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Chem Path > L15 Laboratory investigations of diarrhea and malabsorption > Flashcards

L15 Laboratory investigations of diarrhea and malabsorption Flashcards

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1
Q

In diarrhea, stool weight is greater than 200g/day.

How do we define acute, persistent and chronic diarrhea?

A

Acute: <2 weeks
Persistent: 2-4 weeks
Chronic: > 4 weeks

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2
Q

Acute diarrhea is a sudden alteration in normal bowel habits in terms of frequency and/ or liquidity. It is mostly ___________ in origin (90%).
It can also be classified as __________ and _________ acute diarrhea.

A

infectious’
inflammatory;
non-inflammatory

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3
Q

What are the differences between inflammatory and non-inflammatory diarrhea?

(6)

A
  1. Pathogenesis
    - in: disrupted intestinal mucosal barrier through the direct invasion of cytotoxin
    - non-in: no disruption or damage to the intestinal epithelium
  2. Stool
    - in: bloody, small-volume stool
    - non-in: watery stools without blood
  3. Stool examination
    - in: fecal leukocytes and RBC +++
    - non-in: fecal leukocytes absent
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4
Q

Diagnostic studies for acute diarrhea is for identifying medically significant diarrhea, thus not routinely tested.
They are reserved for patients with? (list 2)

It is also used to detect complications like electrolyte imbalance.

A
  • profuse diarrhea with dehydration
  • fever
  • recent antibiotics use
  • severe abdominal pain
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5
Q

Stool microbiology can be done if needed- list some examples.
Colonoscopy with biopsy can also be done.

A
  • Culture (enteric pathogens)
  • parasites
  • virus
  • C.difficile toxin
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6
Q

Chronic diarrhea is mostly infectious/ non-infectious in nature.

A

non-infectious

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7
Q

How can chronic diarrhea be classified?

(5)

A
  1. Secretory
  2. Osmotic
  3. Steatorhhea
  4. Dysmotility
  5. Inflammatory
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8
Q

What are the causes of secretory diarrhea? (4)

A
  • stimulant laxative
  • cholera
  • VIPoma (vasoactive intestinal peptide)
  • carcinoid syndrome
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9
Q

Secretory diarrhea can be relieved by fasting. T/F?

A

F

- persists with fasting

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10
Q

Stool Osmolar gap calculation?

A

290- 2(Na+K in stool)

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11
Q

Stool Osmolar gap is _________ in secretory diarrhea.

A

reduced, <50 mOsm/kg

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12
Q

What are the causes of osmotic diarrhea? (3)

A
  • osmotic laxatives
  • lactase/disaccharidase deficiencies
  • non-absorbable sugars e.g. sorbitol, lactulose, PEG (percutaneous endoscopic gastrostomy - tube)
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13
Q

Osmotic diarrhea is ceased by fasting. T/F?

A

T

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14
Q

Stool Osmolar gap is _________ in osmotic diarrhea.

A

increased, >100 mOsm/kg

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15
Q

What are the causes for stratorrhea? (6)

  • Greasy, foul-smelling, difficult to flush
A
  • Intraluminal - pancreatic insufficiency, SIBO
  • Mucosa - celiac disease, Whipple’s disease
  • Osmotic effects of fatty acid
  • Weight loss/nutritional insufficiency
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16
Q

Causes for dysmotility-induced chronic diarrhea? (2)

A
  • Hyperthyroid
  • IBS - rapid transit of GI content
    (Irritable bowel syndrome)
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17
Q

Causes for inflammatory chronic diarrhea?(2)

A
  • GI malignancy

- IBD - inflammatory bowel disease (chronic inflammation!)

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18
Q

Symptoms of inflammatory diarrhea (3) and specific lab results (1)?

A
  • Fever, pain, bleeding

- increase in fecal calprotectin

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19
Q

Diagnostic approach for chronic diarrhea?

  1. Directed by Hx, P/E, routine tests (CBC, L/RFT)
  2. Stool microbiology
  • what specific tests can be done to differentiate ddx? (5)
A
  1. Hydrogen breath test
    (SIBO: carbohydrate malabsorption
    e.g. lactose intolerance - lactase deficiency > bacteria flora digest lactose > give H2 and methane)
  2. Fecal elastase
    (marker of pancreatic insufficiency - it is pancreatic enzyme that does not undergo significant degradation)
  3. Urine laxative (abusive use)
  4. Urine 5-HIAA (marker of carcinoid syndrome - produced excessively in carcinoid tumor)
  5. Hormone profile (GI hormones, thyroid function test)
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20
Q

Factors contributing to normal digestion/absorption? (3)

A
  1. Normal speed of passage
  2. Nutrients in absorbable form
  3. Integrity of absorptive cells (intestinal mucosa)
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21
Q

Lipid absorption requires? (2)

A
  1. Hepatobiliary function: bile salts

2. Pancreatic exocrine function: lipase

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22
Q

Carbohydrate absorption requires? (2)

A
  1. Salivary and pancreatic amylase

2. Disaccharidases

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23
Q

Protein absorption requires? (3)

A
  • Gastric and pancreatic exocrine function
    1. Pepsin
    2. Trypsin (protease)
    3. Chymotrypsin (protease)
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24
Q

Vitamin B12 absorption requires? (3)

A
  1. Intrinsic factor (gastric function)
  2. Intestinal flora to consume B12
  3. Intestinal mucosa of lower ileum
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25
Q

Name 4 pancreatic digestion disorder that causes malabsoprtion.

A
  1. Chronic pancreatitis
  2. Zollinger-Ellison syndrome (low pH inactivates lipase) [acidic content of stomach goes to intestines]
  3. Cystic fibrosis
  4. Ca pancreas
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26
Q

Name 3 diseases related to intestinal malabsorption. (also briefly mention their pathology)

A
  1. Celiac disease (reduced absorptive surface)
  2. Crohn’s disease (inflammation of intestinal wall)
  3. Carcinoid syndrome + post gastrectomy (increase rate of passage)
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27
Q

Etiology for B12 malabsorption?

A

Gastric atrophy

- Pernicious anemia

28
Q

Etiology for fat and fat/soluble vitamin malabsorption?

A

Biliary obstruction

29
Q

Etiology for carbohydrate malabsorption?

A

Disaccharidase deficiency

30
Q

Etiology for B12, fat malabsorption?

A

altered bacterial flora (e.g. SIBO, diverticulum)

- deconjugation of bile > fat malabsorption

31
Q

Etiology for B12 and bile acid malabsorption?

A

Terminal ileum defect

  • Chron’s disease
  • Surgery
32
Q

Etiology for protein malabsorption?

A

Protein-losing enteropathy

33
Q 
Which of the following are clinical features for carbohydrate malabsorption?
A. osmotic diarrhea
B. flatulence
C. increase stool osmolar gap
D. pale stool 
E. increased H2 breath test
A

All except D

should be in fat malabsorption

34
Q

What are the lab findings in fat malabsorption? (2)

- with pale stool, steatorrhea

A
  • Fraction fat excretion >6%

- reduced vit A, D, K and Ca due to reduced VitD)

35
Q

Clinical features for protein malabsorption?

A
  • edema, muscle atrophy

- recurrent infection (reduced antibody-mediated immunity)

36
Q

Lab findings in protein malabsorption?

A

Reduced total protein/albumin

37
Q

Clinical features for B12 malabsorption? (2)

A
  • Megaloblastic anemia

- Peripheral neuropathy

38
Q

Lab findings in B12 malabsorption? (3)

A
  • increased MCV
  • reduced B12
  • increased homocysteine, MMA (cobalamin deficiency markers)
39
Q

Clinical features for vit A malabsorption? (2)

A
  • Night blindness
  • Follicular hyperkeratosis
    (skin condition with excessive development of keratin in hair follicles > rough, cone-shaped, elevated papules)
40
Q

Clinical features for VitD malabsorption? (4)

A
  1. Osteomalacia (softening of the bone)
  2. Tetany
  3. Paraesthesia
  4. Chvostek/Trousseau sign+
    (face + hand - see youtube if forgot)
41
Q

Lab findings in VitD malabsorption?

A
  • increase ALP (osteolytic)
  • increase PTH (secondary)
  • reduced Ca
  • reduced PO4
42
Q 
Clinical feature of Vit K malabsorption? (1)
Lab findings (2)?
A

Bleeding

- increased PT and APTT

43
Q

Explain why would disaccharidase deficiency will cause the below symptoms.

A. Diarrhea
B. Failure to thrive
C. Abdominal distention and pain

A

A. Diarrhea - due to osmotic activity of sugars
B. Failure to thrive - lack of sugar precursors
C. Lage volumes of gas within the gut - bacteria in LI will metabolize the malabsorbed sugar produce H2 and methane

44
Q

Diagnostic method for disaccharidase deficiency? (3)

A
  1. Dietary exclusion (e.g. avoid lactose if lactose intolerance)
  2. Endoscopy with biopsy and measurement of enzymes
  3. Breath hydrogen test
    i. e. give the patient a solution containing disaccharide and measure hydrogen gas in the breath
45
Q

Treatment for disaccharidase deficiency?

A

avoid foods containing the specific disaccharide

46
Q

Investigations for testing fat.

  1. Stool exam
    - What stain is used in the stool exam?
    - possible errors?
  2. Faecal fat quantification
    - how is it collected?
    - possible issues?
A
  1. Stool exam
    - Sudan III (fat-soluble stain) > count fat droplets under the microscope
    - false-positive: drugs (orlistat), food additives (mineral oil)
  2. Faecal fat quantification
    - 3-5 days of fecal collection
    - issue: patient compliance
47
Q

One of the old ways to test for carbohydrates is an oral sugar intolerance test.

  • give simple sugars and measure blood glucose
  • no rise in BG suggests mucosal dysfunction: absorption of simple sugar independent onpancreatic enzymes/bile acits

What test is more commonly done now?
How is it done?

A

Hydrogen breath test

  • give fasting patients sugar solution (specific to what you want to test)
  • collect breath sample
  • Q30 mins in 2.5 hours
  • Large bowel bacteria digest unabsorbed sugar to H2 and methane
48
Q

For SIBO

What tests can be done to confirm? (2)

A
  1. Quantitave culture of jejunal aspirate
    - gold standard
  2. Hydrogen breath test (give glucose)
    but not specific, because +ve also for disaccharidase deficiency; confirm by eradicating bacteria using Abx
49
Q

For B12 malabsorption, plasma homocysteine and MMA (methylmalonic acid) are __________ and they are substrates for B12 as co-enzymes.
___________ can be used to diagnose perinicious anemia.

A

increased;

Anti-IF/parietal cell antibody
Serum gastrin

50
Q

Schilling test is not done now to test for B12 deficiency.
1st:
- radioactive B12 PO + non-radioactive B12 IM (to saturate body stores), then measure urine radioacvitivity

2nd:
- Radioactive B12 + IF PO + non-radioactive B12 IM

What are the expected results for both tests if the patient has

i) pernicious anemia
- -) intestinal malabsorption

A

Pernicious anemia: low I, normal II
Intestinal malabsorption: low I and II

*modified Schilling test is to repeat I after Abx, to diagnose SIBO

51
Q

What radiological studies can be done to find out pancreatic causes of malabsorption?

A
  • CT, MRI
  • EUS (endoscopic ultrasound)
  • MRCP (magnetic resonance cholangiopancreatography)
  • ERCP (endoscopic - can also treat)
52
Q

What can endoscopy do in investigating malabsorption?

A
  1. Obtain mucosal biopsy for pan-malabsorption

2. Obtain jejunal aspirate for SIBO

53
Q

Which of the following about celiac disease are correct?
A. it is an autoimmune disease that is triggered by the ingestion of gluten
B. it is an inflammatory disorder
C. it causes generalized malabsorption
D. anti-tissue-transglutaminase Ab, anti-gliadin Ab, anti-endomysial Ab, HLA-DQ2/8 genotypes can be checked
E. small bowel biopsy is the gold standard for investigations
F. Gluten free diet is the treatment

A

All of the above

54
Q

Which of the following about cystic fibrosis are correct?
A. It is due to the abnormal secretions of endocrine glands due to CTFR mutation
B. Patients will have chronic respiratory infections and malabsorption
C. Newborn screening is available - immunoreactive trypsinogen
D. CTFR gene test, sweat test, and caecal trypsin, crymotrypsin or elastase tests are useful
E. Antibiotics, physiotherapy and enzyme replacement are treatment options.

A

All of the above except A

Exocrine glands!

55
Q

What is 5-hydroxyindoleacetic acid? (5-HIAA)

It is used as a _______________ marker.

A

It is a main metabolite of serotonin.
It is derived by the oxidative de-amination of serotonin.

  • Carcinoid tumor
56
Q

What precautions would you give to patients before 24 hour urine collection for 5-HIAA?

A
  • Measurement should be made when the patient is symptomatic

- Avoid certain foods (bananas, plums, tomatoes, walnuts), any drugs, and smoking

57
Q

Where are carcinoid tumors most commonly found?

A

in appendix and ileum

58
Q

Raised ALP can be from? (organs)

A

Bone or liver

59
Q

Why would a patient with carcinoid tumors experience hot flushes?

A
  • due to the vasodilatory effects of serotonin in the systemic circulation
60
Q

How to calculate albumin corrected plasma calcium?

A

Ca+ 0.02 (40-albumin)

61
Q

Common causes of vitamin B12 deficiency? (7)

A
  1. Inadequate intake
  2. Pernicious anemia (gastric)
  3. Gastrectomy
  4. Blind loop syndrome (bacterial overgrowth)
  5. Ileal resection
  6. Celiac disease
  7. Crohn’s disease
62
Q

Common causes of macrocytosis? (7)

A
  1. Vit B12 deficiency
  2. Folate deficiency
  3. Reticulocytosis
  4. Alcoholism
  5. Liver disease
  6. Hypothyroidism
  7. Primary bone marrow disorders (e.g. myelodysplastic syndrome)
63
Q

Macrocytosis in Vit B12 deficiency may be masked by concurrent medical conditions.
Name the conditions and suggest further investigations to exclude them.

A
  1. Iron deficiency
    - order an iron profile: low TSAT, increased TIBC, low ferritin
  2. Thalassemia triat
    - gene karyotyping
    - high performance liquid chromatography
    - hemoglobin electrophoresis
64
Q

Plasma amylase = 1066 U/L =?

What other lab test will you order to establish the diagnosis?

A

Acute pancreatitis

  • Ranson score
  • CRP
65
Q

If patient only presented 5 days after onset of pain (acute pancreatitis) when plasma amylase is 270 U/L, what other tests can be done?

A

Urine amylase

  • elevation remains longer
  • not very specific
  • more sensitive

Lipase
- stays elevated for longer than plasma amylase

66
Q

Causes of chronically elevated amylase?

A
  1. pancreatic pseudocyst
  2. chronic pancreatitis
  3. macroamylasaemia (amylase binds to large molecules like immunoglobulins and polysaccharides > renal clearance of amylase is decreased and the half-life is prolonged)
  4. renal insufficiency
67
Q

Patient with chronically elevated amylase - what investigations to conduct? (3)

A
  1. amylase clearance (plasma and urine amylase + creatitine)
  2. OGD
  3. H.pylori (CLO test/urea breath test)

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