Exam 3 Flashcards
RUQ
- Liver and gallbladder
- liver span is 6-12 cm
- under the right costal ridge
- spans across upper abdomen
LUQ
- Spleen & Pancreas
- pancreas is behind the stomach and liver in the upper quadrants
RLQ
- Appendix and Right ovary (lower)
Epigastric area
bounding pulsation: AAA
Appendicitis Clinical Presentation (3):
- RLQ pain, anorexia, n/v, low-grade fever, McBurney’s point maximum tenderness, tachycardia & diminished bowl sounds
- younger patients have constant colicky mid-abdominal pain which later shifts to RLQ
- Pain is worsened by movement & coughing.
The 3 s/s most predictive of Appendicitis:
- pain that starts in the epigastric or periumbilical area.
- migrates to the RLQ.
- abdominal rigidity
Markle’s sign
- causes peritoneal irritation in the RLQ when dropping to heels from standing on toes with a jarring landing
- associated with Appendicitis
Appendicitis Diagnostics:
- CBC: Leukocytosis
Normal WBC
4,500-11,000
Normal Neutrophil
55-70%
Normal Lymphocytes
20-40%
Normal bands
0-5%
A 26 yo man presents w/acute abdominal pain. As part of the evaluation for acute appendicitis, you order a WBC count w/diff and anticipate the following results:
- total WBC 16,500; neutrophils 66%, bands 8%; and lymphocytes 22%
Leukocytosis with a shift to left (elevated WBC, normal neutrophil, elevated bands)
Appendicitis imaging for suspected rupture:
CT abdomen pelvis
Appendicitis Management:
referral to ED (even if not ruptured) for IV antibiotics and appendectomy
Pancreatitis
- acute or chronic inflammation of the pancreas that is life-threatening
- characterized by elevated pancreatic enzymes d/t autodigestion of the pancreatic tissue
Pancreatic enzymes
- Amylase: 23-45
- Lipase: 0-160
- both >200 in pancreatitis
Pancreatitis RF (4):
- cholecystitis/biliary tract dz (gallstones)
- high fat diet
- hypertriglyceridemia
- excessive alcohol use/ETOH
Pancreatitis Clinical Presentation (2):
- sudden onset of intense, constant, sharp pain in the epigastric or LUQ that radiates to the back (most common sign)
- N/v are common
Pancreatitis Diagnostics (3):
2/3 required for pancreatitis per ACG
- characteristic severe, abdominal pain
- elevated serum amylase or lipase 3 times ULN (lipase stays elevated longer-higher probability)
- characteristic abdominal CT findings (inflamed pancreas)
Pancreatitis Management:
- refer to ED for surgery
- treatment aimed at decreasing pancreatic inflammation and treating underlying cause (removal of cholelithiasis)
- hospital required for IV analgesia and rehydraation
IBD
- Inflammatory Bowel Disease
- Ulcerative Colitis and Crohn’s Disease
Ulcerative Colitis (2)
- Diffuse and continuous inflammation of the large intestine and colon
- Ulcers penetrate inner-lining of gastric mucosa
IBD RF:
Family History
Ulcerative Colitis Clinical Presentation (3)
- bloody diarrhea/rectal bleeding is the hallmark sign and indicates disease severity
- mild to severe lower abdominal pain
- “fullness” in the lower abdomen
- hyperactive BS
Ulcerative Colitis Complications:
increases RF colon cancer
A patient reports lower abdominal cramping and occasional blood in stools. The provider suspects inflammatory bowel disease. Which test will the provider order to determine whether the patient has Ulcerative colitis (UC) or Crohn’s disease (CD)?
Colonoscopy can be useful in differentiating UC or CD. UC mucosal inflammation will be continuous with disease in the rectum up to the point where the inflammation stops. CD can have “skip areas”, patchy sections of normal mucosa intermixed with inflamed mucosa, giving a cobblestone appearance of the mucosa.
Crohn’s Disease (2)
- Patchy inflammation (cobble-stone appearance) of the full gastrointestinal lining (gum to bum)
- Ulcers are full-thickness penetrating the entire gastric mucosa
Crohn’s Disease Clinical Presentation (4):
- Abdominal pain typically in the RLQ
- prolonged diarrhea
- Perianal lesions
- Bowel obstruction
Chron’s Disease Complication:
- can develop a fistulous tract
Gastroenteritis Clinical Presentation & Management:
- N/V, non-bloody diarrhea, abdominal pain, hyperactive BS
- Oral or IV rehydration is important
Colorectal cancer Patho:
- Most colorectal cancers are d/t polyps (2/3rd of polyps become adenomatous)
Colorectal Cancer RF:
- personal or family hx of colorectal cancer of polyps
- IBD (UC)
- Hx of belly/pelvic radiation for previous cancer
Colorectal Cancer Screening (3):
- screening gold standard: Colonoscopy (FOBT too late if present)
- start 10 years earlier than diagnosis age of close relative
- average risk: start screening at 45-75, no longer recommended after 85
Constipation in older adults (3):
secondary to
- Medications (opioids)
- Decreased fluid intake
- Diets low in fiber & protein, but high in fate
Non-Pharm Constipation Management (3):
- Initially, avoid medications and foods known to cause constipation (better to stop a med than add a med to correct med s/e)
- Increase dietary fiber (25-30 g/day) and fluid intake
- Bowel Habits: recommend toileting 30 min after eating a meal and elevate feet on footstool
Diverticulitis:
-common complication of diverticulosis (asymptomatic pooching of intestines) resulting in inflammation that involves 1 or more diverticula (almost always symptomatic)
Clinical Presentation of Diverticulitis:
- intermittent LLQ abdominal pain and tenderness (unusually presents in RUQ)
- leukocytosis
- fever
- also associated with bloating and alternating diarrhea & constipation
Diverticulitis Diagnostic:
- CT of abdomen pelvis (gold standard)
- stool occult
A patient has intermittent left-sided lower abdominal pain and fever associated with bloating and constipation alternating with diarrhea. The provider suspects acute diverticulitis. Which tests will the provider order?
CT abd./pelvis and stool for occult blood
Non-Pharm Management of Diverticulitis (2):
- increase dietary fiber in patient with known diverticulitis
- low residue diet during acute diverticulitis
Pharm management of Diverticulitis (1):
Oral antibiotics: Ciprofloxacin & Flagyl for 7-10 days
Patho of Cholelithiasis/Cholecystitis:
Inflammatory, infectious, neoplastic, metabolic, or congenital conditions causing gallstone formation (cholelithiasis) and bile duct obstruction (biliary colic)
Cholecystitis RF (6):
- age
- female
- obesity
- pregnancy
- drugs
- metabolic disease
Cholecystitis classic Clinical Presentation (2):
- sudden, severe pain in RUQ that can radiate to the Right shoulder (typically within an hour of eating a large meal)
- Tenderness, muscle guarding, rigidity, jaundice, distended gallbladder, hypoactive BS
Murphy’s sign
Elicited in patients with acute Cholecystitis by asking the patient to take in and hold a deep breath while palpating the right subcostal area. If pain occurs on inspiration, when the inflamed gallbladder comes into contact with the examiner’s hand, Murphy’s sign is positive
Which of the following would be usual in a patient with biliary colic?
Pain in the upper abdomen in response to eating fatty foods (Feedback: Biliary colic refers to discomfort produced by contraction of the gallbladder)
Cholecystitis Diagnostic of choice:
ultrasound is the image of choice
Cholecystitis Management
Cholecystectomy
GERD
backward flow of gastric contents from stomach to esophagus d/t decreased lower esophageal sphincter tone caused by certain meds and foods (estrogen-progesterone, CCB, fluoroquinolones-ciprofloxacin)
GERD Clinical presentation (3):
- heartburn is most common complaint, cough, and dysphagia (red flag) which occur after eating and worsened by laying down
- Burning substernal sensation after eating described as “food gets stuck”.
- dyspepsia, CP at rest, postprandial fullness
GERD diagnostic:
- no specific diagnostic, presumptive diagnosis made based on presence of classic s/s and responsiveness to empirical treatment
- If unresponsive to PPI, further evaluation with EGD needed
Non-Pharm Management of GERD (2):
- avoid NSAIDS which worsen GERD and reduce alcohol
- Initial treatment: identify triggers and reducing their intake. Remaining upright for 3 hours after meal, smaller meals, and avoid overeating.
Pharm Management of GERD (4):
- use Antacid 1st, then PPI (they take weeks to work)
Antacid most effective when used 1-3 hours after a meal and at bedtime
H2RA for mild esophageal irritation as maintenance therapy to prevent relapse, if no improvement in 6 weeks, unlikely to be helpful long term
Can go straight to PPI in confirmed dx; treatment for 8 weeks to heal mod-severe esophageal inflammation.
Complications of GERD (3):
- Barrett’s Esophagus: a premalignant lesion to adenocarcinoma. (develops in 6-14% of patients w/GERD)
Endoscopic screening (EGD) is standard worldwide
Screening every 3-5 years in absence of dysplasia
Peptic Ulcer Disease
Disorder of full thickness mucosa in the gastric and duodenum lining d/t imbalance of acid and pepsin production; gastric & duodenal lining unable to protect itself
Most common triggers of duodenal ulcers (4):
H. Pylori
NSAID or low-dose Aspirin use
smoking
old age
PUD RF
- Fm hx & genetic factors
- Tobacco
- COPD
- Major trauma & physiological stress
- Oral steroids
- Alcohol
- Bisphosphonate therapy
- Cirrhosis
PUD Clinical Presentation (2):
- Gnawing epigastric pain or dyspepsia occurring 1.5-3 hours after meals or in the middle of the night and may be relieved by eating
- symptoms are recurring and last hours, days, months
PUD Diagnostic:
Endoscopy with biopsy is the standard diagnostic
Non-Pharm management of PUD:
- Eliminate triggers from diet
- Quit smoking, NSAIDS and COX-2 inhibitors
Pham Management of PUD (1):
1st = H. pylori eradication treatment for 10-14 days (2 wks):
- Amoxicillin (or Metronidazole)
- Clarithromycin
- PPI
Other treatments:
Antisecretory therapy
Histamine2 receptor antagonist (H2RA): famotidine, ranitidine
75-98% healing in 4-6 weeks
PPI: Omeprazole (do not use longer than 2 mo. And tapper off)
Prostaglandin therapy: for individuals who can’t d/c NSAIDS
Hemorrhoids
- rectal protrusion (normal anatomical finding) causing discomfort d/t increased venous pressure, dilation, and inflammation
- RF: ETOH, chronic diarrhea/constipation, obesity, high fat/low fiber diet, sedentary life, receiver of anal sex
Hemorrhoids Clinical Presentation (4):
- Rectal bleeding: described as bright red streaks on stool (dark blood mixed w/stool=refer for colonoscopy, risk for cancer)
- Perianal pain/discomfort
- Pruritus ani-anal itching
- Tender palpable lesion
Hemorrhoids Grades (4):
Grade I: no prolapse
Grade II: prolapse with deification and reduce spontaneously
Grade III: prolapse w/deification and must be manually reduced
Grade IV: prolapsed but cannot be reduced manually
Management of Grade I Hemorrhoid:
- dietary modification increase fiber, stool softener, topical corticosteroid, and sitz bath
Management of Grade II-IV Hemorrhoid:
need referral to GI, rubber band ligation, surgery
Which of the following patients should be evaluated for possible surgical intervention for hemorrhoids?
A 44 yo women who has internal & external hemorrhoids w/recurrent prolapse
5 Typed of viral hepatitis:
A, B, C, D, E
Hepatitis A (3):
- transmitted fecal-oral route from sewage, contaminated water, and shellfish
- HAV IgM is the serological marker for acute HAV infection
- self-limiting, no treatment
Hepatitis B (2):
- transmitted by blood and body fluids
- if AST and ALT normal or mildly elevated and patient is asymptomatic, it’s a chronic infection
Hepatitis B surface antigen
a protein on the surface of Hepatitis B virus, it can be detected in elevated levels during acute or chronic Hep B infection indicating person is infectious.
Hepatitis B surface antibody (anti-HBs or HBsAb):
positive or reactive indicates a person is protected against the virus either from a successful recovery or from immunization.
Hepatitis B core antibody:
Does not provide any protection, means someone has been infected at some time with infection. This begins to appear several weeks after you are infected with HBV.
Hepatitis C
- transmitted via blood & body fluid
- 50% of people with HCV develop a chronic infection
- significant risk of cirrhosis and hepatocellular carcinoma
Hepatitis Clinical Presentation (6):
Malaise, myalgia, fatigue, nausea, and anorexia, jaundice
Elevated serum aminotransferase (ALT) in viral hepatitis:
is 20 or more times the upper limit in infectious/viral hepatitis.
Normal AST:
0-35 units/L
Normal ALT:
4-36 units/L
Causes of elevated liver enzymes:
ETOH, medications, hepatitis
IgM
- In the Minute or Miserable for active dz
- produced as your body’s 1st response to a new infection
IgG
- Gone away, past dz
- produced during an initial infection or other antigen exposure, rising a few weeks after infection began, then decreasing and stabilizing
Active Hep B:
(+) HBsAg
(+) Anti-HBc IgM.
(-) Anti-HBs
Chronic Hep B:
(+) HBsAg
(+) Anti-HBc IgG.
(-) Anti HBc IgM
Recovered Hep B:
(+) Anti-HBsAB
(+) Anti-HBc.
(-) HBsAg
Immunity to Hep B:
(+) HBsAB (positive for nurses since we are immunized)