UWORLD 9 Flashcards
Thyroid nodules management
Biliary Colic
What is it due to?
How does the patient present?
How long does the entire episode usually last for?
Due to hormonal or neural stimuli that contract the gall bladder and force gallstones or sludge into the cystic duct.
The increase pressure within the gallbladder causes pain, which is usually decreased as the gall bladder relaxes and the stone moves back into the cystic duct.
Patient typically develop a constant epigastric or RUQ dullness or discomfort. Pain can radiate to the right shoulder.
The entire episode usually lasts for <6 hours.
Abd. exam is usually benign without peritoneal signs or guarding.
What is initally perferred for diagnosing gallstones?
When is it ideally done?
What if patients have a negative result?
Transabdominal UltraSound is initally preferred for diagnosing gallstones as it is readily available.
Ideally done after an 8-hour fast and can show gallstones (echogenic foci with shadow) or sludge (echogenic foci without shadow)
Patients with negative US and suspected biliary colic usually have a repeat US in a few weeks.
If the repeat is negative, they likely need further testing (ex: endoscopic US) to evaluate for missed gallstones or microlithiasis.
Why is CT less sensitive than ultrasound when it comes to gall bladder disease?
It is frequently done for what purpose?
Gallstones can appear isodense with bile and are difficult to distinguish on CT scan of the abdomen.
As a result CT are less sensitive (~55-80%, in most studies) than Ultrasound (which is ~85% sensitive, > 95% specific).
Abd. CT is frequently done to exclude other causes of abdominal pain (ex: pancreatitis, ischemic colitis)
Pancreatitis versus Biliary colic presentation
Pancreatitis does not usually cause pain that radiates to the shoulder (unlike bilary colic)
Both has midepigastric pain that radiates to the back.
Dyspepsia
How does it present?
Treatment for patients <55?
Treatment for patients >55?
Can present with > or =1 of the following symptoms:
Postprandial fullness, epigastric pain or burning and early satiety.
<55: PPI therapy; can also benefit from H.pylori testing with treatment if positive
>55: Upper GI endoscopy is indicated for patients >55 or those with alarm feature (ex: odynophagia, dysphagia, unintentional weight loss).
Management of gallstones:
Asymptomatic
Typical biliary colic symptoms & Confirmed gallstones
Atypical biliary colic symptoms & Confirmed gallstones
Typical Bililary Colic & NO confirmed gallstones
Asymptomatic: No treatment
Typical biliary colic symptoms & Confirmed gallstones: Acute pain management (ex: NSAIDS) and prophylatic elective cholecystectomy (usually laproscoic) to prevent recurrence.
Poor surgical candidates or refuses surgery - can receive a trial of ursodeoxycholic acid (UDCA)
Atypical biliary colic symptoms & Confirmed gallstones - Patients who respond to UDCA undergo cholecystectomy; nonresponders are evaluated for other causes of abdominal pain.
Typical Bililary Colic & NO confirmed gallstones - Cholecystokinin-stimulated cholescintigraphy. Evaluates gall bladder ejection fraction, which is low in patients with functional gall bladder disease.
Patients with a positive test undergo cholecystectomy; those with a negative test are treated empirically for dyspepsia or IBS.
Lithotripsy uses what?
When is it used?
It is not as effective for?
uses shock waves to fragment and remove difficult bilary and pancreatic duct stones.
However, it is not as effective for gallstones within the gallbladder.
choledocholithiasis
where is the stone located?
Presentation - Uncomplicated vesus Complicated
Common bile duct stone
Can present with typical biliary colic symptoms (ex: RUQ pain, N/V), but have longer duration of pain and elevated serum liver function studies (elevated bilirubin, ALP, GGT, elevated transaminases)
Uncomplicated - Afebrile, symptomatic, have normal CBC and pancreatic enzymes (amylase, lipase)
Complicated
- complete obstruction of the CBD can cause acute cholangitis (ex: fever, hypotension, mental status changes, leukocytosis)
- Obstruction to the pancreatic duct can cause acute biliary pancreatitis with elevated serum amylase and lipase >3 x normal
What is used to diagnose cholelithiasis versus choledocholithiasis?
Transabdominal ultrasound is sensitive and specific for diagnosing cholelithiasis, but has lower sensitivty for diagnosing choledocholithiasis.
Patients with uncomplicated choledocholithasis and CBD stone visualized on abdominal US should have endoscopic retrograde cholangiopancreatography (ERCP) for stone removal followed by elective cholecysteomy.
Ultrasound showing dilated CBD without an apparent CBD stone suggests choledocholithiasis but is not specific. As a result, these patients should also have ERCP to confirm the diagnosis and possibly provide therapy for a confirmed CBD stone before undergoing elective cholecystectomy.
Cholescintigraphy
What does it use?
When is it used?
Uses technetium-labeled heaptic iminodiacetic acid (HIDA) to evaluate for patency of the cystic duct, common bile duct, and ampulla.
Useful for diagnosing suspected cholecystitis in patients with negative or inconclusive ultrasound findings.
Management of acute cholecystitis
How does patients present?
IV antibiotics & supporitve care (ex: IV fluids, pain control) and immediate cholecystectomy.
Presents with gall bladder inflammation, Fever, RUQ pain and leukocytosis.
Thormbotic thrombocytopenia Purpura
Pathophysiology
Presentation
Formation of autoantibodies against ADAMTS13, a plasma metalloprotease responsible for cleaving ultralarge strings of vWF off the vascular endothelial wall.
When levels of ADAMTS13 become severely deficient, uncleaved strings of vWF trap and activate platelets, resulting in diffuse microvascular thrombi.
This causes the following:
- Platelet consumption, leading to severe thrombocytopenia
- Intravascular RBC shearing, leading to signs of MAHA, such as schistocytes and elevated indirect bilirubin, lactate dehydrogenase and aminotransferase.
-Organ ischemia, leading to neurologic and renal dysfunction (classically)
Treatment of Thrombotic thrombocytopenic purpura
Patients who have clinical and laboratory data that supports the diagnosis of TTP require urgent treatment with plasma exchange.
This removes the autoantibody against ADAMTS13 and replenishes the enzyme with ADAMTS13 from donor serum.
Von Willebrand disease versus Thrombotic Thrombocytopenic Purpura
Presentation
Treatment
VDW has easy brusing and petechaie, but microangiopathic hemolytic anemia is uncommon (unlike TTP)
VWD - Desmopressin increases serum concentration of vWF and is often used in VWD to stop minor episodes of bleeding.
TTP- Plasma exchange
DIC versus TTP
patients with DIC usually have signs of thrombocytopenia and MAHA due to coagulation cascade activation.
However DIC is usually associated with prolong coagulation testing.
TTP versus Immune Thrombocytopenia
Antibodies against platelet antigens are responsible for immune thrombocytopenia, which may cause thrombocytopenia, bruising and petechiae.
However, immune thrombocytopenia is not associated with MAHA.
For patients with increased risk due to family history of sporadic colon cancer, what is the screening colonoscopy recommendation?
beginning at age 40 (or 10 years before the age of cancer diagnosis in the relative, whichever comes first) and should be repeated 3-5 year intervals depending on the finiding.
Daily low-dose aspirin is associated with what?
According to the United States Preventive Services Task Force, aspirin can be considered for colon cancer?
small decrease risk in colon cancer, as well as cardiovascular events.
However, it is associated with significant upper GI toxicity.
Aspirin can be considered for prevention of colon cancer in individuals whose 10-year risk of cardiovascular events is > or =10%
When is bariatric surgery appropriate?
patients with BMI > 40 kg/m2 or
with obesity-related comorbidity and BMI > 35 kg/m2
Treatment of DVT or PE
> or = 3 months of an oral factor Xa inhibitor (ex: rivaroxaban) for patients with DVT or PE who do not have cancer.
Factor Xa inhibitors are considered the first-line therapy because they are administered orally (unlike LMWH) and do not require a heparin bridge or laboratory monitoring (unlike warfarin).
Those with underlying malignancy who develop DVT or PE, a LMWH is considered more efficacious than other Factor Xa inhibitors.
Antiplatelet and DVT
Antiplatelet therapy such as aspirin is often used for primary and secondary prevention of cardiovascular disease (ex: coronary artery disease, heart attack, stroke).
Antiplatelet therapy is not commonly used in the treatment of DVT.
Management of patients who develop DVT while on menopausal hormone therapy (MHT)
Should discontinue the MHT and begin an alternative treatment such as SSRI (ex: escitalopram) or SNRI (ex: venlafaxine).
Although the exact mechanism for these medications improve hot flashes is currently unknow, 50-70% of women who receive this therapy have a reduction in symptoms.
Primary Biliary Cirrhosis (PBC)
What is it?
Affects mostly?
Disease onset is usually?
Major pathologic feature is?
Chronic and progressive liver disease, that is autoimmune in nature
90% are women
Disease onset is usually around 30-65 years of age.
Destruction of small-and mid-sized bile ducts.
There is progressive fibrosis, and end-stage liver disease can supervene 5-10 years after diagnosis.
Signs and symptoms of primary billary cirrhosis
How do you diagnose?
Progressive cholestatsis and liver failure evolving over several years.
Other clinical characteristics include hyperlipidemia with xanthomas, bone disease (osteoporeosis and/or osteomalacia), and autoimmune manifestations
Elevated alkaline phosphatase levels and unexplained pruritis
Liver biopsy
What antibodies has high sensivity and specificty for PBC?
Antimitochondrial antibodies (AMA) have high sensitivity (>90%) and 98% specificity for PBC
How does PBC differ from Type I autoimmune hepatitis?
Anti-mitochondrial antibodies are specific for PBC.
Anti-smooth muscle antibodies are mostly associated with type I autoimmune hepatitis.
PBC - elevation of aminotransferases, Elevated ALP
Type I autoimmune hepatitis - elevation of aminotransferases is typical. ALP level is either normal or elevated.
Iron overload
How can it occur?
What does it cause?
How does this differ from PBC?
Can be primary (genetic hemochromatosis) or secondary (due to excess exogenous sources of iron such as repeated transfusions).
Can cause liver disease, skin pigmentation, diabetes mellitus, arthropathy, cardiac involvement and hypogonadism.
More elevated levels of aminotransferase than ALP levels (unlike PBC)
Wilson disease
Have low levels of what?
How does it differ from PBC?
low serum cerulopasmin levels.
Elevatd levels of ALT and AST, along with hepatomegaly, are commonly present in Wilson disease
where as elevated ALP levels are more commonly seen in cholestatic diseaes.
Treatment of PBC?
What is the curative treatment?
Ursodeoxycholic acid
slows progression of PBC, improve overall survival and maybe transplant-free survival.
Curative treatment is liver transplant.
What is a frequent complication of PBC?
Bone disease.
It is important to screen reguarly for osteoporosis and osteomalacia.
Clinical features of impaired gastric emptying related to gastric outlet obstruction or delayed gastric motility.
Nausea, bloating, postprandial fullness and a succession splash
*Succession splash is a splashing sound aucscultated with a stethoscope placed over the LUQ and is suggestive of retained gastric materal.
What is the first step in evaluating impared gatric emptying?
You want to first exclude a mechanical obstruction (intrinsic first)–> if neg. then rule out (exernal) –> then finally motility
Upper Gastrotintestional study can diagnose an intrinstic obstruction and may show signs of external compression as well.
If endoscopy is nondiagnostic, but external malignant compression is still a concern, abdominal imaging with CT or MRI can be performed.
Once mechanical obstruction is ruled out, confirmatory tests for gastric motility disorders, such as scintigraphic gastric emptying study, can be performed.
What are your differentials and diagnostic test for delayed gastric emptying?
Intrinsic obstruction - peptic ulcer stricture, gastric malignancy, foreign body, gastric volvulus
Dx: Endoscopy, Upper GI contrast imaging
Extrinstic obstruction - Usually malignant,
Dx: CT, MRI
Impaired motility - Medication (esp. anticholinergic effect), Autonomic neuropathy (esp. diabetic), nerve injury (esp. post-surgical) and idiopathic.
Dx: Nuclear gastric emtpying study, Gastroduodenal manometry
What is the first step in management of diabetic gastroparesis?
What can then be used if this is ineffective?
Dietary modification - smaller, more frequent meals. Foods that are high in fat or fiber can slow gastric emptying and should be avoided.
Promotility medications can be used if dietary changes are no effective or in those with acute worsening of gastroparetic symtoms - erythromycin and metoclopramide.
What medication is used in the treatment of painful diabetic peripheral neuropathy that can worsen diabetic gastroparesis?
Amitriptyline - TCA
TCAs have significant anti-cholindergic effects and can worsen diabetic gastroparesis.
Receiver-operating characteristic (ROC) curve helps determine what?
What does the area under the curve (AUC) of a ROC curve reflect?
What does a larger AUC mean?
What would an ideal test have for AUC?
best cutoff point to use determine on the optimal desired parameters for sensitivity and specificity.
AUC - reflects better discrimination and diagnostic accuracy.
Larger AUC means better higher diagnostic accuracy.
Ideal: AUC of 1.0 (100% sensitivity and specificity) and a non discriminating test would have an AUC of 0.5 (similar to a coin toss).
Test of choice for diagnosing pneumothorax in the acute setting (ex: trauma bay, ICU)?
What does it allow visualization of?
Bedside ultrasonography
(Can be more rapidly performed than CXR or CT scan)
Allows visualization of the pareital and visceral pleura; inability to detect lung sliding and the 2 layers moving against one another during respiration, is consistent with pneumothroax.
*Sliding of the pleural line indicates the lack of air between the visceral and parietal pleural, and “rules out” an anterior pneumothorax. When pathologic air accumulates in between the parietal and visceral pleura, ultrasound waves are able to image the superficial parietal layer, but cannot visualize the visceral layer. This is because of the small collection of air in the pleural space that causes ultrasound waves to scatter.
When do you highly suspect tension pneumothorax in a patient?
Next step in management?
Chest trauma with hypotension, tracheal deviation
Diagnostic confirmation is not needed and urgent treatment can be given with needle decompression or chest tube placement.
What is the inital test of choice where there is suspicion for pneumothorax in the nonacute setting (low risk of tension physiology)?
Upright PA CXR.
First line agent for treatment for the treatment of childhood
Chest radiograph for Allergic Bronchopulmonary Aspergillosis (ABPA) reveals?
upper lobe opacities, atelectasis due to mucus plugging
signs of bronchiectasis such as bronchial wall thickening
Allergic Bronchopulmonary Aspergillosis (ABPA)
When does it occur?
Inital Evaluation for ABPA should include?
Current diagnostic criteria?
patients with either underlying asthma or CF become sensitized to Aspergillus antigens, resulting in an intense IgE and IgG-mediated immune response.
Skin testing for Aspergillus or analysis of total and specific IgE concentrations.
Diagnosis:
- Elevated Aspergillus-specific IgE & total IgE,
- positive Aspergillus specific IgG,
- eosinophilia
- a positive skin test reactivity for Aspergillus.
Mainstay treatment of Allergic Bronchopulmonary Aspergillosis (ABPA)
What is used to monitor and assess clinical response?
What therapy should also be considered?
Treatment is directed at acutely stopping the underlying inflammation and decreasing fungal burden to reduce the risk of recurrence.
Systemic glucocorticoids are the mainstay therapy and have been shown to improve symptoms during acute exacerbations.
-Speed up the resolution of lung opacities on radiographic imaging, normalize eosinophil levels, and significantly reduce total IgE, which is used to monitor and assess clinical response.
Antifungal therapy with itraconazole or voriconazole should be considered as it has been shown to reduce the Aspergillus load and therefore, the antigenic stimulus for ABPA.
It also been shown to decrease the glucocorticoid requirements.
Acute Hep B infection Management?
Most patients can be managed with supportive care and appropriate patient outpatient follow-up.
Even symptomatic patients are at low risk of fulminant hepatic failure or other significant complications.
Hospitalization is generally recommended for significant fever or hemodynamic instability, impaired hepatic synthetic function (ex: abnormal coagulation markers), or signs of fulminant liver failure (ex: encephalopathy, bilirubin >10 mg/dL).
As patients recover from acute hepatitis B infeciton, there is normally a steady drop in ?
When are they considered chronic HBV infection?
Both aminotransferase and HBV DNA levels.
Aminotransferase levels typically normalize within 2-8 weeks.
Patients who do not clear hepatitis B surface antigen after 6 months are diagnosed with progression to chronic HBV infection.
When do you give Hepatitis B immunoglobulin and Hepatitis B vaccine?
Administered as postexposure prophylaxis to health care workers exposed to contaminated blood or other body fluids.
Must be given as son a possible (ideally within 12-24 hours of exposure) for maximal efficacy.
Approproximate likelihood a patient with acute hepatitis B will develop chronic hepatitis B?
How does this differ from hepatitis C and A?
HEP B:
Patients infected at age 1-5 have 20-50% progression rate.
Adults have < or = 5% progression rate to chronic HBV infection.
HEP C:
Approx. 75-85%
HEP A:
Not known to cause chronic hepatitis
When should levothyroxine be administered on an empty stomach with water at least how long before breakfast to ensure adequate and consistent absorption?
What are common offenders that can affect its absorption?
When should it be seperated from levothyroxine?
at least 30-60 minutes before breakfast
Common offenders include calcium and iron preparation.
Supplements should be seperated from levothyroxine by 3-4 hours.
What can decrease levothyroxine absorption?
- bile acid-binding agents (ex: cholestyramine)
- iron, calcium, aluminum hydroxide
- PPI, sucralfate
Thyroid Nodules management?
Thyroid nodules should be evaluated using TSH level and thyroid ultrasound.
Patients with normal or high TSH and a confirmed nodule >1cm in diameter on ultrasound should undergo fine-needle aspiration with nodule cytology.
Patients with low TSH should have a radionuclide thyroid scan to see if it’s a hot nodule or a cold/indeterminate nodule.
What can increase TPG concentration?
What do you have to do in terms of levothyroxine reuirements?
- pregnancy, estrogen (oral), tamoxifen, raloxifene
- heroin, methadone
They can increase levothyroxine requirments due ot increased blood levels of thryoxine-binding globuin.
Classification of Multiple endocrine neoplasia (MEN)
What can decrease TBG concentration?
- androgens, glucocorticoids
- anabolic steriods
- slow release nicotinc acid
Management of thyroid scan results?
Low TSH levels should be evaluated using thyroid scan, usually with iodine 123.
A hyperfunctioning (hot) nodule (increased isotope uptake in the nodule) with decreased surrounding uptake) is rarely malignant and may be treated as benign hyperthyroidism.
An indterminate or hypofunctioning (“cold”) nodule indicates a higher risk of cancer and requires further evaluation with FNA.
What does all patients with medullary thyroid cancer require?
Serum calcitonin and carcinoembroynic antigen,
neck ultrasound (evaluate regional metastases)
genetic testing for germline RET mutations
and evaluation for coexisting tumors (hyperparathyroidism, pheochromocytomas)
What is usually elevated in Pheochromocytoma?
How do you confirm this?
Plasma-free metanephrines
confirmed with 24-hour urinary fractionated metanephrines, catecholamines and abominal imaging.
Management of breech presentation.
Breech presentaiton occurs when the feet or buttocks are the closest presentating part to the cervix.
Most preterm fetuses are in breech presentation; however, most spontaneously convert to cephalic presentation by term (ex: 37 weeks geestation)
External cephalic version (foward roll) is offered to patients with persistent breech presentation at 37 weeks gestation to rotate the fetus to a cephalic presentation.
What presentation is an absolute contraindication to vaginal delivery?
Footling breech presentation
Inital Management of palpable breast mass in those <30 of age versus >30?
<30 - ultrasound
- If it has benign features, do mammography.
- if atypical features, do core needle biopsy.
>30 - Diagnositic mammogram
*Mammogram has a higher sensitivity and specificity in women over the age of 30.
A mammogram is not as sensitive or specific for inital eval in <30 because breast tissue is usually denser ini those less than 30. An US has better sensitivity and specificity for inital evaluation
A score of less than what point is suggestive of dementia or delirium on the MMSE
Less than 24.
Highest score is 30.
What is the most effective oral emergency contraception?
When may it be taken?
How does it compare to levonorgestrel for emergency contraception?
What is the most effective form of emergency contraception? What is it contraindicated in?
Ulipristal, an antiprogestin, is the most effective oral emergency contraceptive
may be take up to 5 days after unprotected intercourse.
OCP with progesterone doses equivalent to levonorgestrel (second-line treatment) can be used as a form of emergency contraception.
However, OCP are less effective than ulipristal (75% compared to greater than 85%) and have more side effects (ex: nausea, vomiting)
Copper IUD is the most efficous form of emergency contraception, more effective than emergency oral contraceptives, 99% pregnancy prevention, but it is contraindicated in acute cervitiis (ex: friable cervix, multiple polymorphonuclear leukocytes on microscopy)
Postexposure prophylaxis for sexual assault
(infection and medication)
HIV (3-drug regimen (ex: tenofovir-emtricitabline with raltegravir)
Hepatitis B (vaccine & immune globulin)
Chlamydia (Azithromycin)
Gonorrhea (Ceftriaxone
Trichomonas Vaginalis (Metronidazole)
HIV prophylaxis is offered up to 72 hours after the assault.
PEDIATRIC VACCINES
live attenuated?
Inactivated (killed)?
Toxoid (inactivated toxin)?
Subunit/conjugate?
Live attenuated - Rotavirus, MMR, Varicella
*live virus that has been weakened to the point that it is incapable of causing disease
Inactivated (killed) - Polio and Hepatitis A
*Virus that is killed and completely incapable of causing disease
Toxoid (inactivated toxin) - Diphtheria, tetanus
*Toxoids are bacterial toxins that have been inactivated by heat/chemical. When injected, it stimulates production of antitoxins.
Subunit/conjugate - Hep B, Haemophilus Influenzae type B, Pertussis, Pneumococcal, Meningococcal, Influenza (injection)
*connect outer sugar-like coatings found on bacteria to proteins to induce an immune response
Varicella vaccine can be administered safely to a patient who lives with a pregnant women.
Isolation from a pregnant women is unnecessary unless?
The risk of post-vaccination rash is very low. Isolation from a pregnant patient is unncessary unless the vaccinated patient develops a rash.
What vaccine should pregnant women not receive?
what about household members?
Pregnant women should not recieve LIVE vaccines, but their household members should get all routine immunizations on schedule.
Delaying vaccines is not recommended, as vaccines make it less likely that children will contract the disease and expose pregnant women to wild-type infection.
Patients with suspected active TB require?
Patients with abnormal results need what?
What is the gold standard for diagnosing active TB?
Chest imaging to document findings consistent with pulmonary TB (ex: infiltrates, cavitation)
Abnormal imaging should submit 3 sputum specimens for acid-fast bacillus smears and culture (preferably in 8-24 hour intervals, with at least one earl-morning sputum specimen).
Sputum microscopy is the easiest and least invasive procedure for confirming suspected active pulmonary TB.
GOLD standard for diagnosing active TB (98% specific, 81% sensitive)
Bronchoscopy with bronchoalveolar lavage and TB
When is it used?
usually reserved for confirming the diagnosis in patients who
- unable to produce adquate expectorated or induced sputum samples,
- who have a negative sputum studies with high suspicion for active TB or
who have a possible alternate diagnosis.
Latent Tuberculosis infection can be diagnosed by?
Its effects on BCG vaccinated patients?
Positive tuberculin skin test or interferon-gamma release assay (IGRA) in the absence of active TB.
PPD testing can assess previous exposure, but can be negative in 10-25% of patients with active pulmonary TB.
In addition, PPD may be difficult to interpret in Bacillus Calmette-Guerin (BCG) vaccinated patients.
IGRA has no interfernce in BCG vaccinated patients, but also cannot differentiate between latent and active TB.
Neither test would be helpful in patients with suspected active TB.