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Advanced Diagnostics > Acute Abdominal Pain > Flashcards

Acute Abdominal Pain Flashcards

1
Q

Visceral Pain

A

occurs when hollow abdominal organs contract forcefully or are distended and stretched
-May be difficult to localize
Varies in quality: gnawing, burning, cramping, or aching

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2
Q

Parietal pain

A

-inflammation of the parietal peritoneum
-Steady, aching pain that is usually more severe
-Usually precisely located over the affected area
-Causes the tenderness and guarding which progresses to rigidity and rebound as peritonitis evolves

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3
Q

Referred Pain

A

Occurs in more distant regions that innervated at the same spinal levels as the disordered structure
ex: R shoulder pain & RUQ pain secondary to an inflamed liver

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4
Q

Red Flags

A

-Weight loss
-Gastrointestinal bleeding
-Anemia
-Fever
-Frequent nocturnal symptoms
-Onset of symptoms in older patients

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5
Q

Gastric Reflux Disease

A

-Back flow (reflux) of acidic gastric contents into the esophagus

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6
Q

Causes of GERD

A

-Incompetent lower esophageal sphincter
-Delayed gastric emptying

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7
Q

GERD s/s

A

-Retrosternal “burning”
-Bitter taste in the mouth
-Frequent belching, hiccoughs, dysphagia
-Excessive salivation
-Frequently occurs at night or laying flat
-Relieved by sitting up, antacids, water or food

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8
Q

GERD Diagnostics

A

-Outpatient EGD if concern for cancer, Barrett’s esophagus, peptic ulcer disease, etc

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9
Q

GERD Management Non-pharmacological

A

elevating HOB, avoiding ETOH, caffeine, spicey food. Stop smoking, weight reduction if contributory.

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10
Q

GERD Pharmacological Management

A

-Antacids PRN
-H2 blocker
-PPI if H2 blockers are ineffective
-GI/Surgery consult as needed

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11
Q

Peptic Ulcer Disease

A

Chronic disorder in which one is at risk for developing mucosal ulcers that are exposed to gastric acid and pepsin.

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12
Q

Causes of PUD

A

-H. Pylori
-Medications: NSAIDS, ASA, and glucocorticoids
-More common in men (3:1)
-Duodenal ulcers between ages 30-55
-Gastric ulcers between ages 55-65
-More common in > ½ ppd smokers
-Stress (associated with ventilator use, coagulopathy, severe skin burns, and central nervous system injury)
-Low or no association with alcohol, caffeine, acetaminophen, spices

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13
Q

PUD s/s

A

-Gnawing epigastric pain
-Relief of pain with eating (duodenal)
-Pain worsens with eating (gastric)

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14
Q

Physical Exam of PUD

A

-Often unremarkable to mild epigastric discomfort
-GI bleeding
—–Melena (UGI bleed)
—–Hematemesis or coffee ground emesis
-Perforation* severe epigastric pain, rigidity, absent bowel sounds and other s/s of infection
—-Things to look out for and never miss include s/s of perforation

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15
Q

PUD labs/diagnostics

A

-Normal for the most part.
May see anemia on the CBC. Leukocytosis in the setting of penetration or perforation
-GI barium study- uncomplicated dyspepsia
-EGD- if warranted.
—Outpatient versus inpatient
—-If outpatient- start treatment and scope in 4-6 weeks.

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16
Q

BOWED Acronym for EGD

A

-Bleeding
-Odynophagia
-Weight loss- unplanned
-Early Satiety
-Dysphagia

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17
Q

PUD Tx: H2 Receptor Antagonists

A

-decrease gastric acid secretion by blocking histamine 2 receptors on parietal cells
-Cimetidine (Tagament) 800mg (rarely used d/t druf interactions & s/e)
-Ranitidine (Zantac) 300mg
-Famotidine (Pepcid) 40mg

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18
Q

PUD Tx: PPIs (30 min before largest meal)

A

-Lansoprazole (Prevacid) 15mg/day
-Omeprazole (Prilosec) 20mg/day (tolerance can develop)
-Pantoprazole (Protonix) 40mg/day
-Esomeprazole (Nexium) 20mg/day

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19
Q

PUD Tx: Mucosal Protective Agents (2 hours apart from other meds)

A

-Sucralfate (Carafate) 1gm/QID *avoid H2 blocker and PPI
-Bismuth subsalicylate (Pepto-Bismal)
-Misoprostol (Cytotec) QID with food. Preventative in patients with chronic NSAID use. *may stimulate labor
-Antacids (Mylanta, Maalox, MOM)
—-Don’t reduce the amount of gastric acidity

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20
Q

PPIs use

A

-used to treat duodenal ulcers, severe erosive esophagitis, or poorly controlled GERD
-suppress gastric acid secretion by inhibiting the hydrogen/potassium ATP enzyme system at the secretory surface of the gastric parietal cell
-Symptoms are relieved in two weeks of use
-Healing of the ulcer is usually attainable in 8 weeks of therapy
—it takes gastric ulcers 2-4 more weeks of healing compared to a duodenal ulcer

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21
Q

PUD & H Pylori

A

Helicobacter pylori (H. pylori) is present in > 75% of duodenal ulcer or gastric ulcers that were not induced by NSAIDS.

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22
Q

To detect H. Pylori

A

-Endoscopic biopsy*
-Urea breath test
-Serum H. pylori antibody test
-Stool antigen for H. pylori
-Urea breath testing – if positive indicates active infection. PPI can cause false negatives and should be held for 7 days before testing
-Serum H Pylori may be reflective of a previous infection

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23
Q

Treatment of PUD & H. Pylori

A

-MOC: Metronidazole + Omeprazole + Clarithromycin
-AOC: Amoxicillin + Omeprazole + Clarithromycin
-MOA: Metronidazole + Omeprazole + Amoxicillin
-BMT: Bismuth subsalicylate + metronidazole+ tetracycline
-BMT + Prilosec
-Regimens typically range 7-14 days of therapy depending on the regimen followed by 3-7 weeks of antiulcer therapy to ensure healing.

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24
Q

Cholecystitis

A

-Inflammation of the gallbladder, acute or chronic, associated with gallstones (cholelithiasis) in more than 90% of cases

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25
Q

Etiology of Cholecystitis

A

-Gallstone- most common form of GB disease
–Formed from cholesterol
—Stone becomes impacted within the cystic duct
—Inflammation occurs behind the obstruction
-Bacterial agents
-Neoplasm
-Stricture of the common bile duct
-Ischemia
-Torsion (twisting of the duct)

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26
Q

Contributing factors of cholecystitis

A

-Obesity, pregnancy, sedentary lifestyle, low fiber diet
-Risk factors: Female, advanced age, rapid weight loss, fad diets, high cholesterol

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27
Q

cholecystitis signs and symptoms

A

-Often precipitated by a large or fatty meal
-Sudden severe pain in the epigastric or RUQ area
-Vomiting sometimes an alleviating factor
-referred pain in right shoulder or back.

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28
Q

Cholecystitis Physical Exam

A

-Murphy’s sign: Deep pain on inspiration while palpating under the right rib cage
-RUQ tenderness to palpation; palpable gallbladder in 15% of cases
-Muscle guarding and rebound pain
-Fever

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29
Q

Labs/Diagnostics of Cholecystitis

A

-Leukocytosis
-Elevated serum bilirubin
Serum ALT, AST, LDH, and alk phos elevation
-Amylase may be elevated
-Xray may show stones
—RUQ US is the gold standard
-HIDA scan (will show obstructed bile duct)
-ERCP- assesses diagnose stones and assess biliary and pancreatic ducts
-Amylase (rule out concomitant pancreatitis
-EKG- Remember to assess above and below
-CXR- r/o pneumonia

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30
Q

Cholecystitis management

A

-Pain management
-NPO
—If significant vomiting, consider NGT for decompression
-Crystalloids for hydration
-Antiemetics
-Broad spectrum antibiotics (i.e Zosyn)- after blood cultures are obtained
-Surgical consultation for cholecystectomy
-Biliary decompression via endoscopic retrograde cholangiopancreatography (ERCP) with sphincterotomy and extraction of stones

31
Q

Pancreatitis

A

Acute inflammatory autodigestive process of the pancreas

32
Q

Pancreatitis etiology

A

-Gallbladder Disease
-Alcoholism or acute intoxication
-Hypercalcemia
-Hyperlipidemia
-Trauma/Surgery
-Medications- Sulfonamides, Thiazides, Furosemide, Estrogen, Azathioprine
-Ischemia
-PUD
-Pregnancy
-Neoplasm
-Idiopathic

33
Q

Pancreatitis s/s “band like” pain

A

-Abrupt onset of steady severe epigastric pain usually worsened by walking or lying supine
-Pain improves when sitting up and leaning forward or when holding the knees to the chest
-Pain that radiates to the back or elsewhere
-Nausea and Vomiting usually present
-Pending severity: weakness, sweating, anxiety
-Ileus
-Fever
-Tachycardia, hypotension, cool/pale skin (hypovolemia

34
Q

Pancreatitis physical exam

A

-Distended abdomen
-Mild jaundice may occur
-Grey-Turner sign -Flank discoloration
-Umbilical discoloration (Cullen’s sign)
-Absent bowel sound if ileus present

35
Q

Pancreatitis lab/diagnostics

A

-Leukocytosis
-Hyperglycemia
-Elevated LDH, AST
Serum amylase (50-180 U/dL) and lipase (14-280 U/L) are elevated in 90% of cases
-BUN may be elevated
-Hypocalcemia
-Elevated CRP suggests pancreatic necrosis
-CT is preferred over US to assess for pseudocysts, necrosis, and fistulas

36
Q

Pancreatitis dx: For diagnosis 2/3 criteria must be met for pancreatitis

A

-Severe, constant upper abdominal pain
-Elevated amylase and/or lipase levels (≥3 times the upper limit of normal). Due to greater specificity, the measure of lipase is preferred to amylase
-Evidence on imaging studies (CT, ultrasound, or MRI)
-Ranson’s criteria assesses prognosis

37
Q

Pancreatitis management

A

-Maintain NPO
-Aggressive IV volume repletion
—Unless prevented by cardiovascular or renal comorbidities, aggressive IV fluids (250 to 350 cc/hr) should be given to the patient immediately to decrease blood urea nitrogen (BUN). This is the most important goal of initial treatment.
-NG suction if needed d/t ileus
-Pain control
-Once pain free and bowel sounds present may start diet and advance as tolerated
-Stone management if causing blockage
-Manage electrolyte abnormalities
-Failure to improve, consider empiric antibiotics
—Piperacillin-Tazobactam
Cefepime +/- metronidazole

38
Q

Appendicitis

A

Inflammation of the appendix, precipitated by obstruction of the appendiceal lumen, If untreated treatment is delayed it can lead to gangrene and perforation within 36 hours

39
Q

Appendicitis causes

A

-Fecalith (undigested food)
-Foreign body
-Inflammation
-Neoplasm

40
Q

Obstruction of the appendix

A

Obstruction of the appendix caused by fecalith, inflammation, foreign body, intestinal worms, strictures or tumors leads to inflammation of the appendix. If left untreated it can quickly evolve into a life threatening crisis.

41
Q

s/s of appendicitis

A

-Initially subtle and nonspecific
-Anorexia and periumbilical discomfort
-Progresses to RLQ pain
-Nausea and vomiting x 1-2 episodes
Persistent vomiting consider alternative diagnosis

42
Q

Appendicitis physical exam

A

-RLQ guarding with rebound tenderness
-Psoas sign- pain with right thigh extension
-Obturator sign- Pain with internal rotation of flexed right thigh
-Positive Rovsing’s sign- RLQ pain when pressure applied to the LLQ
-Localized (point) abdominal tenderness (McBurney’s point)
-Low grade fever

43
Q

Appendicitis lab/diagnostics

A

-Alvarado Score
-Labs will show leukocytosis
-CT or US is diagnostic
US is 98% accurate as long as it can be visualized
CT can detect perforation, assess for abscess
-UA to rule out urinary tract infection
-Pregnancy test to rule out ectopic pregnancy

44
Q

Appendicitis management

A

-Surgical evaluation
-IV antibiotics
—-A cephalosporin (ceftriaxone or cefazolin) with metronidazole
—-Piperacillin-tazobactam
If penicillin allergic, consider ciprofloxacin or levofloxacin with metronidazole
-IV fluids
-Pain & Nausea management
-Risk of perforation if treatment is delayed
-If on initial presentation appendicitis is ruled out but symptoms persist, patient should have a repeat reevaluation within 12-24 hours

45
Q

Diverticulitis

A

Inflammation or localized perforation of one or more diverticula with abscess formation

46
Q

Diverticulitis etiology

A

-Not clearly proven
-Low fiber diet
-More common in men than women
-Weakness or defect in the colon

47
Q

s/s diverticulitis

A

-Mild to moderate abdominal pain in the LLQ
-Constipation common but may alternate with diarrhea
-Nausea and vomiting
-Abdominal distention
-Dysuria and frequency- inflammatory bowel that causes irritation to the bladder
-Low grade fever
-severity may indicative of perforation

48
Q

Physical exam findings of diverticulitis

A

Patients with diverticulosis are usually asymptomatic. Diverticulitis occurs when a diverticulum becomes inflamed and often presents with:
•Abdominal pain (often left lower quadrant)
•Constipation
•Nausea and fever (systemic symptoms)
•Usually marked tenderness on an abdominal exam due to peritoneal irritation from the microperforation
-can include hematochezia

49
Q

Diverticulitis labs/dx

A

-Leukocytosis
-Elevated ESR and CRP
-Plain Xray- to assess for perforation
-Avoid Barium Enema or Flex Sig in the acute phases
-CT may reveal abscess
-Stool hemoquant + 25% of cases

50
Q

Diverticulitis management for mild cases

A

-can be treated at home
-Bowel rest
Clear liquids and advance to low residue for 24-48 hours
Progress to high fiber diet as bowel function normalizes
-Antibiotics
•Ciprofloxacin 500 mg orally 2 times daily combined with metronidazole 500 mg orally 3 times daily for 10 to 14 days
•Amoxicillin 875 mg and clavulanate 125 mg orally 2 times daily for 10 to 14 days

51
Q

Diverticulitis in severe cases

A

-NPO versus low residue -diet
-IV fluids
-Antibiotics
-Treat GI bleeding if present
-Surgical consult as 20-30% of patients will require surgical management
-Hospitalization: complicated diverticulitis, inability to tolerate orals, high fever or significant leukocytosis, immunocompromised

52
Q

Bowel obstruction

A

-Adhesion- most common (50-70%)
-Hernia (15%)
-Malignancy (15%)
-Volvulus- twisting of bowel on itself
-Stricture- r/t Crohn’s disease, radiation, ischemia
-Hematoma- trauma related, anticoagulation
-Intussusception- slipping of once part of an intestine into another part just below it
-Fecal impaction
-Foreign bodies

53
Q

Bowel obstruction S/S

A

-Cramping periumbilical pain initially but later becomes constant and diffuse
-Vomiting within minutes of pain (think proximal)
-Vomiting hours after onset (think distal)
-Most likely afebrile

54
Q

Bowel obstruction physical exam

A

-Minimal abdominal distention- proximal
-Pronounced abdominal distention- distal
-Mild tenderness but not peritonitic
-High pitched, tinkling bowel sounds
-Unable to pass gas/or stool per rectum
-Watery or mucousy stool may be present in partial obstruction
-Dehydration

55
Q

Bowel obstruction lab/dx

A

-Normal labs in the early stages
-Later stages may see leukocytosis and labs consistent with dehydration
-Plain X-Ray will show dilated loops of bowel and air-filled fluid levels
-A horizontal pattern in a small bowel obstruction
-Frame pattern in large bowel obstruction
-CT is helpful to determine level of obstruction and cause if X-ray is unrevealing
-Key diagnostic sign is finding a transition point between dilated and collapsed, nondistended bowel to locate the obstruction

56
Q

Management of bowel obstruction

A

-Bowel rest. NGT to LIS
-Fluid and electrolyte management
-Surgery consult if complete obstruction or if partial obstruction fails to respond to medical management
-Treat the underlying cause
-Steroids helpful if secondary to malignancy
-PPI, H2 blockers and Octreotide

57
Q

Peritonitis

A

Acute inflammation of the visceral and parietal peritoneum

58
Q

Primary peritonitis

A

-Spontaneous bacterial peritonitis
-E. Coli is most common organism along with Klebsiella, Pneumococcus, and Enterococcus

59
Q

Secondary peritonitis

A

-Following trauma or penetrating wounds
-Peritoneal dialysis
-Perforation
-Postop
-Bowel ischemia
-TB
-Familial Mediterranean fever

60
Q

S/S Peritonitis

A

-Acute abdominal pain- worse with motion
-High fevers
-N/V and Constipation
-Ascites
-Ill appearing, septic

61
Q

Physical Exam Peritonitis

A

-Distention
-Rebound tenderness
-Generalized rigidity
-Decreased bowel sounds
-Hyperresonance to percussion

62
Q

Peritonitis lab/dx

A

-Peritoneal aspirate
—Leukocyte count >10,000/mm3
—LDH >225 mU/ml
—Protein levels >1 g/dl
—Glucose <50 mg/dl
–Presence of multi organisms on gram stain and/or culture
-Blood cultures
-Leukocytosis
-Elevated BUN
-Mixed acidosis
-Elevated serum amylase
-Abdominal XR will show
—Free air in the peritoneal cavity
—Dilation of large or small bowel
-CXR will show elevated diaphragm

63
Q

Peritonitis management

A

-Surgical consult
-Antibiotics- third-generation cephalosporin
—-Cefotaxime (Claforan) 2 g IV q8h
—-Ceftriaxone (Rocephin) 2 g IV q24h
—-Ampicillin or Unasyn should be added if concern for enterococcus
—-Severe cases call for Aminoglycoside such as Gentamycin + Metronidazole
—Caution use of aminoglycosides in chronic liver failure patient’s d/t risk of nephrotoxicity
-Fluid resuscitation
-NPO, NG if needed
-Continuous ambulatory -peritoneal dialysis
-Intraperitoneal vancomycin, —-20 mg/L dialysate + 1 g IV load, plus gentamicin, 6-8 mg/L dialysate
—Intraperitoneal cefazolin (Ancef)

64
Q

Spontaneous Bacterial Peritonitis

A

SBP is an acute bacterial infection of ascites fluid in patients with cirrhotic liver disease. Usually there is no source of infection. Mortality in these patients is high.

65
Q

SBP management

A

-Albumin shown to increase survival rate
25% albumin administered intravenously on day 1 (1.5 g/kg) and on day 3 (1 g/kg) has been shown to decrease mortality
-Repeat paracentesis 48 hours after treatment to ensure decrease in PMN cell count
-Prophylaxis indicated as it is likely to reoccur

66
Q

Mesenteric Ischemia

A

Result of inadequate blood flow through the mesenteric circulation leading to ischemia and gangrene of the bowel

67
Q

Etiology of Mesenteric Ischemia

A

-Thrombus or Embolism
-Surgical complication
-Trauma
-Malignancy
-Occlusion of arterioles with systemic disease
—-i.e. TTP, DIC, Polyarteritis nodosa, SLE
-Nonocclusive mesenteric vascular disease
—i.e. CHF, AS, Shock, Cardiac arrhythmia, vasoconstrictors
-Older adults
-Smokers

68
Q

Mesenteric ischemia s/s

A

-Sudden onset of cramping, colicky pain that is out of proportion to physical exam findings.
-N/V
-Fever
-Abdominal guarding and tenderness
-Bowel sounds can be hyperactive or absent
-Shock- tachycardic and hypotensive
-Rectal bleeding if colonic ischemia

69
Q

Mesenteric Ischemia labs/dx

A

-Leukocytosis
-Lactic acidosis
-Mesenteric Angiography is useful to determine the -location of vascular lesions
-MRA has sensitivity and specificity in detecting mesenteric ischemia
-CT can show mesenteric ischemia, focal or segmental bowel wall thickening, submucosal edema or hemorrhage, pneumatosis, portal venous gas
——The findings of pneumatosis intestinalis or portal venous gas on CT, along with peritoneal signs, indicate a medical and surgical emergency.—–

70
Q

Mesenteric Ischemia management: occlusive disease

A

-surgical consult
-Embolectomy or bypass of the occluded vessel to prevent infarction
-Bowel resection if infarction has occurred

71
Q

Mesenteric Ischemia management: nonocclusive disease

A

-Correct volume deficits
-Treat heart failure
-Reverse digitalis toxicity
-NG tube for decompression
-Antibiotics if peritonitis is suspected
-Vasodilators may be utilized once volume has been restored
-The goal for management is to restore intestinal perfusion, reverse ischemia and prevent infarction.

72
Q

Immediate life-threatening conditions that deserve attention

A

-Abdominal aortic aneurysm
-Mesenteric ischemia
-Perforation of GI tract (peptic ulcer, bowel, eso, appendix)
-Acute bowel obstruction
-Volvulus
-Ectopic pregnancy
-Placental abruption
-Myocardial infarction
-Splenic rupture

73
Q

Abdominal aortic aneurysm

A

-Focal dilatation of at least 50% compared to normal though any measurement >3cm is abnormal. Pulsatile mass on PE in some patients pending body habitus
Some manifest as abdominal, back, or flank pain
-Rupture causes hemorrhage and unstable hypotension
-Most common in men >60yo
-Those with COPD, PVD, HTN, smoking, and a family history of AAA are at higher risk
-US is diagnostic but not helpful in the setting of rupture
-CT abd/pelvis without contrast if the patient is stable
-STAT surgery consult if the patient is unstable
—As AAA can cause back pain and hematuria- there is potential to be misdiagnosed as nephrolithiasis.—-

74
Q

Splenic Rupture

A

Splenic rupture in the setting of Epstein Barr virus (EBV), leukemia, and trauma may present with life-threatening abdominal pain.

Advanced Diagnostics (11 decks)

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