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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Diagnosis of PUD?

A

Upper GI endoscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

Weight loss and anorexia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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+)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

AUB or postmenopausal bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

Combined estrogen/progestin OCs or cyclinc/continuous progestins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Classic presentation fo Friedreich ataxia?

A

Progressive gait ataxia and dysarthria in adolescents or young adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Prognosis of patients with Friedreich ataxia?

A

Mean survival age 30-40

Mortality due to cardiac dysfunction (2/2 HCM)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
G6PD deficiency is ___ (inheritance pattern) and thus primarily affects ___ patients.
X-linked; male Note that female patients who have homozygous mutations or skewed lyonization of heterozygous mutations can also express the disorder
26
What is the most common malignancy of the lip, with 95% of cases occurring where?
Squamous cell carcinoma Lower lip vermillion
27
Diagnosis of squamous cell carcinoma is confirmed with biopsy - typical pathologic findings?
Invasive cords of squamous cells with keratin pearls
28
A Tzanck preparation of vesicular fluid can identify the characteristic giant cells of ___.
HSV infection
29
___ is characterized histologically by invasive clusters of spindle cells surrounded by palisaded basal cells.
Basal cell carcinoma (BCC)
30
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?
Upper (instead of lower)
31
___ are characterized by shallow fibrin-coated ulcerations with underlying mononuclear infiltrates.
Aphthous ulcers (canker sores)
32
What are the three serologic phases of acute HBV?
Early Window Recovery
33
Compare the serologies of the three phases of acute HBV?
``` 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 + ```
34
Expected serology in chronic HBV carrier?
HBsAg + | IgG anti-HBc +
35
Expected serology in acute flare of chronic HBV?
``` HBsAg + HBeAg likely + IgM anti-HBc + IgG anti-HBc + HBV DNA + ```
36
Expected serology if vaccinated for HBV?
Anti-HBS +
37
Expected serology of immune due to natural HBV infection?
IgG anti HBc + | Anti-HBs +
38
Positive ___ antigen indicates a higher risk of transmission of hepatitis B.
HBe
39
Healthcare workers exposed to blood from HB patients should receive what? If unvaccinated?
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
40
Hyperactivity of the ___ axis, resulting in increased ___ levels has been associated with depression. Other findings in depressed patients?
HPA; cortisol Decreased hippocampal and frontal lobe volumes Changes in sleep architecture (REM sleep latency and slow-wave sleep are both decreased)
41
Enlarged lateral cerebral ventricles are associated with what psychiatric illness?
Schizophrenia
42
___ infusion can provoke panic attacks in susceptible patients and has bene used in research to identify those with panic disorder.
Lactate
43
Risk factors for uterine inversion?
Nulliparity Fetal macrosomia Placenta accreta Rapid L&D
44
Uterine inversion can result from excessive ___ and traction on the umbilical cord before placental separation.
Fundal pressure
45
How does uterine inversion present?
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
46
___ occurs when the placental villi attach directly to the myometrium, resulting in a placenta that does not spontaneously separate and deliver.
Placenta accreta
47
Uterine atony only occurs after ___.
Placental delivery (as it is a failure of the uterus to contract and compress the placental bed blood vessels after placental delivery)
48
How is uterine inversion managed?
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
49
Why should the uterus be manually replaced prior to placental removal in the setting of uterine inversion?
Delay can make replacement more difficult as the uterus can become edematous and the cervix can contract around the inverted uterus
50
Following H&P to rule out other causes (oropharyngeal, GI, etc.), what is the appropriate evaluation of mild/moderate hemoptysis?
``` 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
51
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)?
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.
52
What is the greatest danger of massive hemoptysis?
Asphyxiation due to the airway flooding with blood (not exsanguination)
53
How should patients with massive hemoptysis be positioned and why?
With the bleeding lung in the dependent (lateral) position to avoid blood collection in the airways of the opposite lung?
54
The newborn with increased work of breathing and fluid-filled fissures has ___, a condition caused by delayed resorption and clearance of alveolar fluid.
TTN (Transient tachypnea of the newborn)
55
Explain the pathophysiology of TTN.
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
56
Why are breath sounds often clear in TTN?
Fluid remains in the interstitial space rather than in the alveoli
57
Treatment of TTN?
Supportive (supplemental O2 as needed) Resolves spontaneously within a few hours to days as passive fluid resoprtion is completed
58
___ 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.
Dactylitis
59
DDx of bone pain in sickle cell disease?
1. Vaso-occlusive crisis 2. Osteomyelitis 3. Avascular necrosis
60
Compare the presentations of vaso-occlusive crises, osteomyelitis, and avascular necrosis.
``` 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
61
___ most commonly presents with rash, high fever, and large joint involvement in early childhood.
Systemic juvenile idiopathic arthritis
62
___ is a clinical syndrome comprising digital clubbing and bony swelling of the toes and fingers, most commonly caused by pulmonary diseases or malignancy.
Hypertrophic osteoarthropathy
63
What is the most common cause of bacterial osteomyelitis in all patients? Patients with SCD are also at increased risk of ___ osteomyelitis.
S. aureus | Salmonella
64
How does PJP present?
Indolent (HIV) or acute respiratory failure (immunocompromised) Fever, dry cough, decreased oxygen levels
65
Findings on work-up for PJP?
Increased LDH Diffuse reticular infiltrates on imaging Induced sputum or BAL (stain)
66
Rx of PJP?
TMP-SMX for 21 days | Prednisone if decreased O2 levels
67
What is the most common cause of CKD and ESRD requiring dialysis in North America?
Diabetes
68
Diabetic nephropathy typically occurs ___ years after onset of DM1 and 2. What is the mechanism?
10-15 Hyperglycemia -> microangiopathy Advanced glycation end products and other inflammatory mediators damage the glomerulus -> proteinuria, overt glomerular nephropathy, ESRD
69
Histologic changes in the glomerulus in diabetic nephropathy?
Mesangial expansion GBM thickening Glomerular sclerosis
70
Clinical findings of diabetic glomerulosclerosis?
Mild to moderate proteinuria | CKD with elevated creatinine
71
What are the three phases of the natural history of diabetic nephropathy?
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
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?
Lambert-Eaton myasthenic syndrome
73
~50% of cases of LEMS are associated with an underlying ___.
Malignancy, mostly small cell lung cancer
74
Presentation of LEMS?
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
Dx LEMS?
Autoantibodies against voltage-gated calcium channels Electrophysiological studies
76
Rx and manage LEMS?
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
Compare the involved sites of MG, LEMS, and dermatomyositis/polymyositis.
MG: ACh receptor in postsynaptic membrane LEMS: presynaptic membrane voltage-gated calcium channels Dermato/polymyositis: muscle fiber injury
78
Compare the clinical features of MG, LEMS, and dermatomyositis/polymyositis.
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
How does Guillain-Barre present?
Acute ascending muscle weakness with areflexia, often with a preceding viral illness
80
MG is classically associated with ___ rather than small cell lung cancer.
Thymoma
81
Populations of women at increased risk for epithelial ovarian cancer?
Postmenopausal women | Family hx of ovarian or breast cancer (BRCA, etc.)
82
Common presentations of epithelial ovarian carcinoma (acute, subacute, etc.)
Acute: SOB, obstipation/constipation with vomiting, abdominal distention Subacute: pelvic/abdominal pain, bloating, early satiety Asymptomatic adnexal mass (firm, non-mobile, nodular)
83
In the setting of clinical suspicion for epithelial ovarian cancer, what are the next steps?
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
Why is image-guided biopsy contraindicated in a patient with malignant features suggesting epithelial ovarian cancer?
Biopsy could lead to rupture of the mass and spreading of the cancerous cells through the abdomen
85
___ is a condition in which endometrial glands and stroma accumulate abnormally within the uterine myometrium.
Adenomyosis
86
Common presentation of adenomyosis?
Multiparous women >40 y/o New-onset dysmenorrhea Boggy, tender uterus Symmetrically enlarged uterus
87
Explain the pathophysiology of adenomyosis.
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
Initial work-up and definitive diagnosis of adenomyosis?
Pelvic U/S and/or MRI Histologically after hysterectomy (treatment for patients who do not improve with conservative management)
89
What is a confounder?
An extraneous factor which has properties linking it with the exposure and outcome of interest
90
Define Tourette syndorome.
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
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?
ADHD | OCD (typically develops within 3-6 years after tics first appear)
92
What is the most common cause of vesicovaginal fistula?
Obstructed labor in resource-limited areas
93
What is the pathophysiology of vesicovaginal fistula formation?
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
Presentation of vesicovaginal fistula?
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
Diagnose vesicovaginal fistula?
Bladder dye testing
96
Treatment of vesicovaginal fistula?
Surgical repair
97
___ is characterized by encephalopathy and acute liver failure after a viral infection.
Reye syndrome
98
Most cases of Reye syndrome occur with aspirin use in the setting of what three infections?
Influenza B (most common) Influenza A Varicella zoster
99
Clinical features of Reye syndrome?
``` Acute liver failure Encephalopathy AST/ALT increased PT-INR/PTT increased NH3 increased ```
100
Liver biopsy findings in Reye syndrome?
Microvesicular steatosis
101
Aspirin is generally contraindicated in children, except in the treatment of what?
Kawasaki disease and rheumatologic diseases
102
First-line treatment for anorexia nervosa?
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
Which antidepressant is contraindicated in eating disorders and why?
Bupropion, increased risk of seizures
104
Which antidepressant is effective in bulimia nervosa?
Fluoxetine
105
Indications for hospitalization in the setting of anorexia nervosa?
``` BMI <15 Marked vital sign or electrolyte abnormalities Cardiac failure Suicidality Acute food refusal Lack of response to outpatient treatment ```
106
Effects of maternal hyperglycemia in the first trimester?
``` 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
Effects of maternal hyperglycemia in the second and third trimesters?
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
What is the most common complication among infants of diabetic mothers?
Neonatal hypoglycemia
109
What is atlantoaxial instability?
Excessive laxity in the posterior transverse ligament increases mobility between C1 and C2 (atlas and axis)
110
Neurologic comorbidities of Down syndrome?
Intellectual disability | Ealry-onset Alzheimer disease
111
Cardio comorbidities of Down syndrome?
Complete AVSD VSD ASD
112
GI comorbidities of Down syndrome?
Duodenal atresia | Hirschsprung disease
113
Endocrine comorbidities of Down syndrome?
Hypothyroidism DM1 Obesity
114
Hematologic comorbidities of Down syndrome?
Acute leukemia
115
Rheumatologic comorbidities of Down syndrome?
Atlantoaxial instability
116
Presentation of atlantoaxial instability?
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
Diagnosis of atlantoaxial instability?
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
Rx atlantoaxial instability?
C1-C2 surgical fusion
119
3 etiologies of colovesical fistula?
1. Diverticular disease (sigmoid most common) 2. Crohn disease 3. Malignancy (colon, bladder, pelvic organs)
120
Presentation of colovesical fistula?
Fecaluria (stool in urine) Pneumaturia (air in urine) Recurrent UTI (mixed flora)
121
Dx colovesical fistula?
Abdominal CT scan with oral or rectal (NOT IV) contrast - will show contrast material in the bladder with thickened colonic and vesicular walls
122
Rx colovesical fistula?
Surgery after resolution of infection | Colonoscopy recommended to exclude malignancy
123
___ is the single most important prognostic consideration in the treatment of patients with breast cancer and is based on ___.
Tumor burden; TNM staging
124
MRI findings in MS?
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
Rx of patients with an acute attack of MS and disabling symptoms?
High-dose IV glucocorticoids Plasma exchange if no response
126
Long term Rx of MS?
Immunomodulators (IFN beta, natalizumab, glatiramer, etc.) for suppression
127
Rx elevated intracranial pressure in patients with pseudotumor cerebri?
Acetazolamide (CA inhibitor that reduces CSF production)
128
When is an LP indicated in patients with suspected MS? What will it show?
When the diagnosis is not clear Oligoclonal IgG bands
129
Bright red, firm, friable, exophytic nodules in a patient with HIV are most likely ___. What causes this?
Bacillary angiomatosis; Bartonella (GN bacillus)
130
Rx bacillary angiomatosis?
Oral erythromycin
131
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.
Kaposi sarcoma
132
___ may cause nodular and papular cutaneous lesions of the external auditory meatus in immunocompromised patients.
Pneumocystis
133
Cause of Whipple's disease?
Bacillus Trophyerma whippelii
134
Presentation of Whipple's disease?
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
Classic biopsy finding of Whipple's disease?
PAS-positive material in the lamina propria of the small intestine
136
What are the first 2 steps to management of a patient with suspected PE?
1. Stabilize with O2 and IV fluids | 2. Evaluate for absolute contraindications to anticoagulation
137
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?
Positive - consider IVC filter | Negative - no further evaluation needed
138
If there are no absolute contraindications to anticoagulation, what should be done?
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
Clinical features of Huntington disease?
Motor: chorea, delayed saccades, motor impersistence (inability to sustain grip) Psych: depression, irritability, psychosis, obsessive-compulsive symptoms Cognitive: executive dysfunction
140
Genetic findings of Huntington disease?
AD CAG trinucleotide repeat expansion
141
Neuropathology of Huntington disease?
Loss of GABA-ergic neurons
142
Imaging findings of Huntington disease?
Caudate nucleus and putamen atrophy
143
Prognosis of Huntington disease?
10-20 years following initial symptom onset
144
List 5 common running injuries of the foot and ankle.
1. Stress fracture 2. Plantar fasciitis 3. Achilles tendinopathy 4. Morton neuroma 5. Tarsal tunnel syndrome
145
What is a Morton (interdigital) neuroma?
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
Dx - Morton neuroma?
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
Rx - Morton neuroma?
Metatarsal support with a bar or padded shoe inserts to decrease pressure on the metatarsal heads Surgery if failure of conservative treatment
148
___ 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.
Plantar fasciitis
149
___ occur due to a sudden increase in exertion with adequate rest. Presentation?
Stress fractures Sharp, localized pain and tenderness over a bony surface
150
Risk factors for stress fractures?
Abrupt increase in intensity of training Poor running mechanic Female with eating disorder
151
___ 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?
Tarsal tunnel syndrome Burning, numbness, and aching of the distal plantar surface of the foot or toes that sometimes radiate up the calf
152
Presentation of tendinopathies?
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