Mixed 4 Flashcards
What is the cause of primary dysmenorrhea?
Excessive prostaglandin production -> uterine hypercontractility, hypertonicity, ischemia
Risk factors for primary dysmenorrhea?
Age <30 BMI <20 Tobacco use Menarche at age <12 Heavy/long menstrual periods Sexual abuse
Presentation of primary dysmenorrhea?
Pain first 2-3 days of menses (lower abdominal pain, may radiate to back/thighs)
N/V, diarrhea, malaise, dizziness, GI symptoms
Normal pelvic exam
First-line treatment of primary dysmenorrhea?
Non-sexually active patients - NSAIDs (inhibit prostaglandin synthesis)
Sexually active - combined OCs (suppress ovulation)
Routine monitoring for the development of what side effects is recommended in patients taking second-generation antipsychotics. Which 2 are associated with the greatest risk?
Weight gain, hyperglycemia, dyslipidemia
Olanzapine and clazpine
Which labs should be ordered to monitor patients taking second-generation antipsychotics? Schedule?
BMI
Fasting glucose and lipids
Blood pressure
Waist circumference
Baseline, 3 months, annually (earlier and more frequent monitoring is recommended for patients with DM and those who have gained >5% of initial weight)
What maneuvers cause decreased preload?
Valsalva (strain)
Abrupt standing
Nitroglycerin administration
What maneuvers cause increased afterload?
Sustained hand grip
What maneuvers caused increased preload?
Passive leg raise
What maneuvers cause increased afterload and preload?
Squatting
Hypertrophic cardiomyopathy is defined as left ventricular hypertrophy and normal chamber size without a clear etiology. What causes it?
Asymmetrical left ventricular hypertrophy -> left ventricular outflow tract obstruction
Inheritance pattern of HCM?
Autosomal dominant
Physical exam findings of HCM?
Carotid pulse with dual upstroke (due to midsystolic obstruction during cardiac contraction)
Systolic ejection murmur along the left sternal border with a strong apical impulse
Discuss the physiology that causes the changes in murmur intensity in HCM with various physical maneuvers.
Increased preload or afterload -> increased LV cavity size -> decreased outflow obstruction -> decreased murmur
Decreased preload -> decreased cavity size -> increased intensity
Handgrip maneuver decreases murmur intensity in HCM. It also decreases murmur intensity in ___ and increases murmur intensity of ___.
AS; MR
Leg raise/squatting/supine positioning decrease murmur intensity in HCM. It will increase murmurs in what 3 situations?
AR
MR
VSD
Hemoglobin electrophoresis pattern in a normal patient?
A: 95-98%
A2: ~2.5%
F: <1%
S: Absent
Hemoglobin electrophoresis pattern in a patient with beta-thalassemia minor?
A: decreased
A2: increased
F: near normal
S: absent
Hemoglobin electrophoresis pattern in a patient with beta-thalassemia major?
A: absent
A2: increased (++)
F: increased (++)
S: absent
Hemoglobin electrophoresis pattern in a patient with sickle cell trait?
A: decreased (–)
A2: near normal
F: near normal
S: increased
Hemoglobin electrophoresis pattern in a patient with sickle cell disease?
A: absent
A2: near normal
F: increased (++)
S: increased (++)
What is Hgb F?
2 alpha and 2 gamma chains
What is Hgb A2?
2 alpha and 2 delta chains
What is Hgb A?
2 alpha and 2 beta chains
Rx beta-thalassemia major?
Transfusions Chelation therapy (required to avoid damage from additional iron from transfusions)
Why is hydroxyurea used to treat sickle cell disease?
Increases Hgb F by inducing a change in gene expression at the beta globin locus -> reduces the relative concentration of Hgb S and minimizes complications caused by sickling
What is unique about isoniazid-induced hepatic cell injury?
Extrahepatic hypersensitivity manifestations (rash, arthralgias, fever, leukocytosis, eosinophilia) are common in patients with drug-induced liver injury, but are characteristically absent when caused by isoniazid.
What is an idiosyncratic reaction?
Unlike direct toxic effects, which are dose-dependent and have short latent periods, these reactions are NOT dose-dependent and have variable latent periods.
Drug-induced liver disease be broadly categorized according to morphology - what are some examples?
Cholestasis (eg, anabolic steroids) Fatty liver (eg, valproate) Hepatitis (eg, isoniazid) Toxic or fulminant liver (eg, acetaminophen) Granulomatous (eg, allopurinol)
What is the most commonly ingested foreign body?
Coins
First step in evaluation of any foreign body ingestion?
PA and lateral X-Rays
What determines the next step in management of foreign body ingestion after X-rays?
If high-risk features (patient symptomatic, object is a button battery, magnet, or sharp item) -> endoscopic removal
If no high-risk features -> serial X-rays
If a foreign body ingestion is managed with serial X-rays, what determines the next step?
If no transit (24 hours) -> endoscopic removal
If object moving distally -> no intervention
When a radiolucent, low-risk foreign body is suspected but not visualized on x-ray, what should be done next?
CT scan
Intervention of choice for foreign body aspiration?
Rigid bronchoscopy (vs. flexible)
Presentation - theca lutein cysts (multilocular, bilaterally enlarged (10-15cm) ovaries), enlarged uterus, hyperemesis gravidarum?
Complete hydatidiform mole