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IM 3 Flashcards

1
Q

List the 4 major stroke subtypes.

A
  1. Ischemic (thrombotic)
  2. Ischemic (embolic)
  3. Intracerebral hemorrhage
  4. Spontaneous subarachnoid hemorrhage
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2
Q

Clinical characteristics of a thrombotic ischemic stroke?

A
  • Atherosclerotic risk factors (HTN, DM, etc.) +/- history of TIA
  • Local obstruction of an artery (carotid, cerebral, vertebral)
  • Symptoms may alternate with periods of improvement (stuttering progression)
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3
Q

Clinical characteristics of an ischemic embolic stroke?

A
  • History of cardiac disease (eg, AFib, endocarditis) or carotid atherosclerosis
  • Onset of symptoms is abrupt and usually maximal at the start, sometimes results in rapid recovery
  • Multiple infarcts in different vascular territories (patchy neurologic findings)
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4
Q

Clinical characteristics of intracerebral hemorrhage?

A
  • History of uncontrolled HTN, coagulopathy, illicit drug use (eg, amphetamines, cocaine)
  • Symptoms progress over minutes to hours
  • Focal neurologic symptoms (hemiplegia, hemiparesis, hemisensory disturbances) appear early, followed by features of increased ICP (eg, vomiting, headache, bradycardia, reduced alertness)
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5
Q

Clinical characteristics of spontaneous subarachnoid hemorrhage?

A
  • Bleeding from arterial saccular (berry) aneurysm or AV malformation
  • Severe headache at onset
  • Meningeal irritation
  • Focal deficits uncommon
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6
Q

Acute onset of unilateral right-sided weakness and slurred speech suggest a ___ lesion, including which areas?

A

Left cerebral hemisphere (motor cortex and Broca’s area)

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7
Q

In the setting of suspected intracranial hemorrhage, what imaging is indicated?

A

Brain CT (confirms intracerebral and subarachnoid hemorrhage and excludes other causes)

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8
Q

Clinical characteristics of lacunar strokes?

A

Severe focal symptoms depending on the affected area;

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9
Q

Where do hypertensive intracranial hemorrhages occur most commonly?

A

Basal ganglia, thalamus, pons, cerebellum

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10
Q

Risk factors for pressure ulcers?

A
  • Reduced mobility
  • Malnutrition
  • Abnormal mental status
  • Decreased skin perfusion
  • Reduced sensation
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11
Q

Standard interventions to prevent pressure ulcers in high-risk patients?

A 
Proper patient positioning - beds with features that provide pressure redistribution and reduced focal pressure; reposition at regular intervals (less evidence for this intervention)
Mobilization
Careful skin care
Moisture control
Maintenance of nutrition
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12
Q

Medications that effectively reduce the risk of acute coronary events in patients with symptomatic atherosclerotic arterial disease?

A

Aspirins

Statins

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13
Q

___ are useful in the prevention and management of venous insufficiency ulcers, which usually occur in the setting of venous stasis dermatitis.

A

Compression stockings

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14
Q

___ are useful in preventing DVT, particularly in patients with contraindications to anticoagulant therapy.

A

Intermittent pneumatic compression

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15
Q

Describe a stage 1 pressure ulcer.

A

Intact skin

Non-blanchable with localized redness

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16
Q

Describe a stage 2 pressure ulcer.

A

Shallow, open ulcer
Red-pink wound with no sloughing
Possible intact or ruptured blister

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17
Q

Describe a stage 3 pressure ulcer.

A

Full-thickness skin loss with possible visual subcutaneous fat
No exposed bone, tendons, or muscles

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18
Q

Describe a stage 4 pressure ulcer.

A

Full-thickness skin loss with exposed bone, tendon, or muscles

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19
Q

Describe an unstageable pressure ulcer.

A

Full-thickness skin loss

Ulcer base covered by slough or eschar that needs removal to stage

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20
Q

Nomenclature of SJS vs. TEN?

A

<10% of BSA - SJS
10-30%: SJS/TEN overlap
>30%: TEN

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21
Q

Clinical features of SJS and TEN?

A

4-28 days after exposure to trigger (2 days after repeat exposure)
Acute influenza-like prodrome
Rapid-onset coalescing erythematous macules, vesicles, bullae
Necrosis and sloughing of epidermis (desquamation)
Mucosal involvement (mucositis)
Systemic signs are common (fever, tachycardia, hypotension, AMS, seizures, coma)

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22
Q

List 5 common drug triggers of SJS and TEN?

A
  • Allopurinol
  • Antibiotics (eg, sulfonamides)
  • Anticonvulsants (eg, carbamazepine, lamotrigine, phenytoin)
  • NSAIDs (eg, piroxicam)
  • Sulfasalazine
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23
Q

Other common triggers of SJS and TEN?

A

Mycloplasma pneumoniae
Vaccination
GVHD

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24
Q

Treatment of SJS?

A

Supportive - aggressive fluid support and wound care

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25
Q

What is erythema multiforme?

A

Self-limited illness characterized by an acute erythematous rash and usually occurs after herpes simplex infection

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26
Q

Predominant skin lesion in erythema multiforme?

A

Targetoid plaques favoring the distal extremities

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27
Q

Characteristics of impetigo?

A

Red macules and papular lesions with honey-colored crusts

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28
Q

Compare the presentation of SJS to that of pemphigus vulgaris.

A

Like SJS, it can cause mucosal lesions and desquamating bullae; however, systemic signs (eg, fever) are less prominent and the course is typically more chronic, with oral lesions appearing weeks to months prior to skin symptoms

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29
Q

Cause of pemphigus vulgaris?

A

Autoantibodies to desmosomes

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30
Q

Walk through the management steps following identification of a thyroid nodule on exam.

A

1 - clinical evaluation, TSH level, U/S
2a - if cancer risk factors or suspicious US findings, OR no risk/suspicious findings BUT normal or elevated TSH -> fine needle aspiration
2b - if no cancer risk factors or suspicious US findings + LOW TSH -> iodine 123 scintigraphy

If hot nodule -> treat hyperthryoidism
If cold or indeterminate nodule -> FNA

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31
Q

Risk factors for thyroid cancer?

A

+ Family history
Radiation exposure in childhood
Cervical lymphadenopathy

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32
Q

Symptoms concerning for thyroid cancer?

A

Compressive symptoms (eg, hoarseness, difficulty swallowing)

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33
Q

Suspicious U/S findings RE a thyroid nodule?

A

Hypoechoic, microcalcifications, internal vascularity

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34
Q

What type of thyroid nodule function indicates a low cancer risk? A high cancer risk?

A

Low - hot nodule

High - indeterminate or cold nodule

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35
Q

In what classic patient presentation should benign intracranial hypertension (pseudotumor cerebri) be suspected?

A

Young obese female with a headache that is suggestive of a brain tumor, but with normal neuroimaging and elevated CSF pressure; neurological signs are usually absent, except for papilledema, visual field defects, and sometimes CN VI palsy

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36
Q

What medications have been associated with benign intracranial hypertension?

A

Glucocorticoids, vitamin A, OCPs

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37
Q

Pathology of benign intracranial hypertension?

A

Impaired absorption of CSF by the arachnoid villi

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38
Q

Treatment of benign intracranial hypertension?

A

Weight reduction

Acetazolamide (if weight reduction fails)

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39
Q

What may be done to prevent blindness in benign intracranial hypertension (if medical measures fail or visual field defects are progressive)?

A

Shutning or optic nerve sheath fenestration

40
Q

Triad of symptoms in normal pressure hydrocephalus?

A

Ataxia
Urinary incontinence
Dementia

41
Q

Herpes zoster ophthalmicus is an infection caused by ___ virus. Most episodes occur in what populations?

A

VZV; elderly or immunosuppresed

42
Q

Pathophysiology of herpes zoster ophthalmicus?

A

VZ virus is latent in the trigeminal ganglion; during periods of immunosuppression, the virus travels via the ophthalmic branch to the forehead and eye

43
Q

Presentation of herpes zoster ophthalmicus?

A

Fever, malaise, burning/itching in the periorbital region

Vesicular rash in the distribution of the cutaneous branch of the first division of the trigeminal nerve

Conjunctivitis and dendriform corneal ulcers

44
Q

Rx herpes zoster ophtlamicus?

A

High dose acyclovir within 72 hours of eruption - reduces development of complications

45
Q

Presentation of herpes simplex keratitis?

A

Pain, photophobia, decreased vision

Dendritic ulcer (most common presentation); may also have minute clear vesicles in the corneal epithelium

46
Q

___ is an infection of the lacrimal sac due to obstruction of the nasolacrimal duct.

A

Dacryocystitis

47
Q

Bacterial keratitis is usually seen in what populations?

A

Contact lens wearers

Following corneal trauma

48
Q

Presentation of bacterial keratitis?

A

Hazy cornea with a central ulcer and adjacent stromal abscess

Hypopyon may be present

49
Q

4 etiologies of urethritis in men?

A
  1. Neisseria gonorrhoeae (most common)
  2. Chlamydia trachomatis
  3. Mycoplasma genitalium
  4. Trichomonas (rare)
50
Q

Clinical features of urethritis in men?

A

Dysuria, discharge, urgency, increased urinary frequency

51
Q

Diagnosis of urethritis in men?

A
  • UA (pyuria - WBCs 10+/HPF)
  • Gram stain and culture
  • NAAT (C. trachomatis) of a first-catch urine sample without pre-cleaning the area
52
Q

What can cause a culture-negative urethritis?

A

Chlamydia trachomatis - cannot be visualized in Gram-stained material or recovered in conventional culture

53
Q

Rx - urethritis in men?

A

Azithromycin OR doxycycline (covers C. trachomatis)

+Ceftriaxone if gonococcus suspected or not ruled out

54
Q

Gold standard for diagnosing UTI?

A

Urine culture

55
Q

Presentation of reactivated TB?

A
  • Apical cavitary lesion on CXR

- Chronic low-grade fever, night sweats, weight loss, cough productive of blood-tinged sputum

56
Q

Most TB cases in the US occur in foreign-born individuals who recently emigrated from endemic areas, including?

A

Mexico, Phillipines, China, Vietnam, India, Dominican Republic, Haiti

Risk highest for those who lived in the US for 5 or fewer years

57
Q

Pathogenesis of primary biliary cholangitis?

A

AI destruction of intrahepatic bile ducts

58
Q

Clinical features of primary biliary cholangitis?

A

Middle-aged women
Insidious onset of fatigue and pruritis
Progressive jaundice, hepatomegaly, cirrhosis
Cutaneous xanthomas and xanthelasmas

59
Q

Lab findings in primary biliary cholangitis?

A
  • Cholestatic pattern of liver injury (Alk phos and AST/ALT elevated, Alk > AST/ALT)
  • AMA Ab
  • Severe hypercholesterolemia
60
Q

Rx - primary biliary cholangitis?

A
  • Ursodeoxycholic acid (delays progression)

- Liver transplant for advanced disease

61
Q

Complications of primary biliary cholangitis?

A

Malabsorption, fat-soluble vitamin deficiencies
Metabolic bone disease (osteoporosis, osteomalacia)
HCC

62
Q

All patients diagnosed with RA should be started on ___ as soon as possible, as joint damage begins early in its course.

A

Disease-modifying antirheumatic agents (DMARDs)

Include non-biologics (MTX, hydroxychloroquine, sulfasalazine, leflunomide, azathioprine) and biolics (eg, etancercept, infliximab, adalimumab, tocilizumab, rituximab)

63
Q

What is the preferred initial DMARD in patients with moderately to severely active RA?

A

MTX

64
Q

Patients should be tested for ___ before starting therapy with MTX.

A

Hepatitis B and C; TB; pregnancy

Also contraindicated in severe renal insufficiency, liver disease, or excessive alcohol intake

65
Q

If a patient with RA does not respond after 6 months with MTX, what is the next step?

A

Biologic DMARDs such as a TNF-alpha inhibitor like etanercept or infliximab

66
Q

What medications should be used for initial temporary symptomatic relief in RA while awaiting response to DMARD therapy?

A

NSAIDs or steroids

67
Q

An MS plaque in the ___ (location) can result in paraplegia, bladder incontinence, and absent sensation below the level of the lesion. Explain.

A

Upper thoracic spinal cord;

Damage to the:

  • Lateral corticospinal tract -> leg weakness
  • Lateral spinothalamic tract -> decreased pinprick sensation
  • Dorsal columns -> decreased proprioception
  • Descending motor and parasympathetic autonomic fibers -> incontinence
68
Q

A lesion in the ___ can lead to cranial nerve dysfunction ipsilateral to the lesion with contralateral motor weakness and sensory changes of the body.

A

Brainstem

69
Q

A lesion in the ___ can cause dysdiadochokinesia (difficulty with rapid-alternating movements0, dysmetria (past-pointing on finger-to-nose testing), limb ataxia and an intension tremor.

A

Cerebellar hemispheres

70
Q

A lesion in the ___ can cause ataxic gait and trunk dysmetria, saccadic movements of the eye (darting), and horizontal nystagmus.

A

Cervical vermis

71
Q

Causes of spinal cord compression?

A
  1. Spinal injury (eg, motor vehicle crash)
  2. Malignancy (eg, lung, breast, prostate cancers; myeloma)
  3. Infection (eg, epidural abscess)

Disc herniation, compression fractures

72
Q

Signs and symptoms of spinal cord compression?

A
  • Gradually worsening, severe local back pain
  • Pain worse in the recumbent position/at night
  • Early signs: symmetric lower extremity weakness, hypoactive/absent deep-tendon reflexes
  • Late signs: Bilateral Babinski reflex, decreased rectal sphincter tone, paraparesis/paraplegia with increased deep-tendon reflexes, sensory loss
73
Q

Management of spinal cord compression?

A
  • Emergency MRI
  • IV glucocorticoids
  • Rad-onc and neurosurgery consultations
74
Q

What tracts are injured in spinal cord compression?

A
  • Descending corticospinal tracts -> lower-extremity weakness and loss of rectal tone
  • Ascending sensory spinothalamic tracts -> sensory level is often 2 SC segments below the lesion
  • Descending autonomics in the reticulospinal tract -> urinary retention/bladder flaccidity/bladder shock
75
Q

Signs and symptoms of lesions affecting the conus medullaris?

A

Back pain with bladder and rectal dysfunction; weakness and sensory loss are less common

76
Q

Signs and symptoms of cauda equina syndrome?

A

Radicular pain, lower-extremity weakness, saddle anesthesia, and bowel/bladder dysfunction

77
Q

___ excludes cauda equina syndrome.

A

A sensory level at the umbilicus

78
Q

List the 5 most common sites for hypertensive hemorrhage in descending order.

A
  1. Basal ganglia (putamen)
  2. Cerebellar nuclei
  3. Thalamus
  4. Pons
  5. Cerebral cortex
79
Q

How do patients with intraparenchymal hemorrhage usually present?

A

Gradual onset of symptoms (minutes to a few hours) in contrast to brain embolism or subrachnoid hemorrhage

80
Q

Typical features of cerebellar hemorrhage?

A

Occipital headache (may radiate to neck/shoulders), neck stiffness (extension of blood into the 4th ventricle), N/V, nystagmus, ipsilateral hemiataxia of the trunk (cerebellar vermis) and/or limbs (hemispheres)

81
Q

In a patient with suspected cerebellar hemorrhage, what should be done first diagnostically?

A

Non-contrast head CT scan (emergency decompression may be life-saving)

82
Q

Signs and symptoms of TMJ dysfunction?

A

History of nocturnal teeth grinding
Patients often interpret the pain as coming from the ear due to anatomic proximity
Worsened with chewing
Some patients may have audible clicks or crepitus in the TMJ

83
Q

True or false - radiologic imaging of the TMJ is often of limited utility.

A

True

84
Q

Initial treatment of TMJ dysfunction?

A

Conservative measures, such as a nighttime bite guard/ surgical intervention is sometimes necessary

85
Q

What is Ramsay Hunt syndrome?

A

A form of herpes zoster infection that causes Bell’s palsy; vesicles ar etypically seen on the outer ear

86
Q

What is glossopharyngeal neuralgia?

A

Condition in which patients experience intermittent, severe, stabbing pain in areas innervated by CN 9 and 10, which includes the ear

87
Q

Etiologies of SIADH?

A
  1. CNS disturbance (stroke, hemorrhage, trauma, etc.)
  2. Medications (carbamazepine, SSRIs, NSAIDs, etc.)
  3. Lung disease (pneumonia, etc.)
  4. Ectopic ADH secretion (eg, small cell lung cancer)
  5. Pain and/or nausea
88
Q

Clinical features of SIADH?

A

Mild/moderate hyponatremia - nausea, forgetfulness

Severe hyponatremia - seizures, coma

Euvolemia - moist mucus membranes, no edema, no JVD

89
Q

Lab findings in SIADH?

A

Hyponatremia
Serum osmolality <275 mOsm/kg H2O (hypotonic)
Urine osmolality >100 mOsm/kg H2O (inappropiately elevated)
Urine sodium >40 mEq/L

90
Q

Management of SIADH?

A

Fluid restriction +/- salt tablets

Hypertonic (3%) saline for severe hyponatremia

91
Q

Extreme care must be taken with the rate of correction in hyponatremia - what rate and why?

A

Max 8 mEq/L over the first 24 hours

Rapid correction can lead to osmotic demyelination syndrome, a devastating and potentially fatal complication (eg, dysarthria, quadriparesis, coma)

92
Q

IV hydrocortisone is the appropriate treatment for hyponatremia due to ___. How would this present?

A

Adrenal insufficiency (hypovolemia, hypotension, possibly orthostasis)

93
Q

Meta-analysis showed a significantly increased risk of ___ and ___ in patients with infection due to S. gallolyticus (S. bovis biotype 1) compared to patients with S. bovis biotype II infection.

A

Colorectal cancer; endocarditis

94
Q

Diphenhydramine, used for allergic rhinitis, hives, insect bites, and motion sickness, is an antihistamine with ___ properties.

A

Anticholinergic

95
Q

Findings suggestive of anticholinergic excess?

A 
Dry mouth/dry skin
Blurry vision/mydriasis
Hyperthermia from impaired heat dissipation
Urinary retnetion
Decreased bowel sounds
Cutaneous vasodilation (red)
Delirium or hallucinations
96
Q

Management of significant anticholinergic OD?

A

Physostigmine (cholinesterase inhibitor)

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