Clinical Approach to GI Patients Week 2 Flashcards

1
Q

What is the most common cause of occult bleeding with iron deficiency?

What is iron deficiency anemia in premenopausal women most associated with?

A

NEOPLASMS –> colon cancer (> 45 yo)

occult = bleeding that is not apparent to the patient or chronic GI bleeds

PW: associated with menstrual and pregnancy-associated iron loss

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2
Q

How is occult bleeding diagnosed (3) in the absence of visible blood loss?

A

(+) Fecal Occult Blood Test (FOBT), Fecal Immunochemical Test (FIT), and iron deficiency anemia

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3
Q

What are 4 Lower GI Bleed considerations in patients UNDER 50 years old (IC/AD/I/MD) and OVER 50 years old (M/D/A/IC)?

A

U: infectious colitis, anorectal disease, IBD, Meckel diverticulum

O: malignancy, diverticulosis, angiectasias, ischemic colitis

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4
Q

What are Diverticulosis, how do they present, and how are they diagnosed?

What are they the most common cause of?

A
  • herniations of mucosa through muscularis at points nutrient artery penetration, most commonly in SIGMOID COLON (90% are asymptomatic)

P: acute, painless large-volume bright red hematochezia (> 50 yo)

Dx: colonoscopy once bleeding subsides

most common cause of MAJOR lower GI tract bleeding

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5
Q

How do appendectomy and antibiotics use affect Inflammatory Bowel Disease?

Who is IBD most commonly seen in and when?

A
  • appendectomy before appendicitis BEFORE age 20 can protect from Ulcerative Colitis
  • antibiotic use with first year of life = 2.9x inc. risk of IBD in childhood

**common in urban, high socioeconomic settings; white Jews highest risk; bimodal (2nd-4th and 7th-9th decades)

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6
Q

What are serological findings and diagnostic imaging found in Ulcerative Colitis and Crohns Disease?

A

UC: anti-neutrophil cytoplasmic Abs (ANCA) - 70%
- “Lead Pipe” appearance = loss of haustra

CD: Saccharomyces cerevisiae (ASCA) - 60-70%

  • “String Sign” appearance
  • narrowing from inflammation/stricture
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7
Q

How does Crohn’s Disease present and what are 4 findings that are MORE COMMON in CD than UC?

How does smoking affect Crohn’s Disease?

A

P: cramping RLQ pain with diarrhea (may have blood) and MIMICS appendicitis (acute ileitis)

  • more likely to have abscesses, strictures, fistulas, and anorectal fissures

Smoking: recent onset of smoking increases likelihood of Crohn’s Disease onset

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8
Q

How does Ulcerative Colitis present?

How does smoking affect Ulcerative Colitis?

A

P: bloody diarrhea with fecal urgency (tenesmus) with primary sclerosing cholangitis (Severe forms = 6+ bloody BMs/day); LLQ pain

Smoking: more common in non-smokers and former smokers (onset found with cessation of smoking)

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9
Q

Crohn’s Disease vs Ulcerative Colitis

SB appearance, inflammation, and ulcers

Which one has significant radiographical imaging?
Which one is associated with CARD15/NOD2?

A

CD: abdominal mass, thick wall with “Cobblestoning”, transmural inflammation with deep knife-like ulcers; non-caseating granulomas; SKIP LESIONS and CREEPING FAT
- CARD15/NOD2 gene on chromosome 16p

UC: no abdominal mass, thin wall, limited mucosa inflammation with superficial broad-based ulcers; toxic megacolon and malignant potential (CD ONLY with colon involvement); pseudopolyps

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10
Q

What is Ischemic Colitis, where does it commonly occur, and what can be seen on imaging and why?

A
  • acute vascular obstruction causing sudden LLQ pain, desire to defecate with blood passage or bloody diarrhea (basically ONLY poop blood)
  • see in WATERSHED areas (Splenic Flexure) in older adults (atherosclerotic disease) and younger pts (cocaine)

Imaging: “thumb printing” colonic dilation due to submucosal edema

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11
Q

What are four things that should make you consider Hereditary Colorectal cancer or Polyposis Syndromes in a patient?

A
  • family history of cancer affecting multiple family members
  • history of colorectal cancer at an early age (< 50 yo)
  • history of multiple polyps (20+)
  • history of multiple extracolonic malignancies
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12
Q

Familial Adenomatous Polyposis (FAP)

How does it present and what extraintestinal manifestation is detected at birth, what genetics are associated with it, and how is it treated?

A
  • early development of thousands of colonic adenomatous polyps and adenocarcinoma
    • detect congenital hypertrophy of retinal pigment epithelium at birth

G: APC AD mutation (90%), MUTYH AR mutation (8%)

T: complete proctocolectomy with ileoanal anastomosis before age 20 (Prophylactic Colectomy recommended)

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13
Q

Lynch Syndrome (Hereditary Nonpolyposis Colon Cancer)

How does it present, what genetics are associated with it, and how is it treated?

A
  • lifetime risk of colorectal cancer and endometrial cancer with risk of multiple other cancer at a young age
    • rapidly transform over 1-2 years to cancer
    • all colorectal cancers should undergo testing for LS

G: AD mutation of DNA base-pair mismatch genes
- MSH2/MLH1 (confirms diagnosis)

T: subtotal colectomy with ileorectal anastomosis

  • annual surveillance of rectal stump
  • hysterectomy/oophorectomy in women 40 yo
    • used prophylactically once childbearing is over
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14
Q

Hamartomatous Polyposis Syndromes

How do these present and how are they diagnosed:

  1. Peutz-Jeghers Syndrome
  2. Familial Juvenile Polyposis
  3. Cowden Syndrome (PTEN)
A
  1. small intestine polyps (not malignant)
    • mucocutaneous pigmented macules on lips, cheek
    • AD serine threonine kinase 11 gene
  2. several polyps in colon (50% risk of adenocarcinoma)
    • AD defects on loci 18q/10q (MADH4/BMPR1A)
  3. polyps with trichilemmomas and cerebellar lesions
    • inc. malignancy in thyroid, breast, urogenital tract
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15
Q

What is the best way to treat and detect colorectal polyps in pts with Nonfamilial Adenomatous and Serrated Polyps?

A

COLONOSCOPY (endoscopic test)

  • diagnostic and therapeutic
  • follow by Postpolypectomy Surveillance (3-10 yrs)

most pts are completely asymptomatic, but chronic occult blood loss can lead to iron deficiency anemia

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16
Q

Colon Cancer (Adenocarcinoma)

What bacteria is associated with pts who have a family history, where does it commonly metastasize to, and when does cancer usually present?

When should screening be done?

A
  • high prevelance of Streptococcus bovis bacteremia (Strep. gallolyticus)
  • main site of metastasis is LIVER
  • cancer usually develops in pts > 45 yo

screen starting at 45 yo; begin at 40 or at least 10 years earlier that 1st degree relative if family history

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17
Q

Angioectasias (Arteriovenous Malformations or AVM)

What is it and what two things cause it?

What is a diagnostic technique that is ONLY diagnostic?

A
  • angiodysplasias that cause painless bleeding from melena –> occult blood loss (proximal to Ligament of Trietz could present as melena)
  • common in pts OVER 70 yo due to chronic renal failure or aortic stenosis

PILL Capsule = pill camera EGD

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18
Q

Hemorrhoids vs Anal Fissures

A

H: see bright red blood per rectum (drops on tissue or in toilet)

  • Thrombosed External Hemorrhoid
  • bluish, perianal nodule on skin (PAINFUL)

AF: severe, tearing pain during defecation followed by throbbing discomfort; linear, rocket-shaped ulcers
- mild associated hematochezia, blood in stool or TP

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19
Q

What, so far that we have learned, would be on a RUQ Abdominal Pain Differential?

A

Duodenal Ulcers

Future: Gallbladder, Hepatitis, Pancreatitis, Budd-Chiari Syndrome

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20
Q

What are the top 6 differential diagnoses for Epigastic Abdominal Pain? (AA/PUD/HH/G/G/E)

A
  1. Dissecting/Ruptured Aortic Aneurysm
  2. Peptic Ulcer Disease
  3. Hiatal Hernia
  4. GERD
  5. Gastritis
  6. Esophagitis
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21
Q

Aortic Aneurysm

What is the difference between Rupture and Dissection?

A

R: risk of rupture inc. with aneurysm size

  • usually no symptoms, seen on routine examination
  • acute pain and hypotension with rupture (BAD)
  • ultrasound men 65-75 who have ever smoked

D: circumferential (or transverse) tear of the intima

  • usually on right lateral wall of ascending aorta
  • creates false lumen w/widened mediastinum
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22
Q

What are the top 4 differentials for LUQ Abdominal Pain?

A
  1. Gastric Ulcer
  2. Gastritis
  3. Pancreatitis
  4. Perforated Subdiaphragmatic Viscus
    • perforated hollow organ in the abdomen
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23
Q

What are the top 6 differentials for RLQ Abdominal Pain?

A
  1. Appendicitis
  2. Ectopic Pregnancy
  3. Ovarian Torsion
  4. IBD
  5. Ogilvie Syndrome
  6. Meckel’s Diverticulitis
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24
Q

Appendicitis

What is it and how does it present, how can it be diagnosed, and what are complications of it?

A
  • caused by obstruction of appendix by a fecalith (or inflammation, neoplasm, etc) between ages 10-30 yo; pain is colicky periumbilical/epigastric that shifts to RLQ within 12 hrs

D: abdominal ultrasound and CT scanning
- moderate leukocytosis with neutrophilia

C: gangrene and perforation (suppurative peritonitis)

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25
Q

Ectopic Pregnancy

What is it and how does it present, how is it diagnosed, and what are complications of it?

A
  • most common cause of maternal death during first trimester (98% are tubal) presenting as lower quadrant pain (appear 6-8 weeks after last normal menstrual period)

Dx: no intrauterine pregnancy on transvaginal US w/serum beta-hCG > 2000 milli-units/mL

C: shock (10% with pelvic exam), maternal death

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26
Q

Ovarian Torsion

What is it and how does it present, how is it diagnosed, and what are complications of it?

A
  • ovarian cysts/tumor causes enlargement of ovary and twisting of oviduct (70% on right side due to utero-ovarian ligament on right) - ADNEXAL pathology
  • usually sudden-onset, severe, unilateral abdominal pain that develop after episodes of exertion

Dx: Transvaginal US w/Doppler (PRIMARY)
- greater than 4 cm in cyst is most common finding

C: loss of ovarian function (surgical emergency)

27
Q

Acute Colonic Pseudo-Obstruction (Ogilvie Syndrome)

What is it and how does it present, how is it diagnosed, and how is it treated?

A
  • spontaneous MASSIVE dilation of cecum/right colon w/o mechanical obstruction (really sick ICU pts)
  • abdominal distension (1st sign) –> plain film radiography demonstrating colonic dilation (no movements but can pass flatus or stool - 40%)

Dx: X-Ray/CT (cecal diameter > 10-12 cm has inc. risk of perforation)

Tx: conservative (attack underlying illness); nasogastric or rectal tube

28
Q

Ogilvie Syndrome

How often should cecal size be evaluated and what are three possible treatments for pts?

A
  • assess cecal size every 12 hours via radiography
  • intervention (no improvement in 2 days or dilation for 3-4 days)
  • use neostigmine (colonoscopic decompression if neostigmine does not work), and surgery (if colonoscopy doesn’t work)
29
Q

Meckel’s Diverticulitis

What is it and how does it present, how is it diagnosed, and how is it managed?

A
  • remnant of vitelline duct on anti-mesenteric border of ileum that can present with obstruction, rectal bleeding, perforation, and intussusception

Dx: technetium-99m scan

Tx: surgical resection

30
Q

What are the top 6 differentials for LLQ Abdominal Pain? (D/IC/EP/OT/IBD/CC)

A
  1. Diverticulitis
  2. Ischemic Colitis
  3. Ectopic Pregnancy
  4. Ovarian Torsion
  5. IBD
  6. Colon Cancer
31
Q

Diverticulitis

What is it and how does it present, how is it diagnosed, and what are treatment options for Inpatients vs Outpatients?

A
  • macroscopic inflammation of a diverticulum that can become macroperforation with abscess/general peritonitis
  • LLQ pain, constipation (1st), fever; thickened, palpable sigmoid and descending colon

Dx: CBC and CT with contrast (no EGD –> inc. perforation risk)

Outpt: antibiotics, clear liquid diet
Inpt: IV fluids, NPO to start, 7-10 days antibiotics

32
Q

What are the top 5 differentials for Periumbilical Abdominal Pain?

A
  1. early appendicitis
  2. mesenteric artery ischemia
  3. ruptured aortic aneurysm
  4. bowel obstruction
  5. inflammatory bowl disease
33
Q

What is the difference between Acute and Chronic Mesenteric Ischemia?

A

A: periumbilical pain out of proportion to tenderness

  • “thumb-printing” on abdominal X-Ray
    - use CT angiography with IV contrast (BEST choice)

C: abdominal angina (dull, crampy periumbilical in 15-30 min after meal) –> pt. have food fear and weight loss
- use mesenteric arteriography for bypass graft

34
Q

What are Intestinal Obstructions, how are they diagnosed, and how can they be treated? (2)

A
  • peritoneal adhesions with colicky abdominal pain, nausea, vomiting (FECULENT), no farts/poop

Dx: plain radiography or CT scan

Tx: NG tube decompression w/fluids OR laparotomy for lysis of adhesions BEFORE bowel ischemia develops

35
Q

What are the top 7 differentials for Diffuse Abdominal Pain? (IBS/MAI/P/IO/IBD/TM/C)

A
  1. Irritable Bowel Syndrome
  2. Mesenteric Artery Ischemia
  3. Peritonitis
  4. Intestinal Obstruction
  5. Inflammatory Bowel Disease
  6. Toxic Megacolon
  7. Constipation
36
Q

What is the difference between Primary (Spontaneous) Bacterial Peritonitis vs Secondary Peritonitis?

Presentation, Diagnosis, and Treatment

A

P: most common in pts. with cirrhosis

  • enteric gram (-) bacilli or gram (+) organisms
  • Dx: peritoneal fluid contains > 250 PMNs/uL
  • blood cultures –> bacteremia is common
  • Tx: cephalosporin, piperacillin/tazobactum

S: bacteria in peritoneum from spillage of viscus

  • mixed flora w/gram (-) bacilli and ANAEROBES
  • pt. motionless, knees drawn up
  • Dx: radiography, abdominal tap (exclude blood)
  • Tx: antibiotics, surgical intervention
37
Q

What is Toxic Megacolon?

A
  • lethal complication of IBD (ulcerative colitis) or C. difficile
  • characterized by total/segmental nonobstructive colonic dilation PLUS systemic toxicity
38
Q

What are the differentials for Fatigue (OG/C/I/CLD/M) and Unintentional Weight Loss (PD/C/I/M)?

A

F: occult GIB, cancer, IBD, chronic liver disease, malnutrition/malabsorption

UWI: cancer, malabsorption syndromes, IBD, poor dentition

39
Q

What amount of unintentional weight loss should prompt further evaluation?

How should men and women be examined?

What is an oral consideration that should always be asked about it pt. is having unintentional weight loss?

A

loss of 5-10% of body weight over 6 months (important to confirm loss –> 50% cannot be substantiated)

  • get history and weigh pt.; men should have rectal exam + prostate, women should have pelvic exam, and both should have stool tested for occult blood
  • ASK ABOUT DENTITION (check your pts. teeth and mouth –> can compromise oral intake)
40
Q

What is the difference between Non-Inflammatory and Inflammatory Acute Diarrhea?

What are three likely causes (BROAD) of each?

A

acute = diarrhea of < 2 weeks duration

NI: watery, non-bloody, self-limited/mild

  • virus or non-invasive bacterial (NO WORKUP)
  • meds, allergies (abx), artificial sweeteners (sorbitol)

I: blood/pus in stool, fever

  • invasive or toxin-producing bacterium
  • STOOL BACTERIAL CULTURE
  • viral, bacterial, protazoal
41
Q

What is the difference between Osmotic and Secretory Chronic Diarrhea?

What are two findings that can help differentiate the two?

What are 4 common causes of both?

A

chronic = diarrhea of > 4 weeks duration

O: volume dec. with fasting, inc. stool osmotic gap (> 50-75 mOsm)

  • ask about intake of dairy, fruits, EtOH, sweeteners
  • meds, lactose intolerance (hydrogen breath test)
  • laxative abuse, malabsorption syndromes

S: volume same with fasting, normal osmotic gap; dehydration and electrolyte imbalance develop

  • high volume of water diarrhea (>1 L/day)
  • endocrine tumors, bile salt malabsorption
  • facultative diarrhea (laxative), villous adenoma
42
Q

What are the 3 most common causes of chronic diarrhea that should be considered?

What are inconsistent findings that should warrant further evaluation?

A

CC: medications, IBS, lactose intolerance

  • nocturnal diarrhea, weight loss, anemia, (+) FOBT warrant further evaluation (WORK THAT BITCH UP)
  • get routine laboratory tests: CBC/serum electrolytes/liver enzymes/ESR and CRP, etc
43
Q

Chronic Diarrhea

What tests can be run to diagnose:

  1. Inflammatory issues (FC/FL)
  2. Giardia/E. histolytica infection
  3. Cryptosporidium/Cyclospora infection
A

Inflammatory

  • fecal occult blood, fecal leukocytes (IBD)
  • fecal calprotectin, fecal lactoferrin (IBD - BETTER)

Giardia/E. histolytica
- Fecal Antigen (better than wet mount), wet mount

Cryptosporidium/Cyclospora
- modified acid-fast staining

44
Q

Chronic Diarrhea

What findings can you look for if you suspect Pancreatic Insufficiency or Chronic Pancreatitis?

What two things can breath tests be used for?

What are 4 serological tests that can be done if suspecting neuroendocrine tumor?

A

Malabsorption

  • PI: fecal elastase (< 100 mcg/g)
  • CP: calcification on plain abdominal radiography

Breath Tests (for malabsorption)

  • SB bacterial overgrowth: glucose/lactulose BT
  • Carbohydrate malabsorption: hydrogen BT

Neuroendocrine
- VIP (VIPoma), calcitonin (thyroid), gastrin (zollinger), 5-HIAA (carcinoid)

45
Q

What medications are common causes of chronic diarrhea? (CI/S/ARB/PPI/N/M/A)

A
cholinesterase inhibitors
SSRIs
angiotensin II-receptor blockers
proton pump inhibitors
NSAIDS
metformin
allopurinol
46
Q

Irritable Bowel Syndrome

What 3 abnormalities are reported and what are 3 ways that it can present clinically?

A
  • pts have altered colonic/small-intestinal motility, enhanced visceral sensation (low pain tolerance to distension), and inc. frequency of psychological disturbances

absence of detectable organic pathology

CP: spastic colon (abdominal pain, constipation), altering constipation/diarrhea, or chronic/painless diarrhea

47
Q

What “alarm” symptoms should cause you to warrent further investigation in a pt who you thought has IBS?

A
  • acute symptom onset, nocturnal diarrhea, severe constipation/diarrhea, hematochezia, weight loss, fever

family history of cancer, celiacs, inflammatory bowel disease

48
Q

Irritable Bowel Syndrome

What are two ways it can be diagnosed? How is it treated?

A
  1. chronic > 6 months (symptoms for at least 3 months before consideration in differential)
    • diagnosis of exclusion
  2. ROME IV Clinical Diagnostic Criteria

use sigmoidscopy and barium radiography to exclude other possibilities

Tx: medications for symptoms, reassurance, avoidance of stress; avoid fatty foods and caffeine (low FODMAPS diet)

49
Q

What protozoans (G/E/C), nematode (SS), and bacterial infections (CD) cause chronic diarrhea in normal patients?

What are viral, bacterial, and protazoal (M/C/C) microbes that cause diarrhea in immunocompromised pts?

A

Normal:
P - Giardia, E. histolytica, cyclospora
N - Strongyloidiasis stercoralis
B - C. difficile

Immunocompromised
V - CMV/HIV
B - C. difficile, MAC
P - Microsporidia, Cryptosporidium, Cyclospora

50
Q

What is the most common cause of antibiotic-associated colitis?

A

CLOSTRIDIUM DIFFICILE

  • anaerobic, Gram (+), spore-forming bacillus
  • produces Cytotoxins A and B (nosocomial)
51
Q

What 4 antibiotics are more likely to lead to development of C. difficile infection? (A/C/C/F)

A

ampicillin, clindamycin, cephalosporins (3rd generation), fluoroquinolones

52
Q

Clostridium Difficile

What 3 tests can help diagnose it, what does it look like, and how does it present?

A

Test: Stool Assay (for Toxins A and B; also PCR), CBC (leukocytosis w/WBC > 15000), Flexible Sigmoidoscopy (not required in most pts)

  • see pseudomembranouc colitis with “volcano” exudate of fibrin and neutrophils; yellow-adherent plaques

P: mild-moderate greenish, foul-smelling watery diarrhea 5-15 times per day

53
Q

Clostridium Difficile

What helps prevent infection and what are two major complications it can cause?

A

P: WASH HANDS WITH SOAP AND WATER (no alcohol sanitizer); use of disposable gloves

C: Toxic Megacolon and hemodynamic instability (perforation –> death)

54
Q

What are 4 characteristics of Malabsorption Syndromes? (WL/OD/S/ND)

What finding would NOT indicate malabsorption?

A

weight loss, osmotic diarrhea, steatorrhea, nutritional deficiency (Vitamin Deficiencies)

significant diarrhea W/O weight loss NOT likely due to malabsorption

55
Q

What are 5 Small Bowel Mucosal disorders that can lead to Malabsorption Syndromes? (C/C/L/W/S)

A

Crohns Disease, Celiac Sprue, Lactase Deficiency, Whipple Disease, Small Bowel Resection

56
Q

What is Celiacs Disease, what genetics does it affect, and what antibodies does it generate?

A
  • immunologic response to storage protein gluten causing diffuse damage to proximal small intestine muscosa with malabsorption of nutrients (most asymptomatic; present in childhood/adulthood)

Genetics: only affect peeps w/ HLA-DQ2 or DQ8 (5%)

Antibodies: Abs to gluten, tissue transglutaminase (tTG)
- IgA tTG antibody test is RECOMMENDED

57
Q

What are 3 atypical symptoms of Celiacs Disease?

What do you do if patient is IgA deficient?

When do antibody levels become undetectable?

A
  • dermatitis herpetiformis, iron deficiency anemia, osteoporosis

DH: pruritic papulovesicles over extensor surfaces of extremities and trunk/scalp/neck

  • if pt IgA deficient, look for IgG abs to tTG and DGP (deaminated gliadin peptides)

lvls become undetectable after 3-12 months of dietary gluten withdrawal

58
Q

What test is used to screen for osteoporosis in pts. with Celiacs Disease?

A

Dual-Energy X-Ray densitometry

59
Q

What is Bile Salt Malabsorption, what absorption is impaired, and what does it cause clinically?

A
  • resection or disease of TERMINAL ILEUM. or destruction of bile salts, preventing fat-soluble vitamin absorption (ADEK)
  • results in bleeding, osteoporosis, hypocalcemia, and WATERY SECRETORY DIARRHEA

minimal weight loss

60
Q

Whipple Disease

What is it, what does it present with, how is it diagnosed, and how is it treated?

A
  • rare, multi-system disease with Gram (+) bacillus that is NOT acid-fast (Tropheryma whipplei)
  • causes weight loss, malabsorption, and chronic diarrhea

Dx: Endoscopy with Duodenal Biospy (PAS (+) stain = positive macrophages with bacillus)

Tx: antibiotics (cross BBB needed), goal of treatment is to prevent progression (can be FATAL)

61
Q

What is the difference between:

Pseudo-diarrhea
Fecal incontinence
Overflow diarrhea

A

PD: frequent, small volume passages

  • rectal urgency, feeling of incomplete evacuation
  • accompanies IBS or proctitis

FI: involuntary discharge of rectal contents
- neuromuscular disorders or structural problems

OD: severe constipation –> only liquid gets by

  • elderly/nursing home patients
  • fecal impaction detectable by rectal examination
62
Q

Fecal Impaction (Constipation)

What is it, how does it present, how can it be diagnosed, and what is Melanosis Coli?

A
  • partial/complete LB obstruction due to rectal impaction
  • “paradoxical diarrhea” - liquid stool passes around impacted feces (Overflow incontinence)

Dx: digital rectal exam –> firm feces are palpable in rectal vault

MC: chronic use of laxatives lead to benign hyperpigmentation of colon

63
Q

When do you NOT perform a rectal exam? (3)

A
  1. you don’t have a finger
  2. you patient doesn’t have a rectum
  3. patient has leukopenia (don’t want to irritate bacteria)