MALABSORPTION AND MALNUTRITION Flashcards
1
Q
Whats the pH in the small intestine?
A
~5.5 in duodenum
~7.5 in ileum
2
Q
Whats absorbed in the duodenum?
A
Calcium, phosphorous, magnesium
Iron
Thiamin
Riboflavin
Niacin
Biotin
Folate
Vitamin A,D,E,K
Lipids
Monosaccharides
Amino acids
Small peptides
3
Q
Whats absorbed in the jejunum?
A
Thiamin
Riboflavin
Niacin
Biotin
Folate
Vit B6, C,A,D,E,K
Calcium, phosphorous, magnesium
Iron
Zinc
4
Q
Whats absorbed in the ileum?
A
Vit C,D,K
Magnesium
Bile salts and acids
5
Q
Whats absorbed in the large intestine?
A
Water
Sodium
Chloride
Potassium
Short chain acids
6
Q
What are the major disorders of the small intestine that cause malabsorption?
A
Coeliac disease
Dermatitis herpetiformis
Tropical sprue
Bacterial overgrowth
Intestinal resection
Whipples disease
Radiation enteropathy
Parasite infection
Intolerances
Others:
Abetalipoproteinaemia
Biliary atresia
Shwachman diamond syndrome
Chronic pancreatitis
CF
IBD
Alcohol use disorder
Short bowel syndrome
Zollinger-Ellison syndrome
HIV
Intestinal TB
Structural defects
7
Q
What is coeliac disease?
A
An autoimmune condition where there is inflammation of the mucosa of the proximal small bowel that improves when gluten is withdrawn from the diet and relapses when gluten is reintroduced
8
Q
Outline the epidemiology of coeliac disease?
A
Common among Northern Europeans
Prevalence is 1% in UK
F:M 2:1
Can present at any age but commonly starts in childhood - peaks after weaning with gluten in first 2 years of life and other peak is in the 2nd or 3rd decades of life
9
Q
In which group of people is coeliac disease more commonly seen in?
A
Those with diabetes mellitus 1, Down syndrome or turner syndrome
Those with other autoimmune disorders e.g. thyroid disease, autoimmune hepatitis, primary biliary cirrhosis and PSC
Or those with relatives with coeliac disease
10
Q
Outline the aetiological factors for coeliac disease?
A
Genetics - HLA-DQ2 in 95% and HLA-DQ8 in 5% (strong negative predictive value)
Immunology - Activation of T helper cells leads to stimulation of B cells and the release of pro-inflammatory cytokines. The activation of the immune system leads to the recruitment of inflammatory cells in the lamina propria and subsequent hyperplasia in the crypts of Lieberkühn.
Environment - recurrent rotavirus infections in childhood increase the risk of development. Age of introduction of gluten into diet is significant. Breastfeeding is protective
11
Q
Outline the pathophysiology of coeliac disease
A
Prolamins are ingested and cross the epithelial surface into the lamina propria -> tissue transglutaminase can deaminate gliadin making it more immunogenic -> gliadin binds to APCs and is presented to T helper cells via HLA DQ2/8 molecules -> activated T helper cells secrete pro-inflammatory cytokines and activate B lymphocytes which leads to the formation of auto-antibodies
Furthermore, gliadin can irritate endothelial cells -> release of cytokines -> activated intraepithelial lymphocytes -> direct epithelial damage
Overall chronic inflammation and damage to enterocytes results in villus atrophy, crypt hyperplasia and inflammatory infiltrate
12
Q
What are the 3 classical features in the pathophysiology of coeliac disease?
A
Villous atrophy (reduced absorptive surface).
Crypt hyperplasia (increased cellular proliferation).
Inflammatory infiltration (increased intraepithelial lymphocytes, influx of immune cells into lamina propria)
13
Q
Whats the main pro-inflammatory cytokine found in coeliac disease?
A
Interferon gamma
And IL15
14
Q
What are ther 2 antibodies in coeliac disease pathophysiology?
A
anti-tissue transglutaminase (anti-TTG) and anti-endomysial (anti-EMA)
15
Q
Which area of the small bowel is typically most affected by coeliac disease?
A
Jejunum
16
Q
What is gluten found in?
A
Barley
Rye
Oats
Wheat
17
Q
What are prolamins?
A
a group of plant storage proteins having a high proline amino acid content
In wheat its called gliadin
In barley it’s hordeins
In rye it’s secalins
18
Q
Why are prolamins resistant to digestion by pepsin and chymotrypsin?
A
because of their high glutamine and proline content
This means they remain in the intestinal lumen, triggering the immune responses that result in coeliac disease.
19
Q
What is gluten?
A
The general name for the proteins found in wheat rye and barley
20
Q
What type of immunoglobulin are anti-TTG and anti-EMA? Why is this significant?
A
IgA - Some patients have an IgA deficiency. When you test for these antibodies, it is important to test for total Immunoglobulin A levels because if total IgA is low because they have an IgA deficiency then the coeliac test will be negative even when they have coeliacs. In this circumstance, you can test for the IgG version of anti-TTG or anti-EMA antibodies or simply do an endoscopy with biopsies.
21
Q
What are the peaks of age presentation for coeliac disease?
A
In infancy after weaning onto gluten-containing foods in first 2 years of life
2nd or 3rd decade of life
22
Q
How does coeliac disease present?
A
The symptoms/signs of coeliac disease are often non-specific, and it may present with intestinal and extra-intestinal manifestations, or be asymptomatic.
Tiredness and malaise associated with unexplained iron/vit B12/folate deficiency anaemia
GI sympotms are absent or mild - chronic diarrhoea, abdominal pain and distension, acid reflux, steatorrhoea, reduces appetite and constipation and sometimes vomiting.
Weight loss
Mouth ulcer and angular stomatitis
Infertility and neuropsychiatric symptoms of anxiety and depression
Failure to thrive in young children. Faltering growth, idiopathic short stature or delayed puberty
Unexplained recurrent miscarriage or sub fertility. Or delayed period.
Dental enamel defects
Osteoporosis/penia/malacia
Dermatitis herpetiformis
Rarely it can present with neurological symptoms - peripheral neuropathy, cerebella’s ataxia and epilepsy
Irritability and depression
23
Q
What is potential coeliac disease?
A
people who may be symptomatic or asymptomatic with antibody positivity for coeliac disease, but no villous atrophy on duodenal biopsy
24
Q
What is non-responsive coeliac disease?
A
people with persistent symptoms and enteropathy that do not respond after 6–12 months on a self-reported gluten-free diet, and is most commonly due to inadvertent gluten ingestion
25
What is refractory coeliac disease?
people with persistent or recurrence of otherwise unexplained symptoms and villous atrophy on duodenal biopsy, despite strict adherence to a gluten-free diet for at least 12 months
26
What are the associated diseases of coeliac disease?
Atopy
Autoimmune thyroid disease
Type 1 diabetes
Sjögren’s syndrome
IBS
Dermatitis herpetiformis
Primary biliary cholangitis
Chronic liver disease
Interstitial ling disease
Epilepsy
Microscopic colitis
Rheumatoid arthritis
Down’s syndrome
IgA deficiency
27
How is coeliac disease diagnosed?
Examine - heigh, weight, BMI, abdomen pain/distension, skin to look for features of dermatitis herpetiformis
Stool culture, microscopy and sensitivity
FBC, blood film, LFTs, U&E, lipids, Mg, haematinics, bone brofuile, clotting
Coeliac serology testing - check IgA tissue transglutaminase antibody and total IgA
Endoscopy and intestinal biopsy
HLA typing can be done
Arrange referral to gastroenterologist
Arrange referral to dermatologist if diagnosis of dermatitis herpetiformis is suspected
28
Whats important to ensure before carrying out coeliac serology testing?
The person must have eaten gluten-containing goods in more than one meal a day for a minimum of 6 weeks before testing is performed
29
When do you check serum IgA endomysial antibodies instead of tTGA?
If IgA tTGA testing is unavailable or in case where the result is weakly positive
30
What should you do if you get a positive serology test result for coeliac disease?
Arrange referral for young people and adults to a gastroenterologist for specialist endoscopic intestinal biopsy to confirm or exclude the diagnosis.
31
What are the extraintestinal manifestations of coeliac disease?
Anaemia
Oestoporosis and osteomalacia
Hypertransaminasemia
Dermatitis herpetiformis
Bruising (thrombocytosis)
Neurological sequelae - peripheral neuropathy, ataxia, epilepsy
Night blindness (vit A deficiency)
Infertility and recurrent spontaneous abortions
Alopecia
32
Why does coeliac disease cause anaemia?
malabsorption of iron and folate
In severe disease affecting the ileum, B12 malabsorption may occur.
33
Why does coeliac disease cause oestoporosis?
Malabsorption of calcium and vitamin D deficiency
Calcium may also be sequestered to poorly absorbed fatty acids.
34
Why can coeliac disease cause easy bruising?
secondary to failure to absorb vitamin K.
35
Why can coeliac disease cause neurological sequelae?
secondary to hypocalcaemia or vitamin B12 deficiency.
36
Whats the gold standard tool for diagnosing coeliac disease?
Upper GI endoscopy - at least 4 biopsy specimens
37
What would be seen on intestinal biopsy for diagnosing coeliac disease if it’s positive?
Crypt hypertrophy and villus atrophy
38
What classification tool is used for coeliac disease?
Marsh-Oberhuber classification
39
What can cause villous atrophy?
Coeliac disease - most common cause of subtotal villous atrophy
Tropical sprue
Common variable immunodeficiency
Non-coeliac enteropathy
40
Outline the Marsh-Oberhuber classification?
Marsh grade - Histological appearance:
0 - normal mucosa
1 - increase intraepithelial lymphocytes
2 - crypt hyperplasia
3a - partial villous atrophy
3b - subtotal villous atrophy
3c - total villous atrophy
4 - hypoplasia of small bowel architecture
Types 2 and 3 are diagnostically supportive of coeliac disease
41
What are the indications for serological testing of coeliac disease?
Based on clinical features:
Sudden or unexpected weight loss.
Chronic or intermittent diarrhoea.
Recurrent abdominal pain, cramping, or distension.
Unexplained gastrointestinal symptoms (e.g. nausea and diarrhoea).
Prolonged fatigue.
Unexplained anaemia (e.g. iron-deficiency, megaloblastic).
Those at increased risk:
Type 1 diabetes
Dermatitis herpetiformis
Autoimmune thyroid disease.
Irritable bowel syndrome.
Family history (first degree relative)
42
How do we manage coeliac diseasE?
Long term adherence to gluten free diet - selection of gluten-free products can be prescribed on the NHS
Screen thyroid, FBC, ferritin, LFTs, calcium, vit D, vit B12 and folate. Replacement mineral and vitamins may be needed
Manage complications
43
Why should patients with confirmed coeliac disease have pneumococcal vaccinations every 5 years?
there is a potential for people with coeliac disease to develop overwhelming pneumococcal sepsis due to hyposplenism.
44
What are the 2 types of refractory coeliac disease?
Type 1 - the lymphocytes are normal. 5-year survival is 93%.
Types 2 -abnormal population of lympocytes. Can progress to enteropathy-associated T-cell lymphoma. The 5-year survival rate is 40–60%.
45
What are the complications of untreated coeliac disease?
Enteropathy-associated T-cell lymphoma
Malnutrition and malabsorption
Lactose intolerance
Oestoporosos
Infertility and miscarriage
Ulcerative jejunitis
Carcinoma of oesophagus, oropharynx or small intestine
Small bowel adenocarcinoma
Dermatitis herpetiformis
Deficiencies - B12, folate, calcium, vitamin D, vitamin K
46
What is dermatitis herpetiformis?
an IgA-mediated condition strongly associated with coeliac disease
It is a blistering disease of the skin, which presents as an extremely itchy papulovesicular rash on the extensor surfaces. Subepidermal bullae are seen on histology with linear IgA deposits on dermal papillae.
47
How is dermatitis herpetiformis managed?
Dapsone
Gluten free diet
48
What is enteropathy-associated T cell lymphoma?
A complication of coeliac disease - a malignant T-cell lymphoma develops in areas of the small intestine affected by the disease's intense inflammation.
49
What is non-coeliac gluten intolerance?
A group of pt who are sensitive to dietary wheat and gluten-containing foods but do not have coeliac disease as their coeliac serology is negative and duodenal biopsies are normal
50
How do those with non-coeliac gluten intolerance present?
With diarrhoea, bloating and abdominal pain which improve on avoidance of gluten
51
What is tropical sprue?
A GI disease that causes chronic diarrhoea and results in severe malabsorption and malnutrition
52
Where does tropical sprue typically affect people?
The tropics e.g. Caribbean, India and SE Asia, some parts of South America
53
Whats the aetiology of tropical sprue?
Unknown but likely to be infective as the disease occurs in epidemics and pt improve on antibiotics
An acute intestinal infection damages the intestinal lining causing inflammation. In response intestinal cells secrete enteroglucagon which decreases intestinal motility = change in normal bacterial flora = bacterial overgrowth = klebsiella, E.coli and enters after become dominant and release toxic byproducts as they ferment the food that lingers in the gut = toxins damage intestinal lining = more inflammation = over time we get villus atrophy = malabsorption and depletion of vitamin B12 ans folate = folate deficiency further constitutes to mucosal injury
54
Outline the prognosis of tropical sprue?
If left untreated it is a chronic disease with flare ups
Prognosis overall is excellent. Mortality is usually associated with water and electrolyte depletion
55
What is the typical presentation of tropical sprue?
it tends to begin with an acute episode of diarrhoea, fever and malaise before settling into a more chronic presentation of steatorrhea, malabsorption, nutritional deficiency, anorexia, malaise and weight loss
Clinical features can vary in different parts of the world
Epidemics can break out in villages, affecting thousands of people at a time
56
When is the onset of tropical sprue?
A few days or many years after being in the tropics
57
What are the complications of tropical sprue?
Megaloblastic anaemia due to vitamin B12 and folate deficiencies
58
How is tropical sprue diagnosed?
Acute infective causes of diarrhoea must be excluded, particularly giardia
FBC shows macrocytic anaemia, serum K+/iron/albumin low, volume depletion, urea raised, calcium and phosphate may be abnormal
Malabsorption should be demonsated, particularly of fat and vitamin B12
Check stool for cysts, ova and parasites
Endoscopy and Jejunal biopsy - mucosa should show partial villus atrophy - typically less severe than coeliac disease although it affects the whole of the small bowel
59
Whats the most common cause of malabsorption in India?
Tropical sprue
60
How do you test for fat malabsorption?
72 hour stool collection test while on a prescribed diet i.e. pt fed a high fat diet 100g fat a day for 3 days. Collecting stool every time you have a bowel movement for 72 hours. A faecal fat >6g in 24 hours is abnormal.
Sudan 3 stain is used to examine the stool under a microscope.
There will also be a decreased absorption of fat soluble vitamins - ADEK
61
How do you test for carbohydrate malabsorption?
D-xylose absorption test - dose of 25g xylose is given by mouth and normal results are that urine contains >20mg/100ml at 1 hour and 4g total in 5 hours
Lower suggests malabsorption
62
How do you manage tropical sprue?
Most pt improve when they leave the sprue area and take folic acid
Antibiotics 1g daily for 6-12 months
My require resuscitation with fluids and electrolytes if severe and nutritional deficiencies may need to be corrected
Vitamin B12 is given to all acute cases
63
What antibiotic is typically used for tropical sprue?
Tetracycline
64
Outline the normal gut microbiome?
Anaerobic bacteria are 1000 times more abundant than aerobic
More proximal is almost sterile containing only a few organisms derived from the mouth
Terminal ileum contains faecal-type organisms, mainly e.coli and anaerobes
Colon has abundant bacteria
65
What are the functions of the gut microbiome?
fermentation of non-digestible dietary residues into short chain fatty acids as an energy source in the colon
initiate vitamin K production and vitamin B production
Help metabolise bile acids, sterols and xenobiotics
develop and maintain immune system
protect the gut mucosa from colonisation by pathogenic bacteria
66
Why is the stomach and proximal small intestine typically devoid of organisms from the gut flora?
Gastric acid kills some ingested organisms
Intestinal motility
67
Which part of the intestine are the most aerobic bacteria likely found?
The caecum
68
What proportion of faeces is bacteria?
60%
69
What are the main bacterial inhabitants of the stomach?
Streptococcus
Staphylococcus
Lactobacillus
Peptostreptococcus
H. Pylori
70
What are the most common bacteria found in the colon?
Bacteriodes fragilis
Bacteriodes melaninogenicus
Bacteroides oralis
Enterococcus facealis
E.coli
71
What is small bowel bacterial overgrowth syndrome?
a disorder characterised by excessive amounts of bacteria in the small bowel resulting in gastrointestinal symptoms.
72
What are the common symptoms in SIBO?
Chronic diarrhoea
Steatorrhoea
Bloating and flatulence
Abdominal pain
Can occasionally cause weight loss
(Mild B12 deficiency which may cause neurological deficits but this is unlikely)
73
Why can SIBO cause steatorrhoea?
Conjugated bile salt deficiency - bacteria are capable of deconjugating and dehydroxylating bile salts
74
What can be seen on bloods in small intestine bacterial overgrowth?
Anaemia
Low B12
High serum folate
Vitamin deficiencies ADEK
75
Why does SIBO cause vitamin deficiencies?
As a result of incomplete absorption of fats, your body can't fully absorb the fat-soluble vitamins A, D, E and K
Some bacteria can metabolise vitamin B12 and interfere with its binding to intrinsic factor
76
Why might you see a raised serum folate in SIBO?
Some bacteria can produce folic acid
77
How is SIBO diagnosed?
Hydrogen breath test
78
Outline how a hydrogen breath test for diagnosing SIBO works?
Bacteria are present in the oral cavity so the mouth should be rinsed out with an antiseptic mouthwash beforehand.
The appearance of a breath hydrogen peak after oral glucose is used to estimate mouth-to-caecum transit time. An earlier rise in the breath hydrogen after glucose indicates bacterial breakdown in the small intestine.
79
What are risk factors for SIBO?
Small intestine diverticula
Small intestine structures
Surgically created blind loops
Resection of ileocecal valve
Fistulas between proximal and distal bowel
Scleroderma
Gastric resection
Gastroparesis, small bowel dysmotiility, coeliac disease, chronic intestinal pseudo-obstruction
IBS
Diabetes or hypochlorhydria
Age-related changes
Organ system dysfunction
Recurrent antibiotics
Gastric acid suppressing meds
Neonates with congenital GI abnormalities
80
What are the 2 processes that most commonly predispose to SIBO?
Diminished gastric acid secretion
Small intestine dysmotility
81
How is SIBO managed?
Underlying cause corrected if possible
If not possible then rotating courses of antibiotics may be necessary
82
What is the enterohepatic circulation?
the circulation of biliary acids, bilirubin, drugs or other substances from the liver to the bile, followed by entry into the small intestine, absorption by the enterocyte and transport back to the liver.
83
What is bile acid malabsorption?
Problems with reabsorbeing build acid so more bile reaches the colon than normal making the colon releasing more water/electrolytes andincrasing the secretion and colonic motility = chronic watery diarrhoea
84
What are some causes of bile acid malabsorption?
Type I: problem in the ileum e.g. ileal resection, damage by radiation therapy
Type II: idiopathic - primary bile acid malabsorption. Spontaneous.
Type III: secondary to GI diseases that can affect the ileum e.g. coeliac disease, chronic pancreatitis and SIBO
Type 4: excessive bile acid production as a side effect of taking metformin
85
How is diagnosis of bile acid malabsorption made?
Trial of medication
SeHCAT scan
86
What is the SeHCAT scan?
Giving oral SeHCAT (synthetic taurine conjugate) and measuring the retention of the bile acid by whole-body counting at 7 days
Taurine is an amino acid that is involved in forming bile salts from bile acids through conjugation
87
How are bile salts synthesised?
synthesized in the liver from cholesterol, conjugated with glycine or taurine
88
How is bile acid malabsorption?
Bile acid sequestrants e.g. cholestyramine or Colesevelam
89
Whats the moa of Cholestyramine?
Cholestyramine resin adsorbs and combines with the bile acids in the intestine to form an insoluble complex which is excreted in the feces
90
What is lactose intolerance?
a clinical syndrome where ingestion of lactose causes symptoms such as diarrhoea, abdominal pain, bloating and flatulence
91
What causes lactose intolerance?
Lactase deficiency
Can be secondary to lactose malabsorption due to underlying intestinal disease
Typically acquired and rarely congenital
92
How is lactose intolerance diagnosed?
Giving an oral dose of 50g of lactose and serial measurement of blood glucose over 2 hours
Hydrogen breath test - too much hydrogen indicates that you aren't fully digesting and absorbing lactose.
93
What are the consequences of ileal resection?
Malabsorption of bile salts and vitamin B12
Loss of ileal brake causing diarrhoea
Bile salt induced diarrhoea
Steatorrhoea and gall stone formation
Oxaluria and oxalate stones
94
Why does ileal resection cause bile-salt-induced diarrhoea?
Bile salts and fatty acids enter the colon and cause malabsorption of water and electrolytes
95
Why does ileal resection cause steatorrhoea and gallstone formation?
Increased bile salt synthesis can compensate for loss of approximately one-third of the bile salts in the faeces. Greater loss than this results in decreased micelle formation and steatorrhoea, and lithogenic bile and gallstone formation.
96
Why is a jejunal resection often better tolerated than an ileal resection?
Because the ileum can compensate for the loss of jejunal absorptive function in a jejunal resection
Jejunum has a relatively decreased adaptive capacity compared to the ileum
97
What is the main complication of jejunal resection?
Gastrin hypersecretion - unknown mechanism
98
What is short bowel syndrome?
a condition in which your body is unable to absorb enough nutrients from the foods you eat because you don't have enough small intestine - often due to a massive intestinal resection
99
How does lactose intolerance cause bloating and diarrhoea?
Lactase deficiency or inactivity = undigested lactose which undergoes fermentation by normal colonic flora = formation of gases like hydrogen = gas, bloating
Bacteria also produce short chain fatty acids = attract water into gut lumen = diarrhoea and abdominal pain
100
What is whipples disease?
A rare, malabsorption infectious disease caused by tropheryma whipplei
101
Who does whipples disease tend to affect?
87% are males, white middle-aged
Those with ezxposure to faecal matter e.g. sewage workers or farmers at higehr risk
102
What type of bacteria is tropheryma whipplei?
A gram positive, non-acid fast PAS positive bacillus
103
How is tropheryma whipplei transmitted?
Faecal-oral route
104
What are the features of whipples disease?
Cardinal features - diarrhoea, weight loss, abdominal pain, arthralgias
Heart - Endocarditis, pericarditis, myocarditis
Skin hyperpigmentation
Pleural disease
CNS - dementia or psychiatric symptoms
Migratory arthralgias
Weight loss
Hyperpigmentation of skin
Infection with tropheryma whippleii
PAS positive granules in macrophage
Poly arthritis
lymphadenopathy
Enteric involvement
Steatorrhoea
105
How is whipples disease diagnosed?
Blood tests - features of chronic inflammation and malabsorption
Endoscopy - pale, shaggy, duodenal mucosa with eroded, red, friable patches
Small bowel biopsy
Confirmatory PCR-based assay
106
What is seen on biopsy for Whipple disease?
PAS-positive macrophages
On electron microscopy, trilaminar cell wall of T.whipplei can be seen within macrophages
107
What are PAS-positive macrophages?
Periodic acid-Schiff -positive macrophages
108
How is whipples disease managed?
Antibiotics that cross the blood-brain barrier daily for 1 year e.g. trimethoprim and sulfamethoxazole
109
Why do patients need to take antibiotics to manage whipples disease for a year?
As treatment periods of <1 year are associated with relapse in about 40%
And left untreated it can be fatal
110
What is radiation enteritis?
inflammation of the intestines that occurs after radiation therapy.
The chronic effects of radiation are muscle fibre atrophy, ulcerative changes due to ischaemia, and obstruction due to radiation-induced fibrotic strictures.
111
What is chronic radiation enteritis?
Diagnosed if symptoms persist 3 months or more
112
What is radiation proctitis?
inflammation of the rectum that occurs as a result of acute damage to the rectum sustained from pelvic radiation.
113
What parasites can cause malabsorption?
giardiasis
coccidiosis
cryptosporidiosis
strongyloidiasis
capillariasis
and perhaps P. falciparum malaria
114
What are the indications for nutrition support?
The patient has eaten very little amounts for the last 5 days or more, or
the patient is very unlikely to eat more than very little amounts for the next 5 days or more (whatever current BMI or history of weight loss), or
the patient’s BMI is < 18.5 kg/m2, or
the patient has unintentionally lost > 10% body weight within the previous 3–6 months, or
the patient has a BMI < 20 kg/m2 with unintentional weight loss > 5% within the previous 3–6 months, or
the patient has poor absorptive capacity, is catabolic and/or hashigh nutrient losses and or has a condition that increases their nutritional needs, for example hyper mobility
115
Whats the suggested nutritional prescription for total intake for clinically stable patients?
- –30 kcal/kg/day total energy (including that derived from protein)
• 1–1.5 g protein/kg/day
• 30–35 ml fluid/kg (with allowance for extra losses from drains, fistulae, etc. and extra input from other sources, for example IV drugs)
• considered the need for additional electrolytes, minerals and
micronutrients in patients with pre-existing deficits, high losses or increased demands
116
What is refeeding syndrome?
a metabolic disturbance that occurs as a result of reinstitution of nutrition in people and animals who are starved, severely malnourished, or metabolically stressed because of severe illness. When too much food or liquid nutrition supplement is eaten during the initial four to seven days following a malnutrition event, the production of glycogen, fat and protein in cells may cause low serum concentrations of potassium, magnesium and phosphate. Cardiac, pulmonary and neurological symptoms can be signs of refeeding syndrome. The low serum minerals, if severe enough, can be fatal.
117
Outline the pathophysiology behind refeeding syndrome?
During refeeding, insulin secretion resumes in response to increased blood sugar, resulting in increased glycogen, fat, and protein synthesis. Refeeding increases the basal metabolic rate. The process requires phosphates, magnesium and potassium which are already depleted, and the stores rapidly become used up. Formation of phosphorylated carbohydrate compounds in the liver and skeletal muscle depletes intracellular ATP and 2,3-diphosphoglycerate in red blood cells, leading to cellular dysfunction and inadequate oxygen delivery to the body's organs. Intracellular movement of electrolytes occurs along with a fall in the serum electrolytes, including phosphate and magnesium. Levels of serum glucose may rise, and B1 vitamin thiamine may fall.
Abnormal heart rhythms are the most common cause of death from refeeding syndrome, with other significant risks including confusion, coma and convulsions and cardiac failure
118
Whats the most common form of death from refeeding syndrome?
Abnormal heart rhythms
119
What are the 2 types of malabsorption?
Global - all nutrients affected
Partial - only specific nutrients cannot be absorbed
120
Outline the basic aetiology of malabsorption?
Nutrients are no longer effectively absorbed by the small intestine so they linger in the GI lumen = diarrhoea, bloating and flatulence
Since these nutritents are lost in the stool it leads to unintentional weight loss and various nutritional deficiencies
121
What are the symptoms of vitamin A deficiency?
Night blindness
Eye dryness
Corneal ulcerations
Thickened skin
122
What are the main symptoms of vitamin D deficiency?
Child with rickets
Adult with osteomalacia
123
What are the main symptoms of vitamin E deficiency?
Ataxia
Impaired proprioception and vibratory sensation
Muscle weakness
124
What are the main symptoms of vitamin K deficiency?
Easy bruising
Epistaxis or gingivitis
Heavy menstrual periods
Excessive bleeding
125
What are the signs of protein malabsorption
Watery diarrhoea
Oedema - protein loss causes reduces oncotic pressure so fluid leaks out
126
What are the most common digestive disorders?
Exocrine pancreatic insufficiency
Lactose intolerance
Cholestasis
127
What are the common absorption defects?
Coeliac disease
Tropical sprue
Whipples disease
128
What is exocrine pancreatic insufficiency?
When there is a deficiency of pancreatic digestive enzymes e.g. amylase, lipase, elastase. Resulting in malabsorption
129
What are the symptms of exocrine pancreatic insufficiency?
Chronic/recurrent diarrhoea with steatorrhoea
Unintentional weight loss
Abdominal distension
Bloating
130
What is the main cause of exocrine pancreatic insufficiency?
Typically results from chronic pancreatitis
131
Why doesnt acute pancreatitis cause exocrine pancreatic insufficiency but chronic pancreatitis does?
In acute pancreatitis, pancreatic enzymes can leak out from damaged tissues and enter circulation
In chronic pancreatitis there may not be enough healthy pancreatic tissue to make these enzymes so the serum levels remain low
132
Whats the main risk factor for chronic pancreatic?
Alcohol abuse
133
Whats the main cause of chronic pancreatitis in children?
Cystic fibrosis
134
How is exocrine pancreatitis insufficiency diagnosed?
Low serum tripsinogen level
Low bicarbonate in duodenal fluid after stimulation with secretin
135
How is exocrine pancreatic insufficiency managed?
Mix of pancreatic enzymes
136
What is cholestasis?
Impaired bile flow = bile builds up in the liver = not enough bile reaches intestine to emulsify fats and make them easier to reabsorb = fat malabsorption = steatorrhoea and fat-soluble vitamin deficiencies
137
What are the 2 types of cholestasis?
Hepatocellular cholestasis - hepatocytes dont make enough bile
Obstructive cholestasis - physical blockage to bile flow
138
What are the causes of hepatocellular cholestasis?
Pregnancy
Oral contraceptive pills
Cirrhosis
Drug reactions - phenothiazine, chlorpromazine, erythmycin, gold salt, anabolic steroids
Sclerosing cholangitis
Viral/alcoholic hepatitis
Septicaemia
Primary biliary cirrhosis
Alpha-1-antitrypsin deficiency
TPN-association cholestasis
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What are the causes of obstructive cholestasis?
Gallstones
Carcinoma of head of pancreas
Alagilles syndrome
Parasites
Cholangitis
Cholangiocarcinoma
Congenital structure e.g. biliary atresia
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Why does cholestasis result in clay-coloured stool, yellow sclera/skin and dark urine?
As cholestasis prevents conjugated bilirubin secretion into GIT = wont turn into steer boil in which normally gives the stool its darker colour
Instead, bilirubin builds up in the blood and deposits in the skin and sclera
It gets excreted in the urine, turning it dark
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Why can oestrogens cause cholestasis?
Because oestrogen can inhibit the export pumps that usually move bile acids from hepatocytes to biliary tract
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Which ethnic groups are more likely to have lactose intolerance?
African and Asian descent
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What are absorption defects?
When there is damage to the small intestine which reduces the SA and causes symptms of global malabsorption
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How can you differentiate between absorption defects and exocrine pancreatic insufficiency?
D-Xylose test
D-Xylose is directly absorbed from intestinal mucosa without the need of pancreatic enzymes
If mucosa is intact then it can be absorbed and serum/urine levels can increase
If mucosa defect, less D-Xylose is absorbed so serum and urine levels are lower = absorption defects
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Outline the pathophysiology of coeliac disease?
Gliadin binds to secretory IgA on mucosal membranes of duodenal cells
This complex binds to transferrin receptor and gets transcytosed across into the lamina propria
Here, tissue transglutaminase cuts of an amide group. The de-aminated gliadin then gets eaten up by macrophage
CD4+ T cells recognise gliadin and cause B cells to release IgA antibodies against gliadin, tTG and proteins of endomesium
Release of cytokines that damage small intestine
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What causes tropical sprue?
Bacterial overgrowth
Mostly of klebsiella, e.coli and enterobacter
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Whats the difference between primary and secondary lactose intolerance?
Primary is caused by a decreased expression of the lactase gene (most common) - most in Asian and African populations
Secondary artistes in thr setting of inflammatory or infectious damage to the intestines or a congenital lactase deficiency
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What are the cardinal features of gastroparesis?
bloating, early satiety, vomiting and chronic nausea
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How does NICE define malnutrition?
a Body Mass Index (BMI) of less than 18.5; or
unintentional weight loss greater than 10% within the last 3-6 months; or
a BMI of less than 20 and unintentional weight loss greater than 5% within the last 3-6 months
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How is screening for malnutrition done?
using the Malnutrition Universal Screen Tool (MUST) on admission or when there is concern
It takes into account BMI, recent weight chang and the presence of acute disease
It categorises patient into low, medium and high risk
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How does NICE suggest we manage malnutrition?
dietician support if the patient is high-risk
a 'food-first' approach with clear instructions (e.g. 'add full-fat cream to mashed potato'), rather than just prescribing oral nutritional supplements (ONS) such as Ensure
if ONS are used they should be taken between meals, rather than instead of meals
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How do we follow up pt with confirmed coeliac disease?
3-6 months after your initial diagnosis - Assess symptoms, perform a complete physical exam, order celiac serology, repeat routine tests, if previously abnormal
At your 12 month visit, your anti-tTg IgA level should be as close to zero as possible. At this visit, your physician should: assess symptoms, perform an abdominal physical examination, order celiac serology, repeat routine tests, assess hepatitis B immunization status
At your annual visit, your physician should: assess symptoms, perform a complete physical exam, order celiac serology, repeat routine tests, order other tests as clinically indicated, recommend a flu shot, recommend a dietitian to provide education and counseling as clinically indicated, recommend a mental health professional to address the psychosocial aspects of going gluten-free and coping with a chronic disease
Repeat bone densitometry at 2-3 years, if previously abnormal, and for adolescents non-compliant with a gluten-free diet
For adults, consider repeat small intestinal biopsy at 3-5 years to assess dietary compliance and rule-out refractory celiac disease
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How do you manage refractory coeliac disease and what are the issues with this?
Steroids have been tried but these increase your risk of osteoporosis even further!
Immunosuppressants have also been tried e.g. azathioprine however this is also associated with an increased risk of small bowel lymphoma.
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Whats the prognosis of coeliac diseases?
70% of those with symptoms will notice an improvement within 2 weeks of starting a GF diet
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What proportion. Of those diagnosed with IBS are misdiagnosed and actually have coeliac?
5%
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What are the differential diagnoses of coeliac?
IBS
IBD
Lactose intolerance
Giardiasis
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Whats the risk of having coeliac disease if you have a first degree relative with coeliac disease?
10-15%
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What proportion of pt are diagnosed with coeliac after the age of 60? Why is this mor common for women?
20%
Because after menopause women will be found to still have IDA despite no periods
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Whats the cell turnover time in the small bowel?
5-7 days
