Mixed 1 Flashcards

1
Q

PUD refers to ulcerations in the stomach or duodenum that are most commonly caused by ___ or ___.

A

H. pylori infection; NSAIDs

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2
Q

Classic symptoms of a duodenal ulcer?

A

Epigastric pain, nausea, and/or early satiety in association with food
Occur in the absence of a food buffer
Epigastric pain 2-5 hours after meals, on an empty stomach, or at night

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3
Q

Diagnosis of PUD?

A

Upper GI endoscopy

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4
Q

Gastric cancer can cause melena and abdominal pain, but is usually accompanied by ___ and ___.

A

Weight loss and anorexia

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5
Q

Define abnormal uterine bleeding.

A

Deviation from the normal menstrual cycle, which typically occurs every 24-38 days and lasts 7 or fewer days

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6
Q

Although abnormal uterine bleeding can be caused by many problems (pregnancy, anatomic abnormalities, anovulation, coagulpathy, endocrine disorders, infection, etc.), it is also the most common presenting clinical feature of ___.

A

Endometrial hyperplasia and cancer

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7
Q

What are the indications for endometrial biopsy in a patient <45?

A

Abnormal uterine bleeding + one of the following:

  • Unopposed estrogen (obesity, anovulation)
  • Failed medical management
  • Lynch syndrome (hereditary nonpolyposis colorectal cancer)

ALSO:

-Atypical glandular cells on Pap test (anyone 35+)

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8
Q

What are the indications for endometrial biopsy in a patient 45+?

A

AUB or postmenopausal bleeding

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9
Q

True or false - an endometrial stripe of 4 or fewer mm excludes endometrial cancer in pre-menopausal and post-menopausal patients.

A

False - true for postmenopausal patients, cannot reliably do so in premenopausal patients

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10
Q

What is the first-line option for management of AUB in premenopausal patients?

A

Combined estrogen/progestin OCs or cyclinc/continuous progestins

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11
Q

Classic presentation fo Friedreich ataxia?

A

Progressive gait ataxia and dysarthria in adolescents or young adults

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12
Q

Friedreich ataxia is an ___ disorder (genetic) caused by a trinucleotide repeat (___) expansion that results in loss-of-function mutation in the ___ gene.

A

AR; GAA; frataxin

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13
Q

Clinical features of Friedreich ataxia?

A

Neurologic deficits (Cerebellar ataxia, dysarthria, loss of vibration and/or position sense, absent DTRs), HCM, skeletal deformities (eg, scoliosis), DM

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14
Q

Prognosis of patients with Friedreich ataxia?

A

Mean survival age 30-40

Mortality due to cardiac dysfunction (2/2 HCM)

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15
Q

PAD is a coronary artery disease risk equivalent, and the medical therapy for such patients should include what?

A

Aggressive risk factor modification with counseling for smoking cessation, lipid-lowering therapy (statin), low-dose aspirin, evaluation and treatment for HTN and DM

Following this, start a supervised exercise program (minimum of 12 weeks with 30-45 minutes of exercise 3x/week) - all patients with claudication

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16
Q

Percutaneous or surgical revascularization in patients with PAD is generallyer served for what kinds of patients?

A

Persistent symptoms despite initial exercise and/or pharmacologic therapy

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17
Q

What should be considered in patients with PAD who have persistent symptoms despite antiplatelet therapy and adequate supervised exercise programs?

A

Cilostazol (PDE3 inhibitor, vasodilator)

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18
Q

What is the pathophysiology of avascular necrosis?

A

Disruption of circulation of bone through micro-occlusion, abnormal endothelial function, or increased intraosseous pressure

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19
Q

Causes of avascular necrosis?

A
Long-term glucocorticoid use
Alcohol abuse
SLE
Antiphospholipid syndrome
Hemoglobinopathies (eg, sickle cell)
Infections (eg, osteomyelitis, HIV)
Renal transplantation
Decompression sickness
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20
Q

Clinical manifestations of avascular necrosis?

A

Groin pain on weight bearing
Pain on hip abduction and internal rotation
No erythema, swelling, or point tenderness

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21
Q

Lab and radiologic findings in avascular necrosis?

A

Normal WBC, ESR, CRP

XR often normal in the first few months
Crescent sign (advanced stage)
MRI is most sensitive modality

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22
Q

Carcinoembryonic antigen (CEA) is elevated in ___ cancer and in ___ (patient population).

A

Colon; smokers

used to monitor patients after colon resection, not a screening test

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23
Q

List 5 medications that should be avoided in G6PD deficiency (may trigger hemolysis).

A
  1. Diaminodiphenyl sulfone (dapsone)
  2. Isobutyl nitrite
  3. Nitrofurantoin
  4. Primaquine
  5. Rasburicase
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24
Q

In addition to some medications, what are two other common triggers of hemolysis in patients with G6PD deficiency?

A

Any oxidative trigger -> infections (leukocytes release highly oxidative reactive oxygen metabolites), fava beans

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25
Q

G6PD deficiency is ___ (inheritance pattern) and thus primarily affects ___ patients.

A

X-linked; male

Note that female patients who have homozygous mutations or skewed lyonization of heterozygous mutations can also express the disorder

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26
Q

What is the most common malignancy of the lip, with 95% of cases occurring where?

A

Squamous cell carcinoma

Lower lip vermillion

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27
Q

Diagnosis of squamous cell carcinoma is confirmed with biopsy - typical pathologic findings?

A

Invasive cords of squamous cells with keratin pearls

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28
Q

A Tzanck preparation of vesicular fluid can identify the characteristic giant cells of ___.

A

HSV infection

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29
Q

___ is characterized histologically by invasive clusters of spindle cells surrounded by palisaded basal cells.

A

Basal cell carcinoma (BCC)

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30
Q

Like SCC, BCC can form ulcerating lesions and is associated with sun exposure. However, it is much less common than SCC and typically affects what part of the lip?

A

Upper (instead of lower)

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31
Q

___ are characterized by shallow fibrin-coated ulcerations with underlying mononuclear infiltrates.

A

Aphthous ulcers (canker sores)

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32
Q

What are the three serologic phases of acute HBV?

A

Early
Window
Recovery

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33
Q

Compare the serologies of the three phases of acute HBV?

A
Early:
HBsAg +
HBeAg +
IgM anti-HBc +
HBV DNA +++

Window:
IgM anti-HBc +
HBV DNA +

Recovery:
IgG anti-HBc +
Anti-HBs +
Anti-HBe +
HBV DNA likely +
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34
Q

Expected serology in chronic HBV carrier?

A

HBsAg +

IgG anti-HBc +

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35
Q

Expected serology in acute flare of chronic HBV?

A
HBsAg +
HBeAg likely +
IgM anti-HBc +
IgG anti-HBc +
HBV DNA +
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36
Q

Expected serology if vaccinated for HBV?

A

Anti-HBS +

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37
Q

Expected serology of immune due to natural HBV infection?

A

IgG anti HBc +

Anti-HBs +

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38
Q

Positive ___ antigen indicates a higher risk of transmission of hepatitis B.

A

HBe

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39
Q

Healthcare workers exposed to blood from HB patients should receive what? If unvaccinated?

A

Post-exposure prophylaxis (HB Ig) within 24 hours

Both the HB vaccine (first dose within 12 hours, next 2 doses according to standard schedule) and Ig

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40
Q

Hyperactivity of the ___ axis, resulting in increased ___ levels has been associated with depression. Other findings in depressed patients?

A

HPA; cortisol

Decreased hippocampal and frontal lobe volumes
Changes in sleep architecture (REM sleep latency and slow-wave sleep are both decreased)

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41
Q

Enlarged lateral cerebral ventricles are associated with what psychiatric illness?

A

Schizophrenia

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42
Q

___ infusion can provoke panic attacks in susceptible patients and has bene used in research to identify those with panic disorder.

A

Lactate

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43
Q

Risk factors for uterine inversion?

A

Nulliparity
Fetal macrosomia
Placenta accreta
Rapid L&D

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44
Q

Uterine inversion can result from excessive ___ and traction on the umbilical cord before placental separation.

A

Fundal pressure

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45
Q

How does uterine inversion present?

A

Fundus collapses into the endometrial cavity and prolapses through the cervix, result in a smooth, round mass protruding through the cervix or vagina

Uterine fundus no longer palpable transabdominally

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46
Q

___ occurs when the placental villi attach directly to the myometrium, resulting in a placenta that does not spontaneously separate and deliver.

A

Placenta accreta

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47
Q

Uterine atony only occurs after ___.

A

Placental delivery (as it is a failure of the uterus to contract and compress the placental bed blood vessels after placental delivery)

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48
Q

How is uterine inversion managed?

A
  1. Aggressive fluid replacement
  2. Manual replacement of the uterus (if the initial attempt is unsuccessful, uteirne relaxants like nitroglycerine or terbutaline may be administered as an aid; laparotomy if manual replacement fails)
  3. Placental removal and uterotonic drugs (oxytocin, misoprostol) after uterine replacement
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49
Q

Why should the uterus be manually replaced prior to placental removal in the setting of uterine inversion?

A

Delay can make replacement more difficult as the uterus can become edematous and the cervix can contract around the inverted uterus

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50
Q

Following H&P to rule out other causes (oropharyngeal, GI, etc.), what is the appropriate evaluation of mild/moderate hemoptysis?

A
CXR
CBC
Coag studies
Renal function
UA
Rheum work-up (if suspected)

Then CT scan +/- bronchoscopy (depending on imaging and if intervention is needed)

Then treat the cause; persistent bleeding is treated via bronchoscopic interventions, embolization, or resection

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51
Q

Following H&P to rule out other causes (oropharyngeal, GI, etc.), what is the appropriate evaluation of massive hemoptysis (>600 mL/24 hours OR 100 mL/hr)?

A

ABCs
If bleeding stops, proceed to the work-up addressed in the previous card. If it continues, proceed to bronchoscopic interventions. If the source is not found, pulmonary arteriography is next. Last step is urgent thoracotomy and surgical intervention.

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52
Q

What is the greatest danger of massive hemoptysis?

A

Asphyxiation due to the airway flooding with blood (not exsanguination)

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53
Q

How should patients with massive hemoptysis be positioned and why?

A

With the bleeding lung in the dependent (lateral) position to avoid blood collection in the airways of the opposite lung?

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54
Q

The newborn with increased work of breathing and fluid-filled fissures has ___, a condition caused by delayed resorption and clearance of alveolar fluid.

A

TTN (Transient tachypnea of the newborn)

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55
Q

Explain the pathophysiology of TTN.

A

Normally, mature fetal lungs begin to reabsorb liquid in late gestation in response to increased catecholamine signals. This resorption mechanism increases during labor; thus, patients born prematurely or by C-section are at increased risk

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56
Q

Why are breath sounds often clear in TTN?

A

Fluid remains in the interstitial space rather than in the alveoli

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57
Q

Treatment of TTN?

A

Supportive (supplemental O2 as needed)

Resolves spontaneously within a few hours to days as passive fluid resoprtion is completed

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58
Q

___ can be the earliest manifestation of vaso-occlusive disease in sickle cell disease and presents with the acute onset of bilateral hand and foot swelling and tenderness.

A

Dactylitis

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59
Q

DDx of bone pain in sickle cell disease?

A
  1. Vaso-occlusive crisis
  2. Osteomyelitis
  3. Avascular necrosis
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60
Q

Compare the presentations of vaso-occlusive crises, osteomyelitis, and avascular necrosis.

A
Vaso-occlusive: 
Acute severe pain in 1+ sites
\+/- low grade fever
Erythema and warmth
May be preceded by a trigger
Osteomyelitis
Acute or subacute focal pain at 1 site
Prolonged fever
Erythema and warmth
Positive blood culture

Avascular necrosis
Chronic worsening pain
No fever
No warmth/erythema

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61
Q

___ most commonly presents with rash, high fever, and large joint involvement in early childhood.

A

Systemic juvenile idiopathic arthritis

62
Q

___ is a clinical syndrome comprising digital clubbing and bony swelling of the toes and fingers, most commonly caused by pulmonary diseases or malignancy.

A

Hypertrophic osteoarthropathy

63
Q

What is the most common cause of bacterial osteomyelitis in all patients? Patients with SCD are also at increased risk of ___ osteomyelitis.

A

S. aureus

Salmonella

64
Q

How does PJP present?

A

Indolent (HIV) or acute respiratory failure (immunocompromised)

Fever, dry cough, decreased oxygen levels

65
Q

Findings on work-up for PJP?

A

Increased LDH
Diffuse reticular infiltrates on imaging
Induced sputum or BAL (stain)

66
Q

Rx of PJP?

A

TMP-SMX for 21 days

Prednisone if decreased O2 levels

67
Q

What is the most common cause of CKD and ESRD requiring dialysis in North America?

A

Diabetes

68
Q

Diabetic nephropathy typically occurs ___ years after onset of DM1 and 2. What is the mechanism?

A

10-15

Hyperglycemia -> microangiopathy

Advanced glycation end products and other inflammatory mediators damage the glomerulus -> proteinuria, overt glomerular nephropathy, ESRD

69
Q

Histologic changes in the glomerulus in diabetic nephropathy?

A

Mesangial expansion
GBM thickening
Glomerular sclerosis

70
Q

Clinical findings of diabetic glomerulosclerosis?

A

Mild to moderate proteinuria

CKD with elevated creatinine

71
Q

What are the three phases of the natural history of diabetic nephropathy?

A
  1. Hyperfiltration (glomerular hypertrophy, increased GFR)
  2. Incipient DN (mesangial expansion, GBM thickening, arteriolar hyalinosis, moderately increased albuminuria, HTN)
  3. Overt DN (mesangial nodules, tubulointerstitial fibrosis, overt proteinuria, nephrotic syndrome, decreased GFR)
72
Q

What is a neuromuscular disorder caused by autoantibodies against voltage-gated calcium channels in the pre-synaptic motor nerve terminal leading to decreased acetylcholine release and subsequent weakness?

A

Lambert-Eaton myasthenic syndrome

73
Q

~50% of cases of LEMS are associated with an underlying ___.

A

Malignancy, mostly small cell lung cancer

74
Q

Presentation of LEMS?

A

Progressive symmetric proximal limb muscle weakness

DTRs are reduced/absent, although vigorous muscle activity can improve reflexes and muscle strength temporarily

Autonomic dysfunction is also common

75
Q

Dx LEMS?

A

Autoantibodies against voltage-gated calcium channels

Electrophysiological studies

76
Q

Rx and manage LEMS?

A

Evaluate/treat undelrying malignancy

Rx symptoms with guanidine or 3,4-diaminopyridine (increase pre-synaptic ACh levels)

Refractory symptoms may respond to IVIG or oral immunosuppressants

77
Q

Compare the involved sites of MG, LEMS, and dermatomyositis/polymyositis.

A

MG: ACh receptor in postsynaptic membrane
LEMS: presynaptic membrane voltage-gated calcium channels
Dermato/polymyositis: muscle fiber injury

78
Q

Compare the clinical features of MG, LEMS, and dermatomyositis/polymyositis.

A

MG: fluctuating muscle weakness (ocular - ptosis, diplopia, bulbar - dysphagia, dysarthria, facial/neck/limb muscles)

LEMS: proximal muscle weakness, autonomic dysfunction, CN involvement, diminished/absent DTRs

Myositis - symmetrical and more proximal muscle weakness, ILD, esopahgeal dysmotlity, Raynaud phenomenon, polyarthritis, skin findings in dermato

79
Q

How does Guillain-Barre present?

A

Acute ascending muscle weakness with areflexia, often with a preceding viral illness

80
Q

MG is classically associated with ___ rather than small cell lung cancer.

A

Thymoma

81
Q

Populations of women at increased risk for epithelial ovarian cancer?

A

Postmenopausal women

Family hx of ovarian or breast cancer (BRCA, etc.)

82
Q

Common presentations of epithelial ovarian carcinoma (acute, subacute, etc.)

A

Acute: SOB, obstipation/constipation with vomiting, abdominal distention
Subacute: pelvic/abdominal pain, bloating, early satiety
Asymptomatic adnexal mass (firm, non-mobile, nodular)

83
Q

In the setting of clinical suspicion for epithelial ovarian cancer, what are the next steps?

A
  1. Imaging (pelvic U/S) - confirms the presumed clinical diagnosis, may evaluate for mets
  2. CA-125 to correlate with clinical findings and monitor treatment
  3. Exploratory laparotomy with cancer resection and inspection of the entire abdomen for mets is required when there is high clinical suspicion
  4. Chemo with platnium-based agents after surgery
84
Q

Why is image-guided biopsy contraindicated in a patient with malignant features suggesting epithelial ovarian cancer?

A

Biopsy could lead to rupture of the mass and spreading of the cancerous cells through the abdomen

85
Q

___ is a condition in which endometrial glands and stroma accumulate abnormally within the uterine myometrium.

A

Adenomyosis

86
Q

Common presentation of adenomyosis?

A

Multiparous women >40 y/o
New-onset dysmenorrhea
Boggy, tender uterus
Symmetrically enlarged uterus

87
Q

Explain the pathophysiology of adenomyosis.

A

Cyclic shedding of the endometrium within the myometrium -> continued accumulation of endometrial tissue within the myometrium -> increased endometrial cavity surface area (heavy menstrual bleeding) -> chronic pelvic pain

88
Q

Initial work-up and definitive diagnosis of adenomyosis?

A

Pelvic U/S and/or MRI

Histologically after hysterectomy (treatment for patients who do not improve with conservative management)

89
Q

What is a confounder?

A

An extraneous factor which has properties linking it with the exposure and outcome of interest

90
Q

Define Tourette syndorome.

A

Multiple motor and one or more vocal tics that present before age 18

Tics occur many times a day nearly every day or at regular intervals for at least a year

91
Q

Patients with Tourette syndrome have high rates of comorbid conditions that complicate management and affect quality of life. What are the two most prevalent comorbidities?

A

ADHD

OCD (typically develops within 3-6 years after tics first appear)

92
Q

What is the most common cause of vesicovaginal fistula?

A

Obstructed labor in resource-limited areas

93
Q

What is the pathophysiology of vesicovaginal fistula formation?

A

Excessive fetal head compression during obstructed labor causes injury and necrosis to the maternal vagina, rectum, and bladder

Tissue necrosis leads to erosion and fistual development between proximal structures

94
Q

Presentation of vesicovaginal fistula?

A

Continuous watery vaginal discharge, alkaline pH, may be malodorous
Vaginal pooling of urine
Area of raised, red granulation tissue on the anterior vaginal wall

95
Q

Diagnose vesicovaginal fistula?

A

Bladder dye testing

96
Q

Treatment of vesicovaginal fistula?

A

Surgical repair

97
Q

___ is characterized by encephalopathy and acute liver failure after a viral infection.

A

Reye syndrome

98
Q

Most cases of Reye syndrome occur with aspirin use in the setting of what three infections?

A

Influenza B (most common)
Influenza A
Varicella zoster

99
Q

Clinical features of Reye syndrome?

A
Acute liver failure
Encephalopathy
AST/ALT increased
PT-INR/PTT increased
NH3 increased
100
Q

Liver biopsy findings in Reye syndrome?

A

Microvesicular steatosis

101
Q

Aspirin is generally contraindicated in children, except in the treatment of what?

A

Kawasaki disease and rheumatologic diseases

102
Q

First-line treatment for anorexia nervosa?

A

Weight restoration through nutritional rehabilitation and psychotherapy (CBT most effective)

Olanzapine if severe/refractory

Antidepressant medications have not shown efficacy; reserved for those with severe comorbid depression or anxiety that persists despite weight restoration

103
Q

Which antidepressant is contraindicated in eating disorders and why?

A

Bupropion, increased risk of seizures

104
Q

Which antidepressant is effective in bulimia nervosa?

A

Fluoxetine

105
Q

Indications for hospitalization in the setting of anorexia nervosa?

A
BMI <15
Marked vital sign or electrolyte abnormalities
Cardiac failure
Suicidality
Acute food refusal
Lack of response to outpatient treatment
106
Q

Effects of maternal hyperglycemia in the first trimester?

A
Hyperglycemia without the ability to produce insulin, which can lead to disrupted organogenesis
Congenital heart disease
Neural tube defects
Small left colon syndrome
Spontaneous abortion
107
Q

Effects of maternal hyperglycemia in the second and third trimesters?

A

Fetal hyperglycemia and hyperinsulinemia -> polycythemia (via increased metabolic demand, fetal hypoxemia, increased erythropoiesis), organomegaly, neonatal hypoglycemia, and macrosomia, possible shoulder dystocia, and brachial plexopathy/clavicle fracture/asphyxia

108
Q

What is the most common complication among infants of diabetic mothers?

A

Neonatal hypoglycemia

109
Q

What is atlantoaxial instability?

A

Excessive laxity in the posterior transverse ligament increases mobility between C1 and C2 (atlas and axis)

110
Q

Neurologic comorbidities of Down syndrome?

A

Intellectual disability

Ealry-onset Alzheimer disease

111
Q

Cardio comorbidities of Down syndrome?

A

Complete AVSD
VSD
ASD

112
Q

GI comorbidities of Down syndrome?

A

Duodenal atresia

Hirschsprung disease

113
Q

Endocrine comorbidities of Down syndrome?

A

Hypothyroidism
DM1
Obesity

114
Q

Hematologic comorbidities of Down syndrome?

A

Acute leukemia

115
Q

Rheumatologic comorbidities of Down syndrome?

A

Atlantoaxial instability

116
Q

Presentation of atlantoaxial instability?

A

Weakness, gait changes, urinary/fecal incontinence, vertebrobasilar symptoms (dizziness, vertigo, imbalance, diplopia)

UMN findings one xam (spasticity, hyperreflexia, Babinski sign)

Patients with Down syndrome are normally hypotonic; instability may have no effect on low tone or cause hypertonicity

117
Q

Diagnosis of atlantoaxial instability?

A

Lateral X-rays of the cervical spine in flexion, extension, and neutral

Open-mouth x-rays can also be helpful in visualizing the odontoid

118
Q

Rx atlantoaxial instability?

A

C1-C2 surgical fusion

119
Q

3 etiologies of colovesical fistula?

A
  1. Diverticular disease (sigmoid most common)
  2. Crohn disease
  3. Malignancy (colon, bladder, pelvic organs)
120
Q

Presentation of colovesical fistula?

A

Fecaluria (stool in urine)
Pneumaturia (air in urine)
Recurrent UTI (mixed flora)

121
Q

Dx colovesical fistula?

A

Abdominal CT scan with oral or rectal (NOT IV) contrast - will show contrast material in the bladder with thickened colonic and vesicular walls

122
Q

Rx colovesical fistula?

A

Surgery after resolution of infection

Colonoscopy recommended to exclude malignancy

123
Q

___ is the single most important prognostic consideration in the treatment of patients with breast cancer and is based on ___.

A

Tumor burden; TNM staging

124
Q

MRI findings in MS?

A

Multifocal ovoid hyperintense white matter lesions in the CNS, particiularly the periventricular and subpial white matter of the cerebrum and the optic nerves, brainstem, and spinal cord

125
Q

Rx of patients with an acute attack of MS and disabling symptoms?

A

High-dose IV glucocorticoids

Plasma exchange if no response

126
Q

Long term Rx of MS?

A

Immunomodulators (IFN beta, natalizumab, glatiramer, etc.) for suppression

127
Q

Rx elevated intracranial pressure in patients with pseudotumor cerebri?

A

Acetazolamide (CA inhibitor that reduces CSF production)

128
Q

When is an LP indicated in patients with suspected MS? What will it show?

A

When the diagnosis is not clear

Oligoclonal IgG bands

129
Q

Bright red, firm, friable, exophytic nodules in a patient with HIV are most likely ___. What causes this?

A

Bacillary angiomatosis; Bartonella (GN bacillus)

130
Q

Rx bacillary angiomatosis?

A

Oral erythromycin

131
Q

Skin lesions of ___ usually occur on the trunk, face, and extremities. Typically, the lesions are papules that become plaques or nodules. The color changes from light brown to pink to dark violet.

A

Kaposi sarcoma

132
Q

___ may cause nodular and papular cutaneous lesions of the external auditory meatus in immunocompromised patients.

A

Pneumocystis

133
Q

Cause of Whipple’s disease?

A

Bacillus Trophyerma whippelii

134
Q

Presentation of Whipple’s disease?

A

White men, fourth-to-sixth decades of life

Weight loss, GI symptoms (abdominal pain, diarrhea, malabsorption with distension, flatulence, steatorrhea)

Extraintestinal manifestations (migratory polyarthropathy, chronic cough, myocardial or valvular involvement leading to congestive failure or valvular regurgitation)

Later stages: dementia, CNS findings (supranuclear opthalmoplegia, myoclonus)

Intermittent low-grade fever, pigmentation, LA

135
Q

Classic biopsy finding of Whipple’s disease?

A

PAS-positive material in the lamina propria of the small intestine

136
Q

What are the first 2 steps to management of a patient with suspected PE?

A
  1. Stabilize with O2 and IV fluids

2. Evaluate for absolute contraindications to anticoagulation

137
Q

If there are absolute contraindications to anticoagulation, obtain a diagnostic test to evaluate for PE. What should be done if it is positive and negative?

A

Positive - consider IVC filter

Negative - no further evaluation needed

138
Q

If there are no absolute contraindications to anticoagulation, what should be done?

A

Assess clinical suspicion of PE with modified Wells criteria

If unlikely, obtain diagnostic test to evaluate for PE

If likely, consider anticoagulation, especially if the patient has no relative contraindications or if there is moderate to severe distress. Then, proceed to diagnostic testing.

If positive, start or continue anticoagulation. Consider surgery or thrombolytics if needed.

If negative, stop anticoagulation.

139
Q

Clinical features of Huntington disease?

A

Motor: chorea, delayed saccades, motor impersistence (inability to sustain grip)
Psych: depression, irritability, psychosis, obsessive-compulsive symptoms
Cognitive: executive dysfunction

140
Q

Genetic findings of Huntington disease?

A

AD CAG trinucleotide repeat expansion

141
Q

Neuropathology of Huntington disease?

A

Loss of GABA-ergic neurons

142
Q

Imaging findings of Huntington disease?

A

Caudate nucleus and putamen atrophy

143
Q

Prognosis of Huntington disease?

A

10-20 years following initial symptom onset

144
Q

List 5 common running injuries of the foot and ankle.

A
  1. Stress fracture
  2. Plantar fasciitis
  3. Achilles tendinopathy
  4. Morton neuroma
  5. Tarsal tunnel syndrome
145
Q

What is a Morton (interdigital) neuroma?

A

Not a true neuroma but a mechanically induced neuropathic degeneration of the interdigital nerves that causes numbness, aching, and burning in the distal forefoot from the metatarsal heads to the third and fourth toes

146
Q

Dx - Morton neuroma?

A

Clinical

Squeezing the metatarsal joints will cause pain on the plantar surface of the foot along with crepitus between the third and fourth toes (Mulder sign)

147
Q

Rx - Morton neuroma?

A

Metatarsal support with a bar or padded shoe inserts to decrease pressure on the metatarsal heads

Surgery if failure of conservative treatment

148
Q

___ causes focal pain in the plantar area of the rearfoot. It is usually worse with the first steps in the morning, decreases with activity during the day, and often worsens again later in the day with prolonged weight bearing. Point tenderness at the plantar surface of the heel.

A

Plantar fasciitis

149
Q

___ occur due to a sudden increase in exertion with adequate rest. Presentation?

A

Stress fractures

Sharp, localized pain and tenderness over a bony surface

150
Q

Risk factors for stress fractures?

A

Abrupt increase in intensity of training
Poor running mechanic
Female with eating disorder

151
Q

___ is due to compression of the tibial nerve as it passes through the ankle is usually caused by a fracture of the bones around the ankle. Presentation?

A

Tarsal tunnel syndrome

Burning, numbness, and aching of the distal plantar surface of the foot or toes that sometimes radiate up the calf

152
Q

Presentation of tendinopathies?

A

Common in runners

Can involve the anterior tibial, posterior tibial, peroneal, Achilles, or flexor hallucis longus tendons

Localized pain and swelling in the ankle and hindfoot