Q3: Flashcards
Diagnostic /treatment Mallory vs booger have
Mallory
Dx: upper GI endoscopy
Tx: acid suppression , most heal spontaneous
Boerhaave
Dx: esophagography or CT with water soluble contrast
Tx: NPo, abx broad and POI and emergency surgery
Bacterial meningitis in >1 month old
- causes
- symptoms
- management
S. Pneu or N. Mening
- younger babies would have irritable, febrile, bulging/full fontanelas, poor feeding
older kids- increased intracranial pressure signs such as headache , vomiting and AMS - Management
DO blood cultures first
Second - LP If no concerning signs of elevated ICP or if there’s sign of ICP and font are open
Second -closed fontanelles with signs of elevated ICP, or rapid deterioration GIVE EMPIRIC ABX (3rd gen) then do BRAIN CT
Screening for osteoporosis
Dxa starting at 65 BUT if RF for osteoporosis (Weight<127, smoking , parental history of hip fracture, early menopause , increased alcohol do FRAX and if high risk do DXA at earlier age
Cardiovascular , GI and hematologic side effects of androgen abuse
Left ventricular hypertrophy, inc ldl and Dec hdl,
polycythemia (elevated Hematocrit ) erythrocytoctosis maybe hypercoagulabiltiy
Gi/ hepatotoxic so enlarged liver , dyslipidemia
Ehlers vs Marfans
- MOI and Genetics
-Skin
- MSK
-cardiac
-other
Ehlers
- AD/ COL5A1/2 mutation impaired processing of connective tissue
-Skin: hyperextended and transparent, easy brusising bc tissues fragile , poor healing so atrophic cigarette burn scars
MSK- joint hyper mobility, pectins excav, scoliosis, high arched palate
Cardiac- MVP
OTHER- abdominal and inguinal hernias ; uterine prolapse
Marfans
AD/ FBN1 fibrillin 1mutation so CT defects
-Skin: striae
MSK- joint hyper mobility, pectus carinatum/excav, scoliosis, talk with long extremities
Cardiac- MVP, progressive aortic root dilation or other aortic diseases (regurgitation and dissection
OTHER- lens and retinal detachment; spontaneous pneumothorax
52 yo female with vulvar pruiritus for past week plus frequent urination, dysuria and nocturia . Similar symptoms 4 times in past 3 months. Thick white discharge and microscopy reveals pseudohyphae other risk factors for this diagnosis
Which if the following additional testing should be done?
A. FSHIevel
B. Hemoglobin A1c
C. Nucleic acid amplification testing
D. Pap test
E. Vulvar biopsy
Hemoglobin A1c
- vulvovagial candiadias
RF - high estrogen (pregnancy)? Immunosuppressive, DIABETEs
Sxs- itching and dysuria
13440
A 31-year-old woman, gravida 1 para 0, at 8 weeks gestation is brought to the emergency department due to persistent nausea, nonbloody vomiting, epigastric pain, and dizziness. The patient has been unable to toferate any oral intake for tv past day. This pregnancy was conceived through intrauterine insemination with donor sperm. She has a history of esophageal reflux for which she takes an over-the-counter antacid. Temperature is 36.7 C (98 F), blood pressure la/ Im Hig, and pulse is 104/min. Current weight is 55 kg (121.3 b), a decrease of 2 kg (4.4 iD) from her prepregnancy wo Cardiac examination shows tachycardia but a regular rhythm with no murmurs. The thyroid is nonenlarged and has no palpable masses. Abdominal examination shows epigastric tenderness with deep palpation but no rebound, guarding, or palpable masses. Ultrasound confirms an 8-week intrauterine gestation with a normal fetal heartbeat. Wiich of the tollow is the best next step in management of this patient? after what next
A. 24-hour-urine-protein eellection
B. Quantitative-B-AGG-level
C. Serum-F3-and-74 levels
D. Upper endoscopy
E. Urinalysis for ketones
E. Urinalysis for ketones
Hperemesis gravidarum
RF: previous history, multi gestation, mole
-dx: clinically when severe persistent n/v, signs of hypotension (dry MM, orthostatic hypotension, weight loss of >5% prepregnancy weight) but this patient has subtle signs so check ketones in urine. Decreased intake thereforE LOW GLUCOSE which is converted to ketones
Tx: hospitalize especially if there’s KETONURIA
14/40
N-yearold man comes to the office due to vision disturbances. The patient has a history of ankylosing spondylitis and serienced severe pain and redness of the eyes a month ago. Evaluation at that time showed acute anterior uveilie and solone eye drops were prescribed, which the patient sill uses. The eye symptoms resolved within a weak of treatment, er the past several days the patient has had blurry vision and has needed more light to read. He has also exp
The patient has no other medical conditions, and his only other prescribed medication is naproxen
needed. Vital signs are within normal limits. Ocular examination shows nonerythematous conjunctiva, clear comes, and no hypopyon or opäcities of the lenses. Funduscopic examination is normal. The remainder of the physical examination, including neurologic examination, shows no abnormalities. Which of the following is the most appropriate next step in management of this patient?
A Fuorescein eye stain
B. Lumbar-puncture
C. MRIefthe-brain
D. No further- intervention
E Tonometry
Tononetry
- steroid induced open angle glaucoma which raised the IOP because it decreased outflow of aqueous humor
- sxs/ insidious loss of peripheral vision due to atrophy of optic nerve (enlarged optic cup so increased cup to disc ratio )
Maybe central blurriness due to corneal edema
16/40 ~
REVIEW
A 27-year-old woman comes to the office due to a headache over the past 2 weeks. The patient describes the headache as a
“dull ache,” characterizes it as intermittent and associated with nausea and vomiting, and rates the pain as 5 on a scale of O-
10. She is afobrile and has never had a headache like this before. The patient has no visual symptoms. Her only medication
is oral contraceptive
Her menses are regular, and she has never been pregnant. The patient has no family history of
similar conditions. Temperature is 37.1 C (98.8 F), blood pressure is 120/75 mm Hg, pulse Is 80/min, and respirations are 15/min. BMI is 34 kg/mi. Neurologic examination is normal except for papilledema seen on funduscopy: there are no signs of meningeal irritation. MRI and magnetic resonance venography (MRV) of the head are normal. Which of the following complications is likely to develop if this patient is left untreated?
RF, pathophysiology, symptoms diagnostic , treatment
O A. Blindness
O B. Intracranial bleeding
O C. Paralysis
O D. Seizures
O E. Urinary incontinence
BLINDNESS
Idiopathic intrancial hypertension
- impaired CSF Reab in Arac granulation leading to increased ICP
- RF: childbearing age , obese/recent weight gain, meds(vita , retinoids, tetracycline, GH, OCP)
- symptoms : signs of ICP( ha, n/v papilladema), visual changes because optic nerve is compressed with further increased ICP from straining bending over , pulsátiles tinnitus. Retrobulbar pain/neck and back pain
Diag- MRI to rule out hydrocephalus and mass lesions, MR venography to rule out venous thrombosis which can be caused by OBESITY AND OCP, LP: elevated opening pressure, eye exam: papilladema and enlarged blind spots
Tx - weight loss or weight loss surgery , carbonic anhydrase inhibitors(topiramate and acetazolamide
Last resort - shunt or optic nerve sheath fenestratiin if progressive visual problems even with other treatments
patient had nasal packing and subsequently developed rapid-onset shock (fever, hypotension), a diffuse macular rash maybe on palms and soles , and gastrointestinal symptoms (N/V), neurologic (eg, confusion, dizziness, seizure), and hematologic (eg, thrombocytopenia)
Diagnosis
Pathophysiology
Treatment
indicating toxic shock syndrome (TSS).
TSS is most often linked to growth of Staphylococcus aureus in a foreign body (eg, tampons, nasal packing) or skin/wound infection. It is caused by the refease of bacterial exotoxins (eg.
TSS toxin-1) that indiscriminately activate T cells, leading to a massive release of inflammatory cytokines.
Management includes supportive therapy (eg, intravenous fluids), foreign body removal, and broad-spectrum antibiotics.
Pregnant women with SCD are at increased risk of ? + management
PREECLAMPSIA, placental abruption, FGR , preterm delivery
Management: frequent prenatal visits, baseline 24 hour urine collection and protein level, low dose ASA
A 64-year-old woman is brought to the emergéncy department due to sudden-onset double vision for the past few hours. has had no headache, vertigo, or slurring of speech and no focal weakness or numbness. The patient has a history of hypertension, type 2 diabetes mellitus with poor glycemic control, and chronic kidney disease. She smokes cigarettes but does not use alcohol or illicit drugs. Blood pressure is 140/90 mm Hg and pulse is 82/min. Physical examination shows plosis of her right eye. The right eyelid is manually elevated, showing the right eye in a
hdduction
d. Left extraocular movements are normal in all
directions. Bilateral pupils are equal and reactive to light. The remainder of the neurologic examination is normal.
Which of
the following is the most likely cause of this patient’s current condition?
A. Brain demyelination
B. La ar-infaretion
infiltration
D. Myoneural junction diserder
E. Nerve-empression
F. Nerve inflammation
G. Nerve ischemia
NERVE ISCHEMIA
. The most common cause of CN Ill palsy in adults is ischemic neuropathy due to poorly controlled diabetes mellitus.
CN III has 2 major components as follows:
• Inner somatic fibers - innervate the levator muscle of the eyelid and 4 of the extraocular muscles (EOMs) (superior rectus, medial rectus, inferior rectus, inferior oblique)
• Superficial parasympathetic fibers - innervate the sphincter of the iris and the ciliary muscles (controlling pupil constriction).
Because the inner somatic fibers are farther from the blood supply, they are more susceptible to ischemic injury. Therefore patients with ischemic CN III palsy typically have paralysis of the levator muscle (ptosis) and 4 EOMs (*down-and-out-gaze”) with preserved pupillary response.
NERVE INGLAMMATION FROM VASCULITIS OR AI disease
Condylomata accuminata treatment and prevention
Treatment-
• Chemical: podophyllin resin, trichloroacetic acid
Immunologic: imiquimod
Surgical: cryotherapy, laser therapy, excision
Prevention
Vaccination
Barrier contraception
22/40~
REVIE
A 38-year-old woman comes to the office with cough and blood-tinged sputum. She developed malaise, nasal congestion, sore throat, and dry cough 10 days ago. Most of her symptome improved, but the cough persisted and became productive a yellowish aputum. For the past 2 days, she has had several episodes of blood-linged sputum. The patient has no chest pal except the discomfort from coughing. Her appetite Is normal, and she has no weight loss. She feels arious as she has never had blood in the sputum before. She is a nonsmoker, has no other medical problems, and denies international trave Her vaccinations are up to date. The patient’s temperature is 36.7 C (98 F), Staod pressure is 132/80 mm Hg. pulse is 821 and respirations are 18/min. Pulse oximetry is 98% on room air. Her BMI Is 29 kg/m?, and the oropharynx is clear. Scatt bilateral wheezes and crackles that clear with coughing are heard on chest auscultatior. Chest X-ray reveals fields. Which of the following is the most appropriate next step in management of this patient?
A. Bronchoscopy
B. 6F-sean-ofthe chest
C. Pulmonary function tests
D. Sputum acid-fast stain
E. Sputum-eytology
F. Sputum Gram stain and culture
G. Symptomatie treatment only
Supportive **NO ANTIBIOTICS **
Acute bronchitis- caused by recent upper respiratory. Infection now have cough or persistent cough for 5days - 3 weeks without fever or chills, with chest discomfort, with Rhonchi/wheezing , with yellow purulent sputum and/or small amounts of blood in sputum
Following artificial rupture of membranes, this patient developed increasing pain and anxiety with rapid-onset hypotension, tachycardia, and fetal heart rate decelerations. This constellation of findings is concerning for and NBSIM
Send coagulations studies
amniotic fluid embolism syndrome (AFES), a rare but catastrophic obstetric emergency that typically occurs during labor or immediately postpartum.
When amniotic fluid enters maternal circulation, it can initiate a massive anaphylactoid reaction that results in the classic triad of hypoxemia (eg, respiratory failure, pulmonary edema), hypotension, and disseminated intravascular coagulopathy (DIC). This inflammatory reaction generates pulmonary vasoconstrictors (increased respirations and decreased oxygen saturation) and prostaglandins (tense uterus with increasing pain), leading to fetal acidosis (fetal decelerations).
DIC, a hallmark of AFES, occurs when amniotic fluid activates both factor VIl and platelets, triggering the coagulation cascade. Persistent bleeding at line sites (ie, intravenous lines, epidural catheter) is often the earliest clue to a developing coagulopathy, which is confirmed with urgent coagulation studies. This allows for early and aggressive treatment with massive transfusion to reverse the consumptive coagulopathy to prevent devastating hemorrhage.
Additional management focuses on supportive care of the mother to correct the hypoxemia (eg, oxygen, intubation, nechanical ventilation) and hypotension (eg, vasopressors), with prompt delivery of the infant. Despite early recognition, ft romen survive, and those who do have a high incidence of neurologic damage.
