retropharyngeal abscess on a CT scan?
* Hypodense fluid collection with ring enhancement in the retropharyngeal space
* Posterior pharynx wall with anterior displacement
* Spread of infection to other spaces
62
What is the initial screening study in patients with airway compromise for retropharyngeal abscess?
Lateral x-ray neck
63
What are some findings on a lateral x-ray neck for retropharyngeal abscess?
* Widened prevertebral space with gas or air-fluid levels
* Lordosis
* Evidence of foreign body, if present
64
What are the mainstays of therapy for retropharyngeal abscess?
* Systemic IV antibiotics
* Abscess drainage
* Supportive care
65
What should be done for patients with respiratory distress due to retropharyngeal abscess?
Prompt airway management
66
What type of antibiotics should be started for retropharyngeal abscess?
Broad-spectrum empiric antibiotics (e.g., clindamycin or ampicillin/sulbactam)
67
What is a possible complication of retropharyngeal abscess involving the airway?
Airway obstruction
68
What can happen if the infection spreads to the carotid sheath?
Internal carotid artery erosion and jugular vein thrombophlebitis (Lemierre syndrome)
69
What is a serious complication that can arise from a retropharyngeal abscess?
Descending mediastinitis
70
What should be considered to reduce inflammation in retropharyngeal abscess treatment?
Corticosteroids (e.g., dexamethasone)
71
True or False: Patients with retropharyngeal abscess should always be managed as outpatients.
False
72
Fill in the blank: The presence of _______ can help direct therapy for the causative pathogen in retropharyngeal abscess.
Microbiological studies (e.g., bacterial culture of abscess aspirate)
73
What is carbon monoxide (CO)?
A colorless, odorless, tasteless gas
74
What are common causes of CO poisoning?
Smoke inhalation, poorly functioning heating systems, improperly ventilated fuel-burning devices, motor vehicles in poorly ventilated areas
75
When does CO poisoning tend to occur?
During the winter
76
What are some nonspecific symptoms of CO poisoning?
* Headache
* Dizziness
* Fatigue
* Confusion
* Irritability
77
What severe symptoms can CO poisoning lead to?
* Loss of consciousness
* Death
78
How does CO poisoning affect oxygen delivery in the body?
Interferes with oxygen delivery by binding to hemoglobin
79
What is the affinity of CO for hemoglobin compared to oxygen?
250 times that of oxygen
80
What is the antidote for CO poisoning?
Oxygen
81
What is the effect of supplemental 100% normobaric oxygen on CO?
* Reduces half-life of CO to one hour
* Increases amount of dissolved oxygen in the blood
82
What should be the first step for any patient with suspected CO poisoning?
Administer 100% oxygen via a nonrebreather mask
83
What is a common cause of medication-associated priapism?
Trazodone
## Footnote
Trazodone is among the most common causes, occurring in fewer than 0.1% of men treated with the drug.
84
What percentage of men treated with Trazodone experience priapism?
Fewer than 0.1%
## Footnote
This statistic highlights the rarity of priapism associated with Trazodone.
85
Which types of medications have been reported to cause priapism?
Typical and atypical antipsychotic medications, certain antihypertensive, and anticoagulant medications
## Footnote
Priapism can occur after the use of various drug classes.
86
What should be done for men with an erection lasting more than 4 hours?
They should be treated in the emergency department
## Footnote
This is critical to prevent complications such as ischemia and gangrene.
87
True or False: Priapism is a common condition among men using Trazodone.
False
## Footnote
Priapism occurs in fewer than 0.1% of men treated with Trazodone.
88
Fill in the blank: Priapism has been reported following the use of _______ medications.
antipsychotic, antihypertensive, anticoagulant
## Footnote
These medication classes can lead to the occurrence of priapism.
89
What is priapism?
A sustained erection lasting more than four hours not due to sexual excitation
## Footnote
Priapism can lead to serious complications if not treated promptly.
90
How is priapism classified based on etiopathogenesis?
Low-flow and high-flow
## Footnote
This classification is based on the underlying mechanisms causing the condition.
91
What is low-flow priapism caused by?
Inadequate venous outflow from the corpus cavernosum
## Footnote
This results in painful penile ischemia.
92
What is the most common cause of low-flow priapism in adults?
Adverse effects from treating erectile dysfunction (e.g., sildenafil)
## Footnote
Low-flow priapism can also be associated with other medications.
93
What is the most common cause of low-flow priapism in children?
Sickle cell disease
## Footnote
Sickle cell disease leads to vaso-occlusive crises that can result in priapism.
94
What usually causes high-flow priapism?
Perineal trauma
## Footnote
High-flow priapism is less common than low-flow.
95
Is high-flow priapism associated with penile ischemia?
No, it is painless and not associated with ischemia
## Footnote
This differentiates it from low-flow priapism.
96
What diagnostic tools are used to distinguish between low-flow and high-flow priapism?
Penile blood gas analysis and Doppler ultrasound of the penis
## Footnote
These tests help assess blood flow and oxygenation in penile tissues.
97
Why is low-flow priapism considered an acute urological emergency?
It must be treated within 12 hours to prevent complications
## Footnote
Delayed treatment can lead to permanent erectile dysfunction.
98
What is the initial treatment for low-flow priapism?
Aspiration of blood from the corpus cavernosum and injection of phenylephrine
## Footnote
This helps restore normal blood flow and relieve pain.
99
What surgical intervention may be indicated if priapism does not subside?
Surgical therapy to decompress the penis
## Footnote
This is a last resort if other treatments fail.
100
What is the potential outcome if low-flow priapism is treated within 12 hours?
Complete restoration of erectile function is possible
## Footnote
Timely intervention is crucial for preserving erectile ability.
101
What happens if treatment for low-flow priapism is delayed?
Cavernous fibrosis and irreparable damage with erectile dysfunction
## Footnote
Delayed treatment can lead to long-term complications.
102
Does non-ischemic priapism usually require treatment?
No, it usually does not require treatment
## Footnote
Non-ischemic priapism is generally less problematic than ischemic forms.
103
What is Kawasaki disease (KD)?
An acute, necrotizing vasculitis of unknown etiology.
104
What age group is primarily affected by Kawasaki disease?
Children under the age of five.
105
Which ethnic group is more commonly affected by Kawasaki disease?
Those of Asian descent.
106
List the main symptoms of Kawasaki disease.
* High fever
* Desquamative rash
* Conjunctivitis
* Mucositis (e.g., strawberry tongue)
* Cervical lymphadenopathy
* Erythema and edema of the distal extremities
107
What is the most concerning manifestation of Kawasaki disease?
Coronary artery aneurysms.
108
What serious complications can arise from coronary artery aneurysms in Kawasaki disease?
* Myocardial infarction
* Arrhythmias
109
How is Kawasaki disease diagnosed?
It is a clinical diagnosis supported by findings such as elevated ESR or evidence of cardiac involvement on echocardiography.
110
What is the essential treatment for Kawasaki disease?
Intravenous immunoglobulins (IVIG) and aspirin.
111
When should treatment for Kawasaki disease be initiated?
As soon as possible after diagnosis.
112
True or False: Kawasaki disease can affect adults.
False.
113
Fill in the blank: Kawasaki disease is characterized by ________ rash.
desquamative
114
What is a common oral manifestation in Kawasaki disease?
Strawberry tongue.
115
What condition is associated with an increased risk of developing saccular aneurysms?
ADPKD
## Footnote
ADPKD stands for Autosomal Dominant Polycystic Kidney Disease.
116
What symptom did the patient present with that indicated a subarachnoid hemorrhage (SAH)?
Severe headache
## Footnote
Patients typically report having the worst headache of their life.
117
What are other signs of subarachnoid hemorrhage (SAH)?
* Fever
* Xanthochromia
* Meningismus
## Footnote
Xanthochromia refers to the yellow-colored cerebrospinal fluid (CSF), and meningismus includes neck stiffness and positive Kernig sign.
118
True or False: A sudden onset of a severe headache can raise suspicion for SAH.
True
119
Fill in the blank: Xanthochromia is characterized by _______ colored CSF.
yellow
120
What is meningismus?
Neck stiffness and Kernig sign caused by irritation of the meninges by blood
## Footnote
Meningismus is an indication of meningeal irritation, often seen in cases of SAH.
121
What is a traumatic brain injury?
A disruption in normal brain function caused by an external force.
122
What are the inpatient observation indications for traumatic brain injury?
Indications include:
* Skull fracture > 3 mm separation or depressed
* Evidence of traumatic brain injury on imaging (e.g., intracranial hemorrhage)
* Signs of ↑ ICP (e.g., headache, altered mental status)
* Suspected physical abuse
* Caregivers who are unreliable or unable to return if neurological deficits develop within 24 hours after release.
123
When can a patient be released for at-home observation after a traumatic brain injury?
Patients without neurological deficits and non-depressed linear skull fracture < 3 mm separation.
124
What is required of caregivers for at-home observation after traumatic brain injury?
Caregivers must reliably recognize new clinical neurological deficits and return the patient to the hospital if such manifestations arise.
125
True or False: A skull fracture of less than 3 mm separation does not require inpatient observation.
True.
126
Fill in the blank: Evidence of traumatic brain injury on imaging may include _______.
[intracranial hemorrhage].
127
What are signs of increased intracranial pressure (ICP)?
Signs include:
* Headache
* Altered mental status.
128
What is amaurosis fugax?
Transient monocular vision loss
## Footnote
It can sometimes be bilateral.
129
In which condition is amaurosis fugax an early sign of ocular involvement?
Giant-cell arteritis (GCA)
## Footnote
It may indicate potential permanent vision loss.
130
What symptoms are often accompanied by amaurosis fugax in patients with GCA?
Headache and jaw claudication
## Footnote
These symptoms can indicate more serious underlying issues.
131
What is the recommended treatment for patients whose presentation is compatible with GCA?
Immediate glucocorticoid therapy
## Footnote
This treatment is crucial to prevent permanent vision loss.
132
True or False: Amaurosis fugax can only occur in one eye.
False
## Footnote
It can present as bilateral vision loss.
133
What is a life-threatening asthma exacerbation characterized by?
Drowsiness, confusion, silent chest, inability to speak due to dyspnea, paradoxical breathing, bradycardia
## Footnote
Silent chest indicates severe airway obstruction with no audible wheezing.
134
What does the presence of drowsiness and confusion indicate in asthma exacerbation?
Possible severe hypoxia or respiratory failure
## Footnote
These symptoms suggest that the patient may not be getting enough oxygen.
135
What does a silent chest indicate during an asthma attack?
Absence of wheezing
## Footnote
This can signify critical airway obstruction.
136
What is a key sign of inability to speak during an asthma exacerbation?
Dyspnea
## Footnote
This shows the severity of the breathing difficulty.
137
What is paradoxical breathing?
A breathing pattern where the abdomen moves in during inhalation and out during exhalation
## Footnote
This indicates severe respiratory distress.
138
What does bradycardia indicate in the context of asthma exacerbation?
A potentially life-threatening condition
## Footnote
Bradycardia may occur due to hypoxia or vagal stimulation.
139
What are the common symptoms of epiglottitis in adult patients?
Odynophagia, inability to swallow, elevated temperature, sore throat, hoarseness
## Footnote
Stridor is less common but may indicate airway compromise.
140
What is the role of nasal fiberoptic laryngoscopy in diagnosing epiglottitis?
Aids in direct visualization of the supraglottis in a monitored setting
## Footnote
Diagnosis is primarily clinical.
141
How should a patient with airway distress and upper-airway obstruction be managed?
Elective intubation via awake fiberoptic nasotracheal intubation under local anesthesia
## Footnote
A backup tracheotomy/cricothyrotomy kit should always be available.
142
What is the most appropriate care for a patient with acute epiglottitis and signs of airway compromise?
Fiberoptic nasotracheal intubation in a monitored setting with a tracheotomy/cricothyrotomy set at the bedside.
143
True or False: Stridor is a common symptom of epiglottitis.
False
## Footnote
Stridor is associated with impending airway compromise but is less common.
144
What percentage of nontraumatic subarachnoid hemorrhages are caused by ruptured saccular aneurysms?
80%
145
List three risk factors for the development of a saccular aneurysm.
* Age > 40 years
* Female gender
* Hypertension
146
True or False: Cigarette smoking is a risk factor for saccular aneurysms.
True
147
Fill in the blank: Other risk factors for saccular aneurysms include heavy alcohol use, ________, polycystic kidney disease, and family history.
[connective tissue disorders]
148
What is a significant gender-related risk factor for saccular aneurysms?
Female gender
149
Identify a risk factor for saccular aneurysms related to kidney health.
Polycystic kidney disease
150
Name a lifestyle factor that increases the risk of developing a saccular aneurysm.
Cigarette smoking
151
What age is considered a risk factor for saccular aneurysms?
Age > 40 years
152
List two additional risk factors for saccular aneurysms not previously mentioned.
* Heavy alcohol use
* Family history
153
What is the most common type of intracranial hemorrhage in infants with shaken baby syndrome (SBS)?
Subdural hematomas
## Footnote
Subdural hematomas occur due to the violent shaking that causes injury to the brain.
154
What results from violent shaking of a baby in shaken baby syndrome?
Whiplash and rapid rotational head movements
## Footnote
These movements lead to tearing of the intracerebral bridging veins and diffuse axonal injury.
155
List characteristic physical examination findings in children with shaken baby syndrome.
* Irritability
* Lethargy
* Retinal hemorrhages
* Bulging fontanelles
## Footnote
Retinal hemorrhages occur due to rupture of the retinal veins.
156
True or False: Retinal hemorrhages are a characteristic finding in shaken baby syndrome.
True
## Footnote
They result from the tearing of retinal veins during the violent shaking.
157
What additional injuries indicate child abuse in cases of shaken baby syndrome?
* Bruises to the upper torso
* Posterior rib fractures
* Fractures at multiple stages of healing
* Complex, long bone fractures
## Footnote
An example of a bruise pattern is purple discoloration in the T4–T10 dermatomes.
158
Fill in the blank: In shaken baby syndrome, bruises to the _______ torso can indicate child abuse.
upper
## Footnote
Bruises in this area may suggest a forceful grip or other abusive actions.
159
What type of fracture is commonly associated with child abuse in shaken baby syndrome?
Complex, long bone fractures (e.g., spiral humerus fractures)
## Footnote
These fractures indicate potential abusive trauma rather than accidental injury.
160
What is the toxidrome associated with the patient's symptoms?
Tricyclic antidepressant (TCA) toxicity
## Footnote
Symptoms include tachycardia, hyperthermia, blurred vision, mydriasis, dry skin, and impaired intestinal motility.
161
What ECG findings are associated with increased risk for dysrhythmias and seizures in TCA toxicity?
QRS prolongation >100 msec and QTc prolongation >430 msec
## Footnote
The patient had a QRS duration of 120 msec and a QTc interval of 460 msec.
162
What are the elements of anticholinergic syndrome demonstrated by the patient?
* Tachycardia
* Hyperthermia
* Blurred vision
* Mydriasis
* Dry skin
* Impaired intestinal motility
* ECG changes
## Footnote
These symptoms help to distinguish it from sympathomimetic toxidrome.
163
How do TCAs affect alpha-adrenergic and muscarinic receptors?
They block these receptors, causing hypotension and anticholinergic syndrome, respectively
## Footnote
This leads to symptoms like dry skin and impaired intestinal motility.
164
What is the first-line treatment for TCA overdose?
Sodium bicarbonate
## Footnote
It alkalinizes blood pH and increases plasma protein binding of TCAs.
165
What is the goal pH when administering sodium bicarbonate in TCA overdose?
7.50 to 7.55
## Footnote
This goal can be achieved with 1- to 2-mEq/kg boluses.
166
What are the benefits of sodium bicarbonate in TCA overdose treatment?
* Alkalinizes blood pH
* Increases plasma protein binding of TCAs
* Augments myocardial contractility
* Improves intraventricular conduction
## Footnote
These effects can elevate blood pressure and resolve hypotension.
167
What distinguishes the patient's condition from serotonin syndrome?
Normal reflexes and lack of clonus
## Footnote
In serotonin syndrome, increased reflexes and clonus would be present.
168
True or False: A fluid bolus is effective in reversing hypotension caused by TCA overdose.
False
## Footnote
It can help optimize cardiac preload but does not reverse myocardial depression or reduced systemic vascular resistance.
169
What is the best predictor of complications after a tricyclic antidepressant overdose?
An electrocardiogram identifying a QRS duration >100 msec or a QTc interval >430 msec
## Footnote
This is crucial for assessing risk in TCA overdose cases.
170
What condition did the patient have that led to poor oral intake?
Upper respiratory tract infection
## Footnote
Poor oral intake can occur due to symptoms such as sore throat or fatigue associated with the infection.
171
What induced hypovolemia in the patient?
Poor oral intake and increased insensible fluid losses
## Footnote
Insensible fluid losses can be exacerbated by a febrile illness.
172
What medications did the patient take that contributed to acute kidney injury?
ACE inhibitor, diuretic, NSAID
## Footnote
Each of these medications can affect kidney function, especially in the context of volume depletion.
173
What was confirmed by the elevated serum creatinine level?
Acute kidney injury
## Footnote
Elevated serum creatinine is a common marker for kidney dysfunction.
174
What symptoms did the patient experience likely due to uremia?
Nausea, fatigue, anorexia
## Footnote
These symptoms are commonly associated with uremic syndrome.
175
What physiological mechanisms help maintain glomerular filtration in volume depletion?
Prostaglandin-mediated vasodilation of afferent arteriole and angiotensin II-mediated vasoconstriction of efferent arteriole
## Footnote
These mechanisms are part of the kidney's autoregulatory response to maintain filtration pressure.
176
How do NSAIDs and ACE inhibitors affect kidney autoregulation?
They block the autoregulatory defenses
## Footnote
This can lead to decreased glomerular perfusion and potential kidney injury.
177
What is a key learning point regarding NSAIDs and kidney injury?
NSAIDs can precipitate acute kidney injury in the setting of volume depletion and renin-angiotensin-aldosterone axis blockade
## Footnote
This highlights the importance of careful medication management in patients with compromised kidney function.
178
Fill in the blank: The patient's acute kidney injury was likely due to _______ from medication-induced decreased glomerular perfusion.
Uremia
## Footnote
Uremia is a condition that arises when the kidneys cannot adequately filter waste products from the blood.
179
What condition can NSAIDs cause related to kidney function?
Interstitial nephritis
## Footnote
NSAIDs are known to induce interstitial nephritis, which is an inflammation of the kidney's interstitium.
180
What is the mean time from starting medication to signs of acute interstitial nephritis?
10 days
## Footnote
This timeframe can be shorter if the patient has previously taken the medication.
181
What serum creatinine level indicates significant renal dysfunction in this patient?
>4 mg/dL
## Footnote
A serum creatinine level above this threshold suggests severe renal impairment.
182
What does the time course of renal dysfunction in this patient suggest?
Medication-induced decreased glomerular perfusion
## Footnote
The clinical history aligns more with decreased blood flow to the kidneys rather than interstitial nephritis.
183
What features are commonly associated with interstitial nephritis?
* Fever
* Rash
* Eosinophilia
* Pyuria
* White-cell casts
## Footnote
These features can help in diagnosing interstitial nephritis, though their absence does not rule it out.
184
True or False: The absence of fever, rash, eosinophilia, pyuria, and white-cell casts makes interstitial nephritis unlikely.
True
## Footnote
While these symptoms do not exclude interstitial nephritis, their absence in conjunction with the timing makes the diagnosis less likely.
185
The onset of renal dysfunction in this patient would be expected to have occurred at least ______ days earlier.
4
## Footnote
This is based on the patient's serum creatinine level being greater than 4 mg/dL.
186
What are the signs of acute liver failure?
Abnormal liver-enzyme levels, coagulopathy, and encephalopathy
## Footnote
Coagulopathy can be indicated by an elevated international normalized ratio and evidence of gastrointestinal bleeding.
187
Why is determining the underlying cause of liver failure important?
It will affect management
## Footnote
Understanding the cause is crucial for effective treatment strategies.
188
What condition should be suspected in a young patient with liver failure and neurologic symptoms?
Wilson disease
## Footnote
Wilson disease is rare but should be considered based on age and symptoms.
189
What laboratory results suggest Wilson disease?
Low alkaline phosphatase to total bilirubin ratio (<4) and elevated AST and ALT levels with AST-to-ALT ratio >2
## Footnote
Elevated levels should be <2000 U/liter.
190
What additional complications can occur in acute Wilson disease?
Renal failure and Coombs-negative hemolytic anemia
## Footnote
In this context, anemia is likely due to gastrointestinal bleeding.
191
What serum level is suggestive of Wilson disease?
Low serum ceruloplasmin level (<0.1 g/liter)
## Footnote
However, low ceruloplasmin is not sufficient for diagnosis.
192
What factors limit the diagnostic utility of ceruloplasmin levels for Wilson disease?
Low positive predictive values and potential for false elevation in acute settings
## Footnote
Ceruloplasmin is an acute-phase reactant.
193
What confirmatory tests should be conducted before diagnosing Wilson disease?
Serum copper concentration, 24-hour urinary copper excretion, and ocular slit-lamp examination for Kayser-Fleischer rings
## Footnote
These tests help confirm the diagnosis of Wilson disease.
194
What key learning point should prompt evaluation for Wilson disease?
Acute liver failure in a young woman with recent behavioral changes, gastrointestinal bleeding, low alkaline phosphatase, and elevated aminotransferase levels with AST-to-ALT ratio >2
## Footnote
These clinical features are critical for suspicion and further investigation.
195
What are the common clinical presentations of testicular torsion?
Sudden onset of severe hypogastric and left inguinal pain, nausea, vomiting
## Footnote
These symptoms indicate a potential testicular torsion.
196
What physical examination findings are indicative of testicular torsion?
Hypogastric and testicular tenderness, scrotal elevation and swelling
## Footnote
These findings are critical for diagnosing testicular torsion.
197
During which periods does testicular torsion most commonly develop?
Neonatal period and puberty
## Footnote
Understanding these periods helps in identifying at-risk patients.
198
What are two characteristic findings of testicular torsion?
Absent cremasteric reflex and negative Prehn sign
## Footnote
These findings help differentiate testicular torsion from other conditions.
199
Why is testicular torsion considered a medical emergency?
It requires prompt surgical exploration to prevent irreversible ischemia and necrosis of the testis
## Footnote
Timely intervention is crucial for testicular salvage.
200
What surgical procedures are performed for testicular torsion?
Testicular reduction and bilateral orchidopexy
## Footnote
Orchidopexy helps prevent recurrence of torsion.
201
What is the ideal time frame for surgical intervention in testicular torsion?
Ideally within six hours of symptom onset
## Footnote
Delay beyond this time can lead to severe complications.
202
What imaging study can be performed in patients with ambiguous clinical findings before surgical intervention?
Doppler ultrasound of the scrotum
## Footnote
This imaging helps confirm the diagnosis of testicular torsion.
203
True or False: A delay in management of testicular torsion can lead to irreversible ischemia.
True
## Footnote
Immediate treatment is essential to avoid testicular loss.
204
What are the common clinical presentations of testicular torsion?
Sudden onset of severe hypogastric and left inguinal pain, nausea, vomiting
## Footnote
These symptoms indicate a potential testicular torsion.
205
What physical examination findings are indicative of testicular torsion?
Hypogastric and testicular tenderness, scrotal elevation and swelling
## Footnote
These findings are critical for diagnosing testicular torsion.
206
During which periods does testicular torsion most commonly develop?
Neonatal period and puberty
## Footnote
Understanding these periods helps in identifying at-risk patients.
207
What are two characteristic findings of testicular torsion?
Absent cremasteric reflex and negative Prehn sign
## Footnote
These findings help differentiate testicular torsion from other conditions.
208
Why is testicular torsion considered a medical emergency?
It requires prompt surgical exploration to prevent irreversible ischemia and necrosis of the testis
## Footnote
Timely intervention is crucial for testicular salvage.
209
What surgical procedures are performed for testicular torsion?
Testicular reduction and bilateral orchidopexy
## Footnote
Orchidopexy helps prevent recurrence of torsion.
210
What is the ideal time frame for surgical intervention in testicular torsion?
Ideally within six hours of symptom onset
## Footnote
Delay beyond this time can lead to severe complications.
211
What imaging study can be performed in patients with ambiguous clinical findings before surgical intervention?
Doppler ultrasound of the scrotum
## Footnote
This imaging helps confirm the diagnosis of testicular torsion.
212
True or False: A delay in management of testicular torsion can lead to irreversible ischemia.
True
## Footnote
Immediate treatment is essential to avoid testicular loss.
213
What is the etiology of acute-onset monoarthritis with chondrocalcinosis and CPP crystals?
Acute CPP crystal arthritis, previously known as pseudogout.
214
What is the preferred treatment for acute CPP crystal arthritis involving a single joint?
Intra-articular glucocorticoid injection.
215
What systemic therapies can be pursued if multiple joints are involved in acute CPP crystal arthritis?
* Nonsteroidal antiinflammatory drug (e.g., ibuprofen)
* Glucocorticoid (e.g., prednisone)
* Colchicine
216
What are the relative contraindications for alternate therapies in this patient?
Renal impairment and diabetes.
217
In cases of acute CPP crystal arthritis with contraindications, which treatment is preferable?
Intra-articular glucocorticoid injection.
218
True or False: Acute CPP crystal arthritis can also be treated with systemic glucocorticoids.
True.
219
Fill in the blank: Acute CPP crystal arthritis is also known as _______.
[pseudogout]
220
What is leukostasis?
A medical emergency characterized by tissue hypoxia and hypercoagulability due to an excessive number of immature leukocytes causing microvascular obstruction.
221
Define hyperleukocytosis.
A leukocyte count > 100,000/mm3 that may or may not be accompanied by leukostasis.
222
In which type of leukemia is leukostasis most commonly seen?
Acute leukemia, more commonly in AML than ALL.
223
What is the WBC threshold for AML to be associated with leukostasis?
WBC > 150,000/mm3.
224
What is the WBC threshold for ALL to be associated with leukostasis?
WBC > 400,000/mm3.
225
In which phase of chronic myeloid leukemia (CML) is leukostasis almost exclusively seen?
Accelerated phases or blast crisis.
226
What are the clinical features of leukostasis?
Depend on the affected system or organ, but commonly affect lungs and CNS.
227
List common respiratory clinical features of leukostasis.
* Dyspnea
* Tachypnea
* Pulmonary crackles
* Hypoxemic respiratory failure
228
What neurological symptoms may indicate leukostasis?
* Headache
* Confusion
* Dizziness
* Vertigo
* Focal neurological deficits
* Seizures
229
What are potential ophthalmological symptoms of leukostasis?
* Blurry vision
* Retinal hemorrhages
* Papilledema
230
What diagnostic approach is primarily used for leukostasis?
Leukostasis is primarily a clinical diagnosis.
231
What laboratory findings are common in leukostasis?
* ↑ WBC count
* Anemia
* Overestimated platelet count
232
What additional tests may be performed in suspected cases of leukostasis?
* ABG
* Diagnostic microbiology (e.g., blood cultures)
233
What imaging studies may be indicated for leukostasis?
* Chest x-ray
* CT head or MRI head
* Direct fundoscopy
234
What is the treatment goal for leukostasis?
To reduce the WBC count (cytoreduction) and control symptoms.
235
What is the treatment of choice for leukostasis?
Induction chemotherapy.
236
What are the indications for leukapheresis in leukostasis?
* Symptoms of leukostasis
* WBC ≥ 100,000/mm3
* Severe pulmonary and neurological manifestations
237
What is hydroxyurea used for in the context of leukostasis?
As a bridging therapy to induction chemotherapy.
238
True or False: Blood cell transfusions are recommended in leukostasis management.
False.
239
What should be monitored in patients at risk of tumor lysis syndrome (TLS) during leukostasis treatment?
Monitoring for DIC.
240
What is the most likely cause of memory loss in the setting of a possible traumatic experience without known neurologic causes?
Psychogenic cause
## Footnote
This typically indicates a psychological origin rather than a physical one.
241
What is the most likely diagnosis for memory loss due to a psychogenic cause?
Dissociative amnesia
## Footnote
This condition is often linked to trauma or stress.
242
What characterizes dissociative amnesia?
Inability to recall autobiographical information, usually of a traumatic or stressful nature
## Footnote
This type of memory loss is specifically about personal experiences.
243
Does dissociative amnesia involve retrograde amnesia?
No
## Footnote
Patients typically do not have trouble learning new information.
244
What type of memory loss is not involved in dissociative amnesia?
Retrograde amnesia
## Footnote
Patients retain the ability to learn new information.
245
What must be ruled out for a diagnosis of dissociative amnesia?
Physiologic effects of a substance or another medical condition
## Footnote
Memory loss must not be attributable to other medical issues.
246
What is a common underlying cause of orthostatic syncope?
Autonomic dysfunction
## Footnote
Autonomic dysfunction impairs the body's ability to regulate blood pressure when changing positions.
247
What happens to venous return to the heart when a patient with orthostatic syncope stands?
It causes a drop in venous return
## Footnote
This drop leads to decreased preload and decreased cardiac output.
248
What normally occurs in the autonomic response to standing?
Sympathetic tone increases and parasympathetic tone decreases
## Footnote
This response leads to vasoconstriction, increased venous return, and increased heart rate.
249
What can happen if the normal autonomic response to standing is compromised?
Orthostatic hypotension occurs
## Footnote
Compromise can occur due to medications or conditions like neuropathy.
250
Which age-related factor is a risk for baroreceptor dysfunction?
Advanced age
## Footnote
Older individuals may have impaired baroreceptor sensitivity.
251
How does calcium channel blocker use affect orthostatic hypotension?
It blunts peripheral vasoconstriction
## Footnote
This can contribute to decreased blood pressure regulation.
252
What effect do tricyclic antidepressants have related to orthostatic syncope?
They cause autonomic dysfunction
## Footnote
This dysfunction can exacerbate symptoms of orthostatic hypotension.
253
What is the next best step for a patient with clear orthostatic changes and a normal workup?
Adjustment in medications
## Footnote
This includes modifying tricyclic antidepressants and/or calcium channel blockers.
254
True or False: No further diagnostic testing is required for patients with clear orthostatic changes and a highly suggestive history.
True
## Footnote
A thorough workup may often suffice in such cases.
255
What symptoms raise suspicion for stimulant intoxication?
Acute onset of personality and mood changes, formication, tachycardia, and hypertension
## Footnote
These symptoms are indicative of stimulant intoxication from substances like cocaine or amphetamines.
256
List additional signs and symptoms of stimulant use.
* Mydriasis
* Psychomotor agitation
* Nausea
* Diaphoresis
* Loss of appetite
* Weight loss
* Neuropsychiatric symptoms (e.g., hallucinations, delusions)
## Footnote
Neuropsychiatric symptoms can include both visual and auditory hallucinations.
257
True or False: A urine drug screen is always helpful in the acute management of suspected stimulant intoxication.
False
## Footnote
Urine drug screens can yield false positives due to cross-reactivity and prolonged excretion of inactive metabolites.
258
What is the initial management focus for stimulant intoxication?
Stabilizing the patient by controlling agitation and the hyperadrenergic state with benzodiazepines and lowering body temperature
## Footnote
This approach is critical for managing the acute effects of stimulant intoxication.
259
What is the purpose of diagnostic testing in stimulant intoxication?
To assess for alternative diagnoses and/or complications
## Footnote
Examples include ECG to rule out conduction abnormalities and myocardial ischemia.
260
What should be suspected in patients with features of stimulant intoxication but negative urine toxicology?
Bath salt intoxication
## Footnote
Bath salts can produce similar symptoms to stimulants but may not be detected on standard urine drug screens.
261
What is high-altitude pulmonary edema (HAPE)?
A noncardiogenic pulmonary edema occurring shortly after rapid ascent, typically to > 4500 m (∼ 14,500 feet)
## Footnote
HAPE is the most common cause of death in individuals ascending rapidly to high altitude.
262
What triggers the pathophysiology of HAPE?
Decrease in the partial pressure of arterial oxygen causing hypoxic pulmonary vasoconstriction
## Footnote
This leads to increased pulmonary arterial and capillary pressures, resulting in pulmonary hypertension.
263
What are common clinical features of HAPE?
Onset typically 2–4 days after arrival, cough, shortness of breath, weakness, chest tightness, crackles or wheezing, cyanosis, tachypnea, and tachycardia
## Footnote
Cough may initially be dry but can become productive with pink, frothy sputum.
264
What diagnostic methods are used for HAPE?
Lung ultrasound, chest x-ray, ECG, echocardiography
## Footnote
Lung ultrasound shows pulmonary edema and B lines; chest x-ray shows patchy infiltrates.
265
What does a chest x-ray show in HAPE?
Patchy infiltrates
## Footnote
This is one of the diagnostic criteria for HAPE.
266
What are the differential diagnoses for HAPE?
Exacerbation of asthma or COPD, pneumonia, acute heart failure, pulmonary embolism
## Footnote
A normal leukocyte count and rapid improvement with oxygen therapy suggest HAPE over pneumonia.
267
What is the immediate treatment for HAPE?
Descend immediately and provide oxygen therapy
## Footnote
Oxygen therapy should aim for a target SpO2 of > 90%; CPAP may be used if in a hospital setting.
268
What pharmacotherapy options are available for HAPE?
Nifedipine (off-label) or phosphodiesterase inhibitors like sildenafil or tadalafil
## Footnote
These medications are used if immediate descent and oxygen therapy are not feasible.
269
Fill in the blank: Prophylactic medication for altitude illness includes _______.
acetazolamide or dexamethasone
## Footnote
These medications are recommended if risk factors for altitude illness are present.
270
What is the preferred pharmacotherapy for HAPE prevention?
Nifedipine or phosphodiesterase inhibitors
## Footnote
Nifedipine is preferred, especially for individuals with a history of HAPE.
271
What is a common symptom of HAPE related to breathing?
Shortness of breath
## Footnote
This is a significant clinical feature that may develop alongside other symptoms.
272
True or False: HAPE occurs immediately upon ascent to high altitude.
False
## Footnote
HAPE typically has an onset of 2–4 days after arrival at high altitude.
273
What is priapism?
A sustained erection that lasts for more than four hours and is not the result of sexual excitation.
## Footnote
Priapism can lead to serious complications if not treated promptly.
274
How is priapism classified based on etiopathogenesis?
Priapism is classified as either low-flow or high-flow.
## Footnote
This classification helps determine the underlying cause and appropriate treatment.
275
What causes low-flow priapism?
Inadequate venous outflow from the corpus cavernosum, resulting in painful penile ischemia.
## Footnote
Low-flow priapism is an acute urological emergency.
276
What is the most common cause of low-flow priapism in adults?
Adverse effects from treating erectile dysfunction (e.g., sildenafil).
## Footnote
This highlights the importance of monitoring patients on these medications.
277
What is the most common cause of low-flow priapism in children?
Sickle cell disease.
## Footnote
Sickle cell disease can lead to various complications, including priapism.
278
What characterizes high-flow priapism?
It is usually the result of perineal trauma and is not associated with penile ischemia, therefore it is painless.
## Footnote
High-flow priapism is less common than low-flow.
279
How can high-flow priapism be distinguished from low-flow priapism?
Through penile blood gas analysis and Doppler ultrasound of the penis.
## Footnote
These diagnostic tools help determine the appropriate treatment.
280
What is the treatment for low-flow priapism?
Aspiration of blood from the corpus cavernosum and injection of phenylephrine.
## Footnote
Treatment must occur within 12 hours to restore erectile function.
281
What happens if low-flow priapism is not treated within 12 hours?
Leads to cavernous fibrosis and irreparable damage with erectile dysfunction.
## Footnote
Timely intervention is crucial to prevent long-term complications.
282
What is indicated if priapism does not subside after initial treatment?
Surgical therapy to decompress the penis.
## Footnote
This may be necessary in severe cases of low-flow priapism.
283
True or False: Non-ischemic priapism usually requires treatment.
False.
## Footnote
Non-ischemic priapism typically does not require intervention.
284
Fill in the blank: Low-flow priapism is an acute urological emergency that must be treated within _______.
12 hours.
## Footnote
Prompt treatment is essential to prevent complications.
285
What is the outcome if low-flow priapism is treated within 12 hours?
Complete restoration of erectile function is possible.
## Footnote
Early intervention significantly improves prognosis.
286
What is hemolytic uremic syndrome (HUS)?
A thrombotic microangiopathy characterized by the formation of microthrombi that occlude arterioles and capillaries.
287
What are the key components of HUS?
Microangiopathic hemolytic anemia, thrombocytopenia, acute kidney injury (AKI).
288
Which population is predominantly affected by HUS?
Children.
289
What is the most common cause of HUS?
Bacterial toxins, primarily the Shiga-like toxin of enterohemorrhagic E. coli O157:H7.
290
What should be done if there is a suspicion of HUS?
Begin treatment immediately.
291
What are the common clinical features preceding HUS?
Diarrheal illness (usually bloody) for the past 5–10 days.
292
What is the triad of clinical findings in HUS?
* Thrombocytopenia
* Microangiopathic hemolytic anemia
* Impaired renal function
293
What are the symptoms of thrombocytopenia in HUS?
* Petechiae
* Purpura
* Mucosal bleeding
* Prolonged bleeding after minor cuts
294
What are the symptoms of microangiopathic hemolytic anemia in HUS?
* Fatigue
* Dyspnea
* Pallor
* Jaundice
295
What renal symptoms are associated with HUS?
* Hematuria
* Proteinuria
* Oliguria
* Anuria
296
What laboratory findings indicate hemolytic anemia?
* ↓ Hemoglobin
* ↓ Haptoglobin
* ↑ Indirect bilirubin
* ↑ Reticulocytes
* ↑ LDH
* ↑ Schistocytes on blood smear
297
What coagulation profile findings are typical in HUS?
* ↓ Platelets
* Normal/slightly elevated prothrombin time (PT)
* Normal/slightly elevated activated partial thromboplastin time (aPTT)
* Normal/slightly elevated fibrin degradation products and D-dimer levels
* ↑ WBC count
* Negative Coombs test
298
What serum chemistry findings are associated with impaired renal function in HUS?
* ↑ BUN
* ↑ Creatinine
299
What are the treatment options for HUS?
* Supportive care
* Dialysis (up to 50% may require it)
* Plasma exchange therapy (only in refractory cases)
* Eculizumab (effective for aHUS)
300
What is the prognosis of HUS based on treatment timing?
Timely treatment can prevent acute complications and progression to chronic renal failure.
301
What is the mortality rate of HUS with treatment?
< 10%.
302
What percentage of children with HUS may experience long-term renal sequelae?
35–55%.
303
Diagnóstico diferencial de síndrome hemolítico urémico
- púrpura trombótica trombocitopénica
- coagulación intravascular diseminada
- púrpura, inmune trombocitopénica
- síndrome de Bernard-Soulier (problema de adhesión de plaquetas)
- trombastenia de Glanzmann (problema de agregación de plaquetas)
- … y otros
304
What is the primary infectious cause of vision loss in an immunosuppressed patient with vitreous inflammation and necrotizing retinitis adjacent to a retinal scar?
Toxoplasma gondii
## Footnote
This is a key learning point regarding ocular toxoplasmosis.
305
How may ocular toxoplasmosis be acquired?
Congenitally or via ingestion of raw or undercooked meats or oocysts from cats
## Footnote
Ocular toxoplasmosis can be transmitted in utero or through dietary sources.
306
What are the typical results of primary infection of Toxoplasma gondii in children and adults?
Retinochoroidal scars and may be subclinical
## Footnote
Many infections do not present noticeable symptoms.
307
What occurs at the edge of the scar during reactivation of ocular toxoplasmosis?
Reactivation of the disease
## Footnote
This can happen particularly in immunosuppressed individuals.
308
What can elicit reactivation of ocular toxoplasmosis?
Immunosuppression, such as corticosteroid or immunomodulator treatment
## Footnote
Patients on these treatments are at higher risk for reactivation.
309
What is the classic sign of ocular toxoplasmosis?
A nidus of fluffy white necrotizing retinitis near a pigmented chorioretinal scar
## Footnote
This characteristic appearance is crucial for diagnosis.
310
Is vitreous inflammation common in ocular toxoplasmosis?
Yes
## Footnote
Vitreous inflammation is a frequent finding in this condition.
311
What is Fournier gangrene?
A necrotizing fasciitis involving the perineal area, including the scrotum, penis, and anterior abdominal wall
## Footnote
Fournier gangrene is a serious and potentially life-threatening infection.
312
Which patients are at particularly high risk for Fournier gangrene?
Patients with diabetes mellitus
## Footnote
Diabetes mellitus increases susceptibility to infections, including Fournier gangrene.
313
What are the initial symptoms of Fournier gangrene?
Pain, erythema, and swelling
## Footnote
These symptoms may rapidly progress in severity.
314
As Fournier gangrene evolves, what additional symptoms may develop?
Purulent drainage, bullous lesions, tissue necrosis, and subcutaneous crepitus
## Footnote
These symptoms indicate a progression of the infection.
315
What is the most appropriate management for a man with type 2 diabetes and Fournier gangrene?
Surgical debridement
## Footnote
In addition to antibiotic therapy, surgical intervention is critical in managing this aggressive infection.
316
What type of antibiotic therapy is recommended for Fournier gangrene?
Broad-spectrum antibiotic therapy covering gram-positive, gram-negative, and anaerobic organisms
## Footnote
Effective antibiotic coverage is crucial for treating the polymicrobial nature of the infection.
317
True or False: Fournier gangrene can involve the anterior abdominal wall.
True
## Footnote
The infection can extend beyond the perineum to include surrounding areas.
318
Fill in the blank: Fournier gangrene is a type of _______.
necrotizing fasciitis
## Footnote
It is characterized by rapid tissue destruction.
319
What types of wounds can result from a human bite?
Scratches, punctures, lacerations, and avulsions
## Footnote
Human bites can lead to various types of injuries depending on the severity and location of the bite.
320
What is the microbiology of human bite wounds typically characterized by?
Polymicrobial flora reflecting human mouth flora, skin flora, and the environment
## Footnote
The complexity of the microbiome in human bite wounds can complicate treatment.
321
Which pathogens are most commonly isolated from human bite wounds?
* Streptococcus species
* Staphylococcus species
* Eikenella corrodens
* Anaerobes
## Footnote
These pathogens contribute to the risk of infection following a human bite.
322
What factors determine the risk for infection after a human bite?
* Patient’s immunocompetence
* Location of the bite
* Local wound care
## Footnote
Understanding these factors is crucial for assessing and managing bite wounds.
323
Which patients are at the highest risk for infection following a human bite?
Patients with diabetes mellitus, sickle cell anemia, asplenia, and other immunocompromised states
## Footnote
These conditions impair the immune response, increasing infection risk.
324
What types of wounds are particularly high risk for infection?
Wounds over a tendon, joint, or bone
## Footnote
The anatomical location significantly influences infection potential.
325
What is a 'fight bite'?
Human bite wounds on a clenched fist over the knuckles
## Footnote
These injuries can lead to serious complications like septic arthritis or osteomyelitis.
326
How quickly can bite wounds lead to infection?
As quickly as 8 to 12 hours after the bite
## Footnote
Prompt medical evaluation is crucial for timely intervention.
327
What is the recommended antibiotic of choice for treating bite-wound infections?
Amoxicillin-clavulanate
## Footnote
This combination effectively targets the pathogens associated with bite wounds.
328
Why is amoxicillin alone not sufficient for treating bite wounds?
It does not cover beta-lactamase-producing organisms
## Footnote
The addition of clavulanate helps overcome this limitation.
329
What is the alternative antibiotic regimen for penicillin-allergic patients?
Clindamycin combined with trimethoprim-sulfamethoxazole
## Footnote
This combination provides effective coverage for bite-wound infections in allergic individuals.
330
What should be done for patients with bite wounds whose immunization status is unknown?
Administer a tetanus booster
## Footnote
Keeping tetanus immunization up to date is essential in wound management.
331
What are some essential steps in managing an infected bite wound?
* Obtaining cultures
* Irrigating with sterile normal saline
* Exploring the wound
* Debriding devitalized tissue
* Draining fluid collections
* Assessing for bloodborne pathogen transmission
## Footnote
Comprehensive management helps prevent complications and promotes healing.
332
True or False: Antibiotics are typically recommended if a patient is seen more than 24 hours after a bite with no signs of infection.
False
## Footnote
If no signs of infection are present after 24 hours, antibiotics are generally not recommended.
333
What is the most likely diagnosis for a patient with mild chronic bilateral conjunctivitis and pain with urination?
Chlamydial conjunctivitis
## Footnote
This condition can occur due to autoinoculation from a chlamydial infection.
334
What is a common cause of chronic indolent conjunctivitis?
Chlamydia trachomatis
## Footnote
This bacterium is associated with various ocular and genital symptoms.
335
List some symptoms associated with Chlamydia trachomatis infections.
* Injection
* Mucus discharge
* Preauricular lymph-node enlargement
* Follicles on the inferior tarsal conjunctiva
* History of urethritis, cervicitis, or vaginitis
## Footnote
These symptoms can help in diagnosing the infection.
336
What are the diagnostic methods for Chlamydia trachomatis infections?
* Conjunctival culture
* DNA probe
* Microscopic examination
## Footnote
These methods help confirm the presence of the infection.
337
What is the preferred treatment for Chlamydia trachomatis infections?
* Azithromycin
* Doxycycline
## Footnote
Oral antibiotics are the primary treatment options.
338
What are some adjunctive therapies for Chlamydia trachomatis infections?
* Erythromycin
* Tetracycline
## Footnote
These topical antibiotic ointments can support treatment.
339
How do the serotypes of Chlamydia trachomatis differ in terms of disease?
The serotypes causing urethritis and chronic conjunctivitis are different from those causing endemic trachoma
## Footnote
This distinction is important for diagnosis and treatment.
340
Where is endemic trachoma typically seen?
Resource-limited settings
## Footnote
It is rare outside the developing world.
341
What condition should be considered in a patient with conjunctivitis, urethritis, and arthritis?
Reactive arthritis
## Footnote
This diagnosis is relevant in the context of the symptoms presented.
342
What symptoms were absent in the patient that would indicate concomitant uveitis?
* Arthritis
* Photophobia
## Footnote
Their absence suggests that uveitis is not present.
343
What is a key learning point regarding young women with specific symptoms?
A young woman with mild chronic conjunctivitis and pain with urination most likely has a diagnosis of chlamydial conjunctivitis.
344
What is the initial treatment for an episode of anterior uveitis?
A glucocorticoid eyedrop (such as prednisolone) and a mydriatic/cycloplegic eyedrop
## Footnote
Anterior uveitis is an inflammatory condition affecting the middle layer of the eye, and the treatment aims to reduce inflammation and alleviate pain.
345
What are the characteristic symptoms of acute epiglottitis?
Shortness of breath, fever, stridor, odynophagia, inability to swallow secretions
## Footnote
These symptoms are critical for diagnosis and management of acute epiglottitis.
346
What is the classical radiographic finding in acute epiglottitis?
The thumbprint sign
## Footnote
This sign indicates enlargement of the epiglottis with airway narrowing.
347
What is the initial management for adults with acute epiglottitis?
Airway management and intravenous antibiotics
## Footnote
Antibiotics should be started empirically.
348
Name two antibiotics that are commonly used empirically for acute epiglottitis.
Intravenous ampicillin-sulbactam and third-generation cephalosporin
## Footnote
These antibiotics cover common bacterial causes of epiglottitis.
349
If methicillin-resistant Staphylococcus aureus cannot be excluded, which antibiotic should be included?
Vancomycin
## Footnote
This is to ensure coverage against MRSA.
350
What percentage of throat-swab cultures in cases of epiglottitis yield significant microbial growth?
10% to 33%
## Footnote
This indicates that the microbial cause is often not identified.
351
What percentage of acute epiglottitis cases are attributable to Haemophilus influenzae type b?
17%
## Footnote
This suggests that other organisms may be responsible for the majority of cases.
352
Fill in the blank: The most appropriate empiric antibiotic for the treatment of acute epiglottitis is either _______ or an intravenous third-generation cephalosporin.
intravenous ampicillin-sulbactam
## Footnote
This is a key learning point for treatment.
353
What should be considered when children present with unexplained injuries?
Nonaccidental trauma (NAT)
## Footnote
NAT is suspected when injuries are not consistent with the child's level of development or there is a delay in seeking care.
354
What are common symptoms of abusive head trauma in infants?
Symptoms may include:
* poor feeding
* vomiting
* lethargy
* fussiness
* hypotonia
* seizures
## Footnote
Symptoms can be nonspecific.
355
What finding on a nonmobile infant is a sentinel injury for abuse?
Left-ear bruise
## Footnote
This injury should not be overlooked as it may indicate abuse.
356
What can result from a lack of recognition of nonaccidental trauma?
Severe morbidity or possibly death
## Footnote
Early recognition and intervention are crucial.
357
What is a critical next step after suspecting nonaccidental trauma?
Referral to child protective services (CPS)
## Footnote
Reporting suspicion is crucial for child safety.
358
What radiologic evaluations are included for assessing nonaccidental trauma?
Components include:
* CT of the brain (acutely) or MRI (if asymptomatic)
* Skeletal survey
* CT of the abdomen and pelvis (if intra-abdominal damage is suspected)
## Footnote
These evaluations help identify injuries.
359
What is the best method to identify fractures in infants and children under 2 years of age concerning for physical abuse?
Skeletal survey
## Footnote
A complete skeletal survey includes approximately 20 images of the entire body.
360
What should nonradiologic evaluation of nonaccidental trauma include?
Nonradiologic evaluation should include:
* Full physical examination
* Fundoscopic examination
* Basic laboratory testing
* Coagulation studies (if bleeding)
* Hepatic and pancreatic enzyme levels
## Footnote
These help assess for potential injuries.
361
What is the first priority when managing a patient with suspected nonaccidental trauma?
Stabilizing the patient
## Footnote
This is crucial, especially if the patient has a depressed mental status.
362
What may suggest impending brainstem herniation in a patient?
Hypertension, bradycardia, and erratic breathing
## Footnote
These signs require immediate attention.
363
What interventions may reduce the likelihood of brainstem herniation?
Interventions include:
* Consulting the neurosurgery team
* Administering hypertonic saline or mannitol
* Elevating the head of the bed
## Footnote
These measures help manage intracranial pressure.
364
What findings are highly concerning for abusive head trauma?
Presence of a skull fracture and subdural hematoma
## Footnote
These findings necessitate further investigation and reporting.
365
What is the most appropriate next step after stabilizing an infant with an unexplained skull fracture and subdural hematoma?
Notification of child protective services
## Footnote
This step is crucial after acute stabilization and neurosurgery consultation.
366
What is the definition of a suspected case of pertussis?
Cough present for any duration (with a low threshold for suspicion in infants), with ≥ 1 of the following:
* Paroxysmal coughing
* Whooping on inspiration
* Posttussive vomiting
* Apnea
* Known contact with confirmed case
* Living in an area with a pertussis outbreak
## Footnote
The presence of fever suggests an alternative diagnosis.
367
What are the confirmatory studies for pertussis?
PCR and/or cultures for patients who present ≤ 4 weeks since cough onset; Serology for patients who present > 4 weeks after developing symptoms.
## Footnote
These studies help confirm the diagnosis of pertussis based on the duration of symptoms.
368
True or False: A cough of any duration is sufficient to suspect pertussis.
True
## Footnote
There is a low threshold for suspicion in infants.
369
Fill in the blank: The presence of _______ suggests an alternative diagnosis in suspected pertussis cases.
fever
## Footnote
Fever is an important clinical sign that may indicate a different illness.
370
What is electrical alternans?
An ECG finding highly specific to large pericardial effusions
## Footnote
Characterized by cyclical changes in the axis or amplitude of consecutive QRS complexes
371
What causes electrical alternans?
The swinging motion of the beating heart surrounded by pericardial fluid
## Footnote
This motion leads to variations in the ECG readings
372
What are common ECG findings in patients with large pericardial effusion and cardiac tamponade?
Sinus tachycardia and low voltage recording
## Footnote
These findings are typical in such patients
373
What is the management approach for stable patients with pericardial effusion?
Transthoracic echocardiography should be used to confirm the diagnosis
## Footnote
This is essential for assessing the condition further
374
What should be done for unstable patients with suspected cardiac tamponade?
Pericardiocentesis should not be delayed for diagnostic confirmation
## Footnote
Immediate intervention is critical in these cases
375
True or False: Electrical alternans can occur in stable patients without pericardial effusion.
False
## Footnote
Electrical alternans is specifically associated with large pericardial effusions
376
Fill in the blank: In patients with large pericardial effusion, the ECG typically shows _______.
sinus tachycardia and low voltage recording
## Footnote
These are common findings in such patients
377
What is Cryptococcus neoformans?
An opportunistic infection that causes meningoencephalitis in immunosuppressed patients
## Footnote
It commonly affects individuals with weakened immune systems, such as those with HIV.
378
What are common risk factors for Cryptococcus neoformans infection?
* HIV infection
* Glucocorticoid use
* Solid organ transplantation
* Advanced malignancies
* Type 2 diabetes
* Sarcoidosis
* 20% of patients have no identified risk factor
## Footnote
These factors increase susceptibility to the infection.
379
How does the presentation of Cryptococcus neoformans vary?
Symptoms can develop slowly over several weeks, and fever is seen in only 50% of cases
## Footnote
Other symptoms may include headaches, lethargy, cranial-nerve palsies, personality changes, and memory loss.
380
What imaging findings may be seen in cases of Cryptococcus neoformans?
* Normal CT or MRI in 50% of cases
* Atrophy
* Hydrocephalus
* Gyral enhancement
* Nodules (cryptococcomas)
## Footnote
These findings can vary significantly among patients.
381
What diagnostic evaluations are recommended for Cryptococcus neoformans?
* Lumbar puncture
* Measurement of opening pressure of cerebrospinal fluid (CSF)
* Evaluation of CSF with cryptococcal antigen testing
* Fungal cultures
## Footnote
These tests help confirm the diagnosis and assess the condition of the patient.
382
Why are strategies to reduce intracranial pressure important in Cryptococcus neoformans infection?
Many complications of cryptococcal meningitis are due to markedly raised intracranial pressure
## Footnote
Effective management may include large-volume lumbar punctures and neurosurgical shunting.
383
True or False: Fever is a common symptom in all cases of Cryptococcus neoformans infection.
False
## Footnote
Fever is seen in only 50% of cases.
384
Fill in the blank: A common infectious cause of subacute and chronic meningoencephalitis associated with raised intracranial pressure in immunocompromised patients is _______.
Cryptococcus neoformans
## Footnote
This highlights the significance of this pathogen in clinical practice.
385
What is characteristic of a transient aplastic crisis from parvovirus B19 infection in patients with immune deficiency states?
Absence of reticulocytes in the blood and presence of giant pronormoblasts in the bone marrow
## Footnote
This is particularly observed in advanced HIV infections.
386
Why do immunodeficient patients develop persistent severe anemia due to pure red-cell aplasia?
They are unable to form neutralizing antibodies against the virus and parvovirus B19 has a predilection for erythroid progenitor cells
## Footnote
This leads to a lack of red blood cell production.
387
What are the treatment options for pure red-cell aplasia due to parvovirus B19 infection in people with HIV?
Transfusion of blood products, antiretroviral therapy, intravenous immunoglobulin
## Footnote
These treatments help manage the anemia and underlying viral infection.
388
What is the most common clinical presentation of parvovirus B19 infection?
Fifth disease (erythema infectiosum) characterized by the classic 'slapped cheek' rash
## Footnote
This condition is typically seen in children.
389
True or False: Most people are seropositive for parvovirus B19 by late adulthood.
True
## Footnote
This indicates widespread exposure to the virus.
390
Fill in the blank: The most likely infectious cause of pure red-cell aplasia in a patient with advanced HIV infection is _______.
parvovirus B19
391
What is a massive proximal deep-vein thrombosis (DVT) also known as?
Phlegmasia cerulea dolens
## Footnote
This term refers to the severe form of DVT characterized by significant clinical symptoms.
392
What are the symptoms of a massive proximal DVT?
Sudden severe pain, swelling, cyanosis, and arterial compromise.
## Footnote
These symptoms indicate a critical condition that needs immediate attention.
393
What complications can arise from a massive proximal DVT?
Increased venous stasis, extravasation of intravascular fluid, painful swelling, violaceous skin changes, compartment syndrome, soft tissue destruction, infection, and gangrene.
## Footnote
These complications highlight the severe impact of untreated DVT.
394
What should be considered due to the high morbidity and mortality associated with massive proximal DVT?
Catheter-directed thrombolysis or mechanical or surgical thrombectomy.
## Footnote
These interventions are critical for managing severe DVT cases effectively.
395
What key learning point should be noted regarding patients with risk factors for thromboembolic disease?
Sudden onset of leg pain with swelling, purple color, and arterial ischemia with loss of distal pulses raises concern for massive proximal DVT.
## Footnote
Recognizing these signs early can lead to timely intervention.
396
Fill in the blank: A massive proximal DVT can lead to _______ by causing a compartment syndrome.
Arterial ischemia
## Footnote
Compartment syndrome is a serious condition that can occur due to increased pressure within a closed muscle compartment.
397
What is the mortality rate of acute type A aortic dissection after symptom onset?
1% per hour
## Footnote
This highlights the urgency of treatment for this condition.
398
What percentage of patients with type A dissection are initially thought to have another cause of chest pain?
30%
## Footnote
This can delay proper diagnosis and treatment.
399
What physical findings can increase the likelihood of aortic dissection?
Pulse deficits or blood pressure discrepancies between the arms
## Footnote
However, fewer than 20% of patients with type A dissection exhibit these findings.
400
What symptoms are commonly experienced by nearly half of patients with type A aortic dissection?
Pain radiating to the back or a diastolic murmur
## Footnote
The murmur is due to aortic valvular regurgitation.
401
Which imaging modalities can be used to diagnose ascending aortic dissection?
* Contrast-enhanced CT
* Transesophageal echocardiography (TEE)
* MRI
* Invasive aortography
## Footnote
All these modalities are highly accurate.
402
What is the preferred imaging modality for diagnosing acute ascending aortic dissection according to current guidelines?
Contrast-enhanced CT
## Footnote
It is widely available and quick to perform, making it a class I indication.
403
What is a relative contraindication for the use of iodinated contrast in imaging?
Chronic kidney disease
## Footnote
This is due to the risk of contrast nephropathy.
404
What should be considered more important than the potential risk of nephropathy when diagnosing ascending aortic dissection?
The need for urgent diagnosis
## Footnote
This outweighs the potential risk of nephropathy in acute cases.
405
What is the most appropriate procedure for diagnosing acute ascending aortic dissection in hemodynamically unstable patients?
CT angiography
## Footnote
This is highlighted as a key learning point.
406
What is hypokalemia?
A common adverse effect of continuous albuterol therapy
407
What causes hypokalemia in continuous albuterol therapy?
β2-agonist stimulation of the Na+/K+-ATPase, leading to an intracellular K+ shift
408
How does β2-mediated stimulation of the liver affect glucose levels?
It elevates cAMP levels, increasing glycogenolysis and hyperglycemia
409
What role does hyperglycemia play in hypokalemia?
It stimulates insulin secretion, which activates the Na+/K+-ATPase and potentiates the intracellular K+ shift
410
What EKG changes can hypokalemia cause?
T wave flattening, ST depression, and U waves
411
What are other adverse effects of continuous albuterol therapy?
Hypomagnesemia, hypophosphatemia, and increases in heart rate
412
True or False: Continuous albuterol therapy can lead to hypomagnesemia.
True
413
Fill in the blank: Hypokalemia is caused by _______ stimulation of the Na+/K+-ATPase.
β2-agonist
414
What are absolute and relative contraindications to liver transplantation?
Contraindications include:
* Brain death
* Uncontrolled infection or sepsis
* Severe cardiopulmonary disease
* AIDS
* Inadequate social support or inability to adhere to medications
* Certain anatomical abnormalities
* Grade 3 obesity (BMI ≥40)
* Active extrahepatic malignancy
* Hepatocellular carcinoma with metastatic spread
## Footnote
Contraindications may vary according to the policies of individual transplant centers.
415
What is a typical minimum period of abstinence from alcohol and illicit substances before liver transplantation?
6-month minimum period
## Footnote
This period allows time to address substance use disorders and potential recovery from acute alcoholic hepatitis.
416
True or False: Most transplant centers have maintained strict policies regarding abstinence from substances before liver transplantation.
False
## Footnote
Policies have become more flexible over time due to improved survival rates in patients with acute alcoholic hepatitis.
417
What kind of patients have shown dramatically improved survival rates after liver transplantation?
Patients with acute alcoholic hepatitis (AAH)
## Footnote
The benefit is primarily observed in the first month after transplantation.
418
What is the significance of early transplantation in select patients with acute alcoholic hepatitis?
It confirms the utility of early transplantation for patients who do not respond to glucocorticoids
## Footnote
Most benefits were achieved in the first month post-transplant.
419
Fill in the blank: Medical contraindications to liver transplantation include _______.
sepsis or uncontrolled infection, severe cardiopulmonary disease, grade 3 obesity, and active extrahepatic malignancies.
420
What is acute interstitial nephritis (AIN)?
AIN is a kidney disorder characterized by inflammation of the renal interstitium.
421
What percentage of AIN cases are caused by medications?
More than 75%.
422
Name three common causes of drug-induced AIN.
* Antibiotics
* Nonsteroidal antiinflammatory drugs
* Proton pump inhibitors
423
What are the classic symptoms of acute interstitial nephritis?
* Fever
* Rash
* Arthralgias
* Peripheral eosinophilia
* Kidney failure
424
Is it common for all components of the classic triad of AIN to be present?
No, it is uncommon.
425
In a patient with a fever, rash, and acute kidney injury after starting a new medication, what is the most likely diagnosis?
Drug-induced acute interstitial nephritis.
426
What is Guillain-Barré syndrome (GBS)?
An acute immune-mediated polyneuropathy that typically manifests with bilateral ascending flaccid paralysis and sensory involvement
## Footnote
Examples of sensory involvement include paresthesia.
427
What is the pathogenesis of GBS?
Involves autoantibodies against antigens in the myelin sheath, other Schwann-cell antigens, and axon membranes.
428
What percentage of GBS patients have a preceding infection?
Approximately 65%
## Footnote
Infections are typically upper respiratory tract or gastrointestinal.
429
What is the primary method for diagnosing GBS?
Clinical diagnosis; alternative diagnoses should be considered especially in atypical presentations.
430
What findings in cerebrospinal fluid (CSF) analysis support the diagnosis of GBS?
Albuminocytologic dissociation.
431
What are common findings in electrodiagnostic studies for GBS?
Specific findings vary; they help support the diagnosis.
432
What factors influence the medical treatment options for GBS?
The severity of symptoms.
433
What are the available treatment options for GBS?
* Intravenous immunoglobulin (IVIg)
* Plasmapheresis
434
What complications are associated with GBS that can increase mortality?
* Respiratory failure
* Pulmonary embolism
* Cardiac arrest
435
What percentage of GBS patients remain severely disabled after treatment?
Up to 20%.
436
What is the mortality rate for patients with GBS despite medical treatment?
Approximately 5%.
