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.

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2
Q

What are C-peptide and proinsulin?

A

Byproducts of the endogenous production of insulin

They are important for assessing insulin production.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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13
Q

What is the commonality of seizures in children with febrile illnesses?

A

Common and often benign

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14
Q

What severe disease indicators are present in the child described?

A

Focal neurologic deficits, encephalopathy, seizures despite benzodiazepines

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15
Q

What does an analysis of the cerebrospinal fluid (CSF) reveal in this case?

A

Elevated leukocyte count and elevated protein level

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16
Q

What combination of symptoms is suggestive of encephalitis?

A

Aseptic CSF profile, encephalopathy, status epilepticus

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17
Q

What are potential causes of encephalitis in children?

A

Infections, inflammatory disorders, autoantibodies

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18
Q

What suggests an underlying infection in the child?

A

Acute onset of symptoms and fever on presentation

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19
Q

What are the most common infectious causes of encephalitis in children?

A

Herpes simplex virus (HSV) and enterovirus

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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

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21
Q

Why is testing for HSV critical in children with meningoencephalitis?

A

Prompt initiation of acyclovir improves outcomes

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22
Q

Fill in the blank: The CSF profile in encephalitis typically shows _______.

A

Moderate pleocytosis, normal glucose level, moderately elevated protein

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23
Q

True or False: Encephalopathy can present as irritability in children.

A

True

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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

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25
Q

How many types of cryoglobulinemic vasculitis are there?

A

Three types

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26
Q

What is Type I cryoglobulinemic vasculitis associated with?

A

Self-aggregating monoclonal immunoglobulins, usually secondary to B-cell or plasma-cell malignancies such as multiple myeloma or Waldenström macroglobulinemia

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27
Q

What causes Type II cryoglobulinemic vasculitis?

A

A mixture of polyclonal immunoglobulins and monoclonal immunoglobulins with rheumatoid factor activity, often associated with hepatitis C virus (HCV) infection

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28
Q

What diseases are associated with Type II cryoglobulinemic vasculitis besides hepatitis C?

A

Connective tissue diseases or lymphoma

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29
Q

What characterizes Type III cryoglobulinemic vasculitis?

A

Rheumatoid factor activity carried by polyclonal immunoglobulins, often due to HCV and secondary to diseases like Sjögren syndrome, systemic lupus erythematosus, and rheumatoid arthritis

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30
Q

What symptoms did the patient present with?

A

Malaise, headache, progressively worsening constitutional symptoms, palpable purpura, hepatomegaly, and lower-extremity edema

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31
Q

What laboratory findings are consistent with acute glomerulonephritis in this patient?

A

Elevated blood pressure, raised serum creatinine level, proteinuria, and hematuria

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32
Q

What are the relevant factors leading to the diagnosis of cryoglobulinemic vasculitis in this case?

A

Positive rheumatoid factor, hypocomplementemia, HCV infection, and a negative antinuclear antibody

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33
Q

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 _______.

A

cryoglobulinemic vasculitis

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34
Q

True or False: Cryoglobulinemic vasculitis can be caused by a mixture of polyclonal and monoclonal immunoglobulins.

A

True

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35
Q

What is a retropharyngeal abscess?

A

Generally the most dangerous deep neck infection

It is especially concerning due to its potential complications.

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36
Q

Which age group is most commonly affected by retropharyngeal abscess?

A

Children < 5 years of age

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37
Q

What is the gender prevalence for retropharyngeal abscess?

A

♂ > ♀

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38
Q

What pathogens are commonly associated with retropharyngeal abscess?

A
  • Streptococci (viridans streptococci, S. pneumoniae)
  • Staphylococci (including MRSA)
  • Haemophilus influenzae
  • Oral anaerobes (peptostreptococci, Bacteroides species)
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39
Q

What are the common direct or indirect causes of retropharyngeal abscess?

A
  • Contiguous or lymphatic spread from oral or upper respiratory tract infections
  • Local penetrating pharyngeal trauma
  • Spread from other deep neck infections
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40
Q

What are the clinical features of retropharyngeal abscess?

A
  • Features of tonsillitis and trismus
  • Neck asymmetry with unilateral swelling of the posterior pharyngeal wall
  • Torticollis
  • Anterior cervical lymphadenopathy
  • Respiratory distress
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41
Q

What imaging study is preferred for diagnosing retropharyngeal abscess?

A

CT neck with IV contrast

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42
Q

What findings are indicative of retropharyngeal abscess on a CT scan?

A
  • Hypodense fluid collection with ring enhancement in the retropharyngeal space
  • Posterior pharynx wall with anterior displacement
  • Spread of infection to other spaces
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43
Q

What is the initial screening study in patients with airway compromise for retropharyngeal abscess?

A

Lateral x-ray neck

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44
Q

What are some findings on a lateral x-ray neck for retropharyngeal abscess?

A
  • Widened prevertebral space with gas or air-fluid levels
  • Lordosis
  • Evidence of foreign body, if present
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45
Q

What are the mainstays of therapy for retropharyngeal abscess?

A
  • Systemic IV antibiotics
  • Abscess drainage
  • Supportive care
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46
Q

What should be done for patients with respiratory distress due to retropharyngeal abscess?

A

Prompt airway management

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47
Q

What type of antibiotics should be started for retropharyngeal abscess?

A

Broad-spectrum empiric antibiotics (e.g., clindamycin or ampicillin/sulbactam)

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48
Q

What is a possible complication of retropharyngeal abscess involving the airway?

A

Airway obstruction

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49
Q

What can happen if the infection spreads to the carotid sheath?

A

Internal carotid artery erosion and jugular vein thrombophlebitis (Lemierre syndrome)

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50
Q

What is a serious complication that can arise from a retropharyngeal abscess?

A

Descending mediastinitis

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51
Q

What should be considered to reduce inflammation in retropharyngeal abscess treatment?

A

Corticosteroids (e.g., dexamethasone)

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52
Q

True or False: Patients with retropharyngeal abscess should always be managed as outpatients.

A

False

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53
Q

Fill in the blank: The presence of _______ can help direct therapy for the causative pathogen in retropharyngeal abscess.

A

Microbiological studies (e.g., bacterial culture of abscess aspirate)

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54
Q

What is a retropharyngeal abscess?

A

Generally the most dangerous deep neck infection

It is especially concerning due to its potential complications.

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55
Q

Which age group is most commonly affected by retropharyngeal abscess?

A

Children < 5 years of age

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56
Q

What is the gender prevalence for retropharyngeal abscess?

A

♂ > ♀

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57
Q

What pathogens are commonly associated with retropharyngeal abscess?

A
  • Streptococci (viridans streptococci, S. pneumoniae)
  • Staphylococci (including MRSA)
  • Haemophilus influenzae
  • Oral anaerobes (peptostreptococci, Bacteroides species)
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58
Q

What are the common direct or indirect causes of retropharyngeal abscess?

A
  • Contiguous or lymphatic spread from oral or upper respiratory tract infections
  • Local penetrating pharyngeal trauma
  • Spread from other deep neck infections
How well did you know this?
1
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2
3
4
5
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59
Q

What are the clinical features of retropharyngeal abscess?

A
  • Features of tonsillitis and trismus
  • Neck asymmetry with unilateral swelling of the posterior pharyngeal wall
  • Torticollis
  • Anterior cervical lymphadenopathy
  • Respiratory distress
How well did you know this?
1
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2
3
4
5
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60
Q

What imaging study is preferred for diagnosing retropharyngeal abscess?

A

CT neck with IV contrast

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61
Q

What findings are indicative of retropharyngeal abscess on a CT scan?

A
  • Hypodense fluid collection with ring enhancement in the retropharyngeal space
  • Posterior pharynx wall with anterior displacement
  • Spread of infection to other spaces
How well did you know this?
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62
Q

What is the initial screening study in patients with airway compromise for retropharyngeal abscess?

A

Lateral x-ray neck

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63
Q

What are some findings on a lateral x-ray neck for retropharyngeal abscess?

A
  • Widened prevertebral space with gas or air-fluid levels
  • Lordosis
  • Evidence of foreign body, if present
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1
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64
Q

What are the mainstays of therapy for retropharyngeal abscess?

A
  • Systemic IV antibiotics
  • Abscess drainage
  • Supportive care
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65
Q

What should be done for patients with respiratory distress due to retropharyngeal abscess?

A

Prompt airway management

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66
Q

What type of antibiotics should be started for retropharyngeal abscess?

A

Broad-spectrum empiric antibiotics (e.g., clindamycin or ampicillin/sulbactam)

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67
Q

What is a possible complication of retropharyngeal abscess involving the airway?

A

Airway obstruction

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68
Q

What can happen if the infection spreads to the carotid sheath?

A

Internal carotid artery erosion and jugular vein thrombophlebitis (Lemierre syndrome)

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69
Q

What is a serious complication that can arise from a retropharyngeal abscess?

A

Descending mediastinitis

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70
Q

What should be considered to reduce inflammation in retropharyngeal abscess treatment?

A

Corticosteroids (e.g., dexamethasone)

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71
Q

True or False: Patients with retropharyngeal abscess should always be managed as outpatients.

A

False

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72
Q

Fill in the blank: The presence of _______ can help direct therapy for the causative pathogen in retropharyngeal abscess.

A

Microbiological studies (e.g., bacterial culture of abscess aspirate)

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73
Q

What is carbon monoxide (CO)?

A

A colorless, odorless, tasteless gas

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74
Q

What are common causes of CO poisoning?

A

Smoke inhalation, poorly functioning heating systems, improperly ventilated fuel-burning devices, motor vehicles in poorly ventilated areas

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75
Q

When does CO poisoning tend to occur?

A

During the winter

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76
Q

What are some nonspecific symptoms of CO poisoning?

A
  • Headache
  • Dizziness
  • Fatigue
  • Confusion
  • Irritability
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77
Q

What severe symptoms can CO poisoning lead to?

A
  • Loss of consciousness
  • Death
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78
Q

How does CO poisoning affect oxygen delivery in the body?

A

Interferes with oxygen delivery by binding to hemoglobin

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79
Q

What is the affinity of CO for hemoglobin compared to oxygen?

A

250 times that of oxygen

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80
Q

What is the antidote for CO poisoning?

A

Oxygen

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81
Q

What is the effect of supplemental 100% normobaric oxygen on CO?

A
  • Reduces half-life of CO to one hour
  • Increases amount of dissolved oxygen in the blood
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82
Q

What should be the first step for any patient with suspected CO poisoning?

A

Administer 100% oxygen via a nonrebreather mask

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83
Q

What is a common cause of medication-associated priapism?

A

Trazodone

Trazodone is among the most common causes, occurring in fewer than 0.1% of men treated with the drug.

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84
Q

What percentage of men treated with Trazodone experience priapism?

A

Fewer than 0.1%

This statistic highlights the rarity of priapism associated with Trazodone.

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85
Q

Which types of medications have been reported to cause priapism?

A

Typical and atypical antipsychotic medications, certain antihypertensive, and anticoagulant medications

Priapism can occur after the use of various drug classes.

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86
Q

What should be done for men with an erection lasting more than 4 hours?

A

They should be treated in the emergency department

This is critical to prevent complications such as ischemia and gangrene.

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87
Q

True or False: Priapism is a common condition among men using Trazodone.

A

False

Priapism occurs in fewer than 0.1% of men treated with Trazodone.

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88
Q

Fill in the blank: Priapism has been reported following the use of _______ medications.

A

antipsychotic, antihypertensive, anticoagulant

These medication classes can lead to the occurrence of priapism.

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89
Q

What is priapism?

A

A sustained erection lasting more than four hours not due to sexual excitation

Priapism can lead to serious complications if not treated promptly.

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90
Q

How is priapism classified based on etiopathogenesis?

A

Low-flow and high-flow

This classification is based on the underlying mechanisms causing the condition.

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91
Q

What is low-flow priapism caused by?

A

Inadequate venous outflow from the corpus cavernosum

This results in painful penile ischemia.

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92
Q

What is the most common cause of low-flow priapism in adults?

A

Adverse effects from treating erectile dysfunction (e.g., sildenafil)

Low-flow priapism can also be associated with other medications.

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93
Q

What is the most common cause of low-flow priapism in children?

A

Sickle cell disease

Sickle cell disease leads to vaso-occlusive crises that can result in priapism.

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94
Q

What usually causes high-flow priapism?

A

Perineal trauma

High-flow priapism is less common than low-flow.

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95
Q

Is high-flow priapism associated with penile ischemia?

A

No, it is painless and not associated with ischemia

This differentiates it from low-flow priapism.

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96
Q

What diagnostic tools are used to distinguish between low-flow and high-flow priapism?

A

Penile blood gas analysis and Doppler ultrasound of the penis

These tests help assess blood flow and oxygenation in penile tissues.

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97
Q

Why is low-flow priapism considered an acute urological emergency?

A

It must be treated within 12 hours to prevent complications

Delayed treatment can lead to permanent erectile dysfunction.

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98
Q

What is the initial treatment for low-flow priapism?

A

Aspiration of blood from the corpus cavernosum and injection of phenylephrine

This helps restore normal blood flow and relieve pain.

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99
Q

What surgical intervention may be indicated if priapism does not subside?

A

Surgical therapy to decompress the penis

This is a last resort if other treatments fail.

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100
Q

What is the potential outcome if low-flow priapism is treated within 12 hours?

A

Complete restoration of erectile function is possible

Timely intervention is crucial for preserving erectile ability.

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101
Q

What happens if treatment for low-flow priapism is delayed?

A

Cavernous fibrosis and irreparable damage with erectile dysfunction

Delayed treatment can lead to long-term complications.

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102
Q

Does non-ischemic priapism usually require treatment?

A

No, it usually does not require treatment

Non-ischemic priapism is generally less problematic than ischemic forms.

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103
Q

What is Kawasaki disease (KD)?

A

An acute, necrotizing vasculitis of unknown etiology.

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104
Q

What age group is primarily affected by Kawasaki disease?

A

Children under the age of five.

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105
Q

Which ethnic group is more commonly affected by Kawasaki disease?

A

Those of Asian descent.

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106
Q

List the main symptoms of Kawasaki disease.

A
  • High fever
  • Desquamative rash
  • Conjunctivitis
  • Mucositis (e.g., strawberry tongue)
  • Cervical lymphadenopathy
  • Erythema and edema of the distal extremities
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107
Q

What is the most concerning manifestation of Kawasaki disease?

A

Coronary artery aneurysms.

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108
Q

What serious complications can arise from coronary artery aneurysms in Kawasaki disease?

A
  • Myocardial infarction
  • Arrhythmias
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109
Q

How is Kawasaki disease diagnosed?

A

It is a clinical diagnosis supported by findings such as elevated ESR or evidence of cardiac involvement on echocardiography.

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110
Q

What is the essential treatment for Kawasaki disease?

A

Intravenous immunoglobulins (IVIG) and aspirin.

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111
Q

When should treatment for Kawasaki disease be initiated?

A

As soon as possible after diagnosis.

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112
Q

True or False: Kawasaki disease can affect adults.

A

False.

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113
Q

Fill in the blank: Kawasaki disease is characterized by ________ rash.

A

desquamative

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114
Q

What is a common oral manifestation in Kawasaki disease?

A

Strawberry tongue.

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115
Q

What condition is associated with an increased risk of developing saccular aneurysms?

A

ADPKD

ADPKD stands for Autosomal Dominant Polycystic Kidney Disease.

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116
Q

What symptom did the patient present with that indicated a subarachnoid hemorrhage (SAH)?

A

Severe headache

Patients typically report having the worst headache of their life.

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117
Q

What are other signs of subarachnoid hemorrhage (SAH)?

A
  • Fever
  • Xanthochromia
  • Meningismus

Xanthochromia refers to the yellow-colored cerebrospinal fluid (CSF), and meningismus includes neck stiffness and positive Kernig sign.

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118
Q

True or False: A sudden onset of a severe headache can raise suspicion for SAH.

A

True

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119
Q

Fill in the blank: Xanthochromia is characterized by _______ colored CSF.

A

yellow

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120
Q

What is meningismus?

A

Neck stiffness and Kernig sign caused by irritation of the meninges by blood

Meningismus is an indication of meningeal irritation, often seen in cases of SAH.

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121
Q

What is a traumatic brain injury?

A

A disruption in normal brain function caused by an external force.

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122
Q

What are the inpatient observation indications for traumatic brain injury?

A

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.

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123
Q

When can a patient be released for at-home observation after a traumatic brain injury?

A

Patients without neurological deficits and non-depressed linear skull fracture < 3 mm separation.

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124
Q

What is required of caregivers for at-home observation after traumatic brain injury?

A

Caregivers must reliably recognize new clinical neurological deficits and return the patient to the hospital if such manifestations arise.

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125
Q

True or False: A skull fracture of less than 3 mm separation does not require inpatient observation.

A

True.

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126
Q

Fill in the blank: Evidence of traumatic brain injury on imaging may include _______.

A

[intracranial hemorrhage].

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127
Q

What are signs of increased intracranial pressure (ICP)?

A

Signs include:
* Headache
* Altered mental status.

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128
Q

What is amaurosis fugax?

A

Transient monocular vision loss

It can sometimes be bilateral.

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129
Q

In which condition is amaurosis fugax an early sign of ocular involvement?

A

Giant-cell arteritis (GCA)

It may indicate potential permanent vision loss.

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130
Q

What symptoms are often accompanied by amaurosis fugax in patients with GCA?

A

Headache and jaw claudication

These symptoms can indicate more serious underlying issues.

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131
Q

What is the recommended treatment for patients whose presentation is compatible with GCA?

A

Immediate glucocorticoid therapy

This treatment is crucial to prevent permanent vision loss.

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132
Q

True or False: Amaurosis fugax can only occur in one eye.

A

False

It can present as bilateral vision loss.

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133
Q

What is a life-threatening asthma exacerbation characterized by?

A

Drowsiness, confusion, silent chest, inability to speak due to dyspnea, paradoxical breathing, bradycardia

Silent chest indicates severe airway obstruction with no audible wheezing.

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134
Q

What does the presence of drowsiness and confusion indicate in asthma exacerbation?

A

Possible severe hypoxia or respiratory failure

These symptoms suggest that the patient may not be getting enough oxygen.

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135
Q

What does a silent chest indicate during an asthma attack?

A

Absence of wheezing

This can signify critical airway obstruction.

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136
Q

What is a key sign of inability to speak during an asthma exacerbation?

A

Dyspnea

This shows the severity of the breathing difficulty.

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137
Q

What is paradoxical breathing?

A

A breathing pattern where the abdomen moves in during inhalation and out during exhalation

This indicates severe respiratory distress.

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138
Q

What does bradycardia indicate in the context of asthma exacerbation?

A

A potentially life-threatening condition

Bradycardia may occur due to hypoxia or vagal stimulation.

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139
Q

What are the common symptoms of epiglottitis in adult patients?

A

Odynophagia, inability to swallow, elevated temperature, sore throat, hoarseness

Stridor is less common but may indicate airway compromise.

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140
Q

What is the role of nasal fiberoptic laryngoscopy in diagnosing epiglottitis?

A

Aids in direct visualization of the supraglottis in a monitored setting

Diagnosis is primarily clinical.

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141
Q

How should a patient with airway distress and upper-airway obstruction be managed?

A

Elective intubation via awake fiberoptic nasotracheal intubation under local anesthesia

A backup tracheotomy/cricothyrotomy kit should always be available.

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142
Q

What is the most appropriate care for a patient with acute epiglottitis and signs of airway compromise?

A

Fiberoptic nasotracheal intubation in a monitored setting with a tracheotomy/cricothyrotomy set at the bedside.

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143
Q

True or False: Stridor is a common symptom of epiglottitis.

A

False

Stridor is associated with impending airway compromise but is less common.

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144
Q

What percentage of nontraumatic subarachnoid hemorrhages are caused by ruptured saccular aneurysms?

A

80%

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145
Q

List three risk factors for the development of a saccular aneurysm.

A
  • Age > 40 years
  • Female gender
  • Hypertension
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146
Q

True or False: Cigarette smoking is a risk factor for saccular aneurysms.

A

True

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147
Q

Fill in the blank: Other risk factors for saccular aneurysms include heavy alcohol use, ________, polycystic kidney disease, and family history.

A

[connective tissue disorders]

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148
Q

What is a significant gender-related risk factor for saccular aneurysms?

A

Female gender

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149
Q

Identify a risk factor for saccular aneurysms related to kidney health.

A

Polycystic kidney disease

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150
Q

Name a lifestyle factor that increases the risk of developing a saccular aneurysm.

A

Cigarette smoking

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151
Q

What age is considered a risk factor for saccular aneurysms?

A

Age > 40 years

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152
Q

List two additional risk factors for saccular aneurysms not previously mentioned.

A
  • Heavy alcohol use
  • Family history
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153
Q

What is the most common type of intracranial hemorrhage in infants with shaken baby syndrome (SBS)?

A

Subdural hematomas

Subdural hematomas occur due to the violent shaking that causes injury to the brain.

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154
Q

What results from violent shaking of a baby in shaken baby syndrome?

A

Whiplash and rapid rotational head movements

These movements lead to tearing of the intracerebral bridging veins and diffuse axonal injury.

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155
Q

List characteristic physical examination findings in children with shaken baby syndrome.

A
  • Irritability
  • Lethargy
  • Retinal hemorrhages
  • Bulging fontanelles

Retinal hemorrhages occur due to rupture of the retinal veins.

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156
Q

True or False: Retinal hemorrhages are a characteristic finding in shaken baby syndrome.

A

True

They result from the tearing of retinal veins during the violent shaking.

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157
Q

What additional injuries indicate child abuse in cases of shaken baby syndrome?

A
  • Bruises to the upper torso
  • Posterior rib fractures
  • Fractures at multiple stages of healing
  • Complex, long bone fractures

An example of a bruise pattern is purple discoloration in the T4–T10 dermatomes.

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158
Q

Fill in the blank: In shaken baby syndrome, bruises to the _______ torso can indicate child abuse.

A

upper

Bruises in this area may suggest a forceful grip or other abusive actions.

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159
Q

What type of fracture is commonly associated with child abuse in shaken baby syndrome?

A

Complex, long bone fractures (e.g., spiral humerus fractures)

These fractures indicate potential abusive trauma rather than accidental injury.

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160
Q

What is the toxidrome associated with the patient’s symptoms?

A

Tricyclic antidepressant (TCA) toxicity

Symptoms include tachycardia, hyperthermia, blurred vision, mydriasis, dry skin, and impaired intestinal motility.

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161
Q

What ECG findings are associated with increased risk for dysrhythmias and seizures in TCA toxicity?

A

QRS prolongation >100 msec and QTc prolongation >430 msec

The patient had a QRS duration of 120 msec and a QTc interval of 460 msec.

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162
Q

What are the elements of anticholinergic syndrome demonstrated by the patient?

A
  • Tachycardia
  • Hyperthermia
  • Blurred vision
  • Mydriasis
  • Dry skin
  • Impaired intestinal motility
  • ECG changes

These symptoms help to distinguish it from sympathomimetic toxidrome.

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163
Q

How do TCAs affect alpha-adrenergic and muscarinic receptors?

A

They block these receptors, causing hypotension and anticholinergic syndrome, respectively

This leads to symptoms like dry skin and impaired intestinal motility.

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164
Q

What is the first-line treatment for TCA overdose?

A

Sodium bicarbonate

It alkalinizes blood pH and increases plasma protein binding of TCAs.

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165
Q

What is the goal pH when administering sodium bicarbonate in TCA overdose?

A

7.50 to 7.55

This goal can be achieved with 1- to 2-mEq/kg boluses.

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166
Q

What are the benefits of sodium bicarbonate in TCA overdose treatment?

A
  • Alkalinizes blood pH
  • Increases plasma protein binding of TCAs
  • Augments myocardial contractility
  • Improves intraventricular conduction

These effects can elevate blood pressure and resolve hypotension.

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167
Q

What distinguishes the patient’s condition from serotonin syndrome?

A

Normal reflexes and lack of clonus

In serotonin syndrome, increased reflexes and clonus would be present.

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168
Q

True or False: A fluid bolus is effective in reversing hypotension caused by TCA overdose.

A

False

It can help optimize cardiac preload but does not reverse myocardial depression or reduced systemic vascular resistance.

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169
Q

What is the best predictor of complications after a tricyclic antidepressant overdose?

A

An electrocardiogram identifying a QRS duration >100 msec or a QTc interval >430 msec

This is crucial for assessing risk in TCA overdose cases.

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170
Q

What condition did the patient have that led to poor oral intake?

A

Upper respiratory tract infection

Poor oral intake can occur due to symptoms such as sore throat or fatigue associated with the infection.

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171
Q

What induced hypovolemia in the patient?

A

Poor oral intake and increased insensible fluid losses

Insensible fluid losses can be exacerbated by a febrile illness.

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172
Q

What medications did the patient take that contributed to acute kidney injury?

A

ACE inhibitor, diuretic, NSAID

Each of these medications can affect kidney function, especially in the context of volume depletion.

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173
Q

What was confirmed by the elevated serum creatinine level?

A

Acute kidney injury

Elevated serum creatinine is a common marker for kidney dysfunction.

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174
Q

What symptoms did the patient experience likely due to uremia?

A

Nausea, fatigue, anorexia

These symptoms are commonly associated with uremic syndrome.

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175
Q

What physiological mechanisms help maintain glomerular filtration in volume depletion?

A

Prostaglandin-mediated vasodilation of afferent arteriole and angiotensin II-mediated vasoconstriction of efferent arteriole

These mechanisms are part of the kidney’s autoregulatory response to maintain filtration pressure.

176
Q

How do NSAIDs and ACE inhibitors affect kidney autoregulation?

A

They block the autoregulatory defenses

This can lead to decreased glomerular perfusion and potential kidney injury.

177
Q

What is a key learning point regarding NSAIDs and kidney injury?

A

NSAIDs can precipitate acute kidney injury in the setting of volume depletion and renin-angiotensin-aldosterone axis blockade

This highlights the importance of careful medication management in patients with compromised kidney function.

178
Q

Fill in the blank: The patient’s acute kidney injury was likely due to _______ from medication-induced decreased glomerular perfusion.

A

Uremia

Uremia is a condition that arises when the kidneys cannot adequately filter waste products from the blood.

179
Q

What condition can NSAIDs cause related to kidney function?

A

Interstitial nephritis

NSAIDs are known to induce interstitial nephritis, which is an inflammation of the kidney’s interstitium.

180
Q

What is the mean time from starting medication to signs of acute interstitial nephritis?

A

10 days

This timeframe can be shorter if the patient has previously taken the medication.

181
Q

What serum creatinine level indicates significant renal dysfunction in this patient?

A

> 4 mg/dL

A serum creatinine level above this threshold suggests severe renal impairment.

182
Q

What does the time course of renal dysfunction in this patient suggest?

A

Medication-induced decreased glomerular perfusion

The clinical history aligns more with decreased blood flow to the kidneys rather than interstitial nephritis.

183
Q

What features are commonly associated with interstitial nephritis?

A
  • Fever
  • Rash
  • Eosinophilia
  • Pyuria
  • White-cell casts

These features can help in diagnosing interstitial nephritis, though their absence does not rule it out.

184
Q

True or False: The absence of fever, rash, eosinophilia, pyuria, and white-cell casts makes interstitial nephritis unlikely.

A

True

While these symptoms do not exclude interstitial nephritis, their absence in conjunction with the timing makes the diagnosis less likely.

185
Q

The onset of renal dysfunction in this patient would be expected to have occurred at least ______ days earlier.

A

4

This is based on the patient’s serum creatinine level being greater than 4 mg/dL.

186
Q

What are the signs of acute liver failure?

A

Abnormal liver-enzyme levels, coagulopathy, and encephalopathy

Coagulopathy can be indicated by an elevated international normalized ratio and evidence of gastrointestinal bleeding.

187
Q

Why is determining the underlying cause of liver failure important?

A

It will affect management

Understanding the cause is crucial for effective treatment strategies.

188
Q

What condition should be suspected in a young patient with liver failure and neurologic symptoms?

A

Wilson disease

Wilson disease is rare but should be considered based on age and symptoms.

189
Q

What laboratory results suggest Wilson disease?

A

Low alkaline phosphatase to total bilirubin ratio (<4) and elevated AST and ALT levels with AST-to-ALT ratio >2

Elevated levels should be <2000 U/liter.

190
Q

What additional complications can occur in acute Wilson disease?

A

Renal failure and Coombs-negative hemolytic anemia

In this context, anemia is likely due to gastrointestinal bleeding.

191
Q

What serum level is suggestive of Wilson disease?

A

Low serum ceruloplasmin level (<0.1 g/liter)

However, low ceruloplasmin is not sufficient for diagnosis.

192
Q

What factors limit the diagnostic utility of ceruloplasmin levels for Wilson disease?

A

Low positive predictive values and potential for false elevation in acute settings

Ceruloplasmin is an acute-phase reactant.

193
Q

What confirmatory tests should be conducted before diagnosing Wilson disease?

A

Serum copper concentration, 24-hour urinary copper excretion, and ocular slit-lamp examination for Kayser-Fleischer rings

These tests help confirm the diagnosis of Wilson disease.

194
Q

What key learning point should prompt evaluation for Wilson disease?

A

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

These clinical features are critical for suspicion and further investigation.

195
Q

What are the common clinical presentations of testicular torsion?

A

Sudden onset of severe hypogastric and left inguinal pain, nausea, vomiting

These symptoms indicate a potential testicular torsion.

196
Q

What physical examination findings are indicative of testicular torsion?

A

Hypogastric and testicular tenderness, scrotal elevation and swelling

These findings are critical for diagnosing testicular torsion.

197
Q

During which periods does testicular torsion most commonly develop?

A

Neonatal period and puberty

Understanding these periods helps in identifying at-risk patients.

198
Q

What are two characteristic findings of testicular torsion?

A

Absent cremasteric reflex and negative Prehn sign

These findings help differentiate testicular torsion from other conditions.

199
Q

Why is testicular torsion considered a medical emergency?

A

It requires prompt surgical exploration to prevent irreversible ischemia and necrosis of the testis

Timely intervention is crucial for testicular salvage.

200
Q

What surgical procedures are performed for testicular torsion?

A

Testicular reduction and bilateral orchidopexy

Orchidopexy helps prevent recurrence of torsion.

201
Q

What is the ideal time frame for surgical intervention in testicular torsion?

A

Ideally within six hours of symptom onset

Delay beyond this time can lead to severe complications.

202
Q

What imaging study can be performed in patients with ambiguous clinical findings before surgical intervention?

A

Doppler ultrasound of the scrotum

This imaging helps confirm the diagnosis of testicular torsion.

203
Q

True or False: A delay in management of testicular torsion can lead to irreversible ischemia.

A

True

Immediate treatment is essential to avoid testicular loss.

204
Q

What are the common clinical presentations of testicular torsion?

A

Sudden onset of severe hypogastric and left inguinal pain, nausea, vomiting

These symptoms indicate a potential testicular torsion.

205
Q

What physical examination findings are indicative of testicular torsion?

A

Hypogastric and testicular tenderness, scrotal elevation and swelling

These findings are critical for diagnosing testicular torsion.

206
Q

During which periods does testicular torsion most commonly develop?

A

Neonatal period and puberty

Understanding these periods helps in identifying at-risk patients.

207
Q

What are two characteristic findings of testicular torsion?

A

Absent cremasteric reflex and negative Prehn sign

These findings help differentiate testicular torsion from other conditions.

208
Q

Why is testicular torsion considered a medical emergency?

A

It requires prompt surgical exploration to prevent irreversible ischemia and necrosis of the testis

Timely intervention is crucial for testicular salvage.

209
Q

What surgical procedures are performed for testicular torsion?

A

Testicular reduction and bilateral orchidopexy

Orchidopexy helps prevent recurrence of torsion.

210
Q

What is the ideal time frame for surgical intervention in testicular torsion?

A

Ideally within six hours of symptom onset

Delay beyond this time can lead to severe complications.

211
Q

What imaging study can be performed in patients with ambiguous clinical findings before surgical intervention?

A

Doppler ultrasound of the scrotum

This imaging helps confirm the diagnosis of testicular torsion.

212
Q

True or False: A delay in management of testicular torsion can lead to irreversible ischemia.

A

True

Immediate treatment is essential to avoid testicular loss.

213
Q

What is the etiology of acute-onset monoarthritis with chondrocalcinosis and CPP crystals?

A

Acute CPP crystal arthritis, previously known as pseudogout.

214
Q

What is the preferred treatment for acute CPP crystal arthritis involving a single joint?

A

Intra-articular glucocorticoid injection.

215
Q

What systemic therapies can be pursued if multiple joints are involved in acute CPP crystal arthritis?

A
  • Nonsteroidal antiinflammatory drug (e.g., ibuprofen)
  • Glucocorticoid (e.g., prednisone)
  • Colchicine
216
Q

What are the relative contraindications for alternate therapies in this patient?

A

Renal impairment and diabetes.

217
Q

In cases of acute CPP crystal arthritis with contraindications, which treatment is preferable?

A

Intra-articular glucocorticoid injection.

218
Q

True or False: Acute CPP crystal arthritis can also be treated with systemic glucocorticoids.

219
Q

Fill in the blank: Acute CPP crystal arthritis is also known as _______.

A

[pseudogout]

220
Q

What is leukostasis?

A

A medical emergency characterized by tissue hypoxia and hypercoagulability due to an excessive number of immature leukocytes causing microvascular obstruction.

221
Q

Define hyperleukocytosis.

A

A leukocyte count > 100,000/mm3 that may or may not be accompanied by leukostasis.

222
Q

In which type of leukemia is leukostasis most commonly seen?

A

Acute leukemia, more commonly in AML than ALL.

223
Q

What is the WBC threshold for AML to be associated with leukostasis?

A

WBC > 150,000/mm3.

224
Q

What is the WBC threshold for ALL to be associated with leukostasis?

A

WBC > 400,000/mm3.

225
Q

In which phase of chronic myeloid leukemia (CML) is leukostasis almost exclusively seen?

A

Accelerated phases or blast crisis.

226
Q

What are the clinical features of leukostasis?

A

Depend on the affected system or organ, but commonly affect lungs and CNS.

227
Q

List common respiratory clinical features of leukostasis.

A
  • Dyspnea
  • Tachypnea
  • Pulmonary crackles
  • Hypoxemic respiratory failure
228
Q

What neurological symptoms may indicate leukostasis?

A
  • Headache
  • Confusion
  • Dizziness
  • Vertigo
  • Focal neurological deficits
  • Seizures
229
Q

What are potential ophthalmological symptoms of leukostasis?

A
  • Blurry vision
  • Retinal hemorrhages
  • Papilledema
230
Q

What diagnostic approach is primarily used for leukostasis?

A

Leukostasis is primarily a clinical diagnosis.

231
Q

What laboratory findings are common in leukostasis?

A
  • ↑ WBC count
  • Anemia
  • Overestimated platelet count
232
Q

What additional tests may be performed in suspected cases of leukostasis?

A
  • ABG
  • Diagnostic microbiology (e.g., blood cultures)
233
Q

What imaging studies may be indicated for leukostasis?

A
  • Chest x-ray
  • CT head or MRI head
  • Direct fundoscopy
234
Q

What is the treatment goal for leukostasis?

A

To reduce the WBC count (cytoreduction) and control symptoms.

235
Q

What is the treatment of choice for leukostasis?

A

Induction chemotherapy.

236
Q

What are the indications for leukapheresis in leukostasis?

A
  • Symptoms of leukostasis
  • WBC ≥ 100,000/mm3
  • Severe pulmonary and neurological manifestations
237
Q

What is hydroxyurea used for in the context of leukostasis?

A

As a bridging therapy to induction chemotherapy.

238
Q

True or False: Blood cell transfusions are recommended in leukostasis management.

239
Q

What should be monitored in patients at risk of tumor lysis syndrome (TLS) during leukostasis treatment?

A

Monitoring for DIC.

240
Q

What is the most likely cause of memory loss in the setting of a possible traumatic experience without known neurologic causes?

A

Psychogenic cause

This typically indicates a psychological origin rather than a physical one.

241
Q

What is the most likely diagnosis for memory loss due to a psychogenic cause?

A

Dissociative amnesia

This condition is often linked to trauma or stress.

242
Q

What characterizes dissociative amnesia?

A

Inability to recall autobiographical information, usually of a traumatic or stressful nature

This type of memory loss is specifically about personal experiences.

243
Q

Does dissociative amnesia involve retrograde amnesia?

A

No

Patients typically do not have trouble learning new information.

244
Q

What type of memory loss is not involved in dissociative amnesia?

A

Retrograde amnesia

Patients retain the ability to learn new information.

245
Q

What must be ruled out for a diagnosis of dissociative amnesia?

A

Physiologic effects of a substance or another medical condition

Memory loss must not be attributable to other medical issues.

246
Q

What is a common underlying cause of orthostatic syncope?

A

Autonomic dysfunction

Autonomic dysfunction impairs the body’s ability to regulate blood pressure when changing positions.

247
Q

What happens to venous return to the heart when a patient with orthostatic syncope stands?

A

It causes a drop in venous return

This drop leads to decreased preload and decreased cardiac output.

248
Q

What normally occurs in the autonomic response to standing?

A

Sympathetic tone increases and parasympathetic tone decreases

This response leads to vasoconstriction, increased venous return, and increased heart rate.

249
Q

What can happen if the normal autonomic response to standing is compromised?

A

Orthostatic hypotension occurs

Compromise can occur due to medications or conditions like neuropathy.

250
Q

Which age-related factor is a risk for baroreceptor dysfunction?

A

Advanced age

Older individuals may have impaired baroreceptor sensitivity.

251
Q

How does calcium channel blocker use affect orthostatic hypotension?

A

It blunts peripheral vasoconstriction

This can contribute to decreased blood pressure regulation.

252
Q

What effect do tricyclic antidepressants have related to orthostatic syncope?

A

They cause autonomic dysfunction

This dysfunction can exacerbate symptoms of orthostatic hypotension.

253
Q

What is the next best step for a patient with clear orthostatic changes and a normal workup?

A

Adjustment in medications

This includes modifying tricyclic antidepressants and/or calcium channel blockers.

254
Q

True or False: No further diagnostic testing is required for patients with clear orthostatic changes and a highly suggestive history.

A

True

A thorough workup may often suffice in such cases.

255
Q

What symptoms raise suspicion for stimulant intoxication?

A

Acute onset of personality and mood changes, formication, tachycardia, and hypertension

These symptoms are indicative of stimulant intoxication from substances like cocaine or amphetamines.

256
Q

List additional signs and symptoms of stimulant use.

A
  • Mydriasis
  • Psychomotor agitation
  • Nausea
  • Diaphoresis
  • Loss of appetite
  • Weight loss
  • Neuropsychiatric symptoms (e.g., hallucinations, delusions)

Neuropsychiatric symptoms can include both visual and auditory hallucinations.

257
Q

True or False: A urine drug screen is always helpful in the acute management of suspected stimulant intoxication.

A

False

Urine drug screens can yield false positives due to cross-reactivity and prolonged excretion of inactive metabolites.

258
Q

What is the initial management focus for stimulant intoxication?

A

Stabilizing the patient by controlling agitation and the hyperadrenergic state with benzodiazepines and lowering body temperature

This approach is critical for managing the acute effects of stimulant intoxication.

259
Q

What is the purpose of diagnostic testing in stimulant intoxication?

A

To assess for alternative diagnoses and/or complications

Examples include ECG to rule out conduction abnormalities and myocardial ischemia.

260
Q

What should be suspected in patients with features of stimulant intoxication but negative urine toxicology?

A

Bath salt intoxication

Bath salts can produce similar symptoms to stimulants but may not be detected on standard urine drug screens.

261
Q

What is high-altitude pulmonary edema (HAPE)?

A

A noncardiogenic pulmonary edema occurring shortly after rapid ascent, typically to > 4500 m (∼ 14,500 feet)

HAPE is the most common cause of death in individuals ascending rapidly to high altitude.

262
Q

What triggers the pathophysiology of HAPE?

A

Decrease in the partial pressure of arterial oxygen causing hypoxic pulmonary vasoconstriction

This leads to increased pulmonary arterial and capillary pressures, resulting in pulmonary hypertension.

263
Q

What are common clinical features of HAPE?

A

Onset typically 2–4 days after arrival, cough, shortness of breath, weakness, chest tightness, crackles or wheezing, cyanosis, tachypnea, and tachycardia

Cough may initially be dry but can become productive with pink, frothy sputum.

264
Q

What diagnostic methods are used for HAPE?

A

Lung ultrasound, chest x-ray, ECG, echocardiography

Lung ultrasound shows pulmonary edema and B lines; chest x-ray shows patchy infiltrates.

265
Q

What does a chest x-ray show in HAPE?

A

Patchy infiltrates

This is one of the diagnostic criteria for HAPE.

266
Q

What are the differential diagnoses for HAPE?

A

Exacerbation of asthma or COPD, pneumonia, acute heart failure, pulmonary embolism

A normal leukocyte count and rapid improvement with oxygen therapy suggest HAPE over pneumonia.

267
Q

What is the immediate treatment for HAPE?

A

Descend immediately and provide oxygen therapy

Oxygen therapy should aim for a target SpO2 of > 90%; CPAP may be used if in a hospital setting.

268
Q

What pharmacotherapy options are available for HAPE?

A

Nifedipine (off-label) or phosphodiesterase inhibitors like sildenafil or tadalafil

These medications are used if immediate descent and oxygen therapy are not feasible.

269
Q

Fill in the blank: Prophylactic medication for altitude illness includes _______.

A

acetazolamide or dexamethasone

These medications are recommended if risk factors for altitude illness are present.

270
Q

What is the preferred pharmacotherapy for HAPE prevention?

A

Nifedipine or phosphodiesterase inhibitors

Nifedipine is preferred, especially for individuals with a history of HAPE.

271
Q

What is a common symptom of HAPE related to breathing?

A

Shortness of breath

This is a significant clinical feature that may develop alongside other symptoms.

272
Q

True or False: HAPE occurs immediately upon ascent to high altitude.

A

False

HAPE typically has an onset of 2–4 days after arrival at high altitude.

273
Q

What is priapism?

A

A sustained erection that lasts for more than four hours and is not the result of sexual excitation.

Priapism can lead to serious complications if not treated promptly.

274
Q

How is priapism classified based on etiopathogenesis?

A

Priapism is classified as either low-flow or high-flow.

This classification helps determine the underlying cause and appropriate treatment.

275
Q

What causes low-flow priapism?

A

Inadequate venous outflow from the corpus cavernosum, resulting in painful penile ischemia.

Low-flow priapism is an acute urological emergency.

276
Q

What is the most common cause of low-flow priapism in adults?

A

Adverse effects from treating erectile dysfunction (e.g., sildenafil).

This highlights the importance of monitoring patients on these medications.

277
Q

What is the most common cause of low-flow priapism in children?

A

Sickle cell disease.

Sickle cell disease can lead to various complications, including priapism.

278
Q

What characterizes high-flow priapism?

A

It is usually the result of perineal trauma and is not associated with penile ischemia, therefore it is painless.

High-flow priapism is less common than low-flow.

279
Q

How can high-flow priapism be distinguished from low-flow priapism?

A

Through penile blood gas analysis and Doppler ultrasound of the penis.

These diagnostic tools help determine the appropriate treatment.

280
Q

What is the treatment for low-flow priapism?

A

Aspiration of blood from the corpus cavernosum and injection of phenylephrine.

Treatment must occur within 12 hours to restore erectile function.

281
Q

What happens if low-flow priapism is not treated within 12 hours?

A

Leads to cavernous fibrosis and irreparable damage with erectile dysfunction.

Timely intervention is crucial to prevent long-term complications.

282
Q

What is indicated if priapism does not subside after initial treatment?

A

Surgical therapy to decompress the penis.

This may be necessary in severe cases of low-flow priapism.

283
Q

True or False: Non-ischemic priapism usually requires treatment.

A

False.

Non-ischemic priapism typically does not require intervention.

284
Q

Fill in the blank: Low-flow priapism is an acute urological emergency that must be treated within _______.

A

12 hours.

Prompt treatment is essential to prevent complications.

285
Q

What is the outcome if low-flow priapism is treated within 12 hours?

A

Complete restoration of erectile function is possible.

Early intervention significantly improves prognosis.

286
Q

What is hemolytic uremic syndrome (HUS)?

A

A thrombotic microangiopathy characterized by the formation of microthrombi that occlude arterioles and capillaries.

287
Q

What are the key components of HUS?

A

Microangiopathic hemolytic anemia, thrombocytopenia, acute kidney injury (AKI).

288
Q

Which population is predominantly affected by HUS?

289
Q

What is the most common cause of HUS?

A

Bacterial toxins, primarily the Shiga-like toxin of enterohemorrhagic E. coli O157:H7.

290
Q

What should be done if there is a suspicion of HUS?

A

Begin treatment immediately.

291
Q

What are the common clinical features preceding HUS?

A

Diarrheal illness (usually bloody) for the past 5–10 days.

292
Q

What is the triad of clinical findings in HUS?

A
  • Thrombocytopenia
  • Microangiopathic hemolytic anemia
  • Impaired renal function
293
Q

What are the symptoms of thrombocytopenia in HUS?

A
  • Petechiae
  • Purpura
  • Mucosal bleeding
  • Prolonged bleeding after minor cuts
294
Q

What are the symptoms of microangiopathic hemolytic anemia in HUS?

A
  • Fatigue
  • Dyspnea
  • Pallor
  • Jaundice
295
Q

What renal symptoms are associated with HUS?

A
  • Hematuria
  • Proteinuria
  • Oliguria
  • Anuria
296
Q

What laboratory findings indicate hemolytic anemia?

A
  • ↓ Hemoglobin
  • ↓ Haptoglobin
  • ↑ Indirect bilirubin
  • ↑ Reticulocytes
  • ↑ LDH
  • ↑ Schistocytes on blood smear
297
Q

What coagulation profile findings are typical in HUS?

A
  • ↓ 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
Q

What serum chemistry findings are associated with impaired renal function in HUS?

A
  • ↑ BUN
  • ↑ Creatinine
299
Q

What are the treatment options for HUS?

A
  • Supportive care
  • Dialysis (up to 50% may require it)
  • Plasma exchange therapy (only in refractory cases)
  • Eculizumab (effective for aHUS)
300
Q

What is the prognosis of HUS based on treatment timing?

A

Timely treatment can prevent acute complications and progression to chronic renal failure.

301
Q

What is the mortality rate of HUS with treatment?

302
Q

What percentage of children with HUS may experience long-term renal sequelae?

303
Q

Diagnóstico diferencial de síndrome hemolítico urémico

A
  • 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
Q

What is the primary infectious cause of vision loss in an immunosuppressed patient with vitreous inflammation and necrotizing retinitis adjacent to a retinal scar?

A

Toxoplasma gondii

This is a key learning point regarding ocular toxoplasmosis.

305
Q

How may ocular toxoplasmosis be acquired?

A

Congenitally or via ingestion of raw or undercooked meats or oocysts from cats

Ocular toxoplasmosis can be transmitted in utero or through dietary sources.

306
Q

What are the typical results of primary infection of Toxoplasma gondii in children and adults?

A

Retinochoroidal scars and may be subclinical

Many infections do not present noticeable symptoms.

307
Q

What occurs at the edge of the scar during reactivation of ocular toxoplasmosis?

A

Reactivation of the disease

This can happen particularly in immunosuppressed individuals.

308
Q

What can elicit reactivation of ocular toxoplasmosis?

A

Immunosuppression, such as corticosteroid or immunomodulator treatment

Patients on these treatments are at higher risk for reactivation.

309
Q

What is the classic sign of ocular toxoplasmosis?

A

A nidus of fluffy white necrotizing retinitis near a pigmented chorioretinal scar

This characteristic appearance is crucial for diagnosis.

310
Q

Is vitreous inflammation common in ocular toxoplasmosis?

A

Yes

Vitreous inflammation is a frequent finding in this condition.

311
Q

What is Fournier gangrene?

A

A necrotizing fasciitis involving the perineal area, including the scrotum, penis, and anterior abdominal wall

Fournier gangrene is a serious and potentially life-threatening infection.

312
Q

Which patients are at particularly high risk for Fournier gangrene?

A

Patients with diabetes mellitus

Diabetes mellitus increases susceptibility to infections, including Fournier gangrene.

313
Q

What are the initial symptoms of Fournier gangrene?

A

Pain, erythema, and swelling

These symptoms may rapidly progress in severity.

314
Q

As Fournier gangrene evolves, what additional symptoms may develop?

A

Purulent drainage, bullous lesions, tissue necrosis, and subcutaneous crepitus

These symptoms indicate a progression of the infection.

315
Q

What is the most appropriate management for a man with type 2 diabetes and Fournier gangrene?

A

Surgical debridement

In addition to antibiotic therapy, surgical intervention is critical in managing this aggressive infection.

316
Q

What type of antibiotic therapy is recommended for Fournier gangrene?

A

Broad-spectrum antibiotic therapy covering gram-positive, gram-negative, and anaerobic organisms

Effective antibiotic coverage is crucial for treating the polymicrobial nature of the infection.

317
Q

True or False: Fournier gangrene can involve the anterior abdominal wall.

A

True

The infection can extend beyond the perineum to include surrounding areas.

318
Q

Fill in the blank: Fournier gangrene is a type of _______.

A

necrotizing fasciitis

It is characterized by rapid tissue destruction.

319
Q

What types of wounds can result from a human bite?

A

Scratches, punctures, lacerations, and avulsions

Human bites can lead to various types of injuries depending on the severity and location of the bite.

320
Q

What is the microbiology of human bite wounds typically characterized by?

A

Polymicrobial flora reflecting human mouth flora, skin flora, and the environment

The complexity of the microbiome in human bite wounds can complicate treatment.

321
Q

Which pathogens are most commonly isolated from human bite wounds?

A
  • Streptococcus species
  • Staphylococcus species
  • Eikenella corrodens
  • Anaerobes

These pathogens contribute to the risk of infection following a human bite.

322
Q

What factors determine the risk for infection after a human bite?

A
  • Patient’s immunocompetence
  • Location of the bite
  • Local wound care

Understanding these factors is crucial for assessing and managing bite wounds.

323
Q

Which patients are at the highest risk for infection following a human bite?

A

Patients with diabetes mellitus, sickle cell anemia, asplenia, and other immunocompromised states

These conditions impair the immune response, increasing infection risk.

324
Q

What types of wounds are particularly high risk for infection?

A

Wounds over a tendon, joint, or bone

The anatomical location significantly influences infection potential.

325
Q

What is a ‘fight bite’?

A

Human bite wounds on a clenched fist over the knuckles

These injuries can lead to serious complications like septic arthritis or osteomyelitis.

326
Q

How quickly can bite wounds lead to infection?

A

As quickly as 8 to 12 hours after the bite

Prompt medical evaluation is crucial for timely intervention.

327
Q

What is the recommended antibiotic of choice for treating bite-wound infections?

A

Amoxicillin-clavulanate

This combination effectively targets the pathogens associated with bite wounds.

328
Q

Why is amoxicillin alone not sufficient for treating bite wounds?

A

It does not cover beta-lactamase-producing organisms

The addition of clavulanate helps overcome this limitation.

329
Q

What is the alternative antibiotic regimen for penicillin-allergic patients?

A

Clindamycin combined with trimethoprim-sulfamethoxazole

This combination provides effective coverage for bite-wound infections in allergic individuals.

330
Q

What should be done for patients with bite wounds whose immunization status is unknown?

A

Administer a tetanus booster

Keeping tetanus immunization up to date is essential in wound management.

331
Q

What are some essential steps in managing an infected bite wound?

A
  • Obtaining cultures
  • Irrigating with sterile normal saline
  • Exploring the wound
  • Debriding devitalized tissue
  • Draining fluid collections
  • Assessing for bloodborne pathogen transmission

Comprehensive management helps prevent complications and promotes healing.

332
Q

True or False: Antibiotics are typically recommended if a patient is seen more than 24 hours after a bite with no signs of infection.

A

False

If no signs of infection are present after 24 hours, antibiotics are generally not recommended.

333
Q

What is the most likely diagnosis for a patient with mild chronic bilateral conjunctivitis and pain with urination?

A

Chlamydial conjunctivitis

This condition can occur due to autoinoculation from a chlamydial infection.

334
Q

What is a common cause of chronic indolent conjunctivitis?

A

Chlamydia trachomatis

This bacterium is associated with various ocular and genital symptoms.

335
Q

List some symptoms associated with Chlamydia trachomatis infections.

A
  • Injection
  • Mucus discharge
  • Preauricular lymph-node enlargement
  • Follicles on the inferior tarsal conjunctiva
  • History of urethritis, cervicitis, or vaginitis

These symptoms can help in diagnosing the infection.

336
Q

What are the diagnostic methods for Chlamydia trachomatis infections?

A
  • Conjunctival culture
  • DNA probe
  • Microscopic examination

These methods help confirm the presence of the infection.

337
Q

What is the preferred treatment for Chlamydia trachomatis infections?

A
  • Azithromycin
  • Doxycycline

Oral antibiotics are the primary treatment options.

338
Q

What are some adjunctive therapies for Chlamydia trachomatis infections?

A
  • Erythromycin
  • Tetracycline

These topical antibiotic ointments can support treatment.

339
Q

How do the serotypes of Chlamydia trachomatis differ in terms of disease?

A

The serotypes causing urethritis and chronic conjunctivitis are different from those causing endemic trachoma

This distinction is important for diagnosis and treatment.

340
Q

Where is endemic trachoma typically seen?

A

Resource-limited settings

It is rare outside the developing world.

341
Q

What condition should be considered in a patient with conjunctivitis, urethritis, and arthritis?

A

Reactive arthritis

This diagnosis is relevant in the context of the symptoms presented.

342
Q

What symptoms were absent in the patient that would indicate concomitant uveitis?

A
  • Arthritis
  • Photophobia

Their absence suggests that uveitis is not present.

343
Q

What is a key learning point regarding young women with specific symptoms?

A

A young woman with mild chronic conjunctivitis and pain with urination most likely has a diagnosis of chlamydial conjunctivitis.

344
Q

What is the initial treatment for an episode of anterior uveitis?

A

A glucocorticoid eyedrop (such as prednisolone) and a mydriatic/cycloplegic eyedrop

Anterior uveitis is an inflammatory condition affecting the middle layer of the eye, and the treatment aims to reduce inflammation and alleviate pain.

345
Q

What are the characteristic symptoms of acute epiglottitis?

A

Shortness of breath, fever, stridor, odynophagia, inability to swallow secretions

These symptoms are critical for diagnosis and management of acute epiglottitis.

346
Q

What is the classical radiographic finding in acute epiglottitis?

A

The thumbprint sign

This sign indicates enlargement of the epiglottis with airway narrowing.

347
Q

What is the initial management for adults with acute epiglottitis?

A

Airway management and intravenous antibiotics

Antibiotics should be started empirically.

348
Q

Name two antibiotics that are commonly used empirically for acute epiglottitis.

A

Intravenous ampicillin-sulbactam and third-generation cephalosporin

These antibiotics cover common bacterial causes of epiglottitis.

349
Q

If methicillin-resistant Staphylococcus aureus cannot be excluded, which antibiotic should be included?

A

Vancomycin

This is to ensure coverage against MRSA.

350
Q

What percentage of throat-swab cultures in cases of epiglottitis yield significant microbial growth?

A

10% to 33%

This indicates that the microbial cause is often not identified.

351
Q

What percentage of acute epiglottitis cases are attributable to Haemophilus influenzae type b?

A

17%

This suggests that other organisms may be responsible for the majority of cases.

352
Q

Fill in the blank: The most appropriate empiric antibiotic for the treatment of acute epiglottitis is either _______ or an intravenous third-generation cephalosporin.

A

intravenous ampicillin-sulbactam

This is a key learning point for treatment.

353
Q

What should be considered when children present with unexplained injuries?

A

Nonaccidental trauma (NAT)

NAT is suspected when injuries are not consistent with the child’s level of development or there is a delay in seeking care.

354
Q

What are common symptoms of abusive head trauma in infants?

A

Symptoms may include:
* poor feeding
* vomiting
* lethargy
* fussiness
* hypotonia
* seizures

Symptoms can be nonspecific.

355
Q

What finding on a nonmobile infant is a sentinel injury for abuse?

A

Left-ear bruise

This injury should not be overlooked as it may indicate abuse.

356
Q

What can result from a lack of recognition of nonaccidental trauma?

A

Severe morbidity or possibly death

Early recognition and intervention are crucial.

357
Q

What is a critical next step after suspecting nonaccidental trauma?

A

Referral to child protective services (CPS)

Reporting suspicion is crucial for child safety.

358
Q

What radiologic evaluations are included for assessing nonaccidental trauma?

A

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)

These evaluations help identify injuries.

359
Q

What is the best method to identify fractures in infants and children under 2 years of age concerning for physical abuse?

A

Skeletal survey

A complete skeletal survey includes approximately 20 images of the entire body.

360
Q

What should nonradiologic evaluation of nonaccidental trauma include?

A

Nonradiologic evaluation should include:
* Full physical examination
* Fundoscopic examination
* Basic laboratory testing
* Coagulation studies (if bleeding)
* Hepatic and pancreatic enzyme levels

These help assess for potential injuries.

361
Q

What is the first priority when managing a patient with suspected nonaccidental trauma?

A

Stabilizing the patient

This is crucial, especially if the patient has a depressed mental status.

362
Q

What may suggest impending brainstem herniation in a patient?

A

Hypertension, bradycardia, and erratic breathing

These signs require immediate attention.

363
Q

What interventions may reduce the likelihood of brainstem herniation?

A

Interventions include:
* Consulting the neurosurgery team
* Administering hypertonic saline or mannitol
* Elevating the head of the bed

These measures help manage intracranial pressure.

364
Q

What findings are highly concerning for abusive head trauma?

A

Presence of a skull fracture and subdural hematoma

These findings necessitate further investigation and reporting.

365
Q

What is the most appropriate next step after stabilizing an infant with an unexplained skull fracture and subdural hematoma?

A

Notification of child protective services

This step is crucial after acute stabilization and neurosurgery consultation.

366
Q

What is the definition of a suspected case of pertussis?

A

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

The presence of fever suggests an alternative diagnosis.

367
Q

What are the confirmatory studies for pertussis?

A

PCR and/or cultures for patients who present ≤ 4 weeks since cough onset; Serology for patients who present > 4 weeks after developing symptoms.

These studies help confirm the diagnosis of pertussis based on the duration of symptoms.

368
Q

True or False: A cough of any duration is sufficient to suspect pertussis.

A

True

There is a low threshold for suspicion in infants.

369
Q

Fill in the blank: The presence of _______ suggests an alternative diagnosis in suspected pertussis cases.

A

fever

Fever is an important clinical sign that may indicate a different illness.

370
Q

What is electrical alternans?

A

An ECG finding highly specific to large pericardial effusions

Characterized by cyclical changes in the axis or amplitude of consecutive QRS complexes

371
Q

What causes electrical alternans?

A

The swinging motion of the beating heart surrounded by pericardial fluid

This motion leads to variations in the ECG readings

372
Q

What are common ECG findings in patients with large pericardial effusion and cardiac tamponade?

A

Sinus tachycardia and low voltage recording

These findings are typical in such patients

373
Q

What is the management approach for stable patients with pericardial effusion?

A

Transthoracic echocardiography should be used to confirm the diagnosis

This is essential for assessing the condition further

374
Q

What should be done for unstable patients with suspected cardiac tamponade?

A

Pericardiocentesis should not be delayed for diagnostic confirmation

Immediate intervention is critical in these cases

375
Q

True or False: Electrical alternans can occur in stable patients without pericardial effusion.

A

False

Electrical alternans is specifically associated with large pericardial effusions

376
Q

Fill in the blank: In patients with large pericardial effusion, the ECG typically shows _______.

A

sinus tachycardia and low voltage recording

These are common findings in such patients

377
Q

What is Cryptococcus neoformans?

A

An opportunistic infection that causes meningoencephalitis in immunosuppressed patients

It commonly affects individuals with weakened immune systems, such as those with HIV.

378
Q

What are common risk factors for Cryptococcus neoformans infection?

A
  • HIV infection
  • Glucocorticoid use
  • Solid organ transplantation
  • Advanced malignancies
  • Type 2 diabetes
  • Sarcoidosis
  • 20% of patients have no identified risk factor

These factors increase susceptibility to the infection.

379
Q

How does the presentation of Cryptococcus neoformans vary?

A

Symptoms can develop slowly over several weeks, and fever is seen in only 50% of cases

Other symptoms may include headaches, lethargy, cranial-nerve palsies, personality changes, and memory loss.

380
Q

What imaging findings may be seen in cases of Cryptococcus neoformans?

A
  • Normal CT or MRI in 50% of cases
  • Atrophy
  • Hydrocephalus
  • Gyral enhancement
  • Nodules (cryptococcomas)

These findings can vary significantly among patients.

381
Q

What diagnostic evaluations are recommended for Cryptococcus neoformans?

A
  • Lumbar puncture
  • Measurement of opening pressure of cerebrospinal fluid (CSF)
  • Evaluation of CSF with cryptococcal antigen testing
  • Fungal cultures

These tests help confirm the diagnosis and assess the condition of the patient.

382
Q

Why are strategies to reduce intracranial pressure important in Cryptococcus neoformans infection?

A

Many complications of cryptococcal meningitis are due to markedly raised intracranial pressure

Effective management may include large-volume lumbar punctures and neurosurgical shunting.

383
Q

True or False: Fever is a common symptom in all cases of Cryptococcus neoformans infection.

A

False

Fever is seen in only 50% of cases.

384
Q

Fill in the blank: A common infectious cause of subacute and chronic meningoencephalitis associated with raised intracranial pressure in immunocompromised patients is _______.

A

Cryptococcus neoformans

This highlights the significance of this pathogen in clinical practice.

385
Q

What is characteristic of a transient aplastic crisis from parvovirus B19 infection in patients with immune deficiency states?

A

Absence of reticulocytes in the blood and presence of giant pronormoblasts in the bone marrow

This is particularly observed in advanced HIV infections.

386
Q

Why do immunodeficient patients develop persistent severe anemia due to pure red-cell aplasia?

A

They are unable to form neutralizing antibodies against the virus and parvovirus B19 has a predilection for erythroid progenitor cells

This leads to a lack of red blood cell production.

387
Q

What are the treatment options for pure red-cell aplasia due to parvovirus B19 infection in people with HIV?

A

Transfusion of blood products, antiretroviral therapy, intravenous immunoglobulin

These treatments help manage the anemia and underlying viral infection.

388
Q

What is the most common clinical presentation of parvovirus B19 infection?

A

Fifth disease (erythema infectiosum) characterized by the classic ‘slapped cheek’ rash

This condition is typically seen in children.

389
Q

True or False: Most people are seropositive for parvovirus B19 by late adulthood.

A

True

This indicates widespread exposure to the virus.

390
Q

Fill in the blank: The most likely infectious cause of pure red-cell aplasia in a patient with advanced HIV infection is _______.

A

parvovirus B19

391
Q

What is a massive proximal deep-vein thrombosis (DVT) also known as?

A

Phlegmasia cerulea dolens

This term refers to the severe form of DVT characterized by significant clinical symptoms.

392
Q

What are the symptoms of a massive proximal DVT?

A

Sudden severe pain, swelling, cyanosis, and arterial compromise.

These symptoms indicate a critical condition that needs immediate attention.

393
Q

What complications can arise from a massive proximal DVT?

A

Increased venous stasis, extravasation of intravascular fluid, painful swelling, violaceous skin changes, compartment syndrome, soft tissue destruction, infection, and gangrene.

These complications highlight the severe impact of untreated DVT.

394
Q

What should be considered due to the high morbidity and mortality associated with massive proximal DVT?

A

Catheter-directed thrombolysis or mechanical or surgical thrombectomy.

These interventions are critical for managing severe DVT cases effectively.

395
Q

What key learning point should be noted regarding patients with risk factors for thromboembolic disease?

A

Sudden onset of leg pain with swelling, purple color, and arterial ischemia with loss of distal pulses raises concern for massive proximal DVT.

Recognizing these signs early can lead to timely intervention.

396
Q

Fill in the blank: A massive proximal DVT can lead to _______ by causing a compartment syndrome.

A

Arterial ischemia

Compartment syndrome is a serious condition that can occur due to increased pressure within a closed muscle compartment.

397
Q

What is the mortality rate of acute type A aortic dissection after symptom onset?

A

1% per hour

This highlights the urgency of treatment for this condition.

398
Q

What percentage of patients with type A dissection are initially thought to have another cause of chest pain?

A

30%

This can delay proper diagnosis and treatment.

399
Q

What physical findings can increase the likelihood of aortic dissection?

A

Pulse deficits or blood pressure discrepancies between the arms

However, fewer than 20% of patients with type A dissection exhibit these findings.

400
Q

What symptoms are commonly experienced by nearly half of patients with type A aortic dissection?

A

Pain radiating to the back or a diastolic murmur

The murmur is due to aortic valvular regurgitation.

401
Q

Which imaging modalities can be used to diagnose ascending aortic dissection?

A
  • Contrast-enhanced CT
  • Transesophageal echocardiography (TEE)
  • MRI
  • Invasive aortography

All these modalities are highly accurate.

402
Q

What is the preferred imaging modality for diagnosing acute ascending aortic dissection according to current guidelines?

A

Contrast-enhanced CT

It is widely available and quick to perform, making it a class I indication.

403
Q

What is a relative contraindication for the use of iodinated contrast in imaging?

A

Chronic kidney disease

This is due to the risk of contrast nephropathy.

404
Q

What should be considered more important than the potential risk of nephropathy when diagnosing ascending aortic dissection?

A

The need for urgent diagnosis

This outweighs the potential risk of nephropathy in acute cases.

405
Q

What is the most appropriate procedure for diagnosing acute ascending aortic dissection in hemodynamically unstable patients?

A

CT angiography

This is highlighted as a key learning point.

406
Q

What is hypokalemia?

A

A common adverse effect of continuous albuterol therapy

407
Q

What causes hypokalemia in continuous albuterol therapy?

A

β2-agonist stimulation of the Na+/K+-ATPase, leading to an intracellular K+ shift

408
Q

How does β2-mediated stimulation of the liver affect glucose levels?

A

It elevates cAMP levels, increasing glycogenolysis and hyperglycemia

409
Q

What role does hyperglycemia play in hypokalemia?

A

It stimulates insulin secretion, which activates the Na+/K+-ATPase and potentiates the intracellular K+ shift

410
Q

What EKG changes can hypokalemia cause?

A

T wave flattening, ST depression, and U waves

411
Q

What are other adverse effects of continuous albuterol therapy?

A

Hypomagnesemia, hypophosphatemia, and increases in heart rate

412
Q

True or False: Continuous albuterol therapy can lead to hypomagnesemia.

413
Q

Fill in the blank: Hypokalemia is caused by _______ stimulation of the Na+/K+-ATPase.

A

β2-agonist

414
Q

What are absolute and relative contraindications to liver transplantation?

A

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

Contraindications may vary according to the policies of individual transplant centers.

415
Q

What is a typical minimum period of abstinence from alcohol and illicit substances before liver transplantation?

A

6-month minimum period

This period allows time to address substance use disorders and potential recovery from acute alcoholic hepatitis.

416
Q

True or False: Most transplant centers have maintained strict policies regarding abstinence from substances before liver transplantation.

A

False

Policies have become more flexible over time due to improved survival rates in patients with acute alcoholic hepatitis.

417
Q

What kind of patients have shown dramatically improved survival rates after liver transplantation?

A

Patients with acute alcoholic hepatitis (AAH)

The benefit is primarily observed in the first month after transplantation.

418
Q

What is the significance of early transplantation in select patients with acute alcoholic hepatitis?

A

It confirms the utility of early transplantation for patients who do not respond to glucocorticoids

Most benefits were achieved in the first month post-transplant.

419
Q

Fill in the blank: Medical contraindications to liver transplantation include _______.

A

sepsis or uncontrolled infection, severe cardiopulmonary disease, grade 3 obesity, and active extrahepatic malignancies.

420
Q

What is acute interstitial nephritis (AIN)?

A

AIN is a kidney disorder characterized by inflammation of the renal interstitium.

421
Q

What percentage of AIN cases are caused by medications?

A

More than 75%.

422
Q

Name three common causes of drug-induced AIN.

A
  • Antibiotics
  • Nonsteroidal antiinflammatory drugs
  • Proton pump inhibitors
423
Q

What are the classic symptoms of acute interstitial nephritis?

A
  • Fever
  • Rash
  • Arthralgias
  • Peripheral eosinophilia
  • Kidney failure
424
Q

Is it common for all components of the classic triad of AIN to be present?

A

No, it is uncommon.

425
Q

In a patient with a fever, rash, and acute kidney injury after starting a new medication, what is the most likely diagnosis?

A

Drug-induced acute interstitial nephritis.

426
Q

What is Guillain-Barré syndrome (GBS)?

A

An acute immune-mediated polyneuropathy that typically manifests with bilateral ascending flaccid paralysis and sensory involvement

Examples of sensory involvement include paresthesia.

427
Q

What is the pathogenesis of GBS?

A

Involves autoantibodies against antigens in the myelin sheath, other Schwann-cell antigens, and axon membranes.

428
Q

What percentage of GBS patients have a preceding infection?

A

Approximately 65%

Infections are typically upper respiratory tract or gastrointestinal.

429
Q

What is the primary method for diagnosing GBS?

A

Clinical diagnosis; alternative diagnoses should be considered especially in atypical presentations.

430
Q

What findings in cerebrospinal fluid (CSF) analysis support the diagnosis of GBS?

A

Albuminocytologic dissociation.

431
Q

What are common findings in electrodiagnostic studies for GBS?

A

Specific findings vary; they help support the diagnosis.

432
Q

What factors influence the medical treatment options for GBS?

A

The severity of symptoms.

433
Q

What are the available treatment options for GBS?

A
  • Intravenous immunoglobulin (IVIg)
  • Plasmapheresis
434
Q

What complications are associated with GBS that can increase mortality?

A
  • Respiratory failure
  • Pulmonary embolism
  • Cardiac arrest
435
Q

What percentage of GBS patients remain severely disabled after treatment?

A

Up to 20%.

436
Q

What is the mortality rate for patients with GBS despite medical treatment?

A

Approximately 5%.