Exam 3 Flashcards

1
Q

RUQ

A
  • Liver and gallbladder
  • liver span is 6-12 cm
  • under the right costal ridge
  • spans across upper abdomen
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2
Q

LUQ

A
  • Spleen & Pancreas

- pancreas is behind the stomach and liver in the upper quadrants

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3
Q

RLQ

A
  • Appendix and Right ovary (lower)
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4
Q

Epigastric area

A

bounding pulsation: AAA

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5
Q

Appendicitis Clinical Presentation (3):

A
  • 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.
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6
Q

The 3 s/s most predictive of Appendicitis:

A
  1. pain that starts in the epigastric or periumbilical area.
  2. migrates to the RLQ.
  3. abdominal rigidity
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7
Q

Markle’s sign

A
  • causes peritoneal irritation in the RLQ when dropping to heels from standing on toes with a jarring landing
  • associated with Appendicitis
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8
Q

Appendicitis Diagnostics:

A
  • CBC: Leukocytosis
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9
Q

Normal WBC

A

4,500-11,000

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10
Q

Normal Neutrophil

A

55-70%

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11
Q

Normal Lymphocytes

A

20-40%

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12
Q

Normal bands

A

0-5%

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13
Q

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:

A
  • total WBC 16,500; neutrophils 66%, bands 8%; and lymphocytes 22%

Leukocytosis with a shift to left (elevated WBC, normal neutrophil, elevated bands)

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14
Q

Appendicitis imaging for suspected rupture:

A

CT abdomen pelvis

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15
Q

Appendicitis Management:

A

referral to ED (even if not ruptured) for IV antibiotics and appendectomy

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16
Q

Pancreatitis

A
  • acute or chronic inflammation of the pancreas that is life-threatening
  • characterized by elevated pancreatic enzymes d/t autodigestion of the pancreatic tissue
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17
Q

Pancreatic enzymes

A
  • Amylase: 23-45
  • Lipase: 0-160
  • both >200 in pancreatitis
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18
Q

Pancreatitis RF (4):

A
  • cholecystitis/biliary tract dz (gallstones)
  • high fat diet
  • hypertriglyceridemia
  • excessive alcohol use/ETOH
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19
Q

Pancreatitis Clinical Presentation (2):

A
  • sudden onset of intense, constant, sharp pain in the epigastric or LUQ that radiates to the back (most common sign)
  • N/v are common
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20
Q

Pancreatitis Diagnostics (3):

A

2/3 required for pancreatitis per ACG

  1. characteristic severe, abdominal pain
  2. elevated serum amylase or lipase 3 times ULN (lipase stays elevated longer-higher probability)
  3. characteristic abdominal CT findings (inflamed pancreas)
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21
Q

Pancreatitis Management:

A
  • 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
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22
Q

IBD

A
  • Inflammatory Bowel Disease

- Ulcerative Colitis and Crohn’s Disease

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23
Q

Ulcerative Colitis (2)

A
  • Diffuse and continuous inflammation of the large intestine and colon
  • Ulcers penetrate inner-lining of gastric mucosa
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24
Q

IBD RF:

A

Family History

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25
Q

Ulcerative Colitis Clinical Presentation (3)

A
  • 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
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26
Q

Ulcerative Colitis Complications:

A

increases RF colon cancer

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27
Q

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)?

A

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.

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28
Q

Crohn’s Disease (2)

A
  • Patchy inflammation (cobble-stone appearance) of the full gastrointestinal lining (gum to bum)
  • Ulcers are full-thickness penetrating the entire gastric mucosa
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29
Q

Crohn’s Disease Clinical Presentation (4):

A
  • Abdominal pain typically in the RLQ
  • prolonged diarrhea
  • Perianal lesions
  • Bowel obstruction
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30
Q

Chron’s Disease Complication:

A
  • can develop a fistulous tract
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31
Q

Gastroenteritis Clinical Presentation & Management:

A
  • N/V, non-bloody diarrhea, abdominal pain, hyperactive BS

- Oral or IV rehydration is important

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32
Q

Colorectal cancer Patho:

A
    • Most colorectal cancers are d/t polyps (2/3rd of polyps become adenomatous)
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33
Q

Colorectal Cancer RF:

A
  • personal or family hx of colorectal cancer of polyps
  • IBD (UC)
  • Hx of belly/pelvic radiation for previous cancer
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34
Q

Colorectal Cancer Screening (3):

A
  • 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
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35
Q

Constipation in older adults (3):

A

secondary to

  1. Medications (opioids)
  2. Decreased fluid intake
  3. Diets low in fiber & protein, but high in fate
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36
Q

Non-Pharm Constipation Management (3):

A
  1. Initially, avoid medications and foods known to cause constipation (better to stop a med than add a med to correct med s/e)
  2. Increase dietary fiber (25-30 g/day) and fluid intake
  3. Bowel Habits: recommend toileting 30 min after eating a meal and elevate feet on footstool
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37
Q

Diverticulitis:

A

-common complication of diverticulosis (asymptomatic pooching of intestines) resulting in inflammation that involves 1 or more diverticula (almost always symptomatic)

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38
Q

Clinical Presentation of Diverticulitis:

A
  • intermittent LLQ abdominal pain and tenderness (unusually presents in RUQ)
  • leukocytosis
  • fever
  • also associated with bloating and alternating diarrhea & constipation
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39
Q

Diverticulitis Diagnostic:

A
  • CT of abdomen pelvis (gold standard)

- stool occult

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40
Q

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?

A

CT abd./pelvis and stool for occult blood

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41
Q

Non-Pharm Management of Diverticulitis (2):

A
  • increase dietary fiber in patient with known diverticulitis
  • low residue diet during acute diverticulitis
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42
Q

Pharm management of Diverticulitis (1):

A

Oral antibiotics: Ciprofloxacin & Flagyl for 7-10 days

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43
Q

Patho of Cholelithiasis/Cholecystitis:

A

Inflammatory, infectious, neoplastic, metabolic, or congenital conditions causing gallstone formation (cholelithiasis) and bile duct obstruction (biliary colic)

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44
Q

Cholecystitis RF (6):

A
  • age
  • female
  • obesity
  • pregnancy
  • drugs
  • metabolic disease
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45
Q

Cholecystitis classic Clinical Presentation (2):

A
  • 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
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46
Q

Murphy’s sign

A

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

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47
Q

Which of the following would be usual in a patient with biliary colic?

A

Pain in the upper abdomen in response to eating fatty foods (Feedback: Biliary colic refers to discomfort produced by contraction of the gallbladder)

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48
Q

Cholecystitis Diagnostic of choice:

A

ultrasound is the image of choice

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49
Q

Cholecystitis Management

A

Cholecystectomy

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50
Q

GERD

A

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)

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51
Q

GERD Clinical presentation (3):

A
  • 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
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52
Q

GERD diagnostic:

A
  • 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
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53
Q

Non-Pharm Management of GERD (2):

A
  • 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.
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54
Q

Pharm Management of GERD (4):

A
  • 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.
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55
Q

Complications of GERD (3):

A
  • 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
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56
Q

Peptic Ulcer Disease

A

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

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57
Q

Most common triggers of duodenal ulcers (4):

A

H. Pylori
NSAID or low-dose Aspirin use
smoking
old age

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58
Q

PUD RF

A
  • Fm hx & genetic factors
  • Tobacco
  • COPD
  • Major trauma & physiological stress
  • Oral steroids
  • Alcohol
  • Bisphosphonate therapy
  • Cirrhosis
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59
Q

PUD Clinical Presentation (2):

A
  • 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
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60
Q

PUD Diagnostic:

A

Endoscopy with biopsy is the standard diagnostic

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61
Q

Non-Pharm management of PUD:

A
  • Eliminate triggers from diet

- Quit smoking, NSAIDS and COX-2 inhibitors

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62
Q

Pham Management of PUD (1):

A

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

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63
Q

Hemorrhoids

A
  • 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
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64
Q

Hemorrhoids Clinical Presentation (4):

A
  • 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
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65
Q

Hemorrhoids Grades (4):

A

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

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66
Q

Management of Grade I Hemorrhoid:

A
  • dietary modification increase fiber, stool softener, topical corticosteroid, and sitz bath
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67
Q

Management of Grade II-IV Hemorrhoid:

A

need referral to GI, rubber band ligation, surgery

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68
Q

Which of the following patients should be evaluated for possible surgical intervention for hemorrhoids?

A

A 44 yo women who has internal & external hemorrhoids w/recurrent prolapse

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69
Q

5 Typed of viral hepatitis:

A

A, B, C, D, E

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70
Q

Hepatitis A (3):

A
  • transmitted fecal-oral route from sewage, contaminated water, and shellfish
  • HAV IgM is the serological marker for acute HAV infection
  • self-limiting, no treatment
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71
Q

Hepatitis B (2):

A
  • transmitted by blood and body fluids

- if AST and ALT normal or mildly elevated and patient is asymptomatic, it’s a chronic infection

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72
Q

Hepatitis B surface antigen

A

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.

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73
Q

Hepatitis B surface antibody (anti-HBs or HBsAb):

A

positive or reactive indicates a person is protected against the virus either from a successful recovery or from immunization.

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74
Q

Hepatitis B core antibody:

A

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.

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75
Q

Hepatitis C

A
  • transmitted via blood & body fluid
  • 50% of people with HCV develop a chronic infection
  • significant risk of cirrhosis and hepatocellular carcinoma
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76
Q

Hepatitis Clinical Presentation (6):

A

Malaise, myalgia, fatigue, nausea, and anorexia, jaundice

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77
Q

Elevated serum aminotransferase (ALT) in viral hepatitis:

A

is 20 or more times the upper limit in infectious/viral hepatitis.

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78
Q

Normal AST:

A

0-35 units/L

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79
Q

Normal ALT:

A

4-36 units/L

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80
Q

Causes of elevated liver enzymes:

A

ETOH, medications, hepatitis

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81
Q

IgM

A
  • In the Minute or Miserable for active dz

- produced as your body’s 1st response to a new infection

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82
Q

IgG

A
  • Gone away, past dz
  • produced during an initial infection or other antigen exposure, rising a few weeks after infection began, then decreasing and stabilizing
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83
Q

Active Hep B:

A

(+) HBsAg
(+) Anti-HBc IgM.
(-) Anti-HBs

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84
Q

Chronic Hep B:

A

(+) HBsAg
(+) Anti-HBc IgG.
(-) Anti HBc IgM

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85
Q

Recovered Hep B:

A

(+) Anti-HBsAB
(+) Anti-HBc.
(-) HBsAg

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86
Q

Immunity to Hep B:

A

(+) HBsAB (positive for nurses since we are immunized)

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87
Q

Hepatitis D:

A
  • transmitted via blood and body fluids

- Prevent B to prevent D

88
Q

To prevent the outbreak of hepatitis D infection, the NP plans to:

A

immunize at-risk population against hepatitis b

89
Q

A patient has elevated liver enzymes. What is the likely etiology of the elevation? AST 150 & ALT 642

A

Hepatitis

 A diagnosis of hepatitis is far more common when the ALT is elevated. AST becomes the dominant liver enzyme when the patient has consumed a substance that causes the liver to be damaged. Examples of this are acetaminophen, alcohol, and drugs

90
Q

A patient has the following lab results: anti-HCV: reactive. This means?

A

More data are needed

 The anti-HCV is a screening test. A patient who has a reactive screen for hepatitis C may have the disease, but more data are needed to determine this. Once the screen is reactive, a confirmatory test should be performed. The confirmatory test is the HCV RNA. If it is detectable, it indicates past or current infection with hepatitis C. If undetectable the HCV RNA indicates that the screen was a false positive

91
Q

A 44-year-old patient has the following lab results. How should they be interpreted?
HBsAG: negative
anti-HBc: positive
anti-HBs positive.

A

Patient had hepatitis

 This patient has a negative hepatitis B surface antigen (HBsAg) therefore he does not have active hepatitis B. The patient has a positive hepatitis B surface antibody (anti-HBs) therefore he is considered immune. The patient also has a positive hepatitis B core antibody (anti-HBc) therefore he is immune because he has had hepatitis B.

92
Q

A 38 yo man w/current history of IDU presents w/malaise, nausea, fatigue, and “yellow eyes” for the past wk. after ordering diagnostic tests, you conform the diagnosis of acute hepatitis b. anticipated lab results include:

A

the presence of HBsAG

93
Q

Management of exposure to HBV:

A

Post-exposure prophylaxis can prevent HBV infection with HBIG and Hep b vaccine

94
Q

Management of patient with non-alcoholic fatty liver disease:

A

vaccinate against A and B to protect the liver from further damage.

95
Q

Clinical presentation of SBO (5):

A
  • Abdominal pain, distention, constipation, vomiting, peritonitis
96
Q

Initial SBO diagnostic:

A

Initially order abdominal x-rays, Upright and supine x-rays of the abdomen help to determine whether the patient has a partial or complete SBO.

97
Q

Management of SBO:

A

Once SBO is confirmed or suspected, patient will need hospitalization and consult with GI

98
Q

Irritable Bowel Syndrome (IBS) Patho:

A

chronic abdominal pain and altered bowel habits, diarrhea to constipation, in the absence of an organic cause.

99
Q

IBS s/s:

A

Tenesmus is best defined as a sensation of incomplete bowel emptying that is distressing and sometimes painful. Tenesmus is common in patients with constipation and IBS-C

100
Q

ROME III Diagnosis IBS (4):

A

Recurrent abdominal pain/discomfort at least 3 days/month in the first 3 months associated with 2 or more of the following:

  1. Relief with defecation
  2. Onset associated w/change in frequency of stool
  3. Onset associated with change in form or appearance of stool
101
Q

Infantile Colic:

A

PE should confirm the general well-being of an infant. After R/O organic problems, reinforce with parents to stay calm and sooth baby.

102
Q

Intussusception Classic triad:

A
  • Colicky abdominal pain, vomiting, and lethargy
  • Rectal bleeding w/red currant jelly stool
  • Sausage-shaped abdominal mass
103
Q

Pyloric Stenosis:

A
  • Blocks food from entering the small intestine
104
Q

RF for Pyloric Stenosis (3):

A
  • Common in the 1st born male
  • Smoking during pregnancy doubles the risk
  • Premature birth
105
Q

Onset of Pyloric Stenosis:

A
  • Most commonly presents within 3-6 week; rare after 12 wks.
106
Q

Clinical Presentation of Pyloric Stenosis (3):

A
  • Dehydration- fewer wet diapers
  • Nonbilious projectile vomit (“hungry vomiters”)
  • Upper abdominal olive-shaped mass most easily felt after vomiting
     if found, may represent hypertrophy of lateral edge rectus abdominus muscle
107
Q

Chronic Pruitis Ani causes (3):

A
  • Anorectal disorders, diarrhea, and constipation are common causes
108
Q

S/S of Chronic Pruitis Ani:

A

anal itching

109
Q

Non-Pharm Management of Chronic Pruitis Ani (4):

A

stop itch-scratch cycle

anal area should be kept clean and dry (hair dryer on cool setting can help dry)

Barrier creams with zinc oxide

Tight-fitting clothing should be avoided, and constipation prevented.

110
Q

Pharm Management of Chronic Pruitis Ani (23):

A

 Oral antihistamines w/antipruritic properties
 1% hydrocortisone can be used but not for chronic use, should be discontinued after 2 weeks to avoid skin atrophy.
- Patients with persistent symptoms after 2 weeks should be referred to dermatology.

111
Q

Normal Hgb:

A

12-14

112
Q

Normal Hct:

A

35-43%

113
Q

Normal RBC:

A

4.2-5.4

114
Q

Normal MCV

A

80-100

refers to size

115
Q

Normal MCH/MCHC:

A

31-37

refers to color

116
Q

RDW:

A

<15%

1st abnormal cbc finding in evolving micro or macrocytic anemia

117
Q

Reticulocytes

A

1-2%

118
Q

Iron Deficiency Anemia:

A
  • low Hgb d/t iron deficiency

- most common anemia world wide d/t chronic blood loss

119
Q

What is the body’s most important source of iron ?

A

recycled iron from aged RBC

120
Q

Koilonychia:

A

spoon-shaped nails associated w/IDA

121
Q

IDA Clinical Presentation (4):

A

koilonychia
brittle nails
atrophic glossitis
pica

122
Q

IDA s/s (6):

A

Fatigue, exercise intolerance, weakness, palpitations, irritability, and HA

123
Q
You examine a 27-year-old woman with menorrhagia who is otherwise well and note the following results on hemogram:
Hgb = 10.1
Hct = 32%
RBC = 2.9
MCV = 72 
MCHC = 28.2, 
RDW = 18.9%. 

Physical examination is likely to include:

A

no specific anemia related findings

124
Q
-	A 68-year-old man who is usually healthy presents with new onset of “huffing and puffing” with exercise for the past 3 weeks. Physical examination reveals conjunctiva pallor and a hemic murmur. Hemogram results are as follows: 
Hgb = 7.6
Hct = 20.5%
RBC = 2.1
MCV = 76 
MCHC = 28
RDW =18.4%, Reticulocytes =1.8%. 

The most likely cause of these findings is:

A

occult blood loss

125
Q

Which of the following is most consistent with IDA?

A

Low MCV, low MCH

126
Q

IDA most important/initial diagnostic:

A

CBC: microcytic-hypochromic, low RBC, high RDW

127
Q

Other IDA diagnostics:

A

Iron studies (to differentiate)

  • Low serum iron
  • Low serum ferritin
  • high TIBC
128
Q

IDA peripheral blood smear findings:

A

Anisocytosis (abnormal RBC size)

Poikilocytosis (abnormally shaped RBC)

129
Q

IDA initial Management:

A

treat the cause of blood loss & refer (GI, Nutritionist, GYN)

130
Q

Iron rich foods:

A

red meat, poultry, fish, beans, dark green vegetables, raisins, apricots, prunes, and iron-fortified breads and cereals

131
Q

Oral iron supplementations & doses:

A
  • Ferrous sulfate or Ferrous gluconate
  • Elemental iron 50-75 mg /day (150-200 mg/day for adults)
    (3 mg/kg child)
132
Q

 A 48-year-old woman developed IDA after excessive perimenopausal vaginal bleeding, successfully treated by endometrial ablation. Her Hct level is 25%, and she is taking iron therapy. At 5 days into therapy, one possible observed change in laboratory parameters would include:

A

Reticulocytosis within 7-10 days or oral therapy initiation

133
Q

A healthy 34-year-old man asks whether he should take an iron supplement. You respond that:

A

Iron in the absence of deficiency can cause iatrogenic iron overload

134
Q

Iron medication contraindication

A

fluoroquinolones (Cipro)

135
Q

Which of the following is the best advice on taking ferrous sulfate to enhance iron absorption?

A

Take on empty stomach or 30 min before meals w/ascorbic acid (vitamin c) to enhance absorption

136
Q

A 40-year-old woman with pyelonephritis is taking two medications: ciprofloxacin and ferrous sulfate (for IDA). She asks about taking both medications. You advise that:

A

an inactive drug compound is potentially formed if the two medications are taken together.

137
Q

Iron therapy S/E (2):

A

GI upset (n/v) most common complaint; tarry black stools; stool softener for constipation

138
Q

Microcytic-Hypochromic Anemia (2):

A

IDA

Thalassemia

139
Q

Thalassemia:

A

genetic blood disorder that effects how the body makes hgb (reduced or absent globin chains)

140
Q
You examine a 22-year-old woman of Asian ancestry. She has no presenting complaint. Hemogram results are as follows:
Hgb = 9.1 
Hct = 28% 
RBC = 5.6 million MCV = 68 
MCHC = 33.2 
RDW = 13%  Reticulocytes = 1.5%

This is most consistent with the laboratory assessment of:

A

(α-thalassemia minor)

141
Q

Alpha Thalassemia descents:

A

South Asia, middle east, China, Africa

142
Q

Beta Thalassemia descents:

A

Mediterranean

143
Q

Beta Thalassemia Major clinical presentation:

A
s/s @6-12 mo
FTT
fever
hepatosplenomegaly
short
abnormal cranial facial changes d/t cranial marrow expansion
144
Q

Beta Thalassemia Minor clinical presentation:

A

asymptomatic till cbc reveal microcytic RBC

145
Q

Beta Thalassemia Minor diagnostic:

A

CBC:

  • microcytic-hypochromic
  • low hgb & hct
  • normal RDW
146
Q

Hgb electrophoresis

A

gold standard diagnostic used to differentiate SC from thalassemias

147
Q

Which hematologic finding would be expected in an 18-month-old patient diagnosed with beta thalassemia minor?

A

elevated HgbA

148
Q

Which of the following tests would you recommend to patients to confirm the diagnosis of beta thalassemia or sickle cell anemia?

A

Hemoglobin electrophoresis

149
Q

Management of B-Thalassemia

A
  • Major: lifelong blood transfusion, chelation tx in iron overload, splenectomy
  • Intermedia: folic acid (PO 1-2 mg/day), tx iron overload
  • Minor: no tx, avoid inappropriate iron therapy (misdiagnosis of IDA = anemia worsens)
150
Q

Vitamin B12 Deficiency Anemia patho:

A

vitamin B12 is essential for RBC development

deficiency from omnivore diet is uncommon (unless plant-based or vegan, take B12 supplement).

151
Q

Pernicious Anemia patho:

A

a result of autoimmune destruction of gastric parietal cells that produce Intrinsic Factor (IF) which is needed for B12 intestinal absorption

152
Q

Pernicious anemia is usually caused by:

A

lack of production of intrinsic factor by the gastric mucosa

153
Q

Vit. B12 Deficiency anemia clinical presentation (2):

A

Neuro s/s:

  • paresthesia, weakness, clumsy, unsteady gait
  • new onset of mental status change: forgetful/confused
154
Q

Common physical examination findings in patients with pernicious anemia include:

A

Stocking-glove neuropathy of hands & feet

155
Q

Vit. B12 Deficiency anemia PE (4):

A
  • atrophic glossitis (beefy sore tongue)
  • hypoactive DTR
  • loss of vibratory sense
  • tachycardia
156
Q

Vit. B12 Deficiency Diagnostic (2):

A
- CBC: 
macrocytic
normochromic
low hgb
elevated RDW
  • serum cobalamin
157
Q

Medications that effect B12 absorption:

A

PPI & Metformin

158
Q

Prolonged use of PPIs can lead to which micronutrient deficiency that can contribute to anemia?

A

B12

159
Q

Vitamin B12 anemia RF based in Hx (5):

A
  • medications
  • gastric sx
  • UC/CD
  • diet
  • ETOH
160
Q

dietary sources of B12:

A

foods of animal origin

161
Q

Vitamin B12 Therapy:

A
  • Administered orally or parenterally.

- Parenteral therapy is recommended, as the oral form can be absorbed erratically and lead to treatment failure.

162
Q

Vitamin B12 Therapy Management (2):

A
  • Check effectiveness of B12 therapy 2 months after starting by checking hgb
  • Monitor for hypokalemia in the 1st week of B12 supplementation, especially in those taking diuretics & digoxin
163
Q

Vitamin B12 Deficiency complications:

A

If neuro abnormalities persist >6 mo, changes are occasionally permanent.

164
Q

Anemia of Chronic Disease (ACD) patho:

A

Mild-mod anemia d/t inflammation, infection, or malignancy causing reduced erythropoietin response in the marrow (decreased RBC proliferation)

165
Q

ACD etiology (2):

A
  • Inflammatory Dz:
    poorly controlled RA, SLE, UC/CD (IBD), vasculitis, sarcoidosis
  • Infection/Malignancy:
    CKD/renal insufficiency, Cancer, hypothyroidism, organ rejection
166
Q

ACD diagnostics:

A

CBC:

  • normocytic
  • normochromic
  • slightly low Hgb (rarely <9)
  • slightly low Hct (>24%)
  • normal RDW
167
Q

Which of the following is not consistent with ACD?

A

Hct less than 24%

168
Q
	You examine a 57-year-old woman with rheumatoid arthritis who is on a biological disease-modifying antirheumatic drug (DMARD) but continues to have poor disease control, and you find the following results on hemogram: 
Hgb =10.5
Hct =33%
RBC = 3.1
MCV = 88 
MCHC = 32.8
RDW = 12.2%, reticulocytes = 0.8%. 

The laboratory findings are most consistent with:

A

ACD

169
Q

Which of the following conditions is unlikely to result in ACD?

A

Peripheral vascular disease

170
Q

Hemolytic Anemia:

A
  • increased rate of RBC destruction

- most common hemolytic anemia is SC

171
Q

G6PD deficiency (2): (inherited erythrocyte enzyme deficiency)

A
  • causes acute hemolytic anemia, precipitated by infection or oxidant drug or food (aspirin, phenacetin, nitrofurantoin, primaquine)
  • self-limiting, rarely requires treatment
172
Q

Black adult male presents with new onset of jaundice, dark urine, fatigue, and anorexia. He was seen a few days previously and treated for a possible urinary tract infection. He is on the third day of nitrofurantoin (Macrobid) 100 mg PO BID 7 days. The hemoglobin is 11, and hematocrit is 34%. The MCV is 84 fL. The serum indirect bilirubin is elevated. Which of the following conditions is most likely?

A

(GP6D anemia)

173
Q

Hemolytic anemia s/s:

A
  • most are mild and asymptomatic

- severs cases present w/typical anemic s/s (fatigue, weakness, exercise intolerance)

174
Q

Hemolytic anemia diagnostics (3):

A
  • CBC w/diff: slightly low hgb & RBC count
  • Elevated LDH (lactate dehydrogenate); LFTs = hyperbilirubinemia; renal fx: BUN, creatine, eGFR
  • GP6D assay
175
Q

Sickle Cell Anemia diagnostic (2):

A
  • Hemoglobin electrophoresis: required for accurate dx

- HgbS will comprise 85-98% of hgb

176
Q

The nurse practitioner is reviewing the medical record of a 6-month-old infant with normocytic hemolytic anemia and notes an electrophoresis result of hemoglobin S with a 20% concentration of hemoglobin F (fetal hemoglobin). Which additional diagnosis is most likely? Sickle cell anemia

A

Sickle cell anemia

177
Q

Sickle Cell CBC findings (4):

A
  • low hct
  • chronic reticulocytosis
  • hyperbilirubinemia
  • elevated LDH
178
Q

Which hematologic findings on a peripheral smear support a diagnosis of sickle cell anemia?

A

Target cells & Howell-Jolly bodies

179
Q

Hemophilia:

A

X-linked recessive bleeding disorder characterized by low levels of factor VIII (hemophilia A) or factor IX (hemophilia B) resulting in defective fibrin clot formation (cascade)

180
Q

What is the most common type of hemophilia in the United States? Factor VIII deficiency (Hemophilia A)

A

Factor VIII deficiency (Hemophilia A)

181
Q

most common cause of death in hemophilia?

A

intracranial hemorrhage

182
Q

A male patient has a history of recurrent epistaxis. Prior to a scheduled surgery, the provider asks about a family history of bleeding disorders. The patient reports no female relatives who had excessive bleeding episodes, but states that a maternal uncle and his maternal grandfather both had post-surgical complications related to bleeding. Based on this history, which diagnosis is possible?

A

Hemophilia

RF: only males (women are only carriers)

183
Q

Hemophilia diagnostic:

A

Prolonged aPTT

PT, prothrombin time, and PFA-100 are normal

184
Q

A patient is noted to have prolonged bleeding after an intravenous needle is removed. A subsequent laboratory test reveals a prolonged activated partial thromboplastin (aPTT) time with a normal prothrombin time (PT). Based on this result, the provider may suspect alteration in function of which factor?

A

Factor VIII

185
Q

Mild to moderate & moderate to severe Hemophilia

A

may only blead with trauma (joint and muscle hemorrhages are common in mild-mod hemophilia, result in disability )

mod-severe bleed spontaneously

186
Q

Hemophilia management:

A
  • Replacement of coagulation factors, especially with head trauma
  • Patient education: know name of hemophilia they have, s/s of bleed, no contact sports
187
Q

Acute Lymphoblastic Leukemia (ALL) (2):

A

malignancy of the bone marrow

fast-growing cancer of lymphoblasts that causes very high white blood cell (WBC) counts (>50,000)

188
Q

the most common type of cancer in children?

A

ALL

It is more common in boys and in children between the ages of 2 and 4 years;

189
Q

A child has a recent history of leg pain, unexplained bruising, and nosebleeds. The provider notes petechiae and diffuse lymphadenopathy. A complete blood count reveals a white blood cell (WBC) of 30,000 cells/mm3 and near normal red blood cell (RBC) and platelet counts. What will the provider do next to manage this patient?

A

Refer to a specialist for a bone marrow biopsy

190
Q

A patient with acute myelogenous leukemia (AML) who has a high white blood cell count and diffuse lymphadenopathy is hospitalized during the induction phase of chemotherapy. What monitoring and interventions are critical to assess for complications during this phase of care for this patient? Select all that apply.

A
  • Administration of sodium bicarbonate and allopurinol

- daily renal function and chemistry values, - meticulous assessment of hydration.

191
Q

An 18 yo college freshman presents at the campus clinic with reports of severe night sweats, lymphadenopathy, and severe pain over gland areas after drinking alcohol. Further assessment indicates that the patient has a positive Pel–Ebstein sign. Blood work reveals several Reed–Sternberg cells. Which diagnosis is most likely?

A

Hodgkin’s lymphoma

192
Q

A 30 yo male patient is diagnosed with Hodgkin lymphoma. Initial lab work reveals a WBC of 20 × 109/L, hemoglobin of 10.1 gm/dL, a serum albumin of 3 g/dL, and lymphopenia of 0.5 × 109/L. Staging studies identify stage III disease. What is this patient’s prognostic score?

A

4

193
Q

A patient who has non-Hodgkin’s lymphoma reports a dull, aching back pain in the thoracic region for several weeks along with difficulty walking. The provider notes an ataxic gait. What is the immediate treatment for this condition?

A

Steroid therapy

194
Q

Spinal cord compression tx in Non-Hodgkin’s?

A

Dexamethasone to reduce vasogenic edema

195
Q

A patient reports a neck mass that has been present intermittently for 5 or 6 weeks which varies in size. The provider palpates a lymph node measuring 1.25 cm. Which test will provide proper histologic diagnosis for this patient?

A

Lymph node biopsy

196
Q

At what age might a child initially recognize his parents and give a social smile?

A

1-2 months

197
Q

At what age should oral health risk assessment begin?

A

3 months

198
Q

At what age might an infant first be expected to reach for an object and bring an object to the mouth?

A

3-4 months

199
Q

When can an infant be expected to sit without support?

A

6-8 months

200
Q

What would be age-appropriate anticipatory guidance for the parent of a 9-month-old infant?

A

Discuss weaning from a bottle

201
Q

When can an infant be expected to start crawling and possibly start to stand by pulling up on furniture?

A

9-11 months

202
Q

Which patient below is most likely to experience stranger anxiety during a physical exam?

A

12-mo female

203
Q

T/F

It is considered a possible developmental “red flag” if a child does not respond to his or her name by 12 months of age?

A

True

204
Q

When can a child be expected to initially start to take steps, walk with help and use two-word sentences?

A

12-15 months

205
Q

A child who is 18 months old is referred to as a(an):

A

toddler

206
Q

You are examining an 18-month-old boy who is not speaking any discernible words. Mom tells you he has not said “mama” or “dada” yet or babbled or smiled responsively. You:

A

conduct further evaluation of milestone attainment.

207
Q

Risk assessment for dyslipidemia should begin at:

A

2 years

208
Q

A child who can stack a maximum of five blocks is probably:

A

2 years of age

209
Q

At what age should initial blood pressure screening take place in the pediatric patient?

A

3 years

210
Q

When does a child’s vision approximate 20/20?

A

5-6 years

211
Q

Which of the following chromosomal syndromes is a common etiology of social and verbal developmental delays in boys?

A

Fragile X

212
Q

A young female has bilateral breast buds. This represents Tanner Stage:

A

II

213
Q

All of the following would support a diagnosis of Austism Spectrum Disorder (ASD) EXCEPT:

A

the symptoms are absent until the child reaches school age.

214
Q

The initial step in the management of encopresis is:

A

client and family education

215
Q

A 6-week-old infant is found to have positive Barlow and Ortolani maneuvers. What test should the NP order to assess and confirm developmental dysplasia of the hip (DDH)?

A

Ultrasound of the hip