Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Gastrointestinal > Malabsorption > Flashcards

Malabsorption Flashcards

1
Q

What is Maldigestion?

A

impaired breakdown of nutrients, luminal phase (eg pancreatic insufficiency)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is Malabsorption?

A

defective mucosal uptake and transport of adequately digested nutrients. Selective or global.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is Malassimilation?

A

Encompasses maldigestion and malabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the three processes of the luminal phase of absorption?

A
  • Nutrient hydrolysis
  • Fat solubilisation
  • Lumenal availability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe nutrient hydrolysis

A
  • Enzyme deficiency: pancreatic insufficiency
  • Enzyme inactivation: ZE syndrome
  • Inadequacy of mixing: rapid transit, surgical resection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe fat solubilisation

A
  • Decreased bile salts: cholestasis, cirrhosis
  • Bile salt deconjugation: bacterial overgrowth
  • Bile salt loss: ileal disease or resection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe lumenal availability

A
  • Bacterial consumption of nutrients (bacterial overgrowth): B12 deficiency
  • Decreased intrinsic factor (pernicious anaemia): B12 deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the processes of the mucosal phase of absorption?

A
  • Brush border hydrolysis

- Epithelial transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe brush border hydrolysis

A

lactase deficiency (post gastroenteritis, alcohol, radiation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe epithelial transport

A
  • Reduced absorptive surface - resection
  • Damaged absorptive surface – coeliac disease, tropical sprue, Crohn’s disease, ischaemia
  • Infections – Giardia, SIBO
  • Infiltration – lymphoma, amyloid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the post-mucosal phase of absorption

A

Post-absorptive processing – lymphatic obstruction (lymphangectasia, neoplastic, TB)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the clinical features of malabsorption?

A
  • Diarrhoea and weight loss despite adequate intake
  • Bloating, distention, cramps, borborygmi (bowel sounds)
  • Lethargy, malaise
  • Symptoms often mild, non-specific
  • Malabsorption can be global, or specific nutrients
  • Malabsorption syndrome (steatorrhoea, distention, weight loss, oedema) is a RARE presentation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the clues in the history?

A
  • Weight loss
  • Diarrhea/Steatorrhoea (fat, bile salts)
  • Abdominal distension/gas (carbohydrate)= lactose intolerance
  • Intestinal “angina” (vasculopathy, impaired circulation to intestine so mesenteric ischaemia)
  • Metabolic bone disease (calcium and B12)
  • GI surgery
  • Pancreatitis
  • Cystic fibrosis
  • Alcohol
  • FHx coeliac
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the evidence of malnutrition in the skin?

A
  • angular cheilitis (cracking of skin), glossitis
  • dermatitis herpetiformis
  • oedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the evidence of malnutrition neurologically (B12)?

A
  • Peripheral neuropathy
  • Ataxia (posterior column)
  • Psychosis, dementia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How can laboratory results indicate malnutrition?

A
  • Microcytosis: iron deficiency (common in coeliac, otherwise suspect GI blood loss)
  • Macrocytosis (RBC too big): B12, folate deficiency, but also common in coeliac, alcohol
  • Elevated ALP +/- low Ca
  • Hypoalbuminaemia (protein malabsorption)
  • Evidence of multiple nutritional deficiencies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the main causes of malabsorption?

A
  • Coeliac disease
  • Pancreatic insufficiency
  • Small bowel overgrowth (SIBO)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the other causes of malabsorption?

A 
Pernicious anaemia (B12)
Bile acid malabsorption (BAM)
Intestinal resection
Vascular insufficiency
Crohn’s disease
Lactase deficiency
Cholestasis
Giardiasis
Lymphoma
Lymphatic obstruction
TB
Tropical sprue
Whipple’s disease
Zollinger Ellison syndrome
Amyloid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe diagnostic testing for malabsorption

A

-Testing for malabsorption (eg faecal fat, D-xylose test) rarely used / available
-Unless strong pointers to one cause, investigate non-invasively for the 3 commonest causes first
=Tissue Transglutaminase (TTG) – Coeliac disease
=Faecal elastase – Pancreatic insufficiency
=Glucose H2 breath test - SIBO
-Then if clinically suspected move on to more targeted investigation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What other investigations are there for malabsorption?

A
  • Stool microbiology (Giardia)
  • Faecal calprotectin (Crohn’s)
  • 7alpha-cholestenone or SeHCAT test (Bile acid malabsorption)
  • Lactose H2 breath test
  • Small intestinal biopsy (coeliac, Giardia, Crohn’s, Whipples, tropical sprue, lymphangectasia, lymphoma)
  • Small bowel imaging (BaFT, MRI, Capsule)
  • CT/CT angiogram (pancreatic disease, mesenteric ischaemia
21
Q

What is Coeliac Disease?

A 
Small bowel disorder characterized by:
-mucosal inflammation 
-villous atrophy 
-crypt hyperplasia 
which occur upon exposure to dietary gluten and which demonstrate improvement after withdrawal of gluten from the diet.
22
Q

What are the possible causes of coeliac disease?

A

-Genetic predisposition – HLA DQ2, DQ8 (25% population vulnerable)
-Exposure to gluten (gliaden) in wheat, barley, rye
-Gliaden-reactive T lymphocytes
-Tissue transglutaminase antibodies
=Enteropathy
=Prevalence up to 1/100
=Many subclinical or asymptomatic

  • Clinically overt
  • Undiagnosed, silent
  • Latent (potential)
23
Q

What are the clinical symptoms of coeliac disease?

A
  • Diarrhoea
  • Anaemia
  • Dyspepsia
  • Abd pain, bloating
  • Weight loss
  • Mouth ulcers
  • Fatigue
  • Neuropsychiatric symptoms
24
Q

What is the classic presentation of coeliac disease (historical)?

A
  • Childhood
  • FTT / Weight loss
  • Short stature
  • Malnutrition
  • Steatorrhoea
  • Delayed puberty
  • Osteomalacia
  • Myopathy
25
Q

What are the clues on investigation for coeliac disease?

A
  • Anaemia (microcytic, macrocytic)
  • Iron, folate deficiency
  • Macrocytosis without anaemia
  • Hyposplenic blood film
  • Low calcium, elevated Alk Phos
  • Raised transaminases
  • Hypoalbuminaemia
26
Q

What other disease is coeliac disease associated with?

A 
Osteoporosis
Infertility
Dermatitis herpetiformis
Lymphocytic colitis
Ulcerative jejunitis
Lymphoma
Type1 Diabetes
Thyroid disease
Autoimmune liver disease
Sjogren’s syndrome 
Down’s syndrome
Cerebellar ataxia
Other malignancies
27
Q

Describe diagnosis of coeliac disease

A

Serological markers
-Anti-tissue transglutaminase antibody (IgA) (TTG) Sensitivity and specificity >95%
=Anti-endomysial antibody (IgA)
=Anti-gliadin antibody (IgA, IgG)

Small intestinal biopsy

28
Q

What endoscopic changes can be seen in coeliac disease?

A
  • Scalloping
  • Loss of Kerkring’s folds
  • Mosaic pattern
29
Q

What is the treatment for coeliac disease?

A
  • Gluten free diet (life-long)
  • Dietician
  • Nutritional supplements
  • Screen for complications – bone disease
  • Very rarely, need for immunosuppressant medication for refractory cases
30
Q

Describe Pancreatic exocrine insufficiency (PEI)

A
  • Pancreas produces 1.5L/day of bicarbonate and enzyme-rich fluid
  • Enzymes for digestion of fat, protein, CHO
  • Lipolytic activity declines first so fat absorption mainly affected
  • Overt clinical consequences unlikely unless 90% of function lost
  • Steatorrhoea, weight loss, vitamin deficiency (A,D,E,K), also more minor symptoms
31
Q

What are the causes of PEI?

A
  • Chronic pancreatitis
  • Pancreatic cancer
  • Cystic fibrosis (obstruction)
  • Haemochromatosis
  • Pancreatic resection
  • Gastric resection
32
Q

What are the causes of chronic pancreatitis?

A
  • Alcohol – 80% present with pain
  • Duct obstruction – tumours, stones
  • Cystic fibrosis, other genetic causes
  • Systemic disease eg SLE= atrophy
  • Autoimmune (IgG4) pancreatitis
33
Q

Describe cystic fibrosis

A
  • Autosomal recessive, CFTR gene
  • Impairment in bicarbonate and chloride secretion – thick sticky mucus
  • Pancreatic involvement most common GI problem, esp in more severe genotypes
  • 85% affected, starts v early.
  • Commonly leads to PEI in childhood
34
Q

How is PEI diagnosed?

A

-Risk factors (alcohol, CF)
-Symptoms
-Pancreatic imaging (CT, MRI)
-Tests of exocrine pancreatic function
=Direct – eg Secretin stimulation tests (sensitive but cumbersome)
=Indirect – eg Faecal elastase, Pancreolauryl (only reliably detect moderate to severe PEI)

35
Q

What is the treatment for PEI?

A
  • Pancreatic enzyme replacement
  • Taken with meals and snacks
  • Gastric acid suppression
  • Vitamin supplements
36
Q

Describe Small Intestinal bacterial overgrowth (SIBO)

A
  • Normally 105 to 109 bacteria/ml present in distal small bowel
  • Colon has up to 1012 bacteria/ml
  • Mostly Gram- aerobic bacteria in ileum, Gram+ anaerobic bacteria in colon
  • In bacterial overgrowth this balance is lost
  • Increasingly recognised as a feature in other conditions – liver disease, IBS, obesity, CF, coeliac disease
  • Overestimated how many patient have this
37
Q

What are the causes of bacterial overgrowth?

A

-Stasis
– Strictures
=Crohn’s disease
=Tuberculosis
–Hypomotility
=Old age
=Opiate analgesics
=Diabetes
=Systemic sclerosis
-Blind loops, Diverticulae
-Immunodeficiency
-?Obesity

38
Q

What are blind loops?

A
  • Stagnant loop out of continuity with gut so growth
  • Billroth 2 partial gastrectomy
  • Gastric bypass
39
Q

What are the consequences of bacterial overgrowth?

A
  • Vitamin B12 malabsorption
  • Bile acid deconjugation
  • Intraluminal protein utilization
  • Brush border damage
  • Ulceration of mucosa
  • Bowel dysmotility
40
Q

Describe diagnosis of SIBO

A
  • Quantitative culture of jejunal fluid is the gold standard (> 105/mL is abnormal)
  • Glucose/Hydrogen breath test more practical (not accurate)
  • Small bowel radiology to look for anatomical abnormalities
41
Q

What is the treatment for SIBO?

A
  • Treatment with 2 weeks of antibiotics e.g. tetracycline, ciprofloxacin, rifaximin
  • Often needs repeat treatment
42
Q

Describe Bile Acid Malabsorption (BAM)

A
  • Bile acids specifically absorbed in ileum
  • Cause secretory diarrhoea in colon
  • Affected by ileal disease or resection
  • Also impaired in post- cholecystectomy, rapid transit and other malabsorptive states
  • Primary BAM may reflect over-production rather than malabsorption (receptors defective)
43
Q

What are the types of bile acid malabsorption?

A 
-Type 1
=Ileal disease or resection
-Type 2
=Idiopathic
-Type 3
=Assoc with cholecystectomy, rapid transit, coeliac, SIBO, chronic pancreatitis
44
Q

What is used to investigate BAM?

A

Serum 7-alpha cholestenone

SeHCAT retention

45
Q

What is the treatment for BAM?

A

Cholestyramine

Colesevelam

46
Q

Describe Giardia lamblia

A

-Non-invasive pathogen
-Malabsorption due to multiple factors
=Brush border damage
=Reduction in absorptive surface
=Bile acid utilization
=Induction of hypermotility
=Enterotoxin
-Treatment of choice is metronidazole

47
Q

Which other parasites cause malabsorption?

A 
-Protozoa
=Isospora belli
=Cryptosporidium
=Microsporidia (Enterocytozoon bieneusi)
-Tapeworms (blood loss and iron deficiency)
=Taenia saginata (beef tapeworm)
=Hymenolepis nana (dwarf tapeworm)
=Diphyllobothrium latum (fish tapeworm)
-Nematodes
=Strongyloides
=Capilliarasis
48
Q

Describe Whipple’s disease

A
  • Uncommon bacterial infection in older men
  • Caused by Tropheryma whippleii
  • Presents with diarrhoea, arthritis, fever, cough, headache, muscle weakness
  • Intestinal mucosa is infiltrated by foamy macrophages containing PAS-positive material
  • Antibiotic therapy for months to years.

Gastrointestinal (48 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions