Brainscape's Knowledge GenomeTM

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


See full index

Yr 2 - GI & Metabolism > Malabsorption > Flashcards

Malabsorption Flashcards

1
Q

What are the disaccharide sugars, lactose, sucrose and maltose broken down into? What are they broken down by?

A

Their constituent monosaccharides (simple sugars such as glucose)

By the enzymes lactase, sucrase and maltase

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

Where are lactase, sucrase and maltase located?

A

In the apical membrane of the enterocytes lining the small intestine

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

If the necessary enzyme is lacking, what happens to the disaccharides?

A

They cannot be digested or absorbed so remain in small intestine

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

What is result of high conc of sugar due to undigested disaccharides?

A

Creates osmotic force that draws fluid into the small intestine –> causes diarrhoea

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

What then occurs to the unabsorbed sugar? What is the result of this?

A

Fermented by bacteria in the large intestine

Produces acidic stools and gas production, leading to bloating and flatulence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What can cause enzyme deficiency?

A

Primary: Can be congenital

Secondary: Coeliac disease, tropical sprue, infections of intestine, antibiotics (especially neomycin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What occurs in inherited enzyme deficiency?

A

Complete loss of ability to absorb sugar, diarrhoea, baby will die of dehydration if untreated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Why is it possible to screen for mutations regarding the Na+/glucose transporter?

A

The Na+/glucose co-transporter has been cloned (SGLT1)

Every individual studied has missense mutation in gene encoding SGLT1

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

What is result of missense mutation in gene encoding SGLT1?

A

Improper trafficking of protein whilst others result in reduced transport ability –> glucose and galactose transport across the small intestinal epithelium is significantly impaired

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

Why can lactose intolerance increase with age?

A

The extent of synthesis of the enzyme lactase is reduced with age, and is a normal occurrence among people from Mediterranean area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are symptoms of lactose intolerance?

A

Audible bowel sounds (borborygmi), abdominal bloating, flatulence, nausea, urgent need to defecate, abdominal cramps, diarrhoea

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

How can severe diarrhoea lead to malabsorption?

A

Rapid transit time –> pass through gut too quickly to allow adequate absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why do blood glucose levels not rise in lactose intolerance test?

A

Test dose isn’t broken down into glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What can a biopsy of the small intestine show?

A
  • No use in diagnosis of lactase deficiency

- Normal villi virtually excludes celiac disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What can ingestion of large amounts of hexitols (e.g. sorbitol, mannitol), which are used as sugar substitutes, result in?

A

Cause diarrhoea as result of their slow absorption and stimulation of rapid small-bowel motility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the gene responsible for CF? Where is it located?

A

CFTR - located on chromosome 7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What does CFTR code for?

A

cAMP-dependent membrane channel protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does the cAMP-dependent membrane channel protein transport?

A
  • Predominantly transports chloride ions

- Bicarbonate (HCO3-) can also be transported to some extent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How can CF cause lung damage?

A

Cause of recurrent bronchopulmonary infection in children and early adult life –> recurrent infections leads to lung damage

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

How is pancreatic fluid and HCO3- secretion affected in CF?

A

Markedly reduced in CF –> leads to blockage of ducts with mucus and limited or negligible delivery of pancreatic enzymes to duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What can pancreatic insufficiency due to CF be caused by?

A

Inadequate digestion –> steatorrhoea, diarrhoea and wasting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What mutation causes 70% of all CF cases?

A

The delta F508 mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What happens during the delta F508 mutation?

A

Allows protein to be formed but does not get directed to the cell surface, and is destroyed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What do severe/mild alleles in CF cause?

A

Severe –> an incomplete (or no) CFTR protein

Mild –> often missense mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is meconium ileus?

A

One of the most common symptoms of CF –> the inability of a baby to pass meconium (the first faeces) because the meconium is too thick and sticky

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is cholera caused by?

A

Infection with the gram-negative organism Vibrio cholera

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the ‘evacuation phase’ of cholera?

A

Profuse watery diarrhoea ‘rice water’ stools (s called because of presence of mucous flecks in the faecal fluid), and sometimes vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the ‘collapse phase’ of cholera?

A

Caused by dehydration, decreased blood volume leading to circulatory collapse which may be fatal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the mechanism by which the cholera toxin works?

A
  1. Bacteria produce toxin which enters cells of gut lumen and binds to G protein –> activates chloride channel (CFTR)
  2. Activates adenyl cyclase increasing cAMP production
  3. Increases Na+, Cl- and HCO3- secretion into lumen
  4. Osmotic pressure increased –> water and other electrolytes drawn into bowel lumen
  5. Diarrhoea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What does all water absorption occur by?

A

Osmosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is osmosis dependent on?

A

The absorption of electrolytes and nutrients to maintain an osmotic balance with the blood (especially Na+ electrochemical gradient)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the effect of the cholera toxin on enterocytes?

A
  • Activation of a chloride channel (CFTR)
  • Leads to large amounts of Na+, Cl- and HCO3- secretion into lumen
  • Osmotic gradient
  • Profuse watery diarrhoea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Where are digestive enzymes found?

A

Saliva, gastric and pancreatic secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are starches broken down into?

A

a-dextrins and disaccharides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What do brush border enzymes break down?

A
  • a-dextrins and disaccharides are hydrolysed and then absorbed
  • Peptides
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What do long chain fatty acids require for adequate absorption?

A

Bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What can a deficiency in brush border enzymes (e.g. lactase) lead to?

A

A failure of breakdown of disaccharides (e.g. lactose) into glucose and galactose

Not digested and remain in gut

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What do amphipathic bile salts form?

A

Micelles (creates fat droplets)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What happens when fatty acids and monoglycerides reach the epithelial cells of the villi?

A

Diffuse into the cells, leaving micelles behind in the chyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Where are bile salts reabsorbed?

A

At the terminal ileum (enterohepatic circulation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is steatorrhoea and what is it caused by?

A

Presence of excess fat in the faeces caused by fat malabsorption

42
Q

What is appearance of stools in steatorrhoea?

A

Float, difficult to flush, oily appearance, foul smelling

43
Q

What diseases is steatorrhoea seen in?

A

Cholestatic liver disease, pancreatitis, coeliac disease

44
Q

If fat absorption is impaired, what vitamin deficiencies may occur?

A

Vitamins A, D, E and K as they are fat-soluble

45
Q

What is the effect of calcium absorption in a vitamin D deficiency?

A

Calcium absorption greatly reduced

46
Q

What is osteoporosis? What is it caused by?

A

Reduced bone density and increased risk of breaks and fractures

Anorexia, smoking, alcoholism, malabsorption, steroid therapy, vitamin D/calcium deficiency

47
Q

What is osteomalacia?

A
  • Normal amount of bone but mineral content is low (so bone is dense but soft)
  • Rickets occurs if this process is during the period of bone growth (occurs after fusion of the epiphyses)
48
Q

What are the causes of osteomalacia?

A

Vitamin D deficiency, malabsorption, renal disease

49
Q

Where is vit A absorbed? What is a deficiency?

A

Fat-soluble

Absorbed in small intestine

Xerophthalmia

50
Q

Where is vit B2 absorbed? What is a deficiency?

A

Absorbed small intestine

Deficiency angular stomatis, cheilitis

51
Q

Vit B1 (thiamine)

A

Thiamine
Absorbed small intestine
Deficiency –> Beriberi, Wernickes

52
Q

Vit B6

A

Absorbed SI

Deficiency –> polyneuropathy

53
Q

Vit B12

A

Absorbed terminal ileum

Deficiency –> anaemia, SCDC

54
Q

Vit C

A

Absorbed proximal ileum

Deficiency –> scurvy

55
Q

Vit D

A

Absorbed SI/skin

Deficiency –> osteomalacia

56
Q

Vit E

A

Absorbed SI

Deficiency –> Bleeding disorders

57
Q

Vit K

A

Absorbed SI

Deficiency –> Bleeding disorders

58
Q

Where are all minerals absorbed?

A

SI

59
Q

What does Vit B12 require for absorption?

A

Intrinsic factor (IF)

B12/IF complex forms in stomach and is absorbed in terminal ileum

60
Q

What can lead to B12 deficiency?

A
  • Gastric mucosal atrophy (chronic inflammation of gastric mucosa, gastric glandular cells replaced by intestinal-type epithelium, pyloric-type glands, and fibrous tissue)
  • Terminal ileal disease
61
Q

What can vit B12 deficiency lead to?

A
  • Pernicious anaemia –> decrease in RBC

- SCDC (Subacute combined degeneration) –> metabolic disorder of the spinal cord

62
Q

How can vit B12/folate deficiency lead to macrocytic anaemia (large RBC with less Hb)?

A

As normal proliferation of cells depends on adequate folate and vit B12

Folate is necessary for efficient thymidilate synthesis and production of DNA.

63
Q

Where is iron mainly absorbed?

A

In the duodenum

64
Q

What can an iron deficiency be caused by?

A
  • Reduced absorption

- Increased loss (bleeding, sloughed mucosal cells)

65
Q

What is coeliac disease?

A
  • Inflammation of small intestinal mucosa induced by an autoimmune reaction to the ingestion of gluten
  • Villous atrophy / intraepithelial lymphocytosis occurs (flat villi)
66
Q

What is gluten?

A

Protein with a high content of amino acid glutamine; found in wheat, barley, rye

67
Q

How can coeliac disease present in infants?

A

impaired growth, diarrhoea, vomiting, abdominal distension.

68
Q

How can coeliac disease present in older children?

A

anaemia, short stature, pubertal delay, rickets, recurrent abdominal pain or behavioural disturbance.

69
Q

How can coeliac disease present in adult disease?

A

chronic/recurrent iron deficiency anaemia, diarrhoea, abdominal pain, bloating, isolated nutritional deficiencies, reduced fertility, osteoporosis, osteomalacia, abnormal LFT

70
Q

What can cause coeliac disease?

A
  • Intestinal inflammation

- Villous atrophy

71
Q

How can intestinal inflammation lead to coeliac disease?

A
  1. Increased intestinal transit (time traveled in gut)
  2. Decreased macronutrient absorption
  3. Negative calorie/ protein balance → diarrhoea and weight loss
72
Q

How can villous atrophy lead to coeliac disease?

A
  1. Reduced surface area for absorption

2. ↓absorption of osmotically active substances → diarrhoea

73
Q

What can an iron/folate deficiency lead to?

A

Anaemia

74
Q

What can a calcium deficiency lead to?

A

Osteoporosis / osteomalacia

75
Q

What can a fat / vitamins ADEK lead to?

A

Clotting disorders

76
Q

How is coeliac disease diagnosed?

A
  • Serological test –> endomysial (EMA) and tissue transglutaminase (tTG) antibodies

If they are negative and the patient is eating gluten then unlikely they have coeliac

If they are positive then:
- Duodenal biopsy via upper GI endoscopy (sample showing villous atropy)

77
Q

How is coeliac disease managed?

A
  • Gluten Free Diet
  • Replace iron, folate, calcium, vit D
  • Monitor bone mineral density
78
Q

What can cause osmotic diarrhoea?

A

Malabsorption of nutrients

79
Q

What is parasthesia?

A

Tingling in hands

80
Q

What is parasthesia caused by?

A

Malabsorption of calcium

81
Q

What is anaemia caused by?

A

Malabsorption of iron, folate, possibly B12

82
Q

What is pancreatic insufficiency?

A

Reduced delivery of pancreatic enzymes to the duodenum

83
Q

How is CF related to pancreatic insufficiency?

A
  • Reduced HCO3- and pancreatic fluid secretion

- Blockage of ducts due to thicker mucous

84
Q

How is chronic pancreatitis and pancreatic insufficiency related?

A

Irreversible glandular destruction and alteration of anatomy / function due to chronic inflammation

85
Q

What are the symptoms of chronic pancreatitis?

A
  • Epigastric pain, often radiating to the back
  • Food/ alcohol may exacerbate the pain
  • Weight loss
86
Q

What are the causes of chronic pancreatitis?

A
  • Alcohol (>70%)
  • Familial, congenital (pancreas divisum- single pancreatic duct is not formed, but remains as two distinct dorsal and ventral ducts)
  • Autoimmune
  • Genetic
87
Q

What are the effects of exocrine insufficiency related to chronic pancreatitis?

A

Fat malabsorption:

  • Steatorrhoea
  • Fat soluble vitamin deficiency
88
Q

What are the effects of endocrine insufficiency of chronic pancreatitis?

A

Diabetes seen in 40-60%

89
Q

How can chronic pancreatitis be diagnosed?

A
  1. Faecal elastase-1 (low level of elastase seen as produced by pancreas and passed in stool largely unaltered)
  2. Plain abdominal X-ray
  3. Ultrasound/CT
  4. MRCP vs ERCP
90
Q

How can chronic pancreatitis be managed?

A
  1. Stop alcohol
  2. Pain control
  3. Treat diabetes
    Pancreatic enzyme supplements – Creon (pancreatin) (Lipase, protease, amylase)
  4. Vitamin supplementation
91
Q

What is creon?

A

Breaks down in SI and provides enzymes to facilitate digestion

92
Q

Will creon affect elastase levels in faeces?

A

No - don’t make pancreas work but just aid digestion

93
Q

What is cholestatic liver disease?

A

Impairment of bile formation / bile flow

- Steatorrhoea/ fat soluble vitamin malabsorption tends to only occur in prolonged cholestasis

94
Q

How can Primary Sclerosing Cholangitis (PSC) lead to cholestatic liver disease?

A
  • Inflammatory/ fibrotic process affecting intra/extrahepatic bile ducts
  • Leads to bile duct strictures (injury), ~80% associated with IBD
95
Q

How does cholestatic liver disease present?

A

Pruritus, fatigue, jaundice –> ultimately leads to cirrhosis and liver failure

96
Q

What is the only proven treatment in cholestatic liver disease?

A

Liver transplant

97
Q

What drug induces malabsorption?

A

Orlistat: inhibits gastric and pancreatic lipase

98
Q

How can small bowel bacterial overgrowth lead to malabsoption?

A
  • Upper small intestine is almost sterile (lack of bacteria)
  • Normally seen with a structural abnormality (eg. Crohn’s stricture)
  • Bacteria can deconjugate bile salts as well as metabolise B12 in upper SI
99
Q

What is pruritus?

A

An unpleasant sensation of the skin that provokes the urge to scratch (characteristic feature of many skin diseases)

100
Q

What is cirrhosis?

A

A condition in which the liver does not function properly due to long-term damage. This damage is characterised by the replacement of normal liver tissue by scar tissue

Yr 2 - GI & Metabolism (51 decks)

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