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The USMLE Step 2 CK BIBLE The Ultimate Step 2 CK Preparation Guide
Jeffrey Anderson, M.D. The USMLE Step 2 CK BIBLE 2nd Edition
The USMLE Step 2 CK BIBLE Copyright © 2010 Jeffrey Anderson, M.D. All rights reserved. No part of this book may be used or reproduced in any manner whatsoever without written permission except in the case of reprint in the context of reviews and personal education.
CONTENTS
Chapter 1………………………. Surgery Chapter 2………………………. Obstetrics Chapter 3………………………. Gynecology Chapter 4………………………. Pediatrics Chapter 5………………………. Biostatistics Chapter 6………………………. Psychiatry Chapter 7………………………. Cardiovascular Chapter 8………………………. Endocrine Chapter 9………………………. Infectious Disease
Chapter 10……………………… Allergies Chapter 11……………………… Pulmonary Chapter 12……………………… Gastroenterology Chapter 13……………………… Nephrology Chapter 14……………………… Hematology Chapter 15……………………… Rheumatology Chapter 16……………………… Neurology Chapter 17……………………… Oncology Chapter 18……………………… Dermatology Chapter 19……………………… Preventative Med
FOREWORD The USMLE Step 2 CK BIBLE is the culmination of over four months of my own intense personal Step 2 CK preparation. This document contains and all of the notes I made, all of the charts, graphs, and images I put together to create the ultimate study guide, and I guarantee it is more than enough to help you pass, and if used properly can help you achieve a top score on the Clinical Knowledge exam. I used five different study guides as well as all of the notes I took from working in the wards to put together this in-depth study guide. This preparation guide contains the most up-to-date as well as the most commonly asked clinical information, which will help you score high on the Step 2 CK exam. When I put this preparation guide together, I did so with my own score in mind, and I made it so that I would have to study from one source, and that’s exactly what you have here. If you study hard and use the CK BIBLE, you will not only pass, you will do very well. Best of luck on the Step 2 CK exam…
Chapter 1 Surgery
TRAUMA Trauma patients are managed using the ABCDE’s in the primary survey after a traumatic incident. A – Airway • • • •
Ensure patient is immobilized and maintain airway with jaw thrust If airway cannot be established, insert 2 large bore needles into the cricothyroid membrane Never perform tracheotomy in the field If patient is unconscious or you cannot establish an airway otherwise, intubate the patient.
B ‐ Breathing • • • •
Look for chest movement Listen for breathing sounds Observe the respiratory rate Look for life‐threatening injuries (tension pneumothorax, flail chest, open pneumothorax)
C ‐ Circulation • • •
Placement of 2 large‐bore IV’s in the upper extremities If patient is in shock, place a central line in the patient Keep blood on stand‐by in case of hemorrhage
D ‐ Disability • • •
Assess the neurological status with the Glasgow coma scale Check all lab tests (blood, ETOH, electrolytes) Loss of consciousness
A loss of consciousness can be assessed with the mnemonic AEIOU TIPS Alcohol, Epilepsy, Insulin, Overdose, Uremia, Trauma, Infection, Psychogenic, Stroke E – Exposure •
Examine the skin (must remove all clothes)
In the secondary survey, perform the following: • • • •
Check the Glasgow coma scale Check all orifices for trauma and/or injuries (bleeding) Perform checks using ultrasound, XRAY, CT Check for compartment syndrome
GLASGOW COMA SCALE STATUS/FINDING Eye Opening Spontaneous 4 To Voice 3 To Stimulation 2 No Response 1 Verbal Response Oriented 5 Confused 4 Incoherent 3 Incomprehensible 2 No Response 1 Motor Response To Command 6 Localizes 5 Withdraws 4 Abnormal Flexion 3 Extension 2 No Response 1 A coma scale below 8 indicates severe neurologic injury
POINTS
SHOCK The type of shock can be diagnosed by checking the cardiac output (CO), the pulmonary capillary wedge pressure (PCWP), and the peripheral vascular resistance (PVR). Differential Diagnosis of Shock CO PCWP PVR
HYPOVOLEMIC ⇓ ⇓ ⇑
CARDIOGENIC ⇓ ⇑ ⇑
SEPTIC ⇑ ⇓ ⇓
How to correct the different types of shock Hypovolemic Shock
Problem Decreased Preload
Cardiogenic Shock Septic Shock
Cardiac Failure Decreased PVR
Initial Treatment 2 Large bore IV’s, replace fluids 02, dopamine and/or NE 02, NE, IV antibiotics
Recognizing Shock In Chest trauma: • • • • •
The most common type of shock resulting from chest trauma is hypovolemic Patient will be pale, cold, and diaphoretic This patient is likely losing large amounts of blood, thus searching for source of bleeding is imperative Pericardial tamponade can be a result of thoracic trauma, look for distended neck veins In suspected pericardial tamponade, look for an enlarged heart on CXR, perform cardiocentesis, look for electrical alternans on EKG
Management of shock: • • •
Control the site of bleeding Give fluids Prepare for an emergency laparotomy
** If a laparotomy isn’t warranted, simply resuscitate with fluids
HEAD TRAUMA Epidural Hematoma • • •
There will be a history of trauma Sudden loss of consciousness followed by a lucid interval, then followed by rapid deterioration Most commonly bleed is from the middle meningeal artery
Diagnosis: •
With a CT, looking for a lens‐shaped hematoma
Management: •
Emergency craniotomy essential because this is a deadly case within a few hours
Subdural Hematoma • •
Is a low‐pressure bleed coming from the bridging veins There is usually a history of head trauma with fluctuating consciousness
Diagnosis: •
CT showing crescent‐shaped bleed
Management: • •
If there is midline displacement and signs of mass‐effect then do an emergency craniotomy If symptoms are less severe, conservative management includes steroids
Diffuse Axonal Injury • • •
This type of injury occurs after an acceleration‐deceleration injury to the head Patient is usually unconscious There is a terrible prognosis associated with this injury
Management: •
Lower ICP and prevent further injury
Basal Skull Fracture •
This presents with ecchymosis around eyes, behind the ears, or with CSF leak from the nose
Diagnosis: •
CT scan of head and neck
Management: • •
CSF rhinorrhea will stop on its own If facial palsy is present, give steroids
BURNS 1st degree and Seconddegree burns: • • •
Epidermis and superficial dermis Skin is painful, red, and blistered Treatment with ointments and/or pain relievers
Third and Fourth degree burns: • • •
Affects all layers + subcutaneous tissues Painless, dry, charred, and cracked skin Burns affecting all layers of the skin require surgical intervention
Treatment: • • • • •
Depending on severity, resuscitate with fluids Removal of eschars Do a CXR to rule out lung injuries Topical antibiotics after eschar removal Burns that cover more than 20% of the body require admission to a burn center
SURGICAL ABDOMEN The following illustrates the differential diagnosis for abdominal pain in the right upper quadrant, right lower quadrant, left upper quadrant, left lower quadrant.
Right Upper Quadrant Conditions Differentiating Hepatitis • • • •
Presents with RUQ pain and/or tenderness Jaundice is most likely present Fever is present Perform an ultrasound to rule out other causes of pain
Cholecystitis • • •
RUQ pain and tenderness (+) Murphy’s sign (inspiratory arrest during palpation) Perform an ultrasound to detect gallstones, a thickened gallbladder wall, or pericholecystic fluid
Choledocholithiasis • • •
RUQ pain that is worsened with the ingestion of fatty foods Jaundice is often present Perform an ultrasound to detect dilatation of the common bile duct
Biliary Cholic • •
Constant epigastric and RUQ pain Perform an ultrasound to detect the presence of gallstones without any other gallbladder‐related findings
Cholangitis • • • • •
A life‐threatening condition Presence of Charcot’s triad: Fever + Jaundice + RUQ pain If there is also hypotension and mental status changes, this qualifies as Reynold’s pentad Perform and ultrasound and a CT to detect biliary duct dilatation due to gallstone obstruction Confirm diagnosis with ERCP
Pneumonia • •
Presence of pleuritic chest pain Perform a CXR, which will show pulmonary infiltrates
FitzHughCurtis Syndrome • • • •
RUQ pain, fever There is going to be a history of salpingitis Caused by ascending Chlamydia or gonorrhea‐related salpingitis Perform an ultrasound which will show a normal gallbladder and biliary tree with fluid around the liver and gallbladder
Right Lower Quadrant Conditions – Differentiating Appendicitis • • • •
Diffuse abdominal pain that localizes to the RLQ at McBurney’s point (2/3 distance from umbilicus to ASIS) Fever and diarrhea often present Abdominal xray or CT to solidify diagnosis Decision to remove is based on clinical presentation
Ectopic Pregnancy • • • •
Presents with constant lower abdominal pain, crampy in nature Vaginal bleeding Tender adnexal mass Labs will show ⇑ hCG
Salpingitis • • • •
Lower abdominal pain Purulent vaginal discharge Cervical motion tenderness Perform an ultrasound to detect the abscess, and a CT to rule out other conditions
Meckel’s Diverticulitis • • • • • •
Follows the 1‐10‐100 rule 1%‐2% prevalence 1‐10cm in length 50‐100 cm proximal to ileocecal valve Presents with GI bleed, small bowel obstruction (SBO) Technetium pertechnetate scan to detect
Yersinia Enterocolitis • • •
Presents similarly to appendicitis (fever, diarrhea, severe RLQ pain) XRAY will be negative Treat with aggressive antibiotic therapy
Ovarian Torsion • • • • •
Patient develops an acute onset of severe, unilateral pain Pain changes with movement Presence of a tender adnexal mass Ultrasound is done first Confirm with a laparoscopy
Pyelonephritis • •
Classically presents with CVA tenderness, high fever, and shaking chills Best initial diagnostic test is a UA and Urine culture
Intussusception • • • • •
Seen most commonly in infants between 5 and 10 months of age Presence of currant jelly stool (mix of blood and mucus) Vomiting, intense crying Infants will often pull legs into the abdomen to relieve some pain Barium enema is used for both diagnosis and treatment
Left Upper Quadrant Conditions – Differentiating Myocardial Infarction • • •
Crushing chest pain that radiates to the jaw, neck, left arm Nausea, diaphoresis is present Diagnosed by EKG, cardiac enzymes (CKMB, trop I)
Peptic Ulcer • • •
Presents as epigastric pain that is relieved by foods and/or antacids Perforations presents with acute and severe epigastric pain, may radiate to shoulders (Phrenic nerve involvement) Diagnose with an upper GI endoscopy
Ruptured Spleen • • •
Usually a history of trauma Presence of Kehr’s sign (LUQ pain that radiates to the left shoulder) Diagnose with an abdominal CT
Left Lower Quadrant Conditions – Differentiating •
Similar to the RLQ conditions are: Ovarian torsion, Ectopic pregnancy, and Salpingitis
Diverticulitis • •
Patient has LLQ pain, fever, and urinary urgency Diagnose with a CT scan, which shows thickening of the large intestine wall
Sigmoid Volvulus • •
Most commonly seen in an older patient Presents with constipation, distended abdomen, and abdominal pain
•
Contrast enema to diagnose, will see the classic “bird’s beak”
Pyelonephritis Classically presents with CVA tenderness, high fever, and shaking chills Differential Diagnoses for Midline Conditions GERD • • •
Epigastric/substernal burning pain Degree of pain changes with different positions (worse when patient is supine) Diagnosis made with either a barium swallow, pH testing, or upper GI endoscopy
Abdominal Aortic Aneurysm • • • •
Asymptomatic usually until it ruptures If rupture occurs, patient experiences abdominal pain + shock There is usually a palpable pulsatile periumbilical mass Ultrasound done first (least invasive), but can visualize with an xray or CT of the abdomen
Pancreatitis • • •
Epigastric pain that radiates to the back Nausea and vomiting are usually present Patient often has a history of alcoholism
Pancreatic Pseudocyst • • •
Is a result of pancreatitis Consider this if patient had pancreatitis that recurred and/or did not resolve Ultrasound will show a pseudocyst
Surgical Conditions of the Esophagus Achalasia •
A condition where the lower esophageal sphincter fails to relax
Signs and Symptoms: • •
Dysphagia to BOTH solid and liquid Regurgitation of food
Diagnosis: • •
Best initial test its the Barium Swallow, which demonstrates narrowing of the distal esophagus Most accurate test is esophageal manometry, which will demonstrate the lack of peristalsis
Treatment: • • •
The best initial therapy is pneumatic dilation If pneumatic dilation is not successful, surgery should be performed If patient does not want surgery, can attempt to relax the LES with injection of botulinum toxin
Esophageal Diverticula (Zenker’s diverticulum) • •
Most common presentation is a patient with dyphagia that is accompanied by terrible breath Pathology is related to the posterior pharyngeal constrictor muscles with dilate, causing the diverticulum
Signs and Symptoms: • •
Dysphagia Halitosis
Diagnosis: •
The best initial test is the barium swallow
Treatment: •
Surgical resection of the diverticula is the best initial treatment option
Cancer of the Esophagus There are Squamous Cell Carcinoma and Adenocarcinoma Common symptoms to both: • • • • •
Dysphagia to solids 1st, then to liquids 2nd Weight loss Heme (+) stool Anemia Hoarseness
Squamous Cell Carcinoma • • •
Is the 2nd MCC of esophageal cancer Related to chronic use of alcohol and tobacco Most commonly seen in the 6th decade of life and later
Adenocarcinoma • •
Occurs in patients who have chronic GERD Chronic GERD leads to Barrett’s esophagus, which then leads to Adenocarcinoma
Diagnosing: •
The best initial diagnostic test is an endoscopy
Treatment: • •
The best initial treatment is surgical resection as long as there is no metastasis Surgery should be followed with 5‐FU
Diffuse Esophageal Spasms • • •
Patient presents with severe chest pain Often times, they don’t fit the criteria for an MI, but should get the cardiac enzymes and do EKG to rule out an MI Often comes after having a cold drink
Diagnosis: •
Manometry is the most accurate diagnostic test
Treatment: •
Calcium channel blockers and nitrates are the treatment option of choice
Mallory Weiss Tear • •
Violent retching and/or vomiting causes sudden bleeding Most cases resolve spontaneously, if they don’t though give epinephrine to constrict the blood vessels and stop the bleeding
Cancer of the Stomach • • •
Most cancers of the stomach are found to be malignant There is a link of stomach cancers to blood group A, which may indicate a genetic predisposition to the condition Linitis plastica is a diffuse cancer that is fatal within months, and is the most deadly form of gastric cancer
Signs and Symptoms for all: • • • •
GI discomfort and/or pain Weight loss Anemia Anorexia
There is an ⇑ risk when there is: • • • •
Low fiber consumption Excess nitrosamines in the diet (due to smoked meats) Excess salt intake in the diet Chronic gastritis
There are some classic findings in metastatic gastric cancer, they include: Virchow’s node: •
Left supraclavicular node is hard
Krukenberg Tumor: • • •
The metastasis of gastric cancer bilaterally to the ovaries Ovaries are palpable in this case They are signet‐ring cells
Sister Mary Joseph sign: • •
Hard nodule at the umbilicus due to metastasis Indicative of a very poor prognosis
Treatments: • •
Surgery + chemotherapy Palliative care is often the only choice if too advanced
Hernias Inguinal Hernias • •
Is the most common type of hernia Men > women
Direct Inguinal Hernia: •
Protrudes directly through Hasselbach’s triangle (inferior epigastric artery, rectus sheath, and inguinal ligament), medial to the inferior epigastric artery
Indirect Inguinal Hernia: •
More common than the direct hernia, passes laterally to the inferior epigastric artery into the spermatic cord
Signs and Symptoms: •
Groin mass (intermittent) that protrudes with valsalva‐type maneuvers
Diagnosis: • •
Must differentiate from a femoral hernia, which will herniated below the inguinal ligament Diagnosis is based on clinical examination
Treatment: •
Surgical repair
Femoral Hernias • • • •
Women > Men Have a greater risk of incarceration due to the way they herniated Diagnose clinically Surgical correction (do not delay due to risk of incarceration and subsequent strangulation)
Visceral Hernias •
This type of hernia causes intestinal obstruction
Signs and Symptoms: • •
Abdominal pain Obstipation (no flatulence)
Diagnosis: • •
XRAY will show air‐fluid levels, no gas in rectum Differentiate from adhesions
Treatment: •
Surgical repair
Surgical Conditions of the Gallbladder Gallstones (Cholelithiasis) Seen mostly in women with the 4 F’s 1. 2. 3. 4.
Female Fat Forty Fertile
•
It isn’t the presence of gallstones that warrants intervention, but the possible complications associated with them Ultrasound is the test of choice for identifying gallstones
•
Treatment: • • •
Asymptomatic gallstones require no intervention Chronic pain may require a cholecystectomy With an increased risk of cancer, such as in the case of a calcified gallbladder wall, cholecystectomy may be warranted
Cholecystitis • •
Is an infection of the gallbladder that is a result of an obstruction Common causes are: E. Coli, Enterobacter, Enterococcus, and Klebsiella
Note the shadow from the impacted stone.
Signs and Symptoms: • •
Acute onset of right upper quadrant pain that is non‐remitting (+) Murphy’s sign – arrest of inspiration upon palpation
Diagnosis: • • •
Ultrasound to detect stones, a thickened wall, or fluid surrounding the GB Confirm with HIDA scan Labs show WBC’s >20,000, ⇑ Bilirubin, ⇑ AST/ALT
Treatment: • • •
Keep patient NPO, give IV fluids, and give antibiotics to cover gram (‐) rods and anaerobes Do not give morphine for pain because it causes a spasm of the sphincter of oddi If improvements are not seen, cholecystectomy may be warranted
Ascending Cholangitis • •
Obstructed bile flow from an obstructed common bile duct leads to an infection Presence of Charcot’s triad: RUQ, fever, jaundice is commonly seen
Diagnosis: • •
Ultrasound to detect dilation An ERCP can be used after the preliminary US diagnosis
Treatment: • • • •
NPO IV fluids Gram (‐) antibiotics ERCP for decompression of the biliary tree and for removal of the stones
Choledocholithiasis •
An obstruction of the common bile duct
Signs and Symptoms: • • •
Jaundice (obstructive) ⇑ Alkaline phosphatase ⇑ Conjugated bilirubin
Diagnosis: •
Ultrasound to detect CBD obstruction
Treatment: •
Cholecystectomy
Cancer of the GB • • • • •
Is a rare cancer that is associated with a history of gallstones Occurs later in life The MC primary tumor of the gallbladder is the adenocarcinoma Associated with Clonorchis sinensis infestation Has a grave prognosis, with most patients dying within 1yr of diagnosis
Signs and Symptoms: •
Sharp, colicky pain
Diagnosis: •
US or CT to detect the tumor
Treatment: • •
Placement of bile duct stents Surgery as a palliative option, but is not curative
Surgical Conditions of the Pancreas Pancreatitis • •
Autodigestion of the pancreas by it’s own enzymes MCC is alcohol and gallstones
Signs and Symptoms: • •
Severe epigastric pain that radiates to the back ⇑ Serum amylase and lipase
Diagnosis: • •
Clinical suspicion + abdominal CT There may be discoloration of the flank (Grey Turner’s sign) and Cullen’s sign (bluish discoloration of the periumbilicus)
Treatment: • •
NPO, IV fluids, and Demerol for pain relief Be aware of the potential for alcohol withdrawal
Complication: •
There is a risk for abscesses, renal failure, duodenal obstruction, and pancreatic pseudocysts
Pancreatic Pseudocyst • •
Is a complication of chronic pancreatitis Results in a fluid collection within the pancreas that is encapsulated by a fibrous capsule
Diagnosis: • •
Ultrasound Abdominal CT
Treatment: • •
Surgical drainage Creation of a fistula draining the cyst into the stomach
Complications: •
Infection followed by rupture can cause peritonitis
Endocrine Pancreas • •
β‐cell hyperplasia causes an insulinoma α‐cell tumor causes hyperglucagonemia
Cancer of the Pancreas • • • •
More common in African Americans/males/smokers May be more common in diabetics 90% are adenocarcinomas 60% arise from the head of the pancreas
Signs and Symptoms: • •
Weight loss Painless jaundice
Diagnosis: • •
⇑ bilirubin, ⇑ alkaline phosphatase, ⇑CA19‐9 CT scan
Treatment: • •
Although usually a terminal diagnosis, can do a resection of the pancreas, or Whipple’s procedure The 5yr survival rate is only 5%
Surgical Conditions of the Small Bowel Small Bowel Obstruction •
SBO can be caused by a number of conditions
Causes: • • • • • •
Peritoneal adhesions Hernias Crohn’s disease Meckel’s Gallstone ileus Abdominal inflammation
Signs and Symptoms: • • • • •
Nausea/vomiting Abdominal pain Abdominal cramps Tenderness/distention Hyperactive and high‐pitched bowel sounds
Diagnosis: • •
Abdominal xray Air‐fluid levels on upright film
Small Bowel Obstruction (Supine View)
Small Bowel Obstruction (Upright View) Treatment: • • • • •
NG tube decompression NPO IV fluids If only partially obstructed may be able to treat without surgery If surgery is required, must remove both obstruction and dead bowel
Neoplasm of the Small Bowel • • • •
Most commonly is a leiomyoma, second MC is a carcinoid tumor (benign types) Most common malignant types are: adenocarcinoma, carcinoid, lymphoma, and sarcoma Biopsy required for diagnosis Treatment involves surgical resection along with LN’s and metastases
Surgical Conditions of the Large Bowel Polyps • •
Are neoplastic, hamartomas, or inflammatory Neoplastic polyps are MC adenomas
Adenomas can be classified as: • • •
Tubular (these have the smallest potential for malignancy) Tubulovillous Villous (these have the highest risk of malignancy)
Signs and Symptoms: •
MC presents with intermittent rectal bleeding
Diagnosis: •
Colonoscopy or sigmoidoscopy
Treatment: •
Polypectomy
Diverticular Disease General Information: • • • • • •
Up to half of the population has diverticula The risk increases after 50yr of age Only 1/10 people are symptomatic when diverticula are present A TRUE diverticula is rare, and includes full bowel wall herniation A FALSE diverticula is most common, and involves only a herniation of the mucosa The MCC is a low‐fiber diet which causes an increased intramural pressure (this is hypothesis)
Diverticulosis •
This is the presence of multiple false diverticula
Signs and Symptoms: • • • •
Most people are asymptomatic, with diverticula found only on colonoscopy or other visual procedures May have recurrent bouts of LLQ abdominal pain Changes in bowel habits is common Rarely, patient may present with lower GI hemorrhage
Diagnosis: • •
Colonoscopy Barium enema can also be used for diagnosis
Treatment: • •
If patient is asymptomatic, the only therapy should be to increase fiber and decrease fat in the diet If patient has GI hemorrhage, circulatory therapy is warranted (IV fluids, maintenance of hemodynamic stability)
Diverticulitis • •
Inflammation of the diverticula due to infection There are many possible complications, such as abscess, extension into other tissues, or peritonitis
Signs and Symptoms: • • • • •
LLQ pain Constipation OR diarrhea Bleeding Fever Anorexia
Diagnosis: • •
CT demonstrating edema of the large intestine DO NOT perform a colonoscopy or barium enema in an acute case, this might aggravate the problem
Complications: • • • •
Perforation Abscesses Fistula formation Obstructions
Treatment: • • •
If there is an abscess, percutaneous drainage is required Most patients are managed well with fluids and antibiotics For perforation or obstruction, surgery is required
Obstruction of the Large Intestine •
Most common site of colon obstruction is the sigmoid colon
Common causes include: • • • •
Adhesions Adenocarcinoma Volvulus Fecal impaction
Signs and Symptoms: • • •
Nausea/vomiting Abdominal pain with cramps Abdominal distention
Diagnosis: •
XRAY – showing a distended proximal colon, air‐fluid levels, and an absence of gas in the rectum
Treatment: •
If there is severe pain, sepsis, free air, or signs of peritonitis there must be an urgent laparotomy
•
Laparotomy if cecal diameter is >12cm
Volvulus • • • •
Twisting and rotation of the large intestine Can cause ischemia, gangrene, perforation The MC site is the sigmoid colon Occurs most commonly in older patients
Signs and Symptoms: • • •
High‐pitched bowel sounds Distention Tympany
Diagnosis: • •
XRAY – “kidney bean” appearance (ie. Dilated loops of bowel with loss of haustra) Barium enema showing a “bird’s beak” appearance – points to the site of rotation of the bowel
Treatment: • •
Sigmoidoscopy or colonoscopy acts as diagnosis and treatment If this doesn’t work, laparotomy is warranted
Cancer of the Colon • • •
Colon cancer is the 2nd MCC of cancer deaths Believed that a low‐fiber, high‐fat diet increases the risk There are many genetic factors that contribute to colon cancer, such as Lynch syndrome and HNPCC
Lynch Syndrome: • •
LS 1 is an autosomal dominant predisposition to colon cancer that is usually right‐sided LS2 is the same as LS 1 with the addition of cancers outside the colon, such as in the endometrium, stomach, pancreas, small bowel, and ovaries
Screening: • • • • •
Screening should start at 40yr in people with no risk factors If a family member has had cancer of the colon, screening should start 10yr prior to when they were diagnosed (assuming this is less than 40yr) Should have yearly stool occult tests Colonoscopy every 10yr And a sigmoidoscopy every 3‐5yrs
Diagnosis: • •
Obtain preoperative CEA (allows you to follow the progression or recession of the disease) Endoscopy + barium enema
Treatment: • •
Surgical resection + LN dissection If disease is metastatic, add 5‐FU to the post‐operative regimen
Followup: • • •
CEA levels every 3 months for 3 years Perform a colonoscopy at 6 and 12 months, then yearly for 5 years If a recurrence is suspected, a CT should be performed
Surgical Conditions of the Rectum and Anus Hemorrhoids • •
Varicosities of the hemorrhoidal plexus Often related to strenuous bowel movements
Signs and Symptoms: • • • • •
Bright red blood per rectum Itching Burning Palpable anal mass Internal hemorrhoids are NOT painful, while external hemorrhoids ARE painful
Treatment: • • • •
Usually self‐limiting Sitz bath Hemorrhoidal cream Stool softeners to relieve pain
Thrombosed Hemorrhoids • •
These are not a true hemorrhoid, but are external hemorrhoidal veins of the anal canal They are a painful bluish elevation that lie beneath the skin
Classifications: • • • •
1° hemorrhoids involve no prolapse 2° hemorrhoids classically prolapse with defecation but return without manual reduction 3° hemorrhoids prolapse with either straining or defecation and require manual reduction 4° hemorrhoids are not capable of being reduced
Treatment: • •
Conservative therapies Sclerotherapy, rubber band ligation, and surgical hemorrhoidectomy
Anal Fissure • •
A crack or tear in the anal canal Usually occurs after the passage of diarrhea or constipation
Signs and Symptoms: •
The most common presentation is the passage of a painful bowel movement that is accompanied by bright red blood
Diagnosis: •
Perform an anoscopy to diagnose
Treatment: • •
Bulking agents and stool softeners are usually all that is needed If fissures persist despite conservative measurements, a lateral internal sphincterotomy may be required
Anal and Rectal Cancer Anal Cancer: •
The most common form is squamous cell carcinoma
Signs and Symptoms: •
Anal bleeding, pain, and mucus upon evacuation
Diagnose: •
Biopsy
Treatment: •
Chemotherapy + Radiation
Rectal Cancer: •
Seen in males > females
Signs and Symptoms: •
Rectal bleeding, altered bowel habits, tenesmus, obstruction
Diagnosis: •
Colonoscopy
Treatment: • •
Surgery that spares the sphincter If metastasis involved, addition of 5‐FU chemotherapy + radiation
NEUROSURGERY Tumors of the Brain • • • •
Often presents as a headache that is severe enough to awaken the patient during the night Increased intracranial pressure causing nausea, vomiting, and Cushing’s triad (Bradycardia, hypertension, and Cheyne‐Stokes respiration) Presence of focal deficits Often presents with a fixed, dilated pupil
Diagnosing a brain lesion: • •
The most accurate diagnosis comes from biopsy With clinical suspicion a CT and/or MRI can often help make the diagnosis
Treatment: • • • •
Excision is the best treatment for all tumors (except prolactinoma and lymphoma) PROLACTINOMA – give bromocriptine to shrink it, then surgery if this doesn’t work LYMPHOMA – radiation is the treatment of choice If there is metastasis of brain tumors, adjunct therapy is radiation
Differentiating between the different types of brain tumors Glioblastoma Multiforme: • •
The most common 1° CNS neoplasm Is large and irregular with a ring‐enhancing appearance
Meningioma: • • •
The 2nd MC 1° CNS neoplasm Grows slowly Benign
Retinoblastoma: • •
Occurs in children and is often bilateral 40% of cases are familial while the rest are sporatic cases
Medulloblastoma: • •
Common in children Found in the cerebellum/4th ventricle
Prolactinoma: • • •
Is the MC pituitary tumor Presents with many endocrine disturbances such as amenorrhea, impotence, galactorrhea, and gynecomastia. The MC presenting symptoms is visual disturbance (bitemporal hemianopsia)
Lymphoma: • • •
MC CNS tumor in AIDS patients An MRI shows a ring‐enhanced lesion Often confused with toxoplasmosis
Schwannoma: • •
A tumor that affects the 8th cranial nerve Presents with tinnitus, loss of hearing, and increased intracranial pressure
Hydrocephalus •
An increase in CSF causes an enlargement of the ventricles
Signs and Symptoms: • • •
⇑ ICP, ⇓ cognition Headache Focal neurological deficits
Diagnosis: • • • •
A CT or MRI can show the dilation of ventricles A lumbar puncture can help determine the type of hydrocephalus If ICP is normal, it is a communicating hydrocephalus (presents with urinary incontinence, dementia, and ataxia) If ICP is ⇑, it may be either communicating or non‐communicating (Pseudotumor cerebri, congenital)
Treatment: • •
If possible, treat the underlying cause If not possible, a shunt should be placed (usually drained into peritoneum)
Surgical Conditions of the Vascular System Aneurysms • • •
Is a dilatation of an artery to greater than two times its normal diameter “True” aneurysms involve all 3 layers of the vessel, and are caused most commonly by atherosclerosis and congenital disorders “False” aneurysms are covered only by the adventitia of the vessel, and are most commonly caused by trauma
Signs and Symptoms: • • • •
Gastric/epigastric discomfort Back pain Commonly in the abdomen (abdominal aorta aneurysms) Also commonly in the peripheral vessels
Complications: • •
A rupture of an abdominal aneurysm is an emergency Presents with abdominal pain, a pulsatile abdominal mass, and severe hypotension
Diagnosis: • • •
Ultrasound can help detect aneurysms CT is the best test to determine size The most accurate test is the aortogram
Treatment: • • •
Control blood pressure Reduce risk factors Surgery recommended if aneurysms are >5cm
Peripheral Vascular Disease (PVD) •
Due to atherosclerosis
Signs and Symptoms: • •
Presents with claudication Patient may have smooth and shiny skin with a loss of hair in the affected area
Diagnosis: • •
Ankle:Brachial Index (ABI) is the best initial test – normal test is ≥ 0.9 The most accurate test is an angiography
Treatment: • • • • •
Lifestyle modifications such as cessation of smoking and incorporation of exercise Control lipids with an LDL 70%, if patient has recurring TIA’s, or if they have suffered from a previous cerebrovascular accident
Surgical Conditions of the Urinary System Testicular Torsion • • • • • •
Usually occurs in a younger patient Acute edema and severe testicular pain Patient usually experiences nausea and vomiting due to the degree of the pain ABSENCE of the cremasteric reflex Presence of scrotal swelling Testicle may have a horizontal lie
Diagnosis: • •
Ultrasound to assess arterial patency Upon elevation of the teste, the pain is not alleviated
Treatment: • •
1st step is to secure the circulation 2nd step is to evaluate the need for excision of the testicle if it is dead
Epididymitis • • • •
Unilateral pain of the testicle Dysuria Painful and swollen epididymus Less common in prepubertal children as opposed to torsion
Diagnosis: •
Swab for Chlamydia and Gonorrhea
Treatment: •
NSAIDs and antibiotics
Prostate Cancer • •
Obstructive symptoms Rock‐hard nodule in the prostate
Diagnosis: •
PSA
• • •
Serum phosphatase Azotemia Transrectal ultrasound
Treatment: •
The only surgical requirement is a radical prostatectomy in very severe cases – risk of incontinence and/or impotence
Orthopedic conditions requiring surgery Knee Injuries Include: • • • •
Anterior cruciate ligament tears Posterior cruciate ligament tears Collateral ligament tears Meniscus tears
Anterior Cruciate Ligament tears: • • • •
Injury history usually reveals a “pop” sound during the trauma The Lachman test (anterior drawer test) is used in the field to make a diagnosis MRI is the test of choice to determine the severity of the injury Treatment is either with conservative measures, or if severe with arthroscopic repair
Tear of the ACL with associated joint effusion Posterior Cruciate Ligament tears: • • •
Injury usually occurs when the knee is flexed “Posterior dresser drawer sign” MRI is the test of choice to determine severity of the injury
•
Treatment is either with conservative measures, or if severe with arthroscopic repair
Tear of the PCL Collateral Ligament tears: • • • • •
The MCL is the most commonly injured ligament Seen with a direct blow to the lateral knee Is commonly injured in conjunction with the injury to the ACL or PCL MRI to determine severity of the injury Knee brace
Tear of the MCL Meniscus tears: • •
Often seen in older patients and is due to degeneration Injury is most commonly seen in the medial meniscus and is much more common in men
• • •
Diagnose with McMurray’s test MRI to determine the severity of the injury Treatment is usually rest alone, if severe can treat with arthroscopic surgery
Medial meniscus tear Shoulder Injuries Rotator Cuff Injury • •
Can range from mild tendonitis to severe tears Involve the Supraspinatus, Infraspinatus, Teres Minor, Subscapularis
Signs and Symptoms: • • •
Pain and tenderness of the deltoid with movement Pain over the anterior aspect of the humeral head Neer’s sign (+) – pain elicited when the arm is forcefully elevated forward
Diagnosis: • •
Clinical suspicion MRI is used for confirmation
Treatment: • •
NSAIDs Steroids injections
•
For severe diseases that are not successfully treated with steroids, arthroscopic surgery is helpful
Dislocation of the Shoulder • •
Is most commonly an anterior dislocation Posterior dislocation seen when patient is electrocuted and/or experiences a status epilepticus seizure
Anterior dislocation of the humerus Signs and Symptoms: • •
Immobility Extreme pain
Treatment: • •
Traction‐countertraction techniques to put the bone back in the socket Immobilization period (2‐6 weeks)
Hip and Thigh Injuries Dislocations • • •
Dislocations require emergency reduction under sedation Risk of injury to sciatic nerve Avascular necrosis is a severe complication
Femoral Neck Fracture • • • • •
Requires significant force for injury Produces severe pain of the hip/groin that is exacerbated with movement Leg is classically “externally” rotated Diagnose with xray Requires surgical reduction and internal fixation
Fracture of the left femoral neck Wrist Injuries Colles’ Fracture: • • • •
This is a fracture to the distal radius Occurs after falling on an outstretched hand Diagnose with H & P and xray Treat with cast immobilization for 2‐4 wk
Colles’ fracture Scaphoid Fracture: • • • • •
Almost always secondary to a fall Most commonly misdiagnosed as a sprained wrist Diagnosis is classically made when there is pain in the anatomic snuff box Manage with a thumb splint for 10 weeks Complication is avascular necrosis
Scaphoid Fracture
Carpal Tunnel Syndrome •
Presents with pain, numbness, tingling of the hands along the distribution of the median nerve
Diagnosis: Pathognomonic sign is “Tinel’s Sign”, where tapping over the palmar aspect of the wrist elicits shooting pains • “Phalen’s test” is also diagnostic Wrist Splints: Treatment: Holds the wrist in a position of • Treat by avoidance of aggravating activity, use ‘slight wrist splints which hold the wrist in slight extension’ extension • Severe cases should first be managed with steroid injection in the carpal tunnel, if no treatment surgery is performed •
The Breast Workup of a Breast Mass Algorithm (AAFP)
Cancer Risks • • • • •
The #1 risk factor for breast cancer is gender (Female >>> Male) In women, age is the #1 factor for breast cancer risk Late menopause increases the risk of breast cancer (after 50yr) If less than 11yr at menarche, the risk of breast cancer is increased If >30yr at first pregnancy, the risk for breast cancer increases
History of Fibroadenoma and/or Fibrocystic disease does not increase the risk of getting breast cancer
Family History and Breast Cancer: • • •
Only 5% of breast cancers are familial With a 1st degree relative being affected, the risk of cancer increases Autosomal dominant conditions with increased risk: BRCA‐1, BRCA‐2, Li‐ Fraumeni syndrome, Cowden’s disease, Peutz‐Jeghers
Tumors of the Breast Mammogram • •
All women >40yr (controversial as to age to start) should have yearly mammograms Not effective in young patients because the breast tissue is too dense
Fibroadenoma • •
The classic presentation is a firm, non‐tender, mobile breast nodule Most commonly seen in teens and younger women
When to perform certain tests pertaining to breast masses: A palpable mass that feels cystic always requires an ultrasound first. A palpable mass that doesn’t feel cystic requires a FNA (after an US or instead of an US). Any FNA that reveals bloody fluid requires cytology.
Diagnosis: • • •
Breast exam FNA Follow‐up clinical breast exam in 6 weeks
Treatment: •
Not required as this condition is not a cancer precursor and often disappears on its own
Always do a mammogram in patients >40yr who present with almost all pathologies of the breast. A biopsy is required when a cyst recurs more than 2 times within 4 weeks, when there is bloody fluid, when there are signs of inflammatory breast disease, and when a mass does not disappear with FNA.
Fibrocystic Disease • •
This presents with multiple/bilateral painful lumps in the breast that vary in pain with the menstrual cycle Is the most commonly seen breast tumor in women between 35‐50yr of age
Diagnosis: •
Fine‐needle aspiration to drain fluid, and it will collapse after the FNA
Treatment: •
OCP’s can help prevent this from occurring
PreInvasive Breast Cancers Include Ductal Carcinoma In Situ and Lobular Carcinoma In Situ Ductal Carcinoma In Situ (DCIS) • • •
It’s presence increases the risk of invasive breast cancers Usually non‐palpable and seen on mammogram as irregularly shaped ductal calcifications Will lead to invasive ductal carcinoma
Diagnosis: •
Histology shows puched‐out areas in ducts and haphazard cells along the papillae
Treatment: • •
Surgical excision ensuring clean margins Post‐operative radiation is recommended to decrease the risk of recurrence (Can give Tamoxifen in addition to radiation or instead of radiation)
Lobular Carcinoma In Situ (LCIS) •
In contrast to DCIS, this is not precancerous, it does however increase the risk of future invasive ductal carcinoma
Diagnosis: • • •
Hard to diagnose with mammogram Cannot be detected clinically The histology shows mucinous cells in the classic “saw‐tooth” pattern
Treatment: •
Tamoxifen alone is used for treatment
Invasive Breast Cancers Treatment for all invasive cancers: 1. If lump is 5cm, the treatment involves systemic therapy Invasive Ductal Carcinoma • • • •
Is the most common form of breast cancer, seen in almost 85% of all cases Is unilateral Metastasizes to the brain, liver, and bone Important prognosis factors are size of the tumor and the lymph node involvement
Paget’s Disease of the Breast • •
Presents with an erythematous and scaly lesion of the nipple that is pruritic. Nipple may be inverted Nipple discharge common
Inflammatory Breast Cancer • • • •
Less common Rapid growth/progression Early metastasis Red, swollen, pitted, and warm breast (peau d’orange)
Lobular Carcinoma • •
Multifocal and within the same breast (usually) 20% of cases present as bilateral multifocal lesions
BRCA1 and BRCA2 Testing for these genes should be performed if there is a history of the following: •
Family history of early‐onset breast cancer
• • •
Family history of male breast cancer Past history of breast and/or ovarian cancer in that patient Ashkenazi Jewish heritage
Chapter 2 Obstetrics
Terminologies Gravidty = total number of pregnancies Parity = number of births with a gestational age >24 weeks Term delivery = delivery after 37 weeks of gestation Premature delivery = delivery of infant between 20 and 37 weeks
The Uncomplicated Pregnancy Diagnosing Pregnancy The presence of amenorrhea and + urinary ß‐hCG suggests pregnancy. Confirm pregnancy with the following: • • • •
Presence of gestational sac [seen with transvaginal US at 4‐5 weeks. ß‐hCG level approx 1500mIU/ml.] Fetal heart motion [seen by US between 5‐6 weeks.] Fetal heart sounds [heard with Doppler US at 8‐10 weeks.] Fetal movement [on examination after 20 weeks.]
Estimating date of confinement (EDC) Use Nagele’s rule = Last Menstrual Period (LMP) + 7 days – 3 months + 1yr. *Calculation accuracy depends on regular 28‐day cycles. DRUG CATEGORIES DURING PREGNANCY Category A B C D
Description Medication has not shown an increase in risk for birth defects in human studies. Animal studies have not demonstrated a risk, and there are no adequate studies in humans, OR animal studies have shown a risk, but the risk has not been seen in humans. Animal studies have shown adverse effects, but no studies are available in humans, OR studies in humans and animals are not available. Medications are associated with birth defects in humans; however,
X
potential benefits in rare cases may outweigh their known risks. Medications are contraindicated in human pregnancy because of known fetal abnormalities that have been demonstrated in both human and animal studies.
COMMON TERATOGENS IN PREGNANCY Drug Lithium Carbamazepine, Valproate Retinoid Acid ACE Inhibitors Oral hypoglycemics Warfarin NSAIDs
Birth Defect Ebstein’s anomaly (singlechambered right side of heart). Neural tube defects. CNS defects, craniofacial defects, cardiovascular defects. Decreased skull ossification, renal tubule dysgenesis, renal failure in neonate. Neonatal hypoglycemia CNS & Skeletal defects Necrotizing enterocolitis, constriction of ductus arteriosis.
At first visit upon discover of pregnancy Perform the following: • •
Complete physical exam with pelvic and Pap smear. Culture for gonorrhea and Chlamydia
Labs include the following: • • • • • • •
CBC Blood type with Rh status UA with culture RPR for syphilis Rubella titer TB skin test Offer HIV test
Additional testing: • •
Genetic testing if history indicates the need If pt not immune to rubella, DO NOT immunize (live virus).
Recommend: • • • •
Folic acid Iron Multi‐vitamin 25‐35 lb weight gain during pregnancy
What to do during each trimester 1st trimester: Should see patient every 4 weeks. Assess: • • • • • •
Weight gain/loss Blood pressure Edema Fundal height Urine for glucose and protein Estimation of gestational age by uterine size
2nd trimester: Continue to see the patient every 4 weeks Assess: • •
• • • •
At 12 weeks use Doppler US to evaluate fetal heart beat (each visit) Offer triple‐marker screen (ß‐hCG, estriol, α‐fetoprotein(AFP)) at 15‐18 weeks, [AFP decreased in Down’s syndrome], [AFP increased in multiple gestation, neural tube defects, and duodenal atresia]. Document quickening (fetal movement) at 17‐19 weeks and beyond. Amniocentesis if mother is >35yr or if history indicates (hx of miscarriages, previous child with deficits, abnormal triple‐marker screen). Glucose screening at 24wk Repeat hematocrit at 25‐28wk * The most common cause of inaccurate lab results is dating error.
⇑ MS‐AFP: Neural tube defect (NTD), ventral wall defect, twin pregnancy, placental bleeding, renal disease, sacrococcygeal teratoma. ⇓ MS‐AFP: Trisomy 21, Trisomy 18
SECOND TRIMESTER ROUTINE TESTS Screening Diabetes Anemia Atypical antibodies
GBS screening
Test
Diagnostic Significance 1hr 50g OGTT Abn if (2428 wks) >140mg/dL CBC measured Hb 125mg/dL at beginning of test = DM Abnormal plasma glucose is >140mg/dL at 1hr, >155mg/dL at 2hr, and >180mg/dL at 3hr. If 1 post glucose load measurement is abnormal, impaired glucose tolerance is the diagnosis. If 2 or more post glucose load measurements are abnormal, gestational diabetes is the diagnosis.
The following antiemetics are safe to use during pregnancy: • • • • •
Doxylamine Metoclopramide Ondansetron Promethazine Pyridoxine
The Complicated Pregnancy Bleeding after 20 weeks (late pregnancy) Most common causes of late pregnancy vaginal bleeding are: 1. 2. 3. 4.
Abruptio placenta Placenta previa Vasa previa Uterine rupture
* Never perform a digital or speculum exam in any patient with late vaginal bleeding until a vaginal ultrasound has ruled out placenta previa ABRUPTIO PLACENTA • • •
Sudden onset of severely painful vaginal bleeding in patient with history of hypertension or trauma. Bleeding may be concealed, in which case there will be severe, constant pain without the presence of blood. DIC is a feared complication
Management: • •
Emergent C‐section if patient or fetus is deteriorating Admit and observe if bleeding has stopped, vitals and HR are stable, or fetus is 140/90 or ⇑ systolic BP >30 mmHg or diastolic BP >15 mmHg compared to previous BP). • New onset proteinuria and/or edema. • Commonly around week 20 • SBP >160 mmHg or DBP >110 mmHg. • Significant proteinuria (>1g/24hr urine collection or >1+ on dip) • CNS disturbances such as headache or visual disturbance • Pulmonary edema • RUQ pain • CONVULSIONS • 25% occur before labor, 50% during labor, 25% in first 72hr post‐partum
Primiparas – are at greatest risk for eclampsia. Chronic hypertension with superimposed preeclampsia – is diagnosed when there is chronic hypertension with increasingly severe hypertension, proteinuria, and/or warning signs. Eclampsia – is the diagnosis when there is unexplained grand mal seizures in a hypertensive and/or proteinuric in a woman in the last half of pregnancy. Seizures are due to severe diffuse cerebral vasospasm, which cause cerebral perfusion deficits and edema HELLP syndrome – is diagnosis when there is Hemolysis, Elevated Liver enzymes, and Low Platelets. Treatment: • •
BP goal is 140‐150 mmHg (systole) and 90‐100 mmHg (diastole). Don’t treat unless BP is >160/100 mmHg
Maintenance Therapy: • •
First line therapy – Methyldopa Second line therapy ‐ β‐blockers such as labetalol
* β‐blocker use in pregnancy can cause IUGR Acute elevation in BP: •
IV hydralazine or labetolol
Seizure management: • • •
Airway protection first IV Magnesium Sulfate bolus for seizure and infusion for continued prophylaxis Induce labor is fetus is ≥36 weeks with mild preeclampsia and attempt vaginal delivery with IV oxytocin if both mother and fetus are stable
HELLP Syndrome • • •
Occurs in up to 10% of preeclampsia patients Occurs in third trimester, may occur 2 days after delivery Risk factors include: whites, multigravids, older maternal age
Management: • •
• • •
Immediate delivery at any gestational age IV corticosteroids if platelets are 100,000/mm^3 and liver functions normalize Give platelet transfusion if platelets drop below 20,000/mm^3 or platelet count less than 50,000/mm^3 if C‐section will be performed IV Magnesium Sulfate for seizure prophylaxis Steroids for fetal lung maturity.
Complications of HELLP: • • •
DIC Placental abruption Fetal death
• •
Hepatic rupture Ascites
Normal physiologic changes in pregnancy There are many normal physiological changes that occur in pregnancy, these include the following. Hematological – pregnancy creates a state of hypercoagulability • •
⇑ clotting factor levels Venous stasis caused by uterine pressure on lower‐extremity veins
Anemia of Pregnancy: • • • •
Between weeks 6‐30, plasma volume increases approximately 50% Red cell mass increases to a smaller degree, anemia due to 15% dilution Slight leukocytosis Platelets decrease slightly but still remain wnl.
Cardiac – • • • •
CO ⇑ 50% (both HR and SV increase) ⇑ flow causes ⇑ S2 split with inspiration, distended neck veins, systolic ejection murmur, and S3 gallop are normal findings. ⇓ PVR due to progesterone‐mediated smooth muscle relaxation BP ⇓ during first 6 months, then return to normal
Pulmonary – • • • •
Mucosal hyperemia causes nasal stuffiness and nasal hypersecretion Diaphragm elevates due to uterus expansion Tidal volume and minute ventilation ⇑ 30‐40% Functional residual capacity and residual volume ⇓ 20%
• •
Hyperventilation that allows for a pressure gradient so maternal 02 can transfer to fetus Respiratory rate, vital capacity, inspiratory reserve all remain unchanged.
GI – • • • •
⇓ GI motility ⇓ esophageal sphincter tone (leads to GERD) ⇑ alkaline phosphatase Hemorrhoids caused by constipation and ⇑ venous pressure due to enlarging uterus compression on IVC
Renal – • • •
⇓ bladder tone due to progesterone predisposes to urinary stasis and UTI’s/pyelonephritis GFR ⇑ by 50%, thus glucose excretion without increased protein loss Serum creatinine and BUN decrease
Endocrine – • • • • •
⇓ fasting glucose in mother due to fetal utilization ⇑ postprandial glucose in mother due to ⇑ insulin resistance At 9‐11 weeks the fetus produces its own insulin ⇑ maternal thyroid‐binding globulin (TBG) due to ⇑ estrogen, ⇑ total T3 and T4 due to ⇑ TBG. ⇑ cortisol and cortisol‐binding globulin
Skin – • • •
Increased estrogen causes skin changes similar to those in liver disease Spider angiomas, palmar erythema Hyperpigmentation due to ⇑ estrogen and melanocyte‐stimulating hormone
Medical Complications in Pregnancy Cardiac Abnormalities • • •
Heart disorders account for up to 10% of maternal obstetric deaths Women with very high‐risk disorders should be advised against pregnancy due to increased risk of death Cardiovascular physiological changes may unmask and worsen underlying conditions, seen maximally between 28‐34 weeks gestation.
Peripartum Cardiomyopathy • • •
From the 8th month until 5 months post‐partum, heart failure without identifiable cause is possible Risk factors include multiparity, age over 30, history of multiple gestations, and preeclampsia 5‐yr mortality rate is 50%
Managing specific cardiac conditions Heart Failure: • • •
Loop diuretics, nitrates, and β ‐ blockers Digoxin may improve symptoms but does not improve outcome. Never use ACEI’s in pregnancy
Arrhythmias: • •
Rate control as with non‐pregnant patients Never give warfarin or amiodarone
Endocarditis Prophylaxis: • •
Same as in non‐pregnant patient Daily prophylaxis in patient with rheumatic heart disease
Valvular Disease: • • •
Regurgitant lesions do not require therapy Stenotic lesions have increased risk of maternal and fetal mortality Mitral stenosis has increased risk of pulmonary edema and Afib.
Hypercoagulable States Pulmonary Embolus: •
The leading cause of maternal death in US
When to anticoagulate: • • • •
Anticoagulate when DVT or PE in pregnancy Anticoagulate when Atrial Fibrillation is present with underlying heart disease When patient has antiphospholipid syndrome When ejection fraction is 8.5 in the first Monthly biophysical profiles trimester is strongly HbA1c each trimester associated with congenital Triple marker screen at 16‐18 weeks malformations, especially assessing NTD’s. neural tube defects! At 32 weeks start weekly non‐stress tests and amniotic fluid index If gestational DM, do a 2hr 75g OGTT at 6‐12 weeks postpartum to see if diabetes has resolved
Labor in the diabetic patients: • • • • • •
Due to delayed fetal maturity, aim to deliver the baby at 40 weeks If there is poor glycemic control, induce labor at 39‐40 weeks if 2.5 and there is presence of phosphatidyl glycerol this ensures lung maturity If baby is >4,500g, schedule a C‐section Ensure maternal glucose is between 80‐100mg/dL, this can be ensured with D5 (5% dextrose) Insulin resistance decreases rapidly after delivery, so keep an eye on insulin administration and maintain blood‐glucose levels with a sliding scale
Common neonatal problems in diabetic pregnancy: • • • • •
Hypoglycemia Hypocalcemia Polycythemia Hyperbilirubinemia Respiratory distress syndrome
Liver Disease Intrahepatic Cholestasis of Pregnancy: •
A genetic condition most commonly seen in European women
Si/Sx Intractable nighttime pruritis of palms and soles of feet Diagnosis up to 100x increase in serum bile acids Treatment Ursodeoxycholic acid in treatment of choice. Antihistamines also helpful Acute Fatty Liver of Pregnancy: • •
A rare condition caused by disordered metabolism of fatty acids by the fetal mitochondria. Causes HTN, proteinuria, and edema that can mimic preeclampsia.
Diagnosis: • • • • •
⇑ liver enzymes (ALT, AST, GGT) Hyperbilirubinemia DIC Hypoglycemia Increased serum ammonia
Treatment: •
Emergency situation requires ICU admission and aggressive IV fluids + immediate delivery
Urinary Tract Infections, Bacteriuria, and Pyelonephritis Infection Type Symptoms
Treatment
Possible Complications
Asymptomatic Bacteriuria (+) urine culture NO burning NO frequency NO fever NO urgency Outpatient Nitrofurantoin is the DOC
Acute Cystitis
Pyelonephritis
(+) urine culture BURNING FREQUENCY URGENCY NO fever
Acute pyelonephritis if untreated in approximately 30%
Acute pyelonephritis if untreated in approximately 30%
(+) urine culture BURNING FREQUENCY URGENCY FEVER + CVA TENDERNESS Admission, give: IV hydration IV cephalosporin’s Give tocolytics Preterm labor and delivery. Severe cases may progress to sepsis, anemia, and pulmonary dysfunction
Outpatient Nitrofurantoin is the DOC
Ectopic Pregnancy/Tubal Pregnancy The earlier the age of gestation the less there is a risk of complications. 1st trimester: • • • •
D&C is the most common 1st trimester procedure. Give prophylactic antibiotics Perform under twilight anesthesia + paravertebral block Can perform medical abortion as an alternative to D&C with use of oral mifepristone (progesterone antagonist), and oral misoprostol (prostaglandin E1). * Must be performed within 63 of onset of amenorrhea.
Complications: • •
Endometritis (rarely) Retained products of conception (POCs)
2nd trimester: • •
D&C is the most common 2nd trimester procedure. For more advanced pregnancies, an “intact D&C” can be used.
Complications: • •
Retained placenta is the most common immediate complication Cervical trauma/cervical insufficiency is the most common delayed complication
Abortion • • • •
Termination of pregnancy usually ≤ 20 weeks, spontaneously in 15% of all pregnancies. Risk factors = ⇑ paternal age, conception within 3 months of live birth, ⇑ parity 50% are due to chromosomal abnormalities Vaginal bleeding in first half of pregnancy is presumed to be a threatened abortion until proven otherwise
Ectopic Pregnancy: • •
Implantation outside of the uterine cavity PID increases the risk
Risk factors: • • • •
Previous ectopic pregnancy History of gonorrhea, Chlamydia, PID, salpingitis Advanced maternal age (>35) > 3 prior pregnancies
Differential dx of ectopic pregnancy: • • • • • •
Ovarian torsion Endometriosis Surgical abdomen Abortion Salpingitis Ruptured ovarian cyst
Diagnosing: • •
(+) β‐hCH + US to determine intra vs. extra uterine pregnancy Low progesterone level is suggestive of a non‐viable pregnancy that may be located outside of the uterine cavity
Treatment: • • • • •
Laparoscopic removal, tubes usually heal on their own Methotrexate early, especially if size is 5000g in non‐diabetic mother.
Fetal Assessment and Intrapartum Surveillance The following must be assessed and observed closely during pregnancy: • • • • • •
Fetal growth Fetal well‐being Tests of fetal maturity Intrapartum fetal assessment Isoimmunization Genetic testing
1. Fetal Growth • US is most reliable tool for growth assessment • Measure by fundal height, a deviation from expected fundal height during weeks 18‐36 require repeat measurement and/or US • Early pregnancy: Gestational sac + crown‐rump length correlate quite well with gestational age • Later pregnancy: 4 measurements done due to wide deviation of normal range: 1‐ Biparietal diameter of skull 2‐ Abdominal circumference 3‐ Femur length 4‐ Cerebellar diameter 2. Fetal wellbeing • ≥ 4 movements per hr usually indicates fetal well‐being Nonstress test (NST): • • • •
Measures response of fetal heart rate to movement Normal NST when FHR ⇑ by 15 beats per minute for 15 sec following fetal movement (2 of these accelerations within 20min considered to be normal) A non‐reactive NST requires further assessment NST has a high false‐positive rate, thus a repeat within 24hr is a good idea
Biophysical profile: Measures: • • •
Fetal breathing Fetal breathing Fetal tone
• • •
Qualitative amniotic fluid volume Reactive fetal heart rate All measures from 0‐2, a score of 8‐10 is normal, score of 6 requires further evaluation, score of ≤ 4 usually requires immediate intervention
3. Tests of fetal maturity • Since the respiratory system is last thing to develop in the fetus, decisions regarding delivery are usually based on the maturity of this system • Surfactant is still low all the way up to 33 weeks • Lack of surfactant causes neonatal respiratory distress syndrome (RDS) Testing fetal lung maturity: • •
Lecithin : sphingomyelin ratio >2.0 is the safe ratio and suggests lung maturity. Phosphatidylglycerol appears late in pregnancy and its presence indicates fetal lung maturity.
NOTE: Sphingomyelin remains constant throughout pregnancy, while lecithin only elevates when the fetal lungs become mature 4. Intrapartum fetal assessment FHR monitoring: • • • • •
Normal FHR is 120‐160 BPM FHR >160 for ≥ 10 min considered tachycardia (MCC is maternal fever) FHR 30degrees, pt has stress incontinence. ** If patient describes an “urge” and/or “frequency” for urination, it is suggestive of neurogenic incontinence Treatments: Stress Incontinence 1st – attempt kegel exercises, 2nd – surgery (colporaphy) Neurogenic Anti‐spasmotics, anti‐cholinergics Other causes of urinary incontinence: Neuropathic caused by head injury, spinal injury, or peripheral nerve injury. Treatment: catheter, either indwelling or intermittent Anatomical caused by a vesicovaginal fistula. Treatment: repair of defect.
Gynecologic Oncology 1. 2. 3. 4. 5. 6.
Endometrial cancer Fibroids/Leiomyoma Cervical cancer Ovarian neoplasm’s Vulvar and vaginal cancer Gestational trophoblastic neoplasia
Endometrial Cancer: • •
Is the most common reproductive tract cancer with approximately 30,000‐ 40,000 new cases each year. Is an “estrogen‐dependent” cancer
Risk factors: • • • • • • •
Unopposed postmenopausal estrogen replacement therapy Menopause after 52yr of age Obesity Nulliparity PCOS Diabetes Chronic anovulation
Signs & Symptoms: • •
Abnormal uterine bleeding, especially if woman is postmenopausal All women >35yr with abnormal bleeding requires an endometrial sampling for histologic examination.
Diagnosis: • • •
Pap smear not reliable Bimanual exam for masses, nodules, induration, and immobility Endometrial biopsy by endocervical curettage, D&C, hysteroscopy with direct biopsies.
Treatment: •
If simple or complex hyperplasia – give progesterone to reverse hyperplastic process promoted by estrogen (Provera for 10 days)
• •
Atypical hyperplasia – hysterectomy because of likelihood that invasive carcinoma will ensue Endometrial carcinoma Total abdominal hysterectomy + bilateral salpingo‐oophorectomy + lymph node dissection, adjuvant external‐beam radiation, treatment for recurrence is high‐dose progestin’s.
Prognosis: • •
Histologic grade is the most important factor in overall prognosis. Depth of myometrial invasion is 2nd most important factor in overall prognosis
G1 – highly differentiated G2 – moderately differentiated G3 – solid or completely undifferentiated G1 tumor that doesn’t invade the myometrium has a 95% 5‐yr survival G3 tumor with deep myometrial invasion has ~20% 5‐yr survival Uterine Leiomyomas Fibroids • • •
Fibroids are benign tumors whose growth is related to the production of estrogen. Growth is often rapid perimenopausally 30% of cases warrant a hysterectomy
Signs & Symptoms: • • •
Menorrhagia Pelvic pain and pressure (misdiagnosed as dysmenorrheal) Enlarged, firm, asymmetric, non‐tender uterus
Diagnosing Fibroids: •
US initially, confirm with tissue sample by either D&C or biopsy (especially in postmenopausal women).
Treatments: • •
Mild symptoms only require re‐assurance and observation Estrogen inhibitors such as GnRH agonists can shrink the uterus, which help to create a simpler surgical procedure.
• •
Surgery myomectomy recommended in young patients who want to preserve fertility. Hysterectomy is definitive treatment that should be reserved for symptomatic women who have no desire for children and/or any more children.
Adenomyosis • • • •
Abnormal location of endometrial glands and stroma within the myometrium of the uterine wall When symptomatic is causes dysmenorrheal and menorrhagia. Uterus feels soft, globular, tender, and symmetrical. Unlike leiomyomas, there is no change with high or low estrogen states.
Diagnosis Symptoms
Pelvic Exam
Sonogram
Hysteroscopy Histology
Leiomyoma Secondary dysmenorrhea and menorrhagia. (+) or (–) symptoms of bladder, ureter, and/or rectal compression Asymmetrically enlarged, firm, NONTENDER uterus.
Large intramural or subserosal myomas (saline infusion can help visualize this) Direct visualization of tumors Is definitive diagnosis
Adenomyosis Secondary dysmenorrhea and menorrhagia
Symmetrically enlarged, soft, TENDER uterus. May be tender immediately before and during menses Diffusely enlarged uterus with cystic areas within myometrial wall Is definitive diagnosis
Leiomyosarcoma •
A rare cancer that accounts for approximately 3% of uterine cancers
Signs & Symptoms: Sarcoma postmenopausal bleeding, pelvic pain, increasing vaginal discharge Treatment: • • •
Hysterectomy with intraopertive LN biopsy Surgical staging is an important aspect Adjunctive therapies have minimal overall benefit
** Only 50% of patients survive 5 yr
Cervical Cancer • The most important screening tool is the Pap smear • The average age of diagnosis is between 45‐50yr. • The most common diagnosis is squamous cell carcinoma (85%), the other 15% are adenocarcinoma Diagnosis: Cervical Biopsy most commonly is SCC Next step metastatic workup (pelvic exam, CXR, IV pyelogram, cystoscopy, and sigmoidoscopy). ** Imaging studies not required (invasive cervical cancer is the only gynecological cancer that does not get staged clinically). Management: •
Management is simple hysterectomy or modified radical hysterectomy + LN dissection. Survival 4cm, + margins, local recurrence
Ovarian Neoplasms Benign cysts: • • •
Functional growth resulting from failure of normal rupture of follicle Benign tumors are more common than malignant tumors Risk of malignancy increases with age
Signs & Symptoms: • •
Pelvic pain/pressure Acute and severe pain when cyst ruptures
Confirm Diagnosis With US
Benign Neoplasms Neoplasm Epithelial Cell
Germ Cell
Stromal Cell
Characteristics Serous cystadenoma is the most common type. Usually benign (malignancy risk increases when bilateral). Others: mucinous, endometrioid, Brenner tumor (all rarely malignant). Diagnose: Clinical / CT or MRI Most common type is Teratoma (aka dermoid cyst). Almost never malignant. Contains tissues from all 3 germ layers. Unilateral, cystic, mobile, non‐tender adnexal mass, often asymptomatic. Confirm diagnosis with US Are functional tumors secreting hormones. Granulosa tumor makes estrogen (gynecomastia, loss of body hair). Sertoli‐Leydig makes androgens (virilization in females)
Treatment Excision
Excision to prevent torsion or rupture of ovary
Excision
Malignant Tumors: • • • • •
Most commonly seen in women > 50yr OCP use is a protective factor Seen in higher frequency in women of low parity, ⇓ fertility, delayed childbearing Usually asymptomatic until metastasis has occurred Yearly pelvic exams are the most effective screening tools
Signs & Symptoms: • • •
Vague abdominal pains Vague pelvic pains Constipation, early satiety, abdominal distention, urinary frequency
Treatment: •
Debulking surgery + chemo/radiation
Malignant Neoplasms Neoplasms Epithelial Cell
Germ Cell
Stromal Cell
Characteristics The cause of 90% of all ovarian malignancies. Serous cystadenocarcinoma is the most common type (often develops from a benign precursor). Is the most common ovarian cancer in women 80% 5‐yr survival
Total hysterectomy + oophorectomy.
Vulvar and Vaginal Cancers Vulvar Intraepithelial Neoplasia (VIN): VIN 1 & 2 characterized by mild/moderate dysplasia, ⇑ risk of progressing to advanced stages and then carcinoma. VIN 3 = carcinoma in situ Signs & Symptoms: • • •
Pruritis Presence of raised lesions Irritation
Diagnosis: •
Biopsy required for a definitive diagnosis
Differential diagnosis: •
Malignant melanoma and Paget’s disease
Treatment: • •
For VIN 1 and 2 local excision For VIN 3 wide excision
Vulvar Cancer: • •
90% are squamous cell cancers Most often this presents in postmenopausal women
Signs & Symptoms: •
Pruritis (may present with or without an ulcerative lesion)
Treatment: •
Excision
** 5yr survival rate ranges from 70%‐90% depending on LN involvement. ** With the presence of deep pelvic nodes, survival rate drops to 20%
Vaginal carcinoma in situ and carcinoma: •
70% of patients with vaginal CIS have previous genital tract neoplasm
Treatment: • •
Radiation Surgery reserved for extensive disease
Gestational Trophoblastic Disease (GTN) • •
An abnormal proliferation of placental tissue that involves both the cytotrophoblast and/or syncytiotrophoblast. Can be both benign and malignant
Risk factors: • •
Maternal age on low or high spectrum (35yr) Folate deficiency is a risk factor
Signs & Symptoms: • • • • • • • •
Most common sign is a fundus that is larger than dates should show Bilateral cystic enlargement of the ovary Bleeding at 95% cure Single‐agent chemo until after β‐hCG is negative for 3 weeks. Follow‐up for 1 yr on OCP
Metatstatic: Poor Px Brain or liver 65% cure Multiple‐agent chemo until after β‐hCG is negative for 3 weeks. Follow‐up for 5 yrs on OCP.
The Breast Benign Breast Diseases: • • • • •
Fibroadenoma Fibrocystic disease Intraductal Papilloma Fat Necrosis Mastitis
Malignant Breast Diseases: • • • • • •
Ductal carcinoma in situ (DCIS) Lobular carcinoma in situ (LCIS) Ductal carcinoma Lobular carcinoma Inflammatory breast cancer Paget’s disease of the breast
Fibroadenoma • • •
Is the most commonly seen tumor in young women (20’s) Fibroadenomas grow rapidly but have no increased risk for developing cancer Histology shows myxoid stroma and curvilinear/slit ducts
Treatment: Not required and will often resorb within several weeks (re‐evaluate at 1 month)
Fibrocystic Disease • • •
Is the most common tumor in patients between 35‐50 years of age. Arises in terminal ductal lobular units Often arises as multiple bilateral small lumps which are tender during the menstrual cycle
Intraductal Papilloma • •
Presents commonly with serous bloody nipple discharge Multiple nodules in younger patients and solitary growth in perimenopausal patients
•
There is an increased cancer risk with multiple papillomas, but no increased cancer risk with solitary pipillomas
Ductal Carcinoma in Situ (DCIS) • • •
Usually seen on mammography but not clinically palpable Is a premalignancy that will lead to invasive ductal cancer Histology shows haphazard cells along papillae, punched‐out areas in ducts, with cells infiltrating open spaces.
Treatment: • • •
Mass excision ensuring clear margins. If margins are not clear must excise again with wider margins. Give post‐op radiation to prevent recurrences.
Lobular Carcinoma in Situ (LCIS) • • • •
LCIS can’t be detected clinically but mammography is also a weak tool for diagnosis Not precancerous like DCIS but can be a marker for future invasive ductal cancer Mucinous cells are almost always present There is a “saw‐tooth” and clover‐leaf configurations in the ducts
Invasive Ductal Carcinoma (IDC) • • • • • •
Is the most common breast cancer type, seen most commonly in the mid 30’s – late 50’s, and forms solid tumors Most important prognosis factor is the size of the tumor LN involvement is also an extremely important factor in prognosis There are many subtypes of IDC, such as mucinous and medullary Moderately differentiated IDC comes from cribriform or papillary intraductal originators Poorly differentiated IDC comes from intraductal comedo originator.
Invasive Lobular Carcinoma (ILC) • • • •
3%‐5% of invasive cancer is lobular Most commonly seen from 45‐55 yr of age Vague appearance on mammogram Growth pattern single file growth pattern within a fibrous stroma
Treating invasive carcinomas: • • • •
If tumor is 5cm, and METS is systemic therapy
Inflammatory Carcinoma • • •
Classic symptoms are that of inflammation (warm, red, painful) Progresses rapidly and is almost widely metastatic at presentation Has a very poor prognosis
Paget’s Disease of the Breast • •
Very specific presentation of dermatitis + macular rash over the nipple and areola There is almost always an underlying ductal carcinoma
More on the breast: • • • • • •
The most common cause of nipple discharge is intraductal papilloma The presence of discharge + palpable mass increases the likelihood of cancer is greater If discharge is unilateral, further workup is required If discharge is bloody, further workup is required If discharge is associated with a mass, further workup is required For bilateral, milky nipple discharge do a workup for prolactinoma
With discharge: •
Next step is a mammogram to look for underlying masses and/or calcifications
• •
If mammography gives a definitive diagnosis, excision of duct is recommended For nipple discharge, never base diagnosis on cytology
Mastalgia: • •
Is cyclical or noncyclical breast pain that isn’t caused by lumps Treat with danazol (induces amenorrhea)
Gynecomastia: • • • •
Enlargement of the male breast, both unilateral and bilateral No lobules Is caused by an imbalance in estrogens and androgens, most often occurring during puberty May be seen in hyperestrogen states (cirrhosis, drugs inhibiting estrogen breakdown ETOH, marijuana, heroin)
Cancer Risks of Breast Cancers: • • • • • • • • •
#1 risk factor is gender (females make up 99% of breast cancers) In women, age is the #1 factor Menarche 30yr have an increased risk 95% of breast cancer is NOT familial Having a first degree relative with a hx of breast cancer increases the risk of breast cancer Autosomal dominant conditions that have increased risk, such as BRCA‐1, BRCA‐2 Prior cancer in the opposite breast Cancer of the breast occurs most commonly in the upper and outer quadrant of the breast.
What to do for certain breast masses? When to do an ultrasound (US) this is the first step when finding a palpable mass that feels cystic on physical exam. When to do fine needle aspiration (FNA) this is often the first step when finding a palpable mass, and may be done either after an US or instead of an US.
When to do either mammography (if pt >40yr) and biopsy (or biopsy solely if pt is 1cm When the disease is node (+)
When is trastuzumab included in management? • •
Included for metastatic breast cancer that over expresses HER2/neu This is a monoclonal antibody directed against the extracellular domain of the HER2/neu receptor
Tamoxifen: • • •
Competitively binds to estrogen receptors Produces a 50% decrease in recurrence and a 25% decrease in mortality Excellent for both pre and post‐op patients
Aromatase Inhibitors: • • • •
Include drugs such as: Anastrazole, Exemestane, and Letrozole These block the peripheral production of estrogen These are the standard of care in hormone receptor (+) women who are menopausal (more effective than tamoxifen) Will increase the risk of osteoporosis
LHRH analogues: • •
A commonly used drug is Goserelin An alternative or an addition to tamoxifen in premenopausal women
Benefits of Tamoxifen ⇓ incidence of contralateral breast cancer ⇑ bone density in postmenopausal women ⇓ serum cholesterol ⇓ fractures ⇓ cardiovascular mortality rate
Side effects of Tamoxifen Exacerbates menopausal symptoms ⇑⇑ risk of cancer of the endometrium **All women with a history of tamoxifen use + vaginal bleeding should have an evaluation of the endometrium
Treatment review: If case describes HR(‐), pre or post menopausal chemo alone If case describes HR(+), PREmenopausal chemo + tamoxifen If case describes HR(+), POSTmenop chemo + aromatase inhibitor
Chapter 4 Pediatrics
The Newborn The APGAR score: This score measures the newborn’s need for resuscitation and measures 5 criteria at 1‐minute and 5‐minutes. At 1‐minute we can determine how well the baby did during labor and delivery, while at 5‐minutes we can determine the effectiveness of resuscitation (if it was needed) APGAR SCORING TABLE
Managing the Newborn: There are some important things that must be done immediately upon delivery of the newborn, upon delivery give the following: • •
Give 1% silver nitrate eye drops OR 0.5% erythromycin ophthalmic ointment 1mg of intramuscular vitamin K (prevents hemorrhagic disease of the newborn)
Before discharging the newborn from the hospital, do the following: • •
Hearing test to rule out a sensorineural hearing loss Order neonatal screening tests: PKU, galactosemia, hypothyroidism
Abnormalities in the newborn: There are many abnormalities of the newborn that should be recognizable. It is also important to know which are benign and which require further investigation.
Image
Description
Diagnosis
Red, sharply demarcated raised red lesions
Hemangioma
Unilateral red formations on head and neck (unilateral and permanent)
Port Wine Stain
Bluish/gray macules on lower back and/or posterior thigh (most commonly) Firm, yellow‐ white papules/pustul es with erythematous base, peaks on 2nd day of life Tags or pits in front of the ear
Mongolian Spots
Erythema Toxicum
None
Preauricular Tags
Associated US of kidneys with hearing and hearing loss and GU test abnormalities
Defect in the iris
Coloboma of the Iris
Associated with other CHARGE defects
Co‐ morbidities May be associated with high‐ output cardiac failure if very large. Consider underlying involvement of organs when large. May be associated with Sturge‐ Weber syndrome
Management Steroids or laser therapy if it involves underlying organs
Pulsed laser therapy. If Sturge‐ Weber must evaluate for glaucoma and give anti‐ convulsives Rule out child abuse, usually fade within first few years of life None, is self‐ limited
Screen for CHARGE syndrome
An absence of the iris
Aniridia
Associated with Wilm’s tumor
A mass lateral to the midline
Branchial Cleft Cyst
Is a remnant of embryonic development associated with infections May have ectopic thyroid, associated with infections Associated with chromosomal disorders and other malformation s Associated with intestinal atresia
A midline mass Thyroglossal that rises when Duct Cyst swallowing A protrusion of Omphalocele GI contents through umbilicus contained within a sac An abdominal Gastroschisis defect that is lateral to the midline with no sac covering contents Rectus Hernia abdominus (umbilical) weakness that allows bulging of fetal and infant umbilical cord Scrotal swelling that can be transilluminate d
Hydrocele
Congenital hypothyroidis m
Associated with an inguinal hernia
Must screen for Wilm’s tumor every 3 months until 8yr of age Surgical removal
Surgical removal
Screen for trisomies.
This may close spontaneousl y. Screen for hypothyroid with TSH screen. Differentiate from inguinal hernia by shining flashlight
Absence of teste(s) in scrotum
Cryptorchidis m
Associated Surgical with cancer of removal by the teste(s) 1yr
Opening of the urethra on dorsum of the penis
Epispadias
Urinary incontinence
Evaluate for bladder extrophy
Opening of the urethra on ventral surface of penis
Hypospadias
No definitive mgmt, but not supposed to circumcise the infant
Surgical correction
Reducible Inguinal scrotal swelling Hernia
Developmental Milestones Developmental milestones show up over and over again on the board exams. By memorizing the important milestones you are going to get 2‐3 easy points on the CK exam. Milestones refer to both infant and adolescent (puberty) milestones. Developmental Milestones Age Newborn 2 months 4 months 6 months
Gross Motor Fine Motor Moro reflex, grasp reflex Holds head up Swipes at objects Rolls front to Grasps back Objects Rolls from Transfers back to front, objects sits upright
9 months
Crawls, pulls to a stand
12 months
Stands on own
15 months 18 months 24 months
36 months
Pincer grasp, eats with fingers Mature pincer grasp
Language
Social/Cognition
Coos
Social smile
Orients to voice Babbles
Laughs
Nonspecific words
Specific words “mama” Walks Uses a cup Speaks 4‐6 words Throws a ball, Uses spoon Names walks up the for solid foods common stairs objects Starts Uses spoon Speaks 2 running, can for semi‐ word go up and solids sentence down stairs Can ride a Can eat neatly Speaks 3 tricycle with utensils word sentence
Develops stranger anxiety, sleeps all night Waves goodbye, responds to name Recognizes pictures in a book/magazine Throws temper tantrum Begins toilet training Can follow a 2‐ step command Knows first and last names
Puberty: The milestones of puberty are as follows and are based on population averages: MALES Testicular enlargement – 11.5 yrs Genitals increase in size Pubic Hair Growth Begins Peak Growth Spurt – 13.5 yrs
FEMALES Breast buds – 10.5 yrs Pubic Hair Growth Begins Linear Growth Spurt – 12 yrs Menarche – 12.5 yrs
Child Abuse • • •
Suspected child abuse requires your BY LAW to report the suspected abuse. You must also explain to the parents why you suspect abuse and that you are legally obligated to report it to child protective services. If a parent refuses hospitalization or treatment of their child against the best interest of the child, you must get an emergency court order.
Highrisk children: • • • • • • • •
Premature infants Children with chronic medical problems Infants with colic Children with behavioral problems Poverty stricken children Children of teenage parents Single parents Children of substance abusers
Classic findings: • • • • • •
Chip fractures (damage to the corner of metaphysis in long bones) Spiral fractures Rib fractures Burns (immersion in hot water, cigarette burns, stocking‐glove burns on hands and feet) Head injury – MCC of death Sexual abuse
When to hospitalize a child under suspect of being abused: • • •
The hospital is the safest place for the child The diagnosis is still unclear The child has a medical condition requiring hospitalization
Workup for suspected child abuse: • • • •
PT/PTT/BT Full skeletal survey for breaks If injuries are severe, get a CT or MRI + a thorough eye exam If injury is to the abdomen, get an abdominal CT, check for blood in the stool and urine, and check liver and pancreatic enzymes
Treatment: 1st ‐ Address medical and/or surgical issues before all else 2nd – Report abuse to child protective services (CPS) Breast Feeding There are many advantages to breastfeeding: • •
Psychological and emotional bonding between mother and infant Passive transfer of T‐cell immunity decreases risks of allergies and infection
Contraindications to breast feeding: • • • • • • • •
HIV CMV HSV (only if lesions are on breast) HBV (unless vaccination is given prior) Substance abuse Breast cancer Acute illness in mother that is absent in infant Drugs (list below of contraindicated drugs during breastfeeding)
Absolutely Contraindicated Alcohol Nicotine Antineoplastics
Relatively Contraindicated Steroids Neuroleptics Sedatives
Lithium Chloramphenicol Iodide and Mercurial Drugs
Tetracycline Sulfonamides Metronidazole
Highyield Growth & Development Facts • • • • • • •
The height of a child at 2 years of age normally correlates with the final adult height percentile. By 6 months of age the birth weight should double, and by 1 year the birth weight should triple. The absolute best indicator for malnutrition is a child who is 2mg/dL at any time Hyperbilirubinemia is present after the 2nd week of life
Workup for pathologic jaundice: • • •
Total and direct bilirubin Direct Coomb’s test Blood type of infant and mother (ABO or Rh incompatibility)
• •
CBC, retic #, peripheral smear (assessing for hemolysis) U/A and urine culture (if elevated is direct bilirubin – assess for sepsis)
If prolonged >2 weeks, do the following: If ⇑ conjugated bilirubin • •
Initial diagnostic tests LFT’s Most specific test US and liver biopsy
If no elevation of unconjugated bilirubin • • • •
UTI or other type of infection Bilirubin conjugation abnormalities (Gilberts, Crigler‐Najjar) Hemolysis Intrinsic red cell membrane defect or enzyme defect (spherocytosis, elliptocytosis, G6PD def, pyruvate kinase deficiency)
Treatment: • •
When bilirubin is >10‐12 mg/dL phototherapy Exchange transfusion if encephalopathy is suspected or there is failure of improvement with phototherapy
Unconjugated Hyperbilirubinemia •
Caused by hemolytic anemia or congenital deficiency of glucuronyl transferase (Crigler‐Najjar, Gilbert’s syndrome)
Hemolytic anemia: • • •
Congenital or acquired Congenital spherocytosis, G6PD, pyruvate kinase deficiency Acquired ABO/Rh isoimmunization, infection, drugs, twin‐twin transfusion, chronic fetal hypoxia, delayed cord clamping, maternal diabetes
Conjugated Hyperbilirubinemia • • •
Infectious causes are sepsis, ToRCH’s, hepatitis, syphilis, listeria infection Metabolic causes are galactosemia, α1‐antitrypsin def Congenital causes are extrahepatic biliary atresia, Dubin‐Johnson syndrome, Rotor syndrome
Treatment: • •
UV light to break down bilirubin pigments Urgent treatment is imperative in order to prevent kernicterus induced mental retardation
Complications: •
UV light can cause diarrhea, dermatitis, dehydration, and damage to the retina (be cautious of these adverse effects)
Reye Syndrome • •
The use of salicylates in children causes an acute encephalopathy + fatty degeneration of the liver Most commonly occurs in children aged 4‐12yr
Signs and Symptoms: • •
Alternates an asymptomatic interval with abrupt onset of vomiting, delirium, stupor, abnormal LFT’s Rapid progression to seizures, coma, and death
Diagnosis: •
Significantly elevated liver enzymes
Treatment: • •
Urgent ICP management with mannitol and fluid restriction Glucose administration due to rapid depletion of stores
Prognosis: • • •
Bad if serum ammonia levels are increased 3fold, and if there is a decreased PT level that WONT respond to vitamin K If disease is mild the recovery is usually good and rapid A severe disease can result in permanent neuro defects
Seizures • • •
In the newborn, seizures may present as jitters with repetitive sucking movements, tongue thrusting, and apneic spells. Blood counts and chemistries are often WNL Neonatal seizures can be diagnosed by the presence of ocular deviation and failure of jitters to subside with stimulus
Diagnosis: • • • • • • •
EEG – often normal CBC + chemistry panel often the cause is hypoglycemia in case of GDM Amino acid assay looking for inborn errors of metabolism Total cord blood IgM to look for ToRCH infections Urine cultures LP if suspected meningitis US of head if infant is preterm looking for bleeding
Treatment: • •
1st line DOC is Phenobarbital Persistent seizure not responsive to Phenobarbital – give Phenytoin
Febrile Seizures • • • •
Usually between 3mnt – 5yr A fever is present with no other signs of infection Is the MC convulsive disorder in children and rarely develops into epilepsy Seizure occurs during temperature rise (≥ 102F) but not at its peak
Signs and Symptoms: • •
MC is a tonic‐clonic seizure that rarely last more than 10min + a drowsy postictal period is common Seizure lasting >15min is usually due to an infectious process
Diagnosis: • • •
Clinical diagnosis is usually all that is needed Routine labs only required to identify a source of the fever LP to rule out meningitis (only if suspected)
Treatment: • •
Control fever with antipyretics Reassure parents/counsel
•
Always do a careful evaluation for the source of the fever
** 30%‐50% of children experience recurrent febrile seizures
Genetic and Congenital Disorders Failure to Thrive • • • •
Is the failure of children to grow and develop at an appropriate rate May be due to inadequate calories or inability to absorb the calories May be idiopathic or due to other diseases Factors such as poverty, family problems, neonatal problems, and maternal depression should all be included in diagnosis
Diagnosis: Requires 3 criteria for a FTT diagnosis: 1. Child 200 with symptoms OR Two measurement of fasting glucose >125 2hr oral glucose tolerant test >200 with or without symptoms
Treatment: •
Insulin replacement
Complications: •
DKA
Signs and Symptoms of DKA: • • • • •
Hyperglycemia >250 Hyperkalemia (due to transcellular shift out of the cell in exchange for H+) Low pH Elevated levels of acetone, acetoacetate, and β‐hydroxybutyric acid Increased anion gap
DKA treatment: 1st IV fluids 2nd potassium replacement(hyper becomes hypo as DKA is treated), insulin replacement 3rd addition of glucose to insulin drip when pt becomes normoglycemic (keep giving insulin until ketones are gone) ** insulin is given originally to shut down ketogenesis, not decrease glucose, thus keep giving insulin until ketones are gone despite normal glucose.
Type 2 DM • • • •
A peripheral insulin resistance Usually adult onset (changing with the obesity epidemic) Family history often plays a strong role Ketosis is NOT associated with DM2
Signs and Symptoms: • •
Acute 3P’s (polydypsia, polyphagia, polyuria), fatigue, weight loss Subactue infections (yeast infections, Mucor, S. Aureus)
Chronic signs and symptoms: • • •
Macrovascular stroke, CAD Microvascular retinitis, nephritis Neuropathy parasthesia, stocking and glove burning sensation, autonomic insufficiency, ⇓ sensation
Diagnosis: same as type 1 Treatment: • • • • • • • •
FIRST treatment is always diet and lifestyle modifications Oral hypoglycemics for mild/moderate disease 1st line metformin (biguanide), its MOA is blocking gluconeogenesis 2nd line sulfonylurea (glyburide), MOA is ⇑ β‐cell insulin secretion 3rd line Thiazolidinediones (pioglitazone), MOA is increasing tissue sensitivity to insulin If oral drugs don’t work, patient may require insulin Lifelong cases most usually will require insulin treatment ACEI’s important because they slow down the progression of diabetic nephropathy
Monitoring DM with HbA1c: • • •
HbA1c allows us to get a measure of the average glucose level over the past 3 months Tight glucose control is directly responsible for decreasing complications and mortality in both types of insulin An HbA1c 1000mg/dL There is no acidosis (as in type 1 DM)
Treating HHNK: • • •
IV fluids are most important, rehydration is often all that is needed. May require upwards of 10L of fluids Without treatment, mortality rate climbs over 50%
Complications of Diabetes Hypertension Control is essential in DM patients because it causes long‐term complications of the heart, eye, kidney, and brain. Goal is to keep it 15
Renal 20 >2% 5.5 >5.5 early then 3.5g/day Patient has generalized edema Hypercoagulation ⇓ albumin Hyperlipidemia
Diagnosis: • • • •
Best initial test is a urinalysis showing significantly increased levels of protein Next best step is a spot‐urine test for a protein: creatinine >3.5:1 24‐hr urine protein collection >3.5g Most accurate test Renal biopsy
TYPE OF NEPHROTIC DISEASE Minimal Change Disease Focal Segmental Glomerulosclerosis
Membranous Glomerulonephritis
Membranoproliferative Glomerulonephritis
COMMON CHARACTERISTICS/TX This is seen in young children. Treat with prednisone Similar in presentation to MCD but occurs in adults. Most commonly idiopathic. Commonly presents in young hypertensive males. Treat with prednisone and cyclophosphamide Is the most common 1° cause of nephritic syndrome in adults. A slowly progressive disorder. Many causes: HBV, HCV, syphilis, certain drugs, malignancies, SLE. Treat with prednisone + cyclophosphamide. 50% of cases progress to end‐stage renal failure Type 1 is slowly progressive while Type 2 is aggressive. Autoantibody against C3 convertase (⇓C3 levels) Treat with prednisone, plasmapharesis.
Treatment: • •
Protein and salt restriction HMG‐CoA reductase inhibitor for hyperlipidemia
Nephritic: •
This happens when there is diffuse glomerular inflammation
Signs and Symptoms: • • • • • •
There is an acute‐onset of hematuria Oliguria Hypertension Edema ⇓GFR ⇑ Bun:Cr
TYPE OF NEPHRITIC DISEASE Post‐streptococcal Glomerulonephritis
Rapidly Progressive Glomerulonephritis (Crescentic)
Berger’s Disease (IgA nephropathy)
Henoch‐Schonlein Purpura
COMMON CHARACTERISTICS/TX An acute condition. Classically occurs after Strep Pyogenes infection. Immunofluorescence shows coarse granular IgG or C3 deposits. Labs show increased red cells and casts, ⇓ serum C3, ⇑ ASO titer. A nephritic condition that progresses rapidly to renal failure. Goodpasture’s disease is in this category. Immunofluorescence shows smooth and linear IgG deposits. Treat with prednisone and plasmapharesis. Most common type of nephropathy. IgA deposits in mesangium. Presents with recurrent hematuria + low‐grade proteinuria. Usually harmless, however 1 in 4 may progress to renal failure. Treat with prednisone Always in children, is an IgA nephropathy. Presents with abdominal pain, GI bleed, vomiting, and hematuria. Classically find palpable purpura on
Multiple Myeloma
buttocks and legs Is a self‐limiting disease that requires no steroids. There is an increased light‐chain production. Find Bence‐Jones protein in urine. Hypercalcemia seen. Patient becomes succeptible to encapsulated bacteria because there is a defect in normal antibody production. Treatment must be on the underlying myeloma.
Systemic Glomerulonephropathies: DISEASE Diabetes Mellitus
HIV
Renal Amyloidosis
Type 1 Type 2 Type 3 Type 4
Type 5
CHARACTERISTIC NEPHROPATHY Is the MCC of ESRD. Early manifestation is microalbuminuria (give ACEI’s, strict glycemic control). MC seen when HIV is acquired by IV drug use. Presents as focal segmental glomerulonephritis. Early treatment with antiretroviral Diagnose with birefringence on congo red stain. Treat with a transplant LUPUS No renal involvement Is a mesangial disease with focal segmental glomerular pattern. Treatment isn’t typically required Is a focal proliferative disease. Treat aggressively with prednisone and cyclophosphamide Diffuse proliferative disease. Combination of both nephritic and nephritic disease. Wire‐loop abnormality on LM Treat with prednisone and cyclophosphamide Is a membranous disease that is indistinguishable from other primary membranous diseases. Treat with prednisone
Renal Artery Stenosis • • •
Presents with sudden onset of hypertension along with hypokalemia Abdominal bruit heard with stethoscope Can be caused by plaque, fibromuscular dysplasia
Diagnosis: • • •
Best initial test is a renal ultrasound with Doppler If small kidneys are then seen, do an MRA The most accurate test is a renal angiogram
Treatment: •
Angioplasty and stenting
Obstruction of the Urinary Tract • • •
BPH and stones are the MCC in adults There is an increased risk of stasis thus increasing the risks of UTI’s Present with urinary colic, intense pain that radiates from the back around to the pelvis and the groin
Nephrolithiasis: Calcium Pyrophosphate: • • • •
85% of stones are calcium pyrophosphate Are radiopaque and associated with hypercalcemia 50% of time it’s associated with hypercalciuria Treat calcium stones with hydration and loop diuretics (LOOPS eliminate calcium)
Ammonium Mangesium Phosphate (Struvite): • • • • •
2nd MCC of stones Are radiopaque Usually caused by urease (+) Proteus or Staph Saprophyticus May form large staghorn calculi Treatment involves taking care of the underlying infection
Uric Acid Stones: • •
Often secondary to gout or conditions that cause increased cell turnover, such as myeloproliferative disease Treat by alkalinizing the urine and/or treating any underlying conditions
Kidney Tumors • • • • • •
The most common renal malignancy is renal cell carcinoma, which occurs MC in males from 50‐70yr of age Presents with hematuria, flank pain, fever, palpable mass, and secondary polycythemia Treatment involves interleukin and resection The most common childhood renal malignancy is Wilm’s tumor, which occurs MC between 2‐4yr old Presents with a palpable flank mass Part of WAGR complex (Wilms, Aniridia, GU malformation, Retardation – mental and motor)
Treatment: • Removal of kidney plus chemotherapy and/or radiation
Chapter 14 Hematology
Anemias: Mild to moderate anemia presents with:
•
Fatigue, pallor, pale conjunctiva, flow murmur
Severe anemia presents with:
•
SOB, light‐headedness, confusion
Diagnosis: • •
The most reliable test for iron deficiency anemia is serum ferritin, which will be decreased. If a patient has iron‐deficiency anemia and does not respond to treatment, do hemoglobin electrophoresis to look for an α or β thalassemia
LABS for suspected anemias: 1. 2. 3. 4. 5.
Iron studies (most imp) CBC w/ peripheral smear (paying attention to MCV, MCHC) B12/folate(B12 = neuropathies, folate = no neuropathies) RDW (newer smaller RBCs cause change in RDW) Reticulocyte count (determines whether site of problem is bone marrow synthesis of new RBCs) 6. LDH, bilirubin, haptoglobin (all determine whether hemolysis is in play) 7. TSH with T4 (see whether hypothyroidism is cause of fatigue) 8. CXR/blood culture/UA for suspected sickle cell disease
Iron deficiency Anemia Signs and Symptoms:
• • • •
Fatigue Pallor Pale conjunctiva Low ferritin, low iron, increased TIBC
Diagnosis:
• •
Best diagnostic test for iron‐deficiency anemia is iron studies The most accurate test is a bone marrow biopsy
Treatment:
•
Oral ferrous sulfate supplement
Anemia of Chronic Disease Signs and Symptoms: •
Same signs and symptoms with the addition of a history of chronic inflammatory disorder or autoimmune disorder
Diagnosis:
•
Best diagnostic test is iron studies (will come back normal)
Treatment:
•
Correct the underlying disease
Thalassemia Signs and Symptoms:
• • •
Small MCV Presence of target cells Very other symptoms
Diagnosis:
• • • •
Best initial test is an iron study The most accurate test is hemoglobin electrophoresis Beta‐thalassemia has elevated HgA2 and HgF Alpha‐thalassemia has normal levels
There is no treatment for these conditions
Sideroblastic Anemia
Signs and Symptoms: •
Patient has a history of alcohol abuse, exposure to lead, or the use of isoniazid (INH)
Diagnosis:
• •
Best initial test is iron studies The most accurate test is the Prussian blue stain
Treatment:
• •
Minor cases require only pyridoxine replacement Severe cases require the removal of exposure to toxin
Macrocytic Anemia
• Presents similary to microcytic anemia with fatigue, pallor, light‐headedness, but is caused by a deficiency of either vitamin B12 or folic acid
Vitamin B12 Deficiency: Signs and Symptoms:
• Parasthesias • Peripheral neuropathies • Dementia is the least common occurrence
Diagnosis:
• CBC with peripheral smear, paying special attention to neutrophils • Neutrophils are large and hypersegmented • B12 deficiency can also cause glossitis and diarrhea
Treatment:
• Replace either folate or vitamin B12
NOTE: Approx 30% of B12 deficiencies show normal B12 levels because transcobalamine is an acute phase reactant which elevates with any form of stress. Thus is you suspect B12 deficiency and levels are normal, get a methylmalonic acid level.
After finding low B12 or elevevated methylmalonic acid, the best confirmatory test is antiparietal cell antibodies or anti‐intrinsic factor antibodies (both confirm pernicious anemia as the cause of B12 def). Treatment:
•
Replace B12 or folate
** Folate deficiency is most commonly caused by a poor diet, classically described as a “tea and toast diet”. Folate stores deplete within 3 months, thus with poor diets this can be seen quickly. Treat this with diet modifications and immediate folate replacement. Sickle Cell Anemia
• •
•
Patient presents with extreme pain in the chest, back, and thighs When a patient presents with a sickle cell crisis, give immediate oxygen, normal saline, and analgesics. If patient presents with these symptoms + fever, give IV antibiotics as well
When to do exchange transfusion in sickle cell pt? 1. 2. 3. 4.
Presence of visual disturbances due to retinal infarct. Pulmonary infarct leading to pleuritic pain and abnormal xray. Priapism due to infarct of prosthetic plexus of veins. Stroke
What causes sudden drops in hematocrit in sickle cell pt? •
-
Either due to a folate deficiency or parvo B19 virus, which causes an aplastic crisis All Sickle cell pts should be on folate supplements, thus if that’s the case it is due to parvo B19 Do a PCR for DNA of parvo B19
Treatment
•
Transfusion and IVIG
What should all sickle cell patients who are being discharged be given? • • •
Folate replacement Pneumococcal vaccine Hydroxyurea (This increases hemoglobin F, stops sickling of cells, and prevents further crises)
Hemolytic Anemia All forms of hemolytic anemia present with a sudden onset of weakness and fatigue that is associated with anemia. • •
•
Are premature destruction of red blood cells Bone marrow responds appropriately by increasing erythropoiesis and thus there is an increase in reticulocyte count If bone marrow doesn’t work properly, anemia will ensue
Hemolysis will show the following: 1. Increased indirect bilirubin (Gets released with RBC destruction) 2. Increased reticulocyte count (Determines bones marrow’s ability to make new RBCs) 3. Increased LDH 4. Decreased haptoglobin (ordered to distinguish between anemia and hemolytic anemia) Intravascular hemolysis will also show the following: 1. Abnormal peripheral smear (Schistocytes, helmet cells, fragmented cells) 2. Hemoglobinuria 3. Hemosiderinuria (Metabolic, oxidized product or hemoglobin in urine). Causes: Factors external to RBC defects OR intrinsic RBC defects
1. Factors external to RBC defects (Most cases acquired) • Immune hemolysis • Mechanical hemolysis (caused by prosthetic heart valves) • Medications, burns, and toxins
2. Hemolysis due to intrinsic RBC defects (Most cases inherited) • •
•
Caused by sickle cell disease, hemoglobin disease, thalassemias Membrane defects such as hereditary spherocytosis, paroxysmal nocturnal hemoglobinopathy Enzyme defects such as G6PD deficiency and pyruvate kinase deficiency
Autoimmune Hemolysis •
Patient often has a history of autoimmune diseases, cancers, or medication use
Diagnosis:
• • •
Most accurate test is Coomb’s test Look for an increased LDH and increased reticulocyte count Look at the peripheral smear for spherocytes
Treatment:
• • •
The best initial therapy is prednisone With no response to prednisone, IVIG can stop acute episodes With recurring episodes of hemolysis, a splenectomy is most effective
*NOTE: warm antibodies are the cause here, which are always IgG. Only IgG responds to steroids and splenectomy.
ColdInduced Hemolysis (Cold agglutinins)
• • •
Coomb’s test is negative There is often a mycoplasma or EBV infection There is no response to steroids, splenectomy, or IVIG
Hemolysis due to intrinsic defects Glucose6Phosphate dehydrogenase deficiency
• • • •
Presents with a severe and acute onset of hemolysis Is an x‐linked disorder, thus seen in males Most commonly there is a history of sulfa drugs, primaquine, or dapsone use Ingestion of fava beans is classically asked on board exams
Diagnosis: • •
The best initial test is the peripheral smear that shows Heinz bodies and bite cells The most accurate diagnostic test is a glucose-6-phosphate level. The problem with this test is that it will only show up after 2 months, and is not a good test early on in an acute haemolytic episode
Treatment:
•
Avoidance of oxidative stress
Pyruvate Kinase Deficiency Presents the same way as G6PD deficiency, but the cause is unknown
Hereditary Spherocytosis Signs and Symptoms:
• • • •
Jaundince in childhood Splenomegaly Bilirubin gallstones Recurrent episodes
Spherocytes Diagnosis:
• •
The most accurate and best initial test is the osmotic fragility test Peripheral smear showing spherocytes
Treatment:
• •
Folic acid supplementation Splenectomy for severe disease
Hemolytic Uremic Syndrome (HUS)
•
HUS in kids, there is usually a history of E.Coli 0157:H7
Signs and Symptom: • •
Acute renal failure Abdominal pain
• •
Bloody diarrhea Seizures
Treatment: •
Dialysis in children, adults this isn’t useful and there is a much poorer prognosis
Thrombotic Thrombocytopenic Purpura (TTP)
•
Is an idiopathic disease that is often seen in HIV patients
Signs and Symptoms: There is a pentad of:
• • • • •
Haemolytic anemia Renal failure Fever Thrombocytopenia Neurological diseases
Treatment:
• •
Plasma exchange until symptoms subside Without treatment this is fatal
Paroxysmal Nocturnal hemoglobinuria (PNH) Presents with recurring episodes of dark urine, mostly seen in the morning. Signs and Symptoms:
• • • •
Pancytopenia Recurring episodes of dark urine in the morning Portal vein thrombosis is a complication that leads to death May progress to cause aplastic anemia and/or AML
Diagnosis:
•
The most accurate test is the presence of decay accelerating factor antibody
Treatment:
•
Prednisone or other steroids
Methemoglobinemia
• •
Blood locked in the oxidized state cannot pick up and transport oxygen. Patient will present with shortness of breath with no reason
Signs and Symptoms: • •
SOB with no known cause (There will be clear lungs on exam with a normal CXR) Blood (if seen) will have a brownish appearance, which indicates it is locked in the oxidized state.
Diagnosis:
• • •
Look for exposure to drugs like nitroglycerin, amyl nitrate, or nitroprusside CXR and PE show no reason for SOB Look for a history of anesthetic use
Treatment: •
Give methylene blue
Transfusion Reactions 1. ABO incompatibility presents with acute symptoms of hemolysis while the transfusion is happening. Ex: during a transfusion, a patient becomes hypotensive and tachycardic. She has back and chest pain, and there is dark urine. LDH and bilirubin are elevated, and haptoglobin are low. 2. Transfusion related acute lung injury(leukoagglutination rxn) presents with acute SOB from antibodies in the donor blood against recipient white cells. 3. IgA Deficiency presents with anaphylaxis. In future use donation from IgA deficient donor or washed red cells. 4. Febrile nonhemolytic rxn results in a small rise in temperature and needs no therapy, the reaction is against the donor’s white cell antigens. Prevent by using filtered blood transfusion in future. 5. Minor blood group incompatibility results in delayed jaundice, no therapy needed.
Leukemia Acute leukemias present with signs of pancytopenia, such as fatigue, bleeding, and infections from non-functional white blood cells.
Acute Myelogenous Leukemia • •
AUER RODS Mostly occurring in adults (up to 80%)
Diagnosis:
•
The best initial test is peripheral smear showing blasts
Treatment: •
Best initial therapy for AML is Idarubicin (or daunorubicin) and cytosine arabinoside
Acute Lymphoblastic Leukemia
• • • • •
The most common malignancy in children Is the leukemia most responsive to therapy Is a neoplasm of early lymphocytic B cell precursors Histology reveals predominance of lymphocytes Poor prognosis when age 9, WBC’s >10^5, or CNS involvement
Diagnosis:
•
The best initial test is peripheral smear showing blasts
Treatment:
•
Idarubicin + cytosine arabinoside + intrathecal methotrexate.
Acute Promyelocytic Leukemia(M3) This leukemia is associated with disseminated intravascular coagulopathy Treatment:
•
Idarubicin + cytosine arabinoside + all trans retinoic acid(ATRA)
Chronic Myelogenous Leukemia(CML) Signs and Symptoms: • • •
•
Elevated white cells that are predominantly neutrophils Splenomegaly is frequent. Untreated CML has the highest risk of transformation into acute leukemia of all forms of myeloproliferative disorders. Associated with Philadelphia Chromosome
Diagnosis: •
•
Best initial test is Leukocyte alkaline phosphatase score (LAP score). An elevated PMN count with low LAP score is CML. Reactive high white counts from infection give an elevated LAP score, LAP is up in normal cells, not CML. The most accurate test is finding the Philadelphia Chromosome
Treatment: • •
Best initial treatment is Imatinib (Gleevec) Bone marrow transplant is the only cure for CML, but is never the best initial therapy, because Imatinib leads to 90% hematologic remission with no major adverse effects.
Chronic Lymphocytic Leukemia(CLL) Seen in people older then 50yr of age Signs and Symptoms:
• • • •
Often asymptomatic Organomegaly Haemolytic anemia Thrombocytopenia
Diagnosis:
•
Best initial test is the peripheral smear showing ‘smudge cells’
Treatment: • •
At stages 0 and 1, there is no treatment required At advanced stages give fludarabine or chlorambucil
Hairy Cell Leukemia Seen in middle‐aged people and presents with massive splenomegaly and pancytopenia Diagnosis: •
The Most accurate test is the tartrate resistant acid phosphatase(TRAP) smear showing hairy cells
Treatment:
•
The best initial therapy for Hairy Cell leukemia is cladribine or 2‐CDA
Myelofibrosis • •
•
Presents similarly to hairy cell leukemia except there will be a normal TRAP level The key diagnostic feature is the “tear‐drop” shaped cells on peripheral smear There is no specific therapy for myelofibrosis
Polycythemia Vera (Erythrocytosis) This presents with headache, blurred vision, dizziness, and fatigue. All due to thickened blood Signs and Symptoms:
• • •
Everything above Pruritis following hot showers or baths due to histamine release Splenomegaly
Diagnosis:
• •
Very high hematocrit with a low MCV Get an ABG to rule out or in hypoxia as a cause of erythrocytosis
Treatment:
• • •
The best initial therapy is phlebotomy Hydroxyurea can be given to lower the cell count Give daily aspirin
PLASMA CELL DISORDERS
Multiple Myeloma This condition presents most commonly with bone pain due to fractures occurring from normal use Diagnosis: • • •
• • • • •
The most specific test is a bone marrow biopsy Skeletal survey to detect punched out osteolytic lesions Serum protein electrophoresis(SPEP) to look for elevated monoclonal antibody (usually IgG) Urine protein electrophoresis(UPEP) to detects Bence‐Jones proteins Peripheral smear showing “rouleaux” formation of blood cells. Elevated calcium levels due to osteolytic lesions Beta 2 microglobulin level is a prognostic indicator BUN and Creatinine to detect renal insufficiency
Treatment:
• • •
Steroids and Melphalan The most effective therapy is bone marrow transplant Treat all underlying co‐morbidities
Waldenstrom’s Macroglobulinemia This is a hyperviscosity of the blood due to overproduction of IgM Signs and Symptoms:
• • • • •
Blurred vision Confusion Headache Enlarged lymph nodes Splenomegaly
Diagnosis: •
•
The best initial test is the serum viscosity (increased significantly) and SPEP for IgM levels There will be no specific finding on the CBC
Treatment: • •
Plasmapharesis is the best initial therapy Can also give fludarabine or chlorambucil
Aplastic Anemia • • •
Presents as pancytopenia with no identifiable etiology. If pt is 50), give antithymocyte globulin and cyclosporine.
LYMPHOMAS
Present with enlarged lymph nodes that are most commonly seen in the cervical area Hodgkin’s disease occurs in a bimodal age distribution (young and old), and is characterized by Reed-Sternberg cells
Reed-Sternberg Cell
Non‐Hodgkin’s disease is commonly seen in HIV patients Diagnosis: •
The best initial diagnostic test for both types of lymphomas is lymph node biopsy
Once excisional biopsy shows abnormal architecture, further testing to determine stage of the lymphoma needs to be done. 1. 2. 3. 4.
Stage 1 single lymph node group Stage 2 2 LN groups on one side of diaphragm Stage 3 LN involvement on both sides of diaphragm Stage 4 widespread disease
HD and NHL present with stages as follows: HD ‐ 80‐90% pres w/ stage 1 and 2 NHL ‐ 80‐90% pres w/ stages 3 and 4
How to stage: CXR, CT with contrast (Chest/abdomen/pelvis/head), and BM biopsy. Treatment: 1. Localized disease (stage 1,2) without “B” symptoms is treated predominantly with radiation. 2. More advanced stages 3,4 is treated with chemotherapy.
B SYMPTOMS: Are systemic symptoms such as:
FEVER
Specific treatments:
NIGHT SWEATS
1. HD: ABVD (adriamycin[doxorubicin], bleomycin, vinblastine, dacarbazine) WEIGHT LOSS 2. NHL: CHOP (cyclophosphamide, hydroxyadriamycin, oncovin[vincristine], and prednisone) * Also test for anti‐CD20 antigen and if present, add Rituximab, which adds efficacy to CHOP.
COAGULATION DISORDERS
Von Willebrand’s disease (VWD) Is due to platelet dysfunction, not a lower number of platelets •
• • •
Bleeding from PLT dysfunction, superficial bleeds from skin and mucosal surfaces, such as gingival, gums, and vagina. Epistaxis common Bleeding often worsened with use of aspirin PLT count is normal
Diagnosis: • •
Best initial test is platelet function test The most accurate test is a ristocetin cofactor assay and a VWF level (If VWF is normal, ristocetin tells you if it is working properly)
Treatments: •
•
First line treatment is desmopressin or DDAVP, which causes the release of subendothelial stores of VWF and co‐factor VIII If desmopressin doesn’t work, give factor VIII replacement
Platelettype bleeding causes: petechiae, epistaxis, purpura, gingival, gums, vaginal Factortype bleeding causes: hemarthroses, hematoma Idiopathic Thrombocytopenic Purpura (ITP) ITP is a diagnosis of exclusion that presents with platelet‐type bleeding and a platelet count of 95% of time is has one of these features. CERVICAL CANCER • •
•
Start pap smears at 21, or 3yrs after onset of sexual activity Do pap smears every 3 yrs until age 65. Stop at 65 unless there has been no previous screening. Administer HPV quadrivalent vaccine to all women 13‐26yr
Following up an abnormal pap smear:
1. An abnormal pap smear with low‐grade or high‐grade dysplasia should be followed by colposcopy and biopsy. 2. A pap smear showing atypical squamous cells of undetermined significance (ASCUS), do HPV testing. If HPV (+), proceed to colposcopy, if HPV (‐), do repeat pap in 6mnth 3. Once pap smear normal, return to routine testing
* Pap smears lower mortality in screen populations, but still not as much as mammography because incidence of cervical CA is less than that of breast cancer. PROSTATE CANCER • •
No proven screening method that lowers mortality rate. PSA and DRE not proven to lower mortality. Do not routinely offer these tests, however if pt asks for them, you should perform.
Treating prostate cancer: 1. Localized: Surgery and either external radiation or implanted radioactive pellets (nearly equal in efficacy) 2. Metastatic: Androgen blockade is standard of care, use flutamide (testosterone receptor blocker) AND leuprolide or goserelin (GNRH agonists). * There is no good chemotherapy for metastatic prostate cancer, treatment is hormonal in nature. *Remember the 5‐alpha‐reductase inhibitor finasteride is used for BPH, not cancer A man with prostate cancer presents with severe, sudden back pain. MRI shows cord compression, and he’s started on steroids. What’s the next best step in mgmt? FLUTAMIDE (to block temporary flare up in androgen levels that accompanies GNRH agonist treatment
OVARIAN CANCER Key feats are women >50 with increasing abdominal girth at same time as weight loss. Diagnostic testing: • •
There’s no routine screening test CA125 is a marker of progression and response to therapy, not a diagnostic test
Treatment: • •
Treatment is surgical debulking followed by chemotherapy, even in cases of local metastatic disease. Ovarian ca is unique in that surgical resection is beneficial even when there’s a large volume of tumor spread through the pelvis and abdomen. If possible, removing all visible tumors helps.
TESTICULAR CANCER
• • •
Presents with painless scrotal lump in a man 35, Women >45
Chapter 18 Dermatology
Using Topical Steroids Potency Low Moderate
Medication 1% hydrocortisone 0.1% triamcinolone
High
Fluocinonide
Very High
Diflorasone
Use Face, genitalia, and skin Body/Extremities, face, genitalia, and skin folds For thick skin. Never on face Thick skin or severe body needs
Acne •
An infection of the pilosebaceous gland caused by the bacteria Propionibacterium acnes
ACNE Signs and Symptoms: •
Blackheads (open comedones) and whiteheads (closed comedones)
Treatment: • • •
Mild disease should be managed with topical antibiotics such as clindamycin, erythromycin, in addition to benzoyl peroxide Moderate disease should combine benzoyl peroxide with retinoids Severe disease should be managed with oral antibiotics and oral retinoic acid derivatives
Bacterial Infections of the Skin Impetigo A superficial skin infection limited to the epidermis
Impetigo • •
Is often described as being “honey‐colored”, “wheeping”, or “oozing” Usually caused by Staphylococcus, but may also be due to Strep Pyogenes
Treatment: •
Mupirocin (A topical antibiotic) and/or antistaphylococcal oral antibiotics
Erysipelas A skin infection of the epidermis and the dermis, which is usually caused by Strep Pyogenes. This condition is often described as being bright red, angry, and swollen.
Erysipelas •
With erysipelas may come fever and chills
Treatment: •
Penicillin G or ampicillin if diagnosis is Streptococcus
Cellulitis An infection caused by Staphylococcus and Streptococcus that infects the dermis and the subcutaneous tissues. Managed with antistaph drugs such as oxacillin and nafcillin.
Cellulitis
Folliculitis An infection of the hair follicle, may progress to a worse infection called a furuncle. Usually caused by staphylococcus, if acquired from a hot‐tub it can be due to Pseudomonas, fungi, or virus Look for this around the beard area where there are accumulations of pus‐like material.
Folliculitis Treatment: • •
Local care and topical mupirocin Severe cases that progress require systemic antistaphylococcal antibiotics
Necrotizing Fasciitis Is a severe, life‐threatening skin infection. It begins as a cellulitis that dissects into the fascial planes of the skin. MCC by strep and Clostridium Presentation: • • • •
High fever Extreme pain that is worse than it looks Bullae Crepitus
Necrotizing Fasciitis Diagnosis: • •
CT or MRI looking for air in the tissue and/or necrosis Elevated creatine phosphokinase
Management/Treatment: • • •
Surgical debridement Combination beta lactam/beta lactamase medications If it is caused by Strep Pyogenes, give clindamycin + PCN
Scarlet Fever Is caused by Strep Pyogenes, and looks like a combination of a rash and goosebumps
Scarlet Fever Signs and Symptoms: • • • • • • •
Rough skin Strawberry tongue Beefy‐red pharynx Rash is most intense in the axilla and groin (In the creased areas of skin) Desquamation of hands and feet occurs as rash resolves May have fever, chills, sore throat, cervical adenopathy Glomerulonephritis is a complication
Treatment: •
Penicillin
Common Dermatologic Disorders Eczema • • • •
Is a superficial, itchy, erythematous lesion The rash develops after itching Commonly seen on the flexor surfaces Diagosis is clinical
Eczema Treatment: Avoidance of irritants and triggers, keep skins moisturized, antihistamines/steroids are good for relief from inflammation and itching There are many variations of Eczema, including: 1. Atopic Dermatitis – this is the classic where itching causes a rash 2. Contact dermatitis – an itchy rash at the site of contact, classically caused by contact with nickel, chemicals, or poison plants 3. Seborrheic dermatitis – scaling and flaking in areas of sebaceous glands
Psoriasis • • • • •
Presents as pink plaques with silver scaling Occurs on the extensor surfaces such as the elbows and knees There is often pitting of the fingernails The classic finding is known as “Auspitz Sign”, which is pinpoint bleeding when the scale is removed This is diagnosed clinically
Psoriatic Plaque Treatment: 1st line is Topical steroids 2nd line is UVA light and may be used as an adjunct/prophylactic 3rd line is methotrexate and clyclosporin Urticaria • • • • •
Is a condition caused by mast cell degranulation and histamine release Presents with the classic “wheals” that are intensely itchy “Dermographism” is seen where you can write a word with your finger on the skin and it will remain Most lesions are IgE‐mediated (thus a type 1 sensitivity) Diagnose this condition by scrapings
Urticaria Treatment: • • •
Avoid triggers Give antihistamines/steroids This can possibly affect the respiratory tract which would then involve securing an airway
Vitiligo • • • •
There is a loss of melanocytes in discrete areas of the skin Borders are sharply demarcated Usually seen in darker patients Possibly autoimmune in nature
Vitiligo Treatment: •
Mini‐grafting can restore pigment to areas where it is lacking
Albinism • • • •
Failure of melanocytes to produce pigment, due to a tyrosine deficiency Patient has white skin, iris translucency, decreased retinal pigment, nystagmus, and strabismus Avoid sun exposure and use sunscreen all the time There is an increased risk of skin cancer due to lack of protection from the sun
Albinism
Blistering Disorders Pemphigus Vulgaris • • •
A rare autoimmune disorder affecting people between 20‐40yr of age Bullae slough off easily and leave large denuded areas of skin, this is know as “Nikolsky’s sign”, this predisposes to an increased risk of infection Fatal condition if not managed properly
Pemphigus Vulgaris Diagnosis: •
Immunofluorescence of the surrounding epidermal cells shows a “tombstone” fluorescent pattern
Treatment: •
High‐dose oral steroids
Bullous Pemphigoid • • • •
An autoimmune condition that affects mostly the elderly Less severe than pemphigus vulgaris Presents with hard and tense bullae that do not rupture easily Prognosis is much better than that of pemphigus vulgaris
Bullous Pemphigoid Diagnosis: • •
Skin biopsy showing a linear band along the basement membrane on immunofluorescence Increased eosinophils found in the dermis
Treatment: •
Oral steroids
Erythema Multiforme • •
Is a hypersensitivity reaction to drugs, infections, or systemic disorders Presents with diffuse and erythematous target lesions that are highly differing in shape
Erythema Multiforme Diagnosis: •
Is clinical but a history of herpes infection makes this a likely diagnosis
Treatment: •
Stop offending causes and treat if there is a history of herpes with acyclovir
Porphyria Cutanea Tarda • • •
An autosomal disorder of impaired heme synthesis Get blisters on sun‐exposed areas of the face and hands Differentiate this porphyria by the absence of abdominal pain
Porphyria Cutanea Tarda Diagnosis: •
Wood’s lamp of urine, where the urine fluoresces with an orange‐pink color due to the increased levels of uroporphyrins
Treatment: • • • •
Sunscreens used liberally Phlebotomy Chloroquine Avoidance of alcohol
Parasitic Infections of the Skin Scabies • •
Presents as severely itchy papules and burrows that are located along the webs of the fingers Highly contagious
Scabies infection Diagnosis: •
Identify the Sarcoptes Scabiei mite from a skin scraping under the microscope
Treatment: • •
Permethrin 5% create to the entire body for those infected and close contacts for 8‐10hr, repeated in another week Wash all linens and bedding in hot water the same day as cream application
Pediculosis Capitis (Head Lice) • •
Itching and swelling of the scalp Common in school‐aged children
Diagnosis: •
Microscopic exam of the hair shaft will show lice attached to shaft
Treatment: • •
Permethrin shampoo or gel to the scalp Repeat applications are commonly required
Pediculosis Pubis (Crabs) • •
Extremely itchy papules in the pubic region May also be along the axilla, buttocks, eyelashes, eyebrows, and periumbilical area
Diagnosis: •
Microscopic identification of lice
Treatment: •
Permethrin shampoo left on for 10 minutes, and repeated again within a week
Cutaneous Larva Migrans • • •
Is a snake‐like, thread‐like lesion that marks the burrow of the nematode larvae Often seen on the hands, back, feet, and buttocks Is caused by hookworms, namely Ancylostoma, Necatar, and Strongyloides
Cutaneous Larva Migrans Diagnosis: • •
A history of skin being exposed to moist soil or sand Presence of classic lesion
Treatment: •
Ivermectin orally or Thiabendazole topically
Fungal Cutaneous Disorders Disease Tinea
Candida
Tinea Versicolor
Onychomyco sis
Signs and Symptoms Itchy, scaly, well demarcated plaques. Black dots seen on scalp Itchy, scaly plaques, usually in skin fold areas
Pityrosporu m Ovale. Sharply demarcated hypopigment ed macules on face and trunk in the summer. Macules do not tan Thickened, yellowing of the fingernails and toenails.
Diagnosis KOH Prep
Treatmen t Topical Antifungal s
KOH prep showing budding yeasts + pseudohyph ae
Topical Nystatis or Oral Fluconazo le
KOH prep shows the classic “Spaghetti and meatball appearance”
Selenium Sulfide shampoo on affected area for 7 days.
Clinical Fluconazo and/or KOH le or prep Itraconazo le
Skin Cancer Cancer Type Malignant Melanoma
Squamous Cells Carcinoma
Basal Cell Carcinoma
Kaposi’s Sarcoma
Cutaneous T‐ cell Lymphoma
Image
Signs and Symptoms Seen MC in light‐skin people with increased sun exposure. Fits all ABCDE criteria Common in elderly. On sun exposed areas. Ulcerations and crusted MC and looks like a pearly papule with translucent borders Red/purple plaques. Caused by HHV8. Almost exlusively in AIDS patient Total body rash that is very itchy
Treatment
Prognosis
Excision + Poor with chemotherapy metastasis if there is metastasis
Excision + radiation
Moderate prognosis (better than melanoma but worse than basal cell)
Excision
Great prognosis – almost never metastasizes
Chemotherapy Good unless and HIV there is medications associated organ damage
Radiation, 7‐10 yr chemotherapy survival with no treatment.
Chapter 19 High-Yield Preventative Medicine
• • • • • •
• • • •
• •
•
Female patients > 65 yrs of age should receive a one‐time DEXA bone scan for osteoporosis Any female who is at least 60yr old and has 1 risk factor for osteoporosis The T‐score is used to assess bone density A T‐score between [‐1.5 to ‐2.5] is considered to be osteopenia A T‐score 50yr or to adults with chronic diseases (DM, CHF, etc) Pneumococcal vaccine given to all adults >65yr of age or to adults with chronic diseases
•
Screening for cervical cancer with a pap smear should start at 21yr of age or 3yrs after the onset of sexual activity (whichever comes first) If 2‐3 normal pap smears are done in a row and the woman is in a monogamous relationship, you can increase the time between pap smears to every 2‐3 years. Screening can stop at 70yrs of age Bupropion is FDA approved for smoking cessation and must be used in conjunction with counseling and nicotine replacement
• • •
• • • • • • • • •
•
Hepatitis A vaccine is given to men who have sex with men Meningococcal vaccine is given to those who live in close quarters with others Routine cholesterol screening should begin in patients at risk at 35yr of age in men and 45yr of age in women, then every 5yrs after that The most common vaccine‐preventable disease is hepatitis A When CD4 count drops below 200/250, start PCP prophylaxis with TMP‐SMX When CD4 count drops below 50, prophylax for mycobacterium avium complex with amoxicillin Routine screening for Chlamydia is now recommended for all sexually active females who are ≤ 24 yrs of age Mammograms should be done every 1‐2 yrs starting at 40yr in females with an average risk of breast cancer. There is no clear time when they should stop, but it should be no sooner than 70yr of age Pneumococcal vaccine is a capsular polysaccharide of the 23 most common types of pneumococcus, which yield a B‐cell response only, it is T‐cell independent Any female with a history of being treated for CIN2/3 should have pap smears with or without colposcopy and curettage every 6 months until three negative results are obtained (patients may resume standard screen after meeting this milestone)
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Usmlesuccess.net domain is owned by PAUL CIURYSEK and its registration expires in 25 days.
General Get moreUsmlesuccess.net whois history
PAUL CIURYSEK Owner since June 05, 2014 | ||
---|---|---|
25 days ago Expired on May 31, 2019 | 9 years old Created on May 31, 2010 | 1 year ago Changed at May 31, 2018 |
Registrar and Status
Registar | FASTDOMAIN, INC. |
Sponsor | BlueHost.Com |
Status | clientTransferProhibited |
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Usmlesuccess.net uses WordPress CMS and is hosted by Unified Layer.
IP Whois Get moreUsmlesuccess.net server history
- Unified Layer
- 67.20.67.177IP address
Server Technologies
- NginxBackend server
- WordPressCMS
Nameservers
- ns1.bluehost.com
- ns2.bluehost.com
host | value | ttl |
---|---|---|
usmlesuccess.net | 67.20.67.177 | 14399 |
host | value | ttl | pri |
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usmlesuccess.net | mx.spamexperts.com | 14399 | 10 |
usmlesuccess.net | fallbackmx.spamexperts.eu | 14399 | 20 |
usmlesuccess.net | lastmx.spamexperts.net | 14399 | 30 |
host | value | ttl |
---|---|---|
usmlesuccess.net | ns1.bluehost.com | 21599 |
usmlesuccess.net | ns2.bluehost.com | 21599 |
host | value | ttl |
---|---|---|
usmlesuccess.net | Mname: ns1.bluehost.com Rname: root.box412.bluehost.com Serial: 2018010400 Refresh: 86400 Retry: 7200 Expire: 3600000 Minimum-ttl: 300 | 21599 |
host | value | ttl |
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usmlesuccess.net | https://amigreat.weebly.com/j-cole-crooked-smile-free-mp3-download.html. Txt: v=spf1 +a +mx +ip4:69.89.31.212 ?all | 14399 |
Safety status of Usmlesuccess.net is described as follows: Google Safe Browsing reports its status as safe.
MyWOT
Overall reputation | Unknown |
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Trustworthiness | Unknown |
Privacy | Unknown |
Child safety | Unknown |
User reviews
Reputation | Unknown | |
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0 Epsxe isos games download. negative |