TWU FHN 2 Module 2
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| Referred from outside of abdomen Sources of pain: | Pneumonia
Myocardial infarction
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| Sources of pain: Intra-abdominal causes | causes can be referred to other areas
Pain of acute cholecystitis referred to right scapula
Stomach pain to shoulders
Pancreatic pain to back and L shoulder
Ovaries/uterine- inner thighs
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| Acute abdominal pain | is pain of sudden onset and is not always a surgical emergency
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| Chronic abdominal pain | is intermittent or continuous abdominal pain/discomfort lasting longer than 3 to 6 months
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| Acute abdomen | is a sudden (acute) condition of the abdomen requiring immediate surgical intervention
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| Children under 5 Appendicitis uncommon | Diagnosis often missed or delayed
Perforation more common
Disproportionately high percentage of deaths due to appendicitis
Difficult to determine unless abdominal tenderness, guarding, doubling up or vomiting present
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| Intussusception | peak incidence 6 months
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| Children age 5-12 Recurrent abdominal pain | Psychosomatic most common
Organic cause found in less than 10%
Always rule out constipation in children-common cause of GI complaint
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| Acute appendicitis | Common from age 5-15
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| Abdominal Pain - Adolescence | Inflammatory bowel disease
Screen for STD/pregnancy risk
Acute appendicitis
Peak incidence from age 10-15
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| abdominal pain - adult | PUD from 30-50
Nonspecific abdominal pain (NSAP) most common under 40
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| Cholecystitis higher incidence | obese females on estrogen
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| PUD higher incidence | males
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| Women of childbearing age with lower abdominal pain | LMP
Sexual history to assess risk for preg/STD
Contraception use
Vaginal discharge
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| Women of reproductive age at risk for: | Ectopic pregnancy
Endometriosis
Adenexal/Ovarian torsion
More common for UTI/pyelonephritis
PID
Pregnant female: Appendicitis difficult to diagnose due to upward displacement of vermiform appendix
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| Elderly Difficult to elicit accurate description of the pain Concurrent illnesses, complaints make it hard for patient to differentiate new symptoms | Malignancies-assess weight loss
Strangulated hernias
Intestinal obstruction
Diverticulitis
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| Blacks, Mediterranean descent- | sickle cell crisis
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| Native Americans | higher incidence gallbladder disease
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| Biliary colic typically develops | in the evening
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| Abdominal pain child under 5 | Consider poison
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| abdominal pain child 5-15 | consider constipation
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| appendicitis | Colicky, crampy periumbilical progressing to constant pain in RLQ
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| ureterolithiasis | Excruciating pain in R, LUQ, or flank radiating to groin or medial thigh-
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| pain Radiating to L shoulder | renal calculi, splenic rupture, ectopic pregnancy
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| GB disease | RUQ pain radiating to R scapula
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| Surgical scars | possible adhesions
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| Silver colored stools | stools-Carcinoma of Ampulla of Vater
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| Hernias | strangulation, obstruction
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| obstruction | Distention, abnormal peristalsis
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| Bluish periumbilical discoloration (Cullen sign)— | intraabdominal bleeding
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| Ecchymosis of flanks (Gray Turner sign)— | intraabdominal bleeding or pancreatitis
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| peritonitis, ileus | Absent or hypoactive bowel sounds-
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| Absent bowel sounds RLQ- | intussusception
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| Light percussion produces localized pain in presence of | peritoneal inflammation
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| Palpable gall bladder, Murphy’s sign | inspiratory halt
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| Blumberg | rebound tenderness
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| Positive McBurney sign | rebound tenderness over the McBurney point
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| Positive obturator sign | ruptured appendix or pelvic abscess causes irritation of the obturator muscle) With R leg flexed 90 degrees at the hip and knee rotate leg laterally and medially to elicit pain in hypogastric (pubic) region
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| Positive iliopsoas sign | Pain with raising the R leg from the hip while the examiner pushed downward
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| Positive Rovsing sign | RLQ pain intensified with LLQ palpation
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| Positive Markle (heel drop test) | Heel jar raises up to tip toes pain with relaxation when heel touches the floor
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| rectal Tenderness laterally to left | Diverticulitis with abscess
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| rectal Tenderness laterally to rt | Acute appendicitis
Intussusception
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| Upright chest | free intraperitoneal air under diaphragm (pneumoperitoneum
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| Suspected intestinal obstruction | Enlarged loops of bowel/ fluid levels
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| Suspected perforation (intestinal or gastric) | Free air in peritoneum
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| CBC with differential | Never diagnostic of acute appendicitis
Rising leukocyctosis supportive of acute infectious or inflammatory process
Anemia (acute/chronic) (may need corrected prior to surgery)
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| C Reactive Protein | Elevated in acute inflammation states
Nonspecific for location
Sensitivity for acute appendicitis 91%
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| Amylase, lipase, liver function tests | Elevated AST/ALT results from hepatocellular necrosis or inflammation-hepatitis
Elevated alkaline phosphatase seen in cholestasis or infiltrative liver disease
Elevated amylase and lipase associated with pancreatic pathology
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| If suspecting ectopic-order quantitative BhCG | Abnormal pregnancy usually associated with abnormally low beta-hCG
(Remember, qualitative BhCG reveals only positive or negative test result)
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| Stool O &P, C&S | Infection, parasites
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| Fecal occult blood | GI blood loss
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| Role of NP | Perform history and physical, form clinical impression, triage appropriately, order initial noninvasive studies and lab, and consult/refer to physician/surgeon
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| RUQ common causes | Cholecystitis, cholelithiasis
Leaking duodenal ulcer
Renal cell carcinoma/hydronephrosis
Hepatomegaly-Hepatitis
CHF
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| LUQ common causes | Gastroenteritis
Irritable colon
Splenic infarct
Pancreatitis
Aortic aneurysm (also in epigastric region)
Renal pathology
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| Diagnostics to consider in RUQ/LUQ | Chest x-ray and EKG
Upright abdominal films
Upper abdominal US
Serum amylase, lipase, transaminases
Radionuclide scan (HIDA)
Upper GI endoscopy
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| Epigastric pain Most common causes | GERD
Peptic Ulcer Disease
Pancreatitis
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| Diagnostics to consider in epigastric pain | C-xray, EKG
Obtain upright abdominal films
Upper GI endoscopy
RUQ ultrasound
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| Generalized Abdominal Pain Common causes | Peritonitis
Pancreatitis
Sickle cell crisis
Early appendicitis
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| Diagnostics to consider in generalized abdomial pain: | Abdominal films
CT scan
Abdominal angiogram
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| Periumbilical Abdominal Pain Common causes | Appendicitis
Small bowel obstruction
Gastritis
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| Diagnostics to consider in periumbilical pain: | Lab-CBC, Chemistry (CMP)
Abdominal x-rays and ultrasound
Contrast enema (consult with surgeon first)
Colonoscopy if indicated
CT scan
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| RLQ causes | appendicitis
ectopic pregnancy
Renal calculi
Ovarian cyst/torsion
Colon cancer
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| LLQ causes | Most common cause is diverticulitis
Ulcerative colitis/Crohns
Colon cancer
Ovarian cyst/torsion
Endometriosis
uterine fibroids
Renal calculi
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| Diagnostics to consider in RLQ/LLQ pain: | Pelvic and rectal exam is mandatory
UA, C & S, cervical cultures, wet prep, CBC, preg. test
Abodominal/Pelvic sono
CT abdomen/pelvis
IVP if indicated
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| Pelvic pain-pain in hypogastrium or suprapubic region Common causes | Prostatitis-also mid sacral pain
PID-referred to midline
Ectopic pregnancy-referred to midline
Acute cervicitis-also midsacral pain
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| PUD ulcer is | a break in the gastric or duodenal mucosa that arises when the normal mucosal defensive factors are impaired.
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| Peptic Ulcer Three major causes: | H-pylori
NSAID use
Hypersecretory states such as Zollinger-Ellison
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| Other causes of PUD | Stress/trauma
Severe burns
CNS trauma
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| Disease associated with PUD | Cirrhosis
Chronic pulmonary disease
Renal failure
Renal transplant
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| Helicobacter pylori infection | spread person to person, may be fecal-oral route or as a reservoir in water sources.
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| H-pylori causes chronic active inflammation | may resolve spontaneously
may progress to gastritis, PUD, gastric adenocarcinoma or mucosa-associated lymphoid tissue lymphoma
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| PUD symptoms | Epigastric pain
gnawing or burning 1-3 hrs after eating-relieved by food or antacids-may radiate to the back
Nausea/Vomiting
may or may not be present
Heartburn
Chest discomfort
Hematemeis or melena
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| PUD Diagnosis | May have anemia with blood loss
Elevated serum amylase in patient with severe epigastric pain suggests ulcer penetration into the pancreas.
Testing for H-pylori
Serum gastrin to screen for Zollinger-Ellison Syndrome
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| PUD Differential Diagnosis | GERD
Biliary tract disease
Pancreatitis
Musculoskeletal
Gastric cancer/pancreatic cancer
Crohn’s Disease
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| Invasive Testing for H-pylori | endoscopy for biopsy and histology
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| Testing for H-pylori Noninvasive | Serum: Screen for H-pylori IgM, IgA antibodies for active disease-
Urea Breath Test
Fecal antigen test
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| Urea Breath Test | H. pylori produce urease-urea changes to ammonia causing a rise in pH which results in a color change
best for determination between active and resolved infection & is considered the gold standard-useful to confirm eradication
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| Fecal antigen test | The H-pylori antigen is shed in the stool of clients with active disease
Appears to be as sensitive as the breath test.
Should be obtained14 days post treatment for PPI treatment regimens, 1 month for bismuth
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| Treatment for H-pylori Combination AntibioticTherapy Advised | Due to drug resistance to metronidazole (50%) and clarithromycin (7%) resistance
Amoxicillin and tetracycline with less resistance
Now recomending to save metronidazole for PCN allergic patients
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| Histamine (H2) receptor antagonist | Work by reversing the competitive inhibition of histamine that stimulates parietal cells to release gastric acid
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| Histamine (H2) receptor antagonist | Cimetidine (Tagamet) 400-800 po bid
Famotidine (Pepcid) 20mg QD
Ranitidine (Zantac) 150 mg bid
Nizatidine (Axid) 150mg po bid
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| Proton Pump Inhibitors | Provide decrease in acid secretion resulting in faster healing rates and symptom control.
Inhibit parietal H+,K+ ATPase blocking gastric secretion
Slightly more effective than H2 receptor antagonists (Tagamet, Pepcid, Zantac
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| PPI Use to treat PUD Uncomplicated treat for 4 wks, 6 wks with complications | Omeprazole (Prilosec) 20-40mg
Lansoprazole (Prevacid) 15-30mg
Pantoprazole (Protonix) 40mg
Esomeprazole (Nexium) 20-40mg
Rabeprazole (Aciphex) 20mg
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| Agents to enhance mucosal defenses | Sucralfate, bismuth, misoprostol and low doses of aluminum-containing antacids have all been shown to promote ulcer healing through the enhancement of mucosal defensive mechanisms.
Bismuth also has direct antibacterial properties
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| Combination Drug Therapy for H. pylori PUD Triple or quadruple therapies available | Example:
Proton Pump Inhibitor bid
Bismuth Subsalicylate 2 tabs qid
Tetracycline 500mg qid
Metronidazole 250mg qid
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| Prevpac | 1 dose bid x 14 days
lansoprazole (Prevacid) 30mg 1 tab. bid
amoxicillin 500mg 2 tabs. bid
clarithromycin 500mg 1 tab bid
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| NSAID Induced PUD | Prevention:
With chronic conditions that require use of NSAID -give with PPI
Take NSAID with meals
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| Treatment of NSAID PUD | Stop NSAIDs and offending agents: ETOH, smoking
Treat with PPI
Uncomplicated for 4 weeks
Complicated treat for 8 weeks
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| Zollinger-Ellison Syndrome | Caused by gastrin-secreting tumors which result in hypergastrinemia and acid hypersecrection.
90% of pts with syndrome develop PUD
< 1% of PUD is caused by Zollinger-Ellison Syndrome
2/3 are malignant
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| Reflux: | normal physiologic occurrence produced by proximal gastric distention resulting in transient relaxation of the lower esophageal sphincter (LES) with symptoms of heartburn and acid regurgitation (dyspepsia)
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| Gastroesophageal Reflux Disease (GERD): | inappropriate relaxation of the LES with accompanying symptoms
Heartburn and acid reflux
Acid regurgitation
Non-cardiac chest pain
Chronic cough or asthma
Chronic laryngitis and hoarseness
Dysphagia
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| Obesity: doubles risk for GERD | Obesity: increased risk for GERD related complications
Erosive esophagitis
Barrett’s Esophagus
Esophageal adenocarcinoma
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| Lifestyle risk factors that reduce sphincter tone: | Smoking
Alcohol consumption
Coffee and chocolate
Estrogen or progesterone
Other drugs
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| GERD Associated diseases: | Irritable bowel syndrome
Connective tissue disorders (scleroderma)
COPD
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| GERD Presentation: Pediatrics | Vomiting is most common presentation
Hyperirritability
Refusal of feeding
Asthma in children
Although reflux is usually harmless; may lead to FTT or esophagitis
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| GERD Alarm Symptoms: Adults | Weight loss
Persistent vomiting
Difficulty swallowing (dysphagia)
Symptoms of GI bleeding (hematemesis or melena)
Anemia
Refer to gastroenterologist for further evaluation or ER if volume depletion
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| GERD Alarm Symptoms: Children | Failure to gain weight at an appropriate rate
Developmental delays
Projectile vomiting
Persistent respiratory symptoms
Changes in neurobehavior
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| GERD Essentials of diagnosis | Diagnosis is based on patient’s symptom report alone (clinical diagnosis)
CBC and stool for occult blood on all
CBC: Identify anemia
Fecal occult blood: Identify GI bleeding
If anemia or GI bleed (alarm) refer to gastroenterology
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| GERD Diagnostic testing recommended for: | Patients not responding to initial medical therapy
Alarm symptoms
Persistent symptoms
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| GERD Diagnostic Studies | Endoscopy with biopsy is recommended study
Demonstrates abnormalities in < 50% of patients some normal
Ambulatory esophageal pH monitoring-pH probe placed above esphageal sphincter-24hr ph monitoring
Esophageal manometry-to assess esophageal motility
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| GERD Differential diagnosis | Myocardial infarction
Esophageal spasm
Cholelithiasis
Angina pectoris
Children: pyloric stenosis; infections
Peptic ulcer disease
Reflux erosive esophagitis: pill induced damage, radiation esophagitis
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| GERD Complications | Barrett’s esophagus
normal squamous epithelium of esophagus replaced by a metaplastic columnar epithelium
10% of patients
Peptic stricture
10% of patients
solid food dysphagia
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| GERD Lifestyle Changes | Avoid lying down within 3 hrs of eating
Elevate HOB 4-6 inches or foam wedge, (worse with pillows)
Decrease abdominal pressure
Avoid constricting clothing.
Avoid NSAID, ASA
Avoid agents that relax the LES
Alcohol/smoking
Avoid acidic foods-
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| GERD Treatment for infants/children | In 85% self-limited, disappearing between 6-12 months
Frequent small feedings
Burp after each feeding; hold upright 15-30 minutes
Prone position not recommended due to danger of SIDS
Some authorities recommend thickening agents (rice cereal)
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| GERD 2005 American College of Gastroenterology (ACG) guidelines | For patients with history of uncomplicated GERD, 4 week trial of empiric therapy with a proton pump inhibitor
Lifestyle changes alone usually not able to adequately control symptoms
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| ProtonPump Inhibitors | Weak bases that are converted to the active form in highly acidic environments.
substantially decreases acid secretion of the parietal cells.
Can take with antacids
Food decreases absorption.
Much more expensive than H2 blockers
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| Proton Pump Inhibitors dosing for GERD | Once a day dosing
Before breakfast for best efficacy
Switch to bedtime if nocturnal symptoms
BID dosing if incomplete response to once daily
If no response with BID dosing, considered a treatment failure and referral for further investigation
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| Drug-drug Interactions and Cardiac Events | Some PPIs may interfere with clopidogrel (antiplatelet drug) reducing the antiplatelet effect
Conflicting studies
FDA warning in 2009 of possible interaction between clopidrogel and omeprazole and esomeprazole
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| PPI Dosing for GERD | Omeprazole (Prilosec) starting 20mg QD
Lansoprazole (Prevacid) 15-30 mg QD
Rabeprazole sodium (Aciphex) 20 mg QD
Pantoprazole sodium (Protonix) 40 mg QD
Esomeprazole magnesium (Nexium) 40mg QD
Dexlansoprazole (Kapidex) 30-60 mg QD
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| Caution for use of PPIs in liver impairment | Dosage adjustment necessary
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| GERD Long-term maintenance therapy | Erosive esophagitis must have long-term acid suppression to maintain healing
Once daily dose of PPI
Majority need once daily or on-demand PPI therapy
Can try to step-down to H2blocker
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| H2 Receptor Antagonists | Can be used if cost of PPIs is prohibitive
Bind to H2 receptors inhibit histamine and acid secretion on gastric parietal cells
Onset of action-30minutes
Bid dosing
Provide heartburn relief for about 8 hours
Reduce 24 hour acidity by 60%
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| GERD Antacids Provide the most rapid symptom relief (immediate) | Useful for occasional mild symptoms.
Duration only 2 hours
Caution magnesium antacids with renal damage.
Can help with diagnosis if symptoms are controlled with antacids
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| GERD Surgical treatment | Refer children for possible surgery if persistent vomiting with FTT, esophagitis or esophageal stricture, apneic spells or chronic pulmonary disease
Surgical fundoplication: relief of symptoms and healing of esophagitis in > 90% of selected patients
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| GERD Follow up by FNP | Re-evaluate adult in 1-2 weeks; if symptoms controlled, continue full course of therapy
If still symptomatic after course of therapy refer to gastroenterology for further evaluation
If control with Rx after 4-6 weeks, can discontinue and re evaluate.
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| GERD full course of therapy | 4 weeks therapy for proton pump inhibitors
6-8 weeks if H2 blockers
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| Cholelithiasis | The presence of stones within the gallbladder
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| Cholelithiasis - High risk patient | Female
Pregnancy
Crohn’s disease
Obesity
Rapid weight loss
Status post-bariatric surgery
Spinal cord injury
Pima Indian
Diabetes mellitus
Increasing age
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| High risk medications for Cholelithiasis | Estrogen
OCPs and HRT
Fibric acid agents (Lopid) Gemfibrozil
Ceftriaxone
Furosemide
Cyclosporine
Opiates
TPN
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| Risk reducers for cholelithiasis | Low-carbohydrate diet and physical activity may decrease risk.
Aspirin and NSAIDs may decrease risk
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| Clinical presentation Asymptomatic gallstones | No symptoms; gallstones visualized on radiologic exam done for another cause
Previously, cholecystectomy performed on only high risk patients
Currently, cholecystectomy NOT indicated for most asymptomatic patients
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| Symptomatic gallstones Biliary colic | Transient
Steady intense pain in RUQ that subsides gradually over 30 minutes to 2-3 hours
Nausea and vomiting
May be referred to R shoulder or scapula
Midepigastrum or other abdominal area
Atypically, chest pain
No associated lab findings
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| % of acute cases of biliary colic will resolve spontaneously | 60
Recurrent attacks common for years
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| Differential diagnosis of biliary colic | Peptic ulcer disease
Acute hepatitis
Renal colic
Appendicitis
Ileitis
Colitis
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| diagnosis of biliary colic | CBC with diff
Liver function testing (liver profile), CMP (chem profile) for hepatic enzymes
RUQ Ultrasound to confirm presence of gallstones (sensitivity >95%)
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| Management of biliary colic | Referral to surgeon for cholecystectomy
90% of all cholecystectomy is now laparoscopic
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| Medical Management of Biliary colic - referral then | Medical therapy may be indicated for patients at high risk for surgery (10% of symptomatic)
Oral dissolution agents (UDCA, CDCA)
Extracorporeal shock wave lithotripsy (ESWL)
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| Acute cholecystitis | Acute or chronic inflammation of the gallbladder
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| Pathophysiology of cholecystitis | Stone impaction within the cystic duct
Produces inflammation of gallbladder and adjacent peritoneum
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| Clinical presentation of cholecystitis (similar to episode of biliary colic, but additional as underlined): | History of biliary colic
Biliary colic symptoms >6 hours
Nausea/Vomiting
Low grade fever
Tender RUQ
Localized rebound
Positive Murphy’s sign
Mild jaundice (20%)
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| Cholecystitis Labs | Elevated bilirubin levels (jaundice rare)
Transaminase levels (ALT, AST) usually < 3 times the normal
Check CBC: Leukocytosis (12,000-15,000)
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| Complications of cholecystitis | Gangrenous cholecystitis (necrosis of GB wall)
Emphysematous cholecystitis (Severe form cholecystitis from gas-forming bacteria)
Gallbladder perforation caused by above
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| Cholecystitis Treatment | Most respond to conservative treatment
IV’s, antibiotics
Percutaneous cholecystostomy
Cholecystectomy recommended due to high rate of recurrence and complications
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| Choledocholithiasis | The presence of gallstones within the biliary tract
Choledocholithiasis develops in 15 % of patients with cholelithiasis
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| Choledocholithiasis pathophysiology | Stones originate from GB and obstruct ducts
Stones can develop in the ducts (especially if chronically infected)
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| Choledocholithiasis Clinical presentation | Jaundice
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| Choledocholithiasis Labs | Bilirubin 20-30 times normal
Alkaline phosphatase mild to 3-6 times normal
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| Choledocholithiasis Diagnosis | Ultrasound-shows bile duct dilatation, not initial finding so repeat in 2 weeks
Magnetic resonance cholangiography (MRCP)
Cholangiography most sensitive test
Percutaneously, surgically, or endoscopically (ERCP)
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| Choledocholithiasis Treatment | Remove stones at time of endoscopy via basket
Choledocholithotomy
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| Cholangitis: | Inflammation and infection of the biliary tree due to obstruction.
Carries 10% mortality rate
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| Suppurative cholangitis | Severe form of cholangitis.
Emergency requiring immediate surgical intervention
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| Cholangitis patho | Stone or malignancy obstructs biliary tree
Impairment of biliary excretion
Jaundice
Spilling of conjugated bilirubin into the urine
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| Cholangitis Bacteria - proliferate in resultant closed system | E. coli
Klebsiella pneumoniae
Bacteriodes fragilis
Enterococcus faecalis
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| Cholangitis - Clinical Presentation | Charcot’s triad
Jaundice
Abdominal pain
Intermittent fever and rigors
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| Charcot's Triad | Jaundice
Abdominal pain
Intermittent fever and rigors
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| Reynold’s pentad | Charcot’s triad PLUS
Hypotension
Altered mental status
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| Gallstone pancreatitis | Pancreatitis produced by gallstones
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| Gallstone pancreatitis Clinical presentation | Similar to acute cholecystitis
Epigastric pain radiating to back
Nausea vomiting
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| Gallstone pancreatitis Laboratory | Amylase, alk phosphatase, bilirubin elevated
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| Coronary heart disease | Most common cause of CVD and death in the US
Men are more often affected than women
Peak incidence for women is age 60-70, men age 50-60
4:1 before age 40
8 to 1 after age 40
over age 70 1 to 1
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| Ischemic Heart Disease Risk factors | Positive family history (onset prior to age 55 in men and 65 in women)
Age
Male gender
Blood lipid abnormalities
HTN
Physical inactivity
Cigarette smoking
Diabetes mellitus
Elevated blood homocysteine levels
Possibly chronic infection
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| Ratio of LDL to HDL | Ratios below 3 indicate lower risk
Ratios above 5 indicate higher risk
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| Ischemic Heart Disease Other possible risk factors | Elevated apolipoprotein(a)
Small dense LDL particles
Hypertriglyceridemia possibly now independent risk factor: usually associated with low levels of HDL
Elevated serum homocysteine
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|
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| High level of C-reactive protein associated with higher rate of ischemic events | Elevated serum CRP levels with High sensitivity assays i. e., hsCRP
1 mg/L – low risk for vascular events
1-3 mg/L- intermediate risk, > 3 mg /L – high risk
🗑
|
||||
| Possible inflammatory process in vessel wall | In healthy pts without hyperlipidemia but with hsCRP > 2mg/L Statin therapy has been shown to reduce the risk for MI, Stroke , unstable angina
🗑
|
||||
| Coronary arterial calcification correlates with the presence and severity of CAD. | Electron Beam CT or multidetector CT can accurately quantify coronary calcification and can be used as screening tests in asymptomatic patients.
🗑
|
||||
| Kawasaki disease in kids | cause coronary vasculitis and aneurysms which in the setting of a hematological disorder can cause coronary embolism.
🗑
|
||||
| Other causes for myocardial ischemia | Spontaneous coronary spasm resulting in Prinzmetal angina
Cocaine use
Thyrotoxicosis, aortic stenosis, aortic insufficiency, tachyarrhythmia or sepsis: Myocardial O2 Demand significantly exceeds supply
🗑
|
||||
| ANGINA PECTORIS | Increased oxygen demand is the most frequent mechanism
🗑
|
||||
| ACUTE CORONARY SYNDROME-Unstable angina and myocardial infarction | Plaque disruption, platelet plugging and coronary thrombosis
🗑
|
||||
| Stable angina - fairly good prognosis | Typically, chest pain, pressure, or heaviness
Can radiate to jaw, arm, back, abdomen
Silent angina expressed as dyspnea
Atypical symptoms Nausea, diaphoresis, lightheadedness, anxiety
Occurs predictably with exertion
Resolves within minutes with rest
🗑
|
||||
| Progressive angina | Increase in frequency, severity, or duration of anginal episodes during the last 6 weeks but not enough to require hospitalization.
🗑
|
||||
| Unstable angina-poorer prognosis | Described as a “crescendo” pain which occurs with exertion, or at rest, less responsive to medication-may result in complete occlusion or infarction
Episodes usually prolonged greater than 20 min.
Unable to walk 1-2 blocks, climb 1 flight of stairs
🗑
|
||||
| Stable Angina: | Increased oxygen demand-vessels cannot meet demand-responds well to meds and rest.
Normal ECG at rest or may show ST or T abnormalities
ECG abnormalities (depression or elevation of ST segment) with angina episode or with stress testing
🗑
|
||||
| unstable angina | Large blockages or artery; ruptured plaque
Blood clot may form which impedes or blocks flow
ECG shows ST segment depression
🗑
|
||||
| In MI plaque or thrombus completely blocks major coronary artery | Irreversible necrosis and cellular death
🗑
|
||||
| Essentials of diagnosis- stable angina | Precordial chest pain
Stress or exertion precipitates
Nitrates or rest relieves
ECG or scintigraphic evidence of ischemia during pain or stress testing
Angiographic demonstration of significant obstruction of major coronary vessels
🗑
|
||||
| Prinzmetal’s Variant Angina | Clinical syndrome where chest pain occurs without usual precipitating factors-associated with ST segment elevation rather than depression.
Associated more with coronary arterial vasoconstrictions (spasms).
🗑
|
||||
| Women < 50
Early morning symptoms
associated with arrhythmia or conduction defects
Avoid precipitants smoking and cocaine
Responds to calcium channel blockers alone or in combo with nitrate preparations.
Avoid betablockers unless fixed stenosis
🗑
|
|||||
| Costochondritis | pain with palpation borders of sternum, may increase with movement
🗑
|
||||
| Aortic dissection | (asymmetry of pulses and blood pressure in both arms
🗑
|
||||
| Pulmonary emboli | pleuritic chest pain, tachypnea, wheezing, and hemoptysis
🗑
|
||||
| If suspect acute MI | Troponin rises at 3-4 hours after will peak at 12-16 hours.
It is found that measuring troponin increased the number of patients diagnosed with AMI by 10.4% over patients diagnosed using CK and CK-MB levels
CK and CK-MB q 8h
3 negatives exclude MI
🗑
|
||||
| Angina Pectoris: Evaluation Lab | Lipids
Other as indicated by H & P
CBC (check for anemia)
TSH (underlying hypo or hyperthyroidism)
Glucose, complete metabolic profile
🗑
|
||||
| Angina Pectoris: Evaluation Chest x-ray | Heart size
Heart failure
Helps to R/O pulmonary edema, pleural effusion, and aortic aneurysm
🗑
|
||||
| Angina Pectoris: Evaluation ECG | 1/4 have normal; remainder may have
Changes associated with old MI
Nonspecific ST-T changes
A-V or intraventricular conduction defects
Left ventricular hypertrophy
🗑
|
||||
| Angina Pectoris: Evaluation During attack | Characteristic change is horizontal or downsloping ST segment depression
Reverses after ischemia disappears
T wave flattening or inversion
ST segment elevation suggests severe ischemia (coronary spasm)
🗑
|
||||
| Angina Pectoris: Evaluation Exercise ECG | Most useful noninvasive procedure
Carries risk of 1 infarct or death/1000 tests
Aortic stenosis is contraindication for testing
Beta Blockers affect test results
🗑
|
||||
| Indications for Stress Testing | To confirm the diagnosis of angina
To determine the severity of limitation of activity due to angina
To assess the progression of disease
To evaluate response to therapy
Less frequently??--to screen asymptomatic populations for silent coronary disease
🗑
|
||||
| Angina Pectoris Evaluation Coronary Angiography | Definitive diagnostic procedure for CAD
Low mortality/morbidity
High cost
With other noninvasive techniques it is usually not indicated solely for diagnosis
🗑
|
||||
| Angina Pectoris: Evaluation Coronary radionuclide angiography | Radioactive isotope is injected IV and sequential images are obtained to visualize vessels and chambers-evaluates ejection fractions and pulmonary blood volumes.
🗑
|
||||
| Angina Pectoris: Treatment Primary prevention | Smoking cessation
Lipid management
Control HTN
AHA Step II Diet
Regular exercise as tolerated
High intensity exercise especially in the cold (skiing, shoveling snow etc) is not advisable
Ideal body weight
🗑
|
||||
| Angina Pectoris: Treatment Antiplatelet agents | ASA-- 80-325 mg/day (cheap)
Plavix 75 mg (clopidogrel bisulfate)-- slight edge over ASA in reducing of atherosclerotic events (expensive)
ACE inhibitors to patients who have DM or LV dysfunction unless contraindicated.
🗑
|
||||
| Hormone Replacement Therapy is NOT ADVISED FOR PREVENTION or TREATMENT OF CAD | - BLACK BOX WARNING Recent study has indicated an increase risk of heart disease in men who use testosterone therapy. This is under FDA review
🗑
|
||||
| Angina Pectoris: Treatment Infrequent anginal attacks--stable angina | Nitrostat 1 tab (0.3 -0.4 mg) SL or
Nitrolingual 1-2 sprays onto or under tongue
DO NOT USE NITRATES WITH VIAGRA
Causes precipitous drop in blood pressure!
Can take prophylactically--5-10 minutes prior to activity or sex
🗑
|
||||
| Angina Pectoris: Treatment Correct treatable conditions | HTN
Anemia
Valvular disease
Hyperthyroidism
Heart failure
🗑
|
||||
| Angina Pectoris: Treatment Daily attacks--stable angina | Initially Nitrate or B-blocker
B-blocker decreases heart rate and contractility
🗑
|
||||
| B-blocker | First-line therapy in most patients with chronic angina
Advantages: efficacious in prophylaxis
Initial therapy after MI due to cardioprotective effects
🗑
|
||||
| B-blocker Examples for angina tx | Atenolol (Tenormin) 50mg QD; increase to 100mg after 1 wk
Nadolol (Corgard) 40mg QD; increase in 3-7d to 80 (Max dose 240 mg QD)
🗑
|
||||
| B-blocker Disadvantages: | Serious SE’s in patients with COPD, sinus or AV block
Contraindication:
severe bronchospastic diseases
bradyarrhythmias
decompensated heart failure
Contraindicated in vasospastic angina
🗑
|
||||
| Angina Pectoris: Treatment Long acting nitrates Contraindications | Migraine or cluster h/a
Orthostatic hypotension
🗑
|
||||
| Angina Pectoris: Treatment Long acting nitrates | Isosorbide dinitrate (Isordil titradose)
Needs 8-10 h nitrate free interval daily
Initial h/a will abate in 1-2 wk
Isosorbide mononitrate (Ismo) 20mg on awakening and in 7 hrs
Nitroglycerine 2% ointment
Nitroglycerine patch
🗑
|
||||
| Angina: Treatment Calcium Channel Blockers | Block the inward movement of calcium through smooth and cardiac muscle.
Decrease the force of myocardial contraction
Increase exercise tolerance
Improve artery blood flow
Avoid in recent MI and with reduced LV function
🗑
|
||||
| Angina: Treatment Calcium Channel Blockers | Diltiazem HCl (Cardizem CD)
Verapamil HCl (Calan)
Dihydropyridines
Amlodipine (Norvasc); Nifedipine (Procardia XL)
🗑
|
||||
| Angina: Treatment Calcium Channel Blockers Disadvantages: | Disadvantages: Constipation, peripheral edema; no cardioprotective effect after MI; may worsen heart failure , serious SE’s
🗑
|
||||
| Angina: Treatment Calcium Channel Blockers Advantages: | Effective, useful with coronary artery spasm; possible anti-atherogenic effect
🗑
|
||||
| Angina: Treatment Calcium Channel Blockers Dihydropyridine group-do not affect the cardiac conduction system. | Nifedipine (Procardia XL)
Amlopidine (Norvasc)-less edema, decrease systolic B/P
Felodipine (Plendil)
Isradipine (DynaCirc)
Nicardipine SR (Cardene SR)
Nisoldipine (Sular)
🗑
|
||||
| Calcium Channel Blockers | NOT usually first choice for stable angina unless unable to tolerate beta blockers and diuretics
🗑
|
||||
| Calcium Channel Blockers | May be first line for Prinzmetal’s angina-
dihydropydines-do not affect the conduction system
verapamil and diltazem-less reflex tachycardia
🗑
|
||||
| may have AV and SA nodal blockade-don’t give with Beta Blockers: | Verapamil (Calan), Diltiazem (Cardizem)
🗑
|
||||
| Ranolazine (Ranexa) | Selective Inhibitor of late sodium influx:
Reduces sodium induced calcium overload in myocytes- antianginal /anti ischemic
No effects of HR or BP.
May be used as a first line or second line agent for stable angina.
500-1000mg PO BID
🗑
|
||||
| Myocardial Infarction | Irreversible necrosis of myocardial tissue as a result of inadequate blood flow for critical period of time.
🗑
|
||||
| Myocardial Infarction May result from: | Occlusive coronary thrombus *most common cause
More rarely
prolonged vasospasm
inadequate blood flow-shock
cocaine
embolic occlusion, vasculitis, aortic pathology
🗑
|
||||
| Thrombus Pathophysiology | Fibrous cap of an atherosclerotic plaque ruptures, which activate local hemostatic mechanism with the formation of platelet-fibrin thrombus.
Thrombus abruptly occludes the atherosclerotic coronary arteries, resulting in an MI.
🗑
|
||||
| Symptoms of acute MI | Occur at rest, usually in early AM
Similar to angina but more severe
NTG has little effect
Cold sweat, feels weak and apprehensive
Move about seeking position of comfort
Lightheaded, syncopal
Dyspnea, orthopnea
Cough, wheeze, nausea & vomiting
🗑
|
||||
| Signs of acute MI | Brady to tachycardia
BP high or low
Low grade fever after 12 hours
Heart sounds may be normal or include murmurs, gallops
🗑
|
||||
| Acute Myocardial Infarction Lab findings | Leukocytosis of 10,00-20,000 on day 2, resolving in 1 week
Serial cardiac enzymes--CK-MB isoenzymes may be positive within 6 hrs
Troponin I--sensitive at 10-14 hours
Elevated for 5-7 days
Troponin T
🗑
|
||||
| Acute Myocardial Infarction Essentials of Diagnosis | Sudden (but not instantaneous) development of anterior chest discomfort >30 minutes that may produce Arrhythmias, Hypotension,Shock or Cardiac failure
Rarely painless, masquerades as
Acute congestive heart failure
Syncope, stroke or shock
🗑
|
||||
| Acute Myocardial Infarction ECG | ST segment elevation or depression
Evolving Q waves
Symmetric inversion of T waves
🗑
|
||||
| Acute Myocardial Infarction Essentials of Diagnosis | Elevation of cardiac enzymes
CK-MB
Troponin T or
Troponin I
Appearance of segmental wall motion abnormality by imaging techniques
🗑
|
||||
| Acute Myocardial Infarction In Primary Care Setting KNOW THIS | Immediate transport-call 911 or EMS
ASA 325 mg (if not allergic)
Chew if enteric coated
O2 @ 2-4 liters by nasal cannula
Nitro SL or spray
ECG-12 LEAD
IV if available
See ACLS Guidelines
🗑
|
||||
| Acute Myocardial Infarction In Emergency Department Setting Termed Acute Coronary Syndrome | EKG within 5 minutes
ST segment elevation—repeat in 5-10 minutes if no elevation (to R/O a late occurring ST segment elevation)
Determine if ST segment elevation (STEMI)
Determine if non-ST segment elevation
🗑
|
||||
| Acute ST Segment Elevation MI (STEMI) Treatment | Angioplasty in 90 minutes
Currently first choice in therapy
Reduces fatality rate better than thrombolysis alone
Thrombolytics in 30 minutes
Only if NO angioplasty services
🗑
|
||||
| Unstable Angina and Non ST Segment Elevation MI (NSTEMI) Acutely presenting: | Partial occlusion
At high risk for ST Segment Elevation MI (STEMI) and sudden death
Immediate referral to ED
Admit if ischemia on ECG
ST segment deviation
new T wave abnormalities
new Left BBB
🗑
|
||||
| Unstable Angina and Non ST Segment Elevation MI-Chronic Tx In chronic phase, typically following revascularization | Aspirin 75-324 mg daily
Clopidogrel (Plavix) 75 mg daily for 9-12 months
Statins
ACE inhibitors
Beta blockers
Smoking cessation
Lo-fat low carb diet
Diabetes control
🗑
|
||||
| Anti-thrombolytics (used in STEMI) | Accelerates the formation of plasmin from plasminogen
Plasmin degrades:
Fibrin
Plasma proteins
Fibrinogen, prothrombin factors V and VIII
Produces a defective hemostasis
Drugs are clot specific or non-clot specific
🗑
|
||||
| Anti platelet agents Prevent platelet aggregation | ASA
Partially effective
Plavix (clopidogrel)
Acts by blocking ADP receptor
Potent irreversible antiplatelet drug
Others
Intravenous glycoprotein IIb/IIIa inhibitors
Specific indications prior to revascularization procedures or in ischemia
🗑
|
||||
| Antithrombin drugs | Heparin
Xarelto (oral factor Xa inhibitor)
This a new drug being suggested for use in dual antiplatlet therapy in patients with ACS. There are many outcomes studies supporting but it is not yet listed as indicated
Low-molecular-weight heparin (LMW)
🗑
|
||||
| Nursemaid Elbow | Result of being lifted or pulled by the hand
May be symptom of child abuse if recurrent
Symptoms
Presents with painful, fully pronated elbow
Complaint that child’s elbow will not bend
🗑
|
||||
| Nursemaid Elbow Clinical findings | Normal radiograph of elbow
Point tenderness over radial head
Usually normal x ray
Ask about trauma as usually not x rayed to rule out fracture if was trauma
🗑
|
||||
| Nursemaid Elbow Treatment | Place elbow extended in full supination; move to full flexion;
Palpable click felt at level of radial head with instant relief of pain/crying
May immobilize briefly in sling for comfort; immobilize longer if symptoms last for several days
🗑
|
||||
| Hip: Evaluation | General information for hip evaluation
NOTE: Hip pain often refers to the knee
KNEE PAIN should trigger an examination of the hip
🗑
|
||||
| Legg-Calve-Perthes | Legg-Calve-Perthes disease (LCPD)
Vascular supply of proximal femur is precarious, and if interrupted can result in necrosis
Highest incidence is ages 3-12; mean of age 7
Atraumatic, persistent pain and limp or limited motion; more common in boys
🗑
|
||||
| Legg-Calve-Perthes Symptoms : | Atraumatic, persistent pain and limp or limited motion; more common in boys
🗑
|
||||
| Hip: Legg-Calve-Perthes Clinical findings | Radiologic A-P and frog-leg views:
Early findings: effusion of joint, widening of joint space, periarticular swelling
Later findings: decreased bone density or collapse of femoral head; necrotic ossification center with patchwork replacement
🗑
|
||||
| Hip: Legg-Calve-Perthes Treatment | referral to pediatric orthopedist
🗑
|
||||
| Hip: Slipped Capital Femoral Epiphysis SCFE (pronouncec skif-ee) | displacement of proximal femoral epiphysis due to disrupted growth plate
ORTHOPEDIC EMERGENCY!
obese adolescent males
fall or direct trauma
weakened epiphyseal area due to hormonal change
Hypothyroidism or endocrine disorder are risk factors
🗑
|
||||
| Slipped Capital Femoral Epiphysis Stable--Able to bear weight | Symptoms
Hip or knee pain, limp or inability to ambulate
Clinical findings
Limitation of internal rotation of hip
A-P and frog-let radiographs show widened epiphysis and decreased height of the epiphysis
Mismatch between epiphysis and metaphysis
🗑
|
||||
| “Toeing-in” major causes | Internal tibial torsion
Internal femoral torsion (femoral anteversion
🗑
|
||||
| Internal tibial torsion: Rotation of the leg between the knee and the ankle | Normally about 20 degees at birth, but decreases to neutral rotation by age 16 months.
Most common cause of in-toeing in child younger than 2 years
document improvement
Refer if no improvement by age 2
🗑
|
||||
| Internal femoral torsion | Children 2 years or older
Worst at ages 4-6, then typically resolves
Incidence twice as high in girls
Congenital and common in individuals that sit in W-sitting position
🗑
|
||||
| Internal femoral torsion Symptoms | Kissing kneecaps
Running may have egg-beater gain where legs flip laterally
🗑
|
||||
| Internal femoral torsion Clinical Findings | Internal rotation of hip increased with limited external rotation
Radiography not indicated
🗑
|
||||
| Internal femoral torsion Treatment | No orthoses required
Active external rotation such as skating or bicycle riding encouraged
Resolves by ages 7-8
Refer only if no external rotation of hip in extension
🗑
|
||||
| Genu varum (bowleg) Normal from infancy thru age 2 | Criteria for referral to pediatric orthopedist
Persisteng bowing beyond age 2
Bowing that is increasing rather than decreasing
Bowing of one leg only
🗑
|
||||
| Genu valgum (knock-knee) (hint for memorizing: gum sticks things together) Typical from age 2 thru age 8 | Criteria for referral to pediatric orthopedist
Knock-knee associated with short stature
🗑
|
||||
| Osgood Schlatter disease | Common cause of knee pain at insertion of patellar tendon on tibial tuberosity (tubercle)
Quadriceps muscle stresses on developing tibial tubercle
Partial avulsion fracture or micro fracture in the ossification center of tibial tuberosity
🗑
|
||||
| Rates over 150 | SVT
🗑
|
||||
| Junctional | No P wave rate of 40-60
🗑
|
||||
| Accelerated Junctional | No P wave rate of 60-100
🗑
|
||||
| Atrial Flutter | Saw tooth pattern but regular qrs complexes
🗑
|
||||
| A fib | always irregular P waves difficult to identify
🗑
|
||||
| Afib patients | must be anticoagulated
🗑
|
||||
| PVC - Premature Ventricular contraction | Check electrolyte and medications - something is wrong. Non perfusion
🗑
|
||||
| Upper Respiratory Infection (URI)- Definition | An illness caused by an acute infectious agent which
involves the upper respiratory tract, including the nasopharynx and sinuses, and larynx commonly including tonsillitis, pharyngitis, laryngitis, sinusitis, acute otitis media, and the common cold
🗑
|
||||
| The majority of URI are caused by a virus | Bacteria cause about 25% of the cases
🗑
|
||||
| Over 200 different viruses have been isolated in patients with URI; the most common is | rhinovirus; others include coronavirus, parainfluenza virus, adenovirus, enterovirus and RSV
🗑
|
||||
| Streptococcus is a bacterial cause of URI | resulting in tonsillitis, pharyngitis and otitis media and account for more than 20 million primary care provider visits annually; up to 15% of acute pharyngitis may be caused by Group A streptococcus
🗑
|
||||
| Incubation period for most URI | is 1-4 days with onset of symptoms 1-3 days after exposure and lasting 7-10 days
🗑
|
||||
| Acute Bronchitis Definition | Infection of the tracheobronchial tree that causes reversible bronchial inflammation
🗑
|
||||
| Treatment of CAP Clinical factor Points Confusion (new disorientation 1 BUN > 19mg/dl 1 Respiratory rate >30 1 BP systolic <90; diastolic <60 1 Age > 65 1 | Scoring
0-1 - low risk; consider home treatment
2 - short in-patient hospitalization or closely monitored outpatient treat
>3 - Sever pneumonia, hospitalize, consider ICU
🗑
|
||||
| Streptococcus pneumoniae Penicillin nonresistant | Penicillin G, amoxicillin
Alternative
Macrolide, cephalosporins (oral [cefpodoxime,cefprozil, cefuroxime, cefdinir, cefditoren]
or parenteral [cefuroxime, ceftriaxone, cefotaxime]),
clindamycin, doxycyline, respiratory fluoroquinolone
🗑
|
||||
| Streptococcus pneumoniae Penicillin resistant | Agents chosen on the basis of susceptibility,
including cefotaxime, ceftriaxone,
fluoroquinolone
Alternative
Vancomycin, linezolid, high-dose amoxicillin
(3 g/day with penicillin)
🗑
|
||||
| Haemophilus influenzae Non–b-lactamase producing | Amoxicillin
Alternative
Fluoroquinolone, doxycycline, azithromycin,
Clarithromycin
🗑
|
||||
| Haemophilus influenzae b-lactamase producing | 2nd or 3rd generation cephalosporin,
amoxicillin-clavulanate
alternate
Fluoroquinolone, doxycycline, azithromycin,
Clarithromycin
🗑
|
||||
| Mycoplasma pneumoniae/ Chlamydophila pneumoniae | Macrolide, a tetracycline
alternate
Fluoroquinolone
🗑
|
||||
| Legionella species | Fluoroquinolone, azithromycin
alternate
Doxycyline
🗑
|
||||
| CAP Antibiotic Recommendations Outpatient Management For previously healthy patients who have not taken antibiotics with the past 3 months: | A Macrolide (clarithromycin, 500 mg orally bid; or Azithromycin, 500 mg day 1, then 250 mg daily x 4 days or 500 mg daily x 3 days or
Doxycycline, 100 mg po bid
🗑
|
||||
| CAP Antibiotic Recommendations Outpatient Management For patients with such comorbid medical conditions as chronic hear, lung, liver, or renal disease, DM, alcoholism, malignancy, asplenia, immunosuppressant conditions or use of immunosuppressive drugs | A respiratory fluoroquinolone (moxifloxacin, 400 mg po daily; Gemifloxacin 320 mg qd, Levofloxacin 750 mg qd or
A macrolide plus a B-lactam (amoxicillin, 1 g po tid; amoxicillin-clavulante, 2 g po bid are preferred to cefpodoxime, 200 mg bid:
🗑
|
||||
| Acute Life Threatening Event | Observer of event brings infant to ER or clinic
Apnea, cyanosis or pallor, limpness, choking
or gagging
Event is frightening to observer; fears infant
has died
🗑
|
||||
| ALTE | Peak age 2-4 months (same as SIDS)
🗑
|
||||
| Cough is an important reflex in clearing the lungs of debris and secretions. | The loss of the ability to cough results in decreased secretion clearance and predisposes to atelectasis and pneumonia.
🗑
|
||||
| Ventilation inadequate to keep Pco2 from increasing above normal is | hypoventillation
🗑
|
||||
| The lungs are repeatedly exposed to particles and infectious particles. The ________ is responsible for filtering larger particles. | nasopharynx
🗑
|
||||
| Hypoxemia | reduction in the oxygen content of the blood.
🗑
|
||||
| Airway resistance | is influenced by the diameter and length of the airways, the viscosity of gas and the nature of the airflow.
🗑
|
||||
| Functional residual volume | is the volume of gas in the lung when mechanical forces acting on the lung are at equilibrium (at the end of a normal relaxed breath).
🗑
|
||||
| Lung compliance | is a measure of the ease at which the lung can be inflated.
🗑
|
||||
| Residual volume (RV) | is the volume of gas left in the lungs at the end of a maximal exhalation.
🗑
|
||||
| Total lung capacity (TLC) | is the volume of gas in the lungs at the end of maximal inhalation.
🗑
|
||||
| Vital capacity (VC) | is the maximal amount of air that can be expelled from the lungs.
🗑
|
||||
| Acute Life Threatening Event Etiology | Gastroesophageal reflux and laryngospasm
are the most common causes of ALTE
Epidemiology
Peak age 2-4 months (same as SIDS)
🗑
|
||||
| Differential Diagnosis for ALTE | Viral: RSV and others
Bacterial: sepsis, pertussis, chlamydia GERD with or without obstructive apnea, midgut volvulus, shockHypoglycemia, medium-chain acyl-coenzyme A dehydrogenase deficiency, carnitine deficiency, urea cycle defect
🗑
|
||||
| Subjective Data for ALTE Careful history most important element of exam | Chronically ill or essentially well, pre-term, prior apnea
Feeding pattern, febrile, respiratory or GI symptoms
“Trying or struggling to breathe” implies airway obstruction
Association with feeding or crying, breath-holding
🗑
|
||||
| Subjective Data for ALTE Careful history most important element of exam | Social situation of the family
Episodes of sleep apnea
Duration of episode (often difficult to assess)
Resuscitative measures at home
🗑
|
||||
| Objective Data for ALTE | Fever or hypothermia suggests infection
Bruising or injury
Nutritional status
Altered state of consciousness suggests seizure or overdose
Respiratory distress implies cardiac or pulmonary involvement
🗑
|
||||
| Diagnostics:ALTE | CBC, metabolic profile, ABG’s, CXR, RSV, pertussis, chlamydia, fiber optic bronchoscopy, CT or barium swallow, esophageal pH monitoring, EEG, MRI brain, polysomnographs (sleep studies)
🗑
|
||||
| Treatment Plan for ALTE | Infant is hospitalized for observation and prompt evaluation and continuous cardiorespiratory monitoring for 12-24 hours
Alleviate parental fears and anxiety surrounding event
Reassess home situation
Treatment in directed at underlying cause
🗑
|
||||
| Oxygen, nasal CPAP for reduction of periodic breathing; | immature breathing pattern causing desaturation
🗑
|
||||
| Caffeine or aminophylline | for central apnea or periodic breathing
🗑
|
||||
| Sudden Infant Death Syndrome (SIDS) | is the unexplained death of an infant younger than one year of age in which the cause cannot be determined either by autopsy, death scene investigation and review of clinical history.
🗑
|
||||
| greatest risk for SIDS. | Premature, low-birth-weight infants, infants of young impoverished mothers of cigarette smokers, African-American and Native-American infants and infants born to mothers who have abused drugs
🗑
|
||||
| Incidence of SIDS | Highest during the winter months
Increases 3-5 fold to infants whose siblings have died of SIDS
Most common between 2-4 months of age
🗑
|
||||
| Incidence has dramatically decreased since the 1990’s since the AAP educational promotion of “Back to Sleep” | where supine sleeping positions are advocated
🗑
|
||||
| A variety of causes for SIDS have been proposed, however none have been proven to explain SIDS | SIDS is associated with the prone position and soft bedding
Cellular brainstem abnormalities and maturational delays
Prolongation of Q-T interval resulting in dysrhythmias
Abnormal CNS control of respiration
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| SIDS Pathological Findings | Intrathoracic petechiae
Mild inflammation and congestion of the respiratory tract
Other, subtler changes suggest an intermittent or chronic hypoxia before death
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| Upper Airway Obstruction Foreign Body Aspiration | Blockage of any part of the airway located above the thoracic inlet, ranging from nasal obstruction due to the common cold to life-threatening obstruction of the larynx or upper trachea (subglottic space)
Epidemiology: children 6 months to 4 years of age
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| Upper Airway Obstruction Foreign Body Aspiration Presentation and diagnosis: | Acute onset of cyanosis or choking
Inability to vocalize or cough (complete obstruction)
More pronounced on inspiration
Drooling and stridor (partial obstruction)
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| Epiglottitis (Supraglottitis) | inflammation of the soft tissue above the glottis
This illness is relatively rare but it is a medical emergency that requires immediate lifesaving intervention due to the risk of total airway obstruction
Early recognition is critical
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| Clinical Presentation of Epiglottitis | Abrupt onset of severe sore throat
usually voice is muffled
sniffing position
Difficulty swallowing
Copious oral secretions or drooling
Symptoms may progress to stridor and respiratory distress, anxiety, sternal retractions and later exhaustion
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| sniffing position | Have a preference for sitting with head held forward, hyperextended, the mouth open and the jaw thrust forward;
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| If epiglottitis is suspected | , DO NOT attempt to examine the pharynx with a tongue depressor because this may result in occlusion of the airway; also do not attempt to place the patient in the supine position; keep the patient in the sitting position
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| Treatment Plan - Epiglottitis | Immediate ACLS transport to the hospital
Keep the patient in the sitting position
Attempt to keep the patient calm
Alleviate parental fears
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| Croup Definition | Laryngeal obstruction caused by subglottic edema
Laryngotracheal airway inflammation disproportionately affects children because a small decrease in diameter secondary to mucosal edema and inflammation
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| Croup Pathophysiology | The most common causes of croup are parainfluenza viruses (type 1,2 and 3)
RSV in younger children
Influenza virus and Mycoplasma pneumoniae are other causes
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| Croup Epidemiology | Most common in children 3 months to 5 years with a peak at 2 years
Higher incidence in males
Occurs in fall and winter months
It typically follows a common cold
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| Presentation of Croup | Onset
3-5 days
Absent or low grade fever
Barking cough
Inspiratory stridor
Hoarseness
Is usually worse at night
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| Treatment of Croup For mild symptoms with no stridor at rest | give oral hydration, minimal handling, provide comfort measures to calm child, breathing of cool, dry, night air, acetaminophen for fever reduction,
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| Treatment of Croup Consider hospitalization if severe symptoms such as stridor at rest, dehydration, hypoxia, respiratory distress | For significant airway compromise nebulized racemic epinephrine 0.05ml/kg/dose diluted to 3 ml NS over 15 minutes not to exceed q 1-2 hour dosing; may cause HTN, cardiac arrhythmias; a rebound effect may occur, with worsening of symptoms after dissipates
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| Treatment of Croup - Pharmacological | Oxygen therapy if hypoxic or desaturating
Dexamethasone 0.6 - 1 mg/kg once IM or 0.6 - 1mg/kg po once or oral prednisalone 2mg/kg in 2-3 divided doses
Nebulized Budesinide (Pulmicort) 0.5 – 1 mg daily or bid
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| Treatment of Croup Education of parents | Assess for respiratory distress, changes in level of activity, increased somnolence
Assess for hydration
When to return to ER if symptoms intensify
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| Treatment of Croup Follow-up | Phone contact in 8-24 hours
Return visit if no improvement in 48 hours
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| Treatment of Croup Prognosis | Most children clinically improve in a few days
Recurrence of croup implies airway hyperreactivity (asthma)
Viral pneumonia may occur in 1 – 2% of children with croup and in immunocompromised children, parainfluenza viral pneumonia or secondary bacterial
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| Bronchiolitis - etiology | Inflammation of the bronchioles resulting in small airway obstruction leading to inadequate expiratory airflow
A term used for first time wheezing with a viral respiratory infection
Bronchiolitis is potentially life threatening
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| Respiratory synctial virus (RSV) is the primary cause of | bronchiolitis
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| Bronchiolitis is extremely contagious | spread by contact with infected respiratory secretions through coughing and hand carriage of contaminated secretions
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| Bronchiolitis Epidemiology | Bronchiolitis is the leading cause of hospitalization of infants
Approximately 50% of children will experience bronchiolitis during the first 2 years of life with a peak age at 2-6 months.
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| Bronchiolitis - Clinical presentation | Usually presents as a progressive respiratory illness similar to the common cold in its early phase associated with cough, coryza and rhinorrhea
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| Young infants with RSV may not have prodromal symptoms and can present with | apnea as the first sign of infection
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| Bronchiolitis Treatment Plan | Indications for hospitalization include infants <6mos, marked respiratory distress, hypoxemia with PO2 < 60mm Hg or SaO2 < 92% on room air; intolerability of oral feeding and inadequate care at home
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| environmental irritants | tobacco smoke, wood burning fires, stoves
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| Bronchiolitis Prevention | Palivizumab (Synagis) 15 mg/kg/ IM once per month November-April
Palivizumab is a RSV monoclonal antibody
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| correlation between RSV infection | future airway hyperreactivity as well as abnormalities in pulmonary function tests (incidence of asthma is higher in hospitalized children)
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| Treatment Plan CAP | Neonates, age < 1 month:
Ampilcillin +Gentamicin + Cefotaxime
If MRSA is a concern add Vancomycin
For Chlamydia trachomatis – Erythromycin 12.5 mg/kg po or IV x 14 days
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| Treatment Plan CAP Infants age 1-3 months |
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|
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