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IM 2 Flashcards

1
Q

Early findings of Alzheimer disease?

A

Anterograde memory loss (ie, immediate recall affected, distant memories preserved)
Visuospatial deficits (eg, lost in own neighborhood)
Language difficulties (eg, difficulty finding words)
Cognitive impairment with progressive decline

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2
Q

Late findings in Alzheimer disease?

A

Neuropsychiatric (eg, hallucinations, wandering)
Dyspraxia (eg, difficulty performing learned motor tasks)
Lack of insight regarding deficits
Non-cognitive neurologic deficits (eg, pyramidal and extrapyramidal motor, myoclonus, seizures)
Urinary incontinence

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3
Q

Death usually occurs within ___ years of a diagnosis of AD regardless of treatment offered.

A

10

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4
Q

Dx Lewy body dementia?

A

Presence of dementia
Presence of 2+ of the following: parkinsonism, fluctuating cognition, visual hallucinations, rapid eye movement sleep behavior disorder

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5
Q

Presentation of frontotemporal dementia?

A

Early and prominent behavioral/personality change
Late prominent memory deficits
Manifests around age 60, much earlier than AD

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6
Q

Features of normal pressure hydrocephalus?

A

Abnormal gait (most prominent feature, appears early, broad-based and shuffling), cognitive impairment, urinary incontinence

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7
Q

In vascular dementia, deficits in ___ function are much more severe than memory deficits early in the course of the disease.

A

Executive

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8
Q

Rome diagnostic criteria - IBS

A

Recurrent abdominal pain/discomfort 3+ days/month for the past 3 months AND 2+ of the following:

  • Symptom improvement with bowel movement
  • Change in frequency of stool
  • Change in form of stool
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9
Q

Warning signs/symptoms suggesting etiologies other than IBS?

A

Rectal bleeding
Nocturnal (awakens from or prevents sleep) or worsening abdominal pain
Weight loss
Abnormal lab findings (eg, anemia, electrolyte disorders, elevated inflammatory markers)

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10
Q

What is the most common GI diagnosis in North America? Prevalence?

A

IBS; 10-15%

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11
Q

Common presentation of IBS?

A

Young women with chronic, crampy abdominal pain with alternating episodes of constipation and diarrhea; passage of stool relieves the pain; may present with non-specific symptoms (reflux, dysphagia, early satiety, chest pain)

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12
Q

Criteria for diagnosing IBS without excluding other causes?

A
  • ROME III criteria
  • No alarm features
  • No family Hx IBD or colorectal cancer
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13
Q

Colonoscopic findings on IBS patients?

A

Normal colonic mucosa

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14
Q

Crypt abscesses are characteristic for what disease? How does it present?

A

Ulcerative colitis; fever, colicky abdominal pain, chronic diarrhea with bloody stool, weight loss

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15
Q

Presentation of duodenal ulcer?

A

Epigastric pain, GI bleeding, anemia

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16
Q

Intestinal villous atrophy is the hallmark of what? How does it present?

A

Celiac disease (AI disease resulting in gluten intolerance); GI distress (diarrhea, abdominal distention, etc.), malabsorption, nutritional deficiencies

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17
Q

Perianal fistulas suggest possible ___ - presentation?

A

Crohn’s disease; abdominal pain, weight loss, extra-intestinal manifestations (eg, arthritis, skin disorders, nephrolithiasis)

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18
Q

Once ESRD develops, there are only two treatment options available - what are they? The choice depends on the patient and co-morbid conditions; if both options are available which is preferred and why?

A

Dialysis
Renal transplant

Renal transplant is preferred, as it is associated with better survival and quality of life

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19
Q

Discuss advantages of renal transplantation over dialysis.

A
  1. Better survival and quality of life
  2. Anemia, bone disease, and hypertension persist in spite of dialysis; better controlled with transplantation
  3. Transplant patients have a return of normal endocrine, sexual, and reproductive functions, and enhanced energy levels (return to full-time employment, more strenuous activity possible)
  4. In diabetics, autonomic neuropathy persists or worsens after dialysis (vs. stabilizes or improves with transplant)
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20
Q

Expected survival rate after kidney transplantation is ___% at 1 year and ___% at 5 years.

A

95; 88

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21
Q

Major disadvantages of renal transplantation?

A

Difficulty finding a donor
Surgical risk
Cost
Side effects of immunosuppression

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22
Q

Types of dialysis?

A 
Hemodialysis (home or in-center)
Peritoneal dialysis (chronic ambulatory or cyclic peritoneal dialysis)

In the US, 85% have in-center hemodialysis, 15% have peritoneal, 1% have home.

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23
Q

5-year survival rate in non-diabetic patients who are on dialysis? Diabetes?

A

30-40%; 20%

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24
Q

List 5 primary causes of nephrotic syndrome.

A
  1. Focal segmental glomerulosclerosis (FSGS)
  2. Membranous nephropathy
  3. Membranoproliferative glomerulonephritis
  4. Minimal change disease
  5. IgA nephropathy
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25
Q

Define nephrotic syndrome.

A

Heavy proteinuria (>3.5 g/24 hr)
Hypoalbuminemia (periorbital edema, peripheral edema, ascites)
Edema

Other findings include hyperlipidemia, lipiduria

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26
Q

Secondary causes of nephrotic syndrome?

A

DM, amyloidosis, etc.

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27
Q

Most common cause of nephrotic syndrome in adults?

A

FSGS

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28
Q

Clinical associations of FSGS?

A

African American and Hispanic ethnicity
Obesity
HIV and heroin use

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29
Q

IgA nephropathy can present with nephrotic syndrome (<10%), but more commonly presents with what?

A

Hematuria following a URI (40-50% of patients)

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30
Q

Second leading cause of nephrotic syndrome overall?

A

Membranous nephropathy

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31
Q

Clinical associations of membranous nephropathy?

A

Adenocarcinoma (eg, breast, lung)
NSAIDs
Hepatitis B
SLE

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32
Q

Which nephrotic syndrome is more common in children? In adults, what is it associated with?

A

Minimal change disease; NSAIDs and lymphoma (usually Hodgkin)

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33
Q

Amyloidosis is usually associated with ___ or ___.

A

Multiple myeloma; chronic inflammatory disease (RA, bronchiectasis, etc.)

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34
Q

Clinical associations of membranoproliferative glomerulonpheritis?

A

Hepatitis B and C

Lipodystrophy

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35
Q

Presentation concerning for native valve bacterial endocarditis with acute cardioembolic stroke?

A

Fever, aortic valve vegetation, cerebral infarct; high risk for complications including TIA or stroke due to septic emboli

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36
Q

Where does cardioembolic stroke due to bacterial endocarditis typically occur?

A

MCA

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37
Q

Treatment of infective endocarditis?

A 
IV antibiotics (significantlyr educe the risk of septic cardioembolism)
Aortic valve surgery IF there is significant valvular dysfunction resulting in heart failure, if infection is persistent or difficult to treat medically, or if septic embolization is recurrent
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38
Q

Early (within 48 hours) use of ___ in acute ischemic stroke due to atherosclerotic thrombosis or embolism is associated with a lower risk of recurrent stroke and decreased mortality.

A

Aspirin

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39
Q

Early use of ___ is generally not recommended in acute ischemic stroke due to atherosclerotic thrombosis or embolism as it is associated with an increased risk of symptomatic intracranial hemorrhage.

A

IV heparin

40
Q

___ is indicated for secondary prevention in patients with cardioembolic stroke due to AFib.

A

Warfarin

41
Q

What is the purpose of randomization?

A

To make the distribution of all potential confounders even; unlike other methods of controlling confounding (matching, stratified analysis, etc.), randomization potentially controls known AND unknown confounders

42
Q

Causes of cauda equina syndrome?

A 
Disc herniation or rupture
Spinal stenosis
Tumors
Infection
Hemorrhage
Iatrogenic injury
43
Q

In adults, the spinal cord ends at the ___ vertebral level. The nerve roots below this level form the ___, which floats in CSF.

A

L1-L2; cauda equina

44
Q

What does the cauda equina innervate?

A

Sensory innervation to the saddle area, motor innervation to the sphincters (anal and urethral), and parasympathetic innervation to the bladder and lower bowel

45
Q

Presentation of cauda equina syndrome?

A
  • Usually bilater,a severe radicular pain
  • Saddle hypo/anthesia
  • Asymmetric motor weakness
  • Hypo/areflexia
  • Late-onset bowel and bladder dysfunction
46
Q

Compare cauda equina and conus medullaris syndrome.

A

Cauda: usually bilateral, severe RADICULAR pain
Conus: sudden-onset severe back pain

Cauda: Saddle hypo/anesthesia
Conus: Perianal hypo/anthesthesia

Cauda: asymmetric motor weakness
Conus: symmetric motor weakness

Cauda: hypo/areflexia
Conus: hyperreflexia

Cauda: late-onset bowel and bladder dysfunction
Conus medullaris: early-onset bowel and bladder dysfunction

47
Q

Why does a cauda equina lesion cause LMN signs vs. conus medullaris, which causes both UMN and LMN signs?

A

Cauda equina - nerve roots are part of the PNS

Conus medullaris - conus is part of the spinal cord

48
Q

Management of cauda equina and conus medullaris syndrome?

A

Emergency MRI
Neurosurgical evaluation
Possible IV glucocorticoids

49
Q

Presentation of tick-borne paralysis?

A

Progressive ascending paralysis over hours to days; may be more pronounced in 1 leg or arm

Typically no fever (history of fever/prodrome makes diagnosis unlikely)

Normal sensation

No autonomic dysfunction (unlike patients with GBS)

CSF exam is typically normal

50
Q

Etiology of paralysis due to a tick?

A

Neurotoxin release (tick needs to feed for 4-7 days for the release of neurotoxin)

51
Q

Presentation fo GBS?

A

Ascending symmetrical paralysis over days to week (not usually hours)

Sensation is usually normal to mildly abnormal

Autonomic dysfunction (tachycardia, urinary retention, arrhythmias) occur in 70%

CSF is typically abnormal (may show albuminocytologic dissociation - high protein, few cells) -> may not be present early in disease course, but in 80-90% at 1 week

52
Q

Rx GBS?

A

IVIG or plasmapheresis

53
Q

Presentation of botulism?

A

Descending paralysis, early CN involvement; pupillary abnormalities are common

54
Q

Presentation of spinal cord tumors?

A

Ascending paralysis over days to weeks (not hours)

Sensation is either mildly or grossly abnormal

55
Q

Rx spinal cord tumor?

A

IV steroids (+ other stuff probably…)

56
Q

What are the 3 general treatment options in Graves hyperthyroidism?

A
  1. Antithyroid drugs
  2. Radioactive iodine
  3. Thyroidectomy
57
Q

When are antithyroid drugs (propylthiouracil, methimazole) indicated in treating Graves hyperthyroidism?

A
  • Mild hyperthyroidism (mild disease, small goiters, low TSH receptor Ab titers)
  • Older age with limited life expectancy
  • Preparation for radioactive iodine or thyroidectomy
  • Pregnancy (PTU in T1)
58
Q

When is radioactive iodine indicated in treating Graves hyperthyroidism?

A
  • Moderate to severe hyperthyroidism with/without mild ophthalmopathy
  • Patient preference in mild hyperthryoidism
59
Q

When is thyroidectomy indicated in treating Graves hyperthyroidism?

A
  • Very large goiter
  • Suspicion of thyroid cancer
  • Coexisting primary hyperparathyroidism
  • Pregnant patients who cannot tolerate thionamides
  • Severe ophthalmopathy
  • Retrosternal goiter with obstructive symptoms
60
Q

In patients who have significant symptoms and thyroid hormone levels 2-3 (or more) times normal, what is the initial and definitive treatment?

A

Initial - ATD with a beta blocker (stabilize pt); pretreatment is also recommended for those at increased risk for complications due to transient worsening of hyperthyroidism following RAI

Definitive - RAI or thyroidectomy

61
Q

___ inhibits thyroid hormone synthesis and release and is used mainly in preparation for thyroidectomy in Graves and for treating thyroid storm.

A

Potassium iodide

62
Q

Asthma and COPD are inflammatory diseases of the respiratory tract characterized by ___ and ___.

A

Cough; dyspnea

63
Q

Why is differentiating between asthma and COPD important?

A

Primary long-term intervention for asthma - inhaled corticosteroids vs. COPD - long-acting anticholinergic inhaler

64
Q

What is the most efficient test to differentiate asthma and COPD?

A

Spirometry before and after administration of a bronchodilator

Asthma - significant reversal (>12% increase in FEV1) in airway obstruction after bronchodilator

COPD - may have partial reversibility; restoration of airflow after administration effectively rules out COPD

65
Q

Compare FVC in asthma vs. COPD vs. late-stage COPD.

A

Asthma and COPD: normal/decreased

Late-stage COPD: decreased/very decreased

66
Q

Compare FEV1 and FEV1/FVC ratio in asthma vs. COPD.

A

Asthma/COPD: both decreased

Late-stage: both very decreased

67
Q

Compare CXR appearance in asthma vs. COPD vs. late-stage COPD.

A

Asthma/COPD: normal

Late-stage COPD: hyperinflation, loss of lung markings

68
Q

Compare DLCO in asthma vs. COPD vs. late-stage COPD.

A

Asthma: Normal/increased
COPD: Normal/decreased
Late-stage COPD: Decreased

69
Q

Nocturnal pulse oximetry is a non-specific test used primarily to screen for ___.

A

OSA

70
Q

Define exudative pleural effusions by Light criteria.

A
  • Pleural fluid protein/serum protein ratio > 0.5
  • Pleural fluid LDH/serum LDH ratio > 0.6
  • Pleural fluid LDH > 2/3 of the upper limit of normal for serum LDH
71
Q

Most parapneumonic effusions are uncomplicated; they are small, sterile, free-flowing, and resolve with antibiotics. However, if bacteria cross into the pleural space, what can happen and how is this determined with lab values?

A

Complicated parapneumonic effusion or empyema may develop; both marked by pleural fluid with a very low pH (<7.2), glucose (<60 mg/dL), WBC > 50,000

72
Q

How are complicated parapnuemonic effusions and empyemas treated?

A

Drainage + anitbiotics

73
Q

Treatment of uncomplicated acute cystitis in non-pregnant women?

A
  1. Nitrofurantoin for 5 days (avoid in suspected pyelonephritis or creatinine clearance <60 mL/min)
  2. TMP-SMX for 3 days (avoid if local resistance rate >20%)
  3. Fosfomycin for 1 day
  4. FQ only if above options not available
  5. Urine culture ONLY if treatment fails
74
Q

Treatment of complicated acute cystitis in non-pregnant women?

A
  1. FQ (5-14 days), extended-spectrum antibiotic (eg, amp/gent) for more severe cases
  2. Obtain sample for urine culture prior to initiating therapy and adjust antibiotic as needed.
75
Q

Treatment of pyelonephritis in non-pregnant women?

A
  1. Outpatient - FQ (eg, ciprofloxacin, levofloxacin)
  2. Inpatient - IV antibiotics (eg, FQ, aminoglycoside +/- ampicillin)
  3. Obtain sample for urine culture prior to initiating therapy and adjust antibiotic as needed
76
Q

Define complicated cystitis.

A

Infection associated with factors that increase the risk of antibiotic resistance or treatment failure (DM, CKD, pregnancy, immunocompromise, urinary tract obstruction, hospital-acquired infection, infection associated with a procedure or indwelling foreign body)

77
Q

Beta-thalassemia is the most common thalassemia in patients of ___ descent. Alpha-thalassemia is more common in patients from ___.

A

Mediterranean; Southeast Asia

78
Q

Pathophysiology - beta-thalassemia major?

A

Impaired production of beta-globins, leading to excess alpha-globins. These chains are unstable and lead to chronic hemolysis and transfusion-dependent anemia

79
Q

Presentation of patients with alpha- or beta-thalassemia minor?

A

Majority are asymptomatic, have varying degrees of anemia, microcytosis, and target cells on peripheral smear, MCV <75, and normal RBC distribution width

80
Q

Compare MCV RDW, and RBCs in iron-deficiency anemia vs. alpha-thalassemia minor vs. beta-thalassemia minor.

A

MCV: decreased in all three
RDW: increased in iron deficiency, normal in thalassemia minors
RBCs: decreased in iron deficiency anemia, normal in thalassemia minors

81
Q

Compare peripheral smear in iron-deficiency anemia vs. alpha-thalassemia minor vs. beta-thalassemia minor.

A

Iron-deficiency: microcytosis, hypochromia

Thalassemia minors: target cells

82
Q

Compare serum iron studies and response to iron supplementation in iron deficiency anemia vs. alpha-thalassemia minor vs. beta-thalassemia minor.

A

Iron-deficiency: decreased iron and ferritin, increased TIBC, iron supplementation increases Hgb

Thalassemia minors: normal/increased iron and ferritin due to RBC turnover; no improvement with iron supplementation

83
Q

Compare hemoglobin electrophoresis in iron deficiency anemia vs. alpha-thalassemia minor vs. beta-thalassemia minor.

A

Iron-deficiency and alpha: normal

Beta: increased Hgb A2

84
Q

Peripheral blood smear in B12 deficiency?

A

Macro-ovalocytes
Megaloblasts
Hypersegmented nuetorphils

85
Q

What is the treatment for iron overload states (transfusion-dependent thalassemia major, sickle cell disease)?

A

Deferoxamine (iron chelator)

86
Q

Treatment of choice for anemia of chronic disease, anemia associated with CKD, and transient bone marrow failure after chemo/BM transplant?

A

EPO

87
Q

Why is folic acid supplementation used in severe forms of hemolytic anemia and beta-thalassemia major?

A

Increased demand for EPO

88
Q

Treatment of choice for autoimmune hemolytic anemia?

A

Prednisone

89
Q

What is used to decrease the frequency and severity of pain crises in patients with sickle cell anemia? MOA?

A

Hydroxyurea; increases hemoglobin F levels

90
Q

Treatment of choice for moderate, symptomatic hereditary spherocytosis?

A

Splenectomy

91
Q

Compare presenting symptoms of an acute MS attack vs. TIA.

A

Neuro deficits related to an acute demyelinating plaque of MS usually last for days to weeks

Transient symptoms lasting for <24 hours in a patient with multiple vascular risk factors are more suggestive of TIA

92
Q

Rx - TIA?

A

Modifying identifiable risk factors
Initiate aspirin
Start statin for hyperlipidemia
Reduce BP

93
Q

When is TPA given?

A

Acute ischemic stroke that causes a significant neurological deficit and presents within 4.5 hours from onset of symptoms

94
Q

What causes warfarin-induced skin necrosis?

A

Warfarin inhibits production of vitamin K-dependent clotting factors II, VII, IX, and X, and natural anticoagulant proteins C and S. Protein C activity decreases to 50% within the first day; levels of procoagulant factors decline more slowly, leading to a transient hypercoagulable state.. The risk is higher in patients with hereditary protein C deficiency.

95
Q

Rx warfarin-induced skin necrosis?

A

Stop warfarin immediately

Give protein C concentrate

96
Q

What causes heparin-induced thrombocytopenia?

A

Autoantibodies to platelet factor 4 (PF4) complexed with heparin

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