nmdc221 session 2: gastrointestinal & alimentary disease ......drug action side effects...

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NMDC221 Session 2:

Gastrointestinal & Alimentary

Disease Part II


Topic Overview

Recommended Reading

Mahan, L.K., & Raymond, J.L. (2016). Krause’s food & the nutrition

care process (14th ed.). St. Louis, MO: Elsevier.

P518-520; 525-557. (prescribed text).

Gastrointestinal & Alimentary Disease: Part II

o Nutritional management & consideration of drug-nutrient

interactions

• Hypochlorhydria

• Gastritis

• Peptic ulcer disease


Hypochlorhydria


Hypochlorhydriao A deficient level of hydrochloric acid (HCL) from the parietal cells of

the stomach resulting in poor dietary protein breakdown (HCL &

pepsin) and reduced liberation of protein bound nutrients (e.g. B12

and iron). HCl also activates important enzymes and hormones, and

can help protect against bacterial overgrowth in the gut.

o Ongoing hypochlorhydria increases the risk of gastric ulcerations,

malabsorption, infections, gastritis, gastric cancers, GORD, and

gastric bacterial overgrowth (Prousky J 2001)

o Can be associated with Sjogren’s syndrome, Addison's disease,

asthma, SLE, osteoporosis, gastritis (Prousky J 2001)

o Results in the malabsorption of protein, vitamin B12, folic acid,

calcium, iron and trace minerals.

o Predisposes a person to malnutrition which increases risk of

degenerative disease

o Leads to amino acid deficiencies


Risk factors1. Age

o hydrochloric acid secretion declines with advancing age

o In one study US researchers found that over 30 percent of men and

women past the age of 60 suffer from atrophic gastritis, a condition

marked by little or no acid secretion. A second study found that up

to 40% of post-menopausal women have no basal gastric acid

secretions (Krasinski SD et al 1986)

2. Lifestyle

o Drinking water with meals; vegetarian diets (or diets low in protein)

can reduce HCL production.

3. Nutrient deficiencies

4. Food allergies and /or sensitivities (although they may be they are a

result of the condition itself).


Risk Factors Cont.

5. Stress

o Sympathetic nervous system dominance (high stress) decreases

parasympathetic vagal nerve innervation of stomach (Pizzorno &

Murray, 2006, p168)

6. Helibacter pylori.

o Can cause atrophic changes to the gastric mucosa (Carter RE

1992)

7. Drugs - can be induced through the repeated administration of acid-

reducing agents, such as proton-pump inhibitors (PPIs); H2-receptor

antagonists (H2-RAs)

8. Others – early weaning onto refined and processed foods; genetics

(Pro-inflammatory IL-1 polymorphisms are associated with

hypochlorhydria) (Furuta T et al 2002)


Signs and Symptoms

o Bloating after eating

o Sense of fullness

o Nausea when taking supplements

o Burping and feeling of ‘upset

stomach’

o Dyspeptic symptoms

o Burning sensations, especially of

the mouth

(English J 2013)


Nutritional treatment

Initial Nutritional Considerations:

o Assess current diet and make necessary modifications

o Consider :- meal size, adequate protein at each meal, small frequent

meals, fluids away from meal times. Suggest - apple cider vinegar

in water before meals or 100ml lemon juice, 15 minutes before main

meals (increases saliva output & stimulation of exocrine secretion of

the pancreas) (Benny 2010)

o Assess microbiome status and support with fermented foods,

probiotics

o Design aims around – providing mucosal repair to tissue (treartment

pplan would then suggest nutrients such as Mucosal– Zinc, Vitamin

A, Glutamine, Vitamin E would be beneifical)

o Assess if there’s any contributing factors – drugs/medications, food

allergies/sensitivities that may need attention.


HypochlorhydriaFurther Nutritional Considerations:

o Provide adequate dietary support

o Consider referring on for H pylori infection (HPSA) testing; assess if

there’s any underlying pathology

o Assess patients digestive secretions – apple cider vinegar, lemon

juice water, fermented foods

o Consider supplementations – Betaine hydrochloride, B complex,

Vitamin C, Probiotics

o Support digestive tissue repair – mucosal repair nutrients, anti-

inflammatory nutrients (see slides 15,16)

o Assess patient’s lifestyle – reduce stress and consumption of acid

reducing agents, avoid smoking, alcohol and poor food choices

(refined, processed). Support physical activity (PA) especially in

those with advancing age to support digestive ,motility


Key Nutrients to Consider

o Betaine hydrochloride

o Vitamin B3

o Enzymes – Bromelain, Papain

o Zinc


Betaine Hydrochloride

Mechanism of

action

• The chloride component is directly used to increase stomach acid

production. (Eklund et. al. 2005)

• Substrate for HCL production.

Evidence of

clinical

application

• “If low stomach acid is the cause of reflux symptoms, betaine hydrochloride

may be useful.” (Hechtman, 2012)

• “Betaine hydrochloride was successful in lowering gastric pH.”

(Yago MR et al 2013)

Dosage• There is no typical dosage for betaine hydrochloride. Practitioners should

follow manufacturers guidelines. However, a general guide is 100-400mg

before or with a protein rich meal.

Other

considerations

• “Betaine hydrochloride dose should be built up slowly”. (Hechtman, 2012)

• Patients may feel a warming sensation in their abdomen.

• “Consider the following before prescribing :- B3 deficiency, Malabsorption,

Age, drugs (proton pump inhibitors, H2 receptor antagonists H2-RAs)”

(Prousky J, 2001)

• Often combined with pepsin


Vitamin B3

Mechanism of

action

• Adequate B3 is required for healthy release of PGD2 that leads to the

binding of the prostaglandin to receptors on parietal cells stimulating the

release of HCL

(Prousky J 2001)

Evidence of

clinical

application

• Hypochlorhydria is an early sign of increased metabolic need for vitamin

B3. There will often be other disturbances in mood (anxiety, depression,

fatigue) evident.

(Prousky J 2001)

Dosage• 100-200mg (up to 3,000mg can be used with caution)

Other

considerations

• Best taken in a B complex

• Niacin flush at high doses


Enzymes and other nutrients

Pepsin 10-100mg / Meal Cleaves peptide bonds

Bromelain 150-400mg / Meal Protein Digestion

Papain 10-100mg / Meal Protein Digestion

Glutamic Acid 500-3,000mg Raises stomach acid,

Substrate for HCl

Zinc 10-100mg Cofactor required for HCl

production

Iron

Vitamin C (ascorbic acid)

EFA’s

15-50mg

500-5,000mg

Up to 6,000mg

Impaired absorption

Anti-inflammatory, supports

acid production

Anti-inflammatory

(Osiecki 7thed, p.16, 26, 47,

139, 162, 170-1, 266;

Rodwell-Williams &

Schlenker, 2003, p 90)


Gastritis


Gastritis

Gastritis = inflammation, irritation, or erosion of the lining of the

stomach. It can occur suddenly (acute) or gradually (chronic).

Types:

1. Acute

o Sudden onset of inflammation and symptoms usually caused by

severe stress, viral infections, alcohol abuse or the use of iron

supplementation, aspirin or NSAID’s

2. Chronic

o Helicobacter pylori infection is the main aetiological factor for

chronic gastritis worldwide (Varbanova M et al. 2014)

o Bile reflux following gastric surgery


Signs and symptomsMay be asymptomatic or present with symptoms such as :-

o abdominal pain and bloating

o indigestion

o loss of appetite

o nausea

o Vomiting +-blood

(Padmavathi et al 2013)


Risk factorso Smoking

o Diet - spicy food, caffeinated beverages, alcohol (Ethanol exposure

alters motility and inflames the mucosa leading to potential for

nutrient deficiencies, particularly folate

(Shils et al 2006, p1525).

o Medications/drugs

o Stress

(Padmavathi GV et al 2013)

o Helibacter pylori -It is thought that all individuals with H. pylori

infection will develop some degree of gastritis. This will depend on

the degree of interplay of bacterial virulence factors, host

susceptibility, genes and environmental factors.

(Varbanova M et al 2014).


Nutritional Treatment

Nutritional Considerations:-

Ask yourself:-

o Are there potential lifestyle factors compromising the patients and lifestyle factors – consider alcohol excess, smoking, caffeine, spicy foods, drugs/med’s, excessive stress etc.

o Are there enough nutrients to support GIT lining?

o Is there effective digestive breakdown of foods? Look at Cofactors for HCL production

o Is a referral required - Consider Helibacter pylori infection (HPSA test)


Gastritis – nutrients

Garlic 0.4 -

1gm(dried) or

2-5g (fresh)

H. pylori overgrowth (implicated in gastritis) (Cardelle-Cobas et al 2010)

Antibacterial against H. pylori

The antibacterial properties of allicin from garlic have been found to reduce the

risk of stomach cancer, lower gastric nitrite (nitrosamine precursor) & inhibit H.

pylori.

Vitamin C 500-5,000mg Ascorbic acid deficiency is found in those with gastritis

Diets high in ascorbic acid are associated with protection from gastric atrophy

and a ‘reduction in the incidence of gastric cancer (possibly through the ability

of ascorbic acid to reduce oxidative damage to the gastric mucosa by

scavenging carcinogenic N-nitroso compounds) thereby attenuating the H.

pylori-induced inflammatory cascade’ (Aditi A et al 2012)

Pharmacologic doses of ascorbic acid also may improve the effectiveness of

H. pylori-eradication therapy significant in gastritis (Aditi A et al 2012)

Glutamine 500-3,000mg

Repairs epithelial cells

Anti-inflammatory protection.

Supports glutathione production and therefore antioxidant

Folate 400mcg Alcohol or sodium bicarbonate consumption for gastritis depletes folate

absorption

Vitamin B12 300-800mcg Deficient in H Pylori patients. Decreases with age, intrinsic factor, anti-

inflammatory

(Shils et al. 2006, p. 1633; Braun & Cohen 2010, p.469)

(Plessas et al, 2012)


Gastritis – nutrients

Probiotics 10-40 billion

organisms

p/day

Antibiotic association (L. Acidophilus & B. Brevi)

Zinc 10-100mg HCl production, immune, healing


GastritisDrug Action Side Effects Interaction

Antacids Neutralizes acid by

increasing

bicarbonate and

mucous .

Inactivates pepsin.

Binds bile salts

Diarrhoea (Mg),

constipation (Al),

hypophosphataemia,

hypercalcaemia

Vitamin C increases aluminium

absorption. Separate doses by 2

hrs.

Folate & Iron – reduces

absorption of both. Separate

doses by 2 hours

‘Raft’

Antacids

(Alginic Acid,

Sucralfate)

When combined

with stomach acid

it forms a slimy

jelly ‘raft’

Sucralfate – nausea,

headache, rash,

dizziness and

indigestion.

Constipation (rare)

Vitamin E & Calcium – reduces

absorption of both

(Braun & Cohen, 2010, p. 1096; Bryant & Knights, 2011, p. 538)


GastritisDrug Action Side effects Interaction

H2-Antagonists Blocks H2 receptors on

parietal cells (Bryant et

al 2007,p541)

Diarrhoea, nausea,

constipation, headache,

dizziness, skin rash

Folate, B12 & Iron –

reduces absorption of

both. Separate doses

by 2 hrs

Proton Pump

Inhibitors (PPI’s)

Reduces gastric output

via non-competitive

bonds

Diarrhoea, nausea,

abdominal pain,

headache

Folate B12 & Iron –

reduces absorption of

both. Separate doses

by 2 hrs

Dopamine 2

Antagonists

(Metoclopramide,

Domperidone)

Enhanced effect on gut

motility. Increases

gastric emptying.

Increases sphincter

tone. Reduces nausea

and vomiting

Metaclopramide –

drowsiness, fatigue,

nervousness, anxiety,

diarrhoea, insomnia.

Domperidone- less side

effects (minimal BBB

crossover)

None known

(Braun & Cohen 2010, p1097; Bryant et al 2011,p541)


Helicobacter Pylori


Helicobacter Pylori

Features:o 50% of the worlds population is thought to be infected. More

common in underdeveloped countries. The prevalence of H. pylori

infection varies widely by geographic area, age, race, ethnicity, and

SES (Brown L 2000)

• Currently there is no biomarker that can reliably predict the outcome

of the infection (Varbanova M et al 2014)

• H. pylori infection leads to chronic gastritis, peptic ulceration, gastric

adenocarcinoma, and gastric mucosa-associated lymphoid tissue

lymphoma (Brown L 2000)

• May also be asymptomatic or present as gastritis, ulcer, or another

GIT pathology (Gastric adenocarcinoma, lymphoma)

• Ulcer recurrence is dramatically reduced following the eradication of

H. pylori

• Treatment protocol is usually Triple therapy (Proton pump inhibitor,

antibiotic & antiprotozoal medication).

(Kumar & Clark 2005)


The exact routes of H. pylori transmission

remain unclear. However, epidemiologic studies

have shown that exposure of food to

contaminated water or soil may increase the

risk of H. pylori infection, suggesting that

person-to-person transmission by oral-oral,

faecal-oral, or gastro-oral exposure is the most

likely path for H. pylori infection

(Brown LM 2000)



Treatment plans must be in line with your treatment

goals. Consider the following as an example:-

- Provide antimicrobial support to reduce h.pylori infection

and further colonisation. Treatment plan may then

include prescribing nutrients such as Vitamin C, Zinc,

Garlic etc.

- Support healthy digestive function – therefore your plan

may include modifying the diet to small frequent meals,

no water with foods and nutrients to support breakdown.

- Ensuring healthy microorganism populations – you may

consider prescribing probiotics to help establish healthy

GIT flora.

. (Jamison 2003, p385; Shils et al, 2006, p1638)


Helicobacter pylori – Vitamin C

Mechanism of

action

Appears to inhibit H. pylori growth (interferes with its colonisation) and

is a free radical scavenger and antioxidant (Zhang HM et al 1997)

Evidence of

clinical

application

High doses of vitamin C inhibits the growth of H. pylori in vitro as well

as in vivo in animal studies (Zhang HM et al 1997)

Appears there’s a causal association between H. pylori infection and

low ascorbic acid levels in gastric juice due to increased oxidation and

decreased secretion of ascorbic acid (Pal J et al 2011)

H. Pylori impairs the bioavailability of Vitamin C (Woodard M et al

2001)

Dosage 500-5,000mg (ascorbic acid)

Other

considerations

Studies have been mixed on the type of Vitamin C exhibiting benefits -

ascorbic acid and sodium ascorbate.

Japan has one of the highest incidences of H. pylori infection rates

(estimated at 70% of the population), the US one of the lowest (but

coincidently a high vitamin C supplement rate exists in the US?)


Helibacter pylori – further nutrients to consider

Probiotics 10-50 billion

org/day

Lactobacillus acidophilus has antibacterial properties that reduces H.

pylori colonization and growth

(Vitor JM, Vale FF 2011)

Garlic

Zinc

50-100mg

10-40mg

Cardelle-Cobas et al 2010 found that the antibacterial properties of

Garlic (allicin) inhibited H. pylori growth.

Aqueous garlic extract effectively inhibited 16 clinical isolates and 3

reference strains of Helicobacter pylori

Concentrated ethanol garlic extract (5mg/ml) was responsible for a 90%

inhibition of the microbes

Long term ethanol garlic extract treatment would be an effective therapy

against H. pylori bacteria (Vitor JM, Vale FF 2011)

Mucosal membrane support, immune support, HCl production


Helicobacter PyloriDrug Action Side effects Interaction

Omeprazole /

Esomeprazole

Proton Pump

Inhibitor

Abdominal pain, dizziness,

headache, GIT symptoms,

diarrhoea, flatulence, skin

rash

Iron, zinc, Vitamin B12:

increasing gastric pH

reduces absorption

Nitroimidazole:

Metronidazole

Antiprotozoal Dizziness, headache, GIT

symptoms, discoloured urine,

vaginal candidiasis, peripheral

neuropathy, leukopenia

Alcohol must be avoided.

Macrolide:

Clarithromycin

Bacteriostatic

– inhibits RNA

synthesis in

bacteria

Anorexia, headache, GIT

symptoms, lethargy, severe

anaemia, fever, rash,

abnormal taste

CYP450 metabolism

Vitamin B12: loss of bowel

flora reduces bacterial

production

Probiotics reduces GIT &

UT side effects of drugs

(Bryant & Knights, 2011,p770)


Helicobacter Pylori

Drug Action Side effects Interaction

Beta-lactam:

Amoxycillin

Medium spectrum

antibiotic (Penicillin

family)

Diarrhoea, GIT

symptoms, headache,

oral & vaginal

candidiasis, hives

Vitamin B12: loss of

bowel flora reduces

bacterial production

Probiotics reduces GIT

& UT side effects of

drugs

Misoprostal

(Cytotec ®)

Prostaglandin synthetic

analogue (PGE1) –

protects the stomach by

decreasing gastric acid

secretions thus helping

to heal the ulcerations

Infrequent –

constipation, flatulence,

headache, GIT

symptoms, diarrhoea.

Can lower blood

pressure.

Dose dependant

diarrhoea.

Contra-indicated in

pregnancy

(Katzung 2001, p1068; Bryant & Knights, 2011, p770)


Peptic Ulcer


Peptic ulcer disease (PUD) = mucosa is eroded due to exposure of

acid and pepsin leading to ulceration.

o Can be either seen as gastric or duodenal ulcers (or both

gastroduodenal).

o Helicobactor pylori seen as the primary causal agent (H. pylori is

present in 95% of patients with duodenal ulcers and in 70% of those

with gastric ulcers).

(Ford AC et al 2006)

o Ulcerations are at risk of serious complications of haemorrhage or

intestinal stricture.

(Davidson & Haslett 2002, p784;

Jamison 2003,p.383;

Shils et al,2006,p1185).

Peptic Ulcer


Risk factors

o Helibacter pylori

o Drugs – NSAID’s

o Smoking

o Stress (Psychosocial factors can be estimated to contribute to 30%

to 65% of ulcers. Heightened stress response -> increases duodenal

acid load results in HPA axis activation altering healing & mucosal

blood flow & Impairment of gastro-duodenal mucosal defences

(Levenstein 2000)


Treatment plans around diet and lifestyle should emphasis the

importance of :

o Ceasing cigarettes.

o Avoiding alcohol, coffee, tea and sugar

o Avoiding NSAIDs and aspirin

o Eating 5/6 small meals daily

o Drinking 2-3 litres of water daily

o Avoiding spicy/hot/ fatty foods

o Consuming cabbage juice

o Further testing – H.pylori infection.



Peptic Ulcers

Nutrients with possible benefits:

Cabbage juice

o Vitamin U (S-methyl methionine sulfonium or MMSC)

has a cytoprotective mechanism on the surface mucosal

mucin of the stomach.

o MMSC was found to increase activity of S-adenosyl-L-

homocysteine that in turn stimulates the methylation

process.

o Trials have found efficacy in treating gastric and

duodenal inflammation and ulceration.

o Cabbage juice has a role in preventive therapy.

(Patel & Prajapati 2012).


Therapeutic Actions

Soluble Fibre

o Reduces disease risk. Inverse relationship with duodenal ulcer rates (Aldoori et al, 1997)

Phosphatidylcholine

o Protection by strengthening mucous-phospholipid layer

Vitamin E

o Anti-ulcer activity, and effective in preventing aspirin

induced gastric lesions

Peptic Ulcer


Peptic Ulcer

Nutrient Dosage Therapeutic Actions

Turmeric 300mg caps x 5/day

30-60 minutes

before food

Antioxidant, anti-inflammatory, positively compared to

liquid antacid therapy, efficacy with ulcer eradication

Glutamine 500-3000mg/day GIT support, mucous membrane trophorestorative,

improves gut immunity and IgA levels, maintains acid

base balance

Cabbage Juice

(Glutamine)

1 litre/day fresh juice

in divided doses

Mucin synthesis stimulation

Probiotics 10-40 billion org/day Recolonization of beneficial gut bacteria.

Saccharomyces spp., Lactobacillus spp.,

Bifidobacterium spp.

Mahan, Raymond 2017; Prucksunand et al 2001; Shils et al,2006,p1638; Braun & Cohen

2010, p902


Peptic Ulcer


Soluble Fibre 30-60g Cancer prevention, optimizes gut bacteria

Phosphatidyl-

choline

3-6g Cell signalling, structural element in membranes

Omega 3 1000-

6,000mg

Increases the adhesion of gut bacteria, regulates inflammation

Vitamin A 5000iu Promotes mucosal healing. Short term use of 50,000IU/day

improves ulcer healing

Vitamin C 500 –

5000mg

Gastric mucosal healing after eradication of H pylori, protective

effect against aspirin induced duodenal injury

Vitamin E 100-1000iu Antioxidant and anti-ulcer activity (used with caution)

Zinc 10-100mg Healing and repair of lesions

(Osiecki 7thed,p47, 59, 185; McAlindon et al 1996; Prucksunand et al 2001; Jamison

2003,p385; Shils et al,2006,p533)


Key Nutrients to Consider: Gastritis, H. pylori, Peptic Ulceration

o Vitamin C

o Glutamine

o Zinc

o Vitamin B12

o Garlic

o Probiotics


Glutamine in Gastritis, H. pylori, Peptic Ulceration

Mechanism

of action

• “The underlying mechanism of action of glutamine-induced gastric

protection is still unclear.” (Hagen, 2009)

Evidence

of clinical

application

• Mostly animal studies – found to protect gastric mucosal cells from

ammonia induced cell death (Hagen 2009)

Dosage1000 – 1500mg twice to three times per day, depending on the level of

severity.

Other

considerations

• None known


Case Study Discussion


Case Study

27 year old female.

Presenting Symptoms

o Gastric Ulcer diagnosed at 16 years old treated but

symptoms still mildly apparent.

o These include: mild ‘warm’ gnawing pain worse for

eating.

o GIT: bloating within 15 minutes of eating, lasts for a

couple of hours or until she eats again, burping

constantly. Heartburn after eating (5/7 days per week)

better for antacids. Loose bowel motions if really anxious

(at least 1 every second day). Undigested food in stool,

odorous.


Case Study

Medications / Supplements

o OCP- Yasmin (Endometriosis)

o Efexor

o Lamictal

o Antacids

o Antibiotics if a UTI is present

Allergies

o Wheat (intolerance)


Case Study

Family History

o Mother: Depression, Bi-polar disorder

o Father: High blood pressure, cholesterol

Past Medical History

o Infant: Vaginal delivery, breast fed. Cradle cap eczema

as a baby.

o Childhood: frequent stomach aches, bouts of

constipation,

o Adolescence: gastric ulcer diagnosed at 16, wisdom

teeth removed at 17.


Case Study

System Presentation

o Nervous system & Endocrine: Depression diagnosed

2003 and hospitalized for two weeks. Tried various drugs

but feels stable on the Efexor & Lamictal. Ongoing anxiety

– presents all of the time. Can’t remember a time when she

did not feel anxious. Insomnia: trouble getting to sleep &

when asleep will wake between 3-5am. Dreams frequently

& wakes unrefreshed.

o Urinary: gets 1 UTI per year, doesn’t clear without

antibiotics

o Circulatory: cold hands & feet

o Reproductive: NAD


Case Study

Physical Examination Results

o Nails: pale, no moons, poor capillary return, white spots

on 5 fingers, vertical ridging, peeling

o Skin: pale, bluish tint

o Appearance: dark circles under eyes, thin, gaunt

o Height: 170cm Weight: 52kg Waist: Hip 0.70

(Female>0.85)

o Tongue: pointed, quivering, thick white coat, pale

o Zinc tally: tastes like ‘water’


Case Study

Time Daily Dietary Intake

8 am Gluten free muesli (1 cup), almonds (handful), Greek low-fat

yoghurt (pot set)

1 cup green tea

12.30

pm

Left overs – last night’s left-overs, sushi

5.30 pm Meat & vegetables (potatoes, corn, beans), stir-fry

Snacks Chocolate

Water – 1.5 litre per day


Group Discussion/tutorial

o Break off into small groups

o Using this case, form a schematic understanding of the

case. Be sure to consider body systems involved in the

presentation, link contributing factors.

o Suggest 3 suitable treatment aims for this client with a

treatment plan on how this may be accomplished.


Constipation


o Infrequent passage of hard stools accompanied by

straining, peri-anal or abdominal discomfort with a

feeling of incomplete evacuation.

o Can be related to food intake, as a result of medical

(neurological/metabolic/endocrine), GIT disorders or

lifestyle factors (mobility) or past laxative abuse.

o Certain drug classes, age & depression can be factors.

(Mahan & Escott-Stump, 2012, p.611)

Constipation


Constipation

Consider:

o Investigate possible cause (food intolerances/drugs)

o adequate water intake (2-3 litres/day)

o caffeine & alcohol intake

o Increase insoluble fibre (fruits & vegetables)

o Flaxseed oil or olive oil

o Probiotic therapy

(Osiecki 2006,p.628; Sarris & Wardle 2010, p55; Sygo &

Oh 2010; Mahan & Escott-Stump, 2012, p.612 & 617;

Toner & Claros 2012)


Constipation

Consider the effect and significance of :-

Probiotics

o The addition of Lactobacillus rhamnosus &

Propionibacterium freudenreichii into the diet has been

shown to increase stool frequency by 24%

(Ouwehand et al, 2002)

Fibre

o A higher intake of dietary fibre was shown to be

associated with a decreased risk of constipation in

women & children

(Roma et al, 1999; Dukas, Willet & Giovannucci, 2003;

Anderson et al 2009).


Constipation


Probiotics 10-40billion

org/day

Gut bacteria stability

Omega 3 1-10gm Lipotropic – supports bile synthesis and hepatic

function

Magnesium 300-1,000mg Muscle relaxant

Vitamin C 500-5,000mg Laxative effect, digestive function & healthy gut

microflora,

Betaine HCl 500-650mg Increases digestive function

Insoluble

Fibre

30-60gm Insoluble : increase moisture and content of faecal

matter for transit

(Osiecki 7thedn, p. 47 & 170; Shils et al, 2006, p533; Sarris & Wardle 2010, p 55; Braun

& Cohen 2010, p689; Asif 2011; Skinner et al 2011; Mahan et al 2012, p612)


ConstipationDrug Action Side Effects Interaction

Bulk forming

laxatives:

Psyllium

Absorbs water to

increase bulk

Flatulence

& bulky

stools

Calcium, Vitamin B12:

decreases absorption. Separate

doses by 2 hours for all

medications.

Hypoglycaemic agents :

additive effects.

Faecal

Softening

Agents:

Docusate &

Poloxamer

Softens stool,

stimulant, detergent-

like & maintains

water & fats in the

stool.

Detergent like action increases

drug absorption in GIT if taken

concurrently.

Liquid Paraffin Coat stool & reduces

water absorption.

Impairs absorption of fat soluble

vitamins

(Bullock et al, 2007 ; Braun & Cohen 2010,p769; Bryant et al, 2011,p548)


Constipation

Drug Action Side Effects Interaction

Stimulant

Laxatives:

Bisacodyl and

Sodium

Picosulphate

Reduces water

absorption & increases

excretion into lumen.

Directly stimulate

nerves in wall lining to

increase peristalsis

Cramping, water and

electrolyte

imbalances, rebound

constipation

Increased

peristalsis and

reduced water

absorption reduces

vitamin & mineral

absorption.

Osmotic

Laxative

Lactulose,

Glycerol,

Sorbitol

Not absorbed & create

osmotic gradient

drawing water into the

lumen = bulk which

stimulates peristalsis

Flatulence, abdominal

discomfort may occur

with lactulose.

Electrolyte

disturbances with

long term daily use.

(Bullock et al, 2007, Bryant et al 2011,p 548)


Constipation

Drug Action Side Effects Interaction

Saline Laxatives:

Magnesium salts,

Sodium salts,

Polythylene glycol

electrolyte solution

Not absorbed & =

osmotic gradient

drawing water into

the lumen.

This creates bulk

stimulating

peristalsis

Long term use of

saline laxatives

linked with

electrolyte

disturbances.

Electrolyte

disturbances with

long term daily use.

Sodium salts should

be avoided in

patients with

congestive cardiac

failure.

(Bullock et al 2007, Bryant et al 2011, p549)


Constipation

Liver Function

o Bile acids have a role in intestinal transport

o A specific bile acid, CDCA, is used medically in the

treatment of functional constipation

o There is a hypothesis that bacterial overgrowth in the

colon leads to deconjugation of CDCA, and therefore

reduces its laxative effect

(Hofmann & Hagey, 2008, p. 2461)


Diarrhoea


Diarrhoea

o Frequent evacuation of liquid stools with subsequent

loss of fluid & electrolytes (particularly sodium,

potassium & magnesium). There may be decreased

enzymatic digestion.

o May be due to infection, drugs, food reaction, over

consumption of sugars, inflammatory diseases,

abnormalities of mucosal cell transport (coeliac).

(Shils et al 2006 p1204, Mahan & Escott-Stump, 2012 p613)


Diarrhoea

• Osmotic: un-absorbable, water-soluble solutes remain in

the bowel, where they attract water

• Secretory: when the small and large bowel secrete more

electrolytes and water than they absorb.

• Exudative: occurs with several mucosal diseases that

cause mucosal inflammation and ulceration.

• Decreased absorption time: chyme is not in contact with

an adequate absorptive surface of the GI tract for a long

enough time so that too much water remains in the

faeces

• Malabsorption: osmotic or secretory causes of diarrhoea

due to malabsorption of various substances


Diarrhoea

Nutritional Considerations

o Diarrhoea related fluid loss leads to dehydration &

electrolyte loss; even vascular collapse may occur

o Hypokalemia may occur in severe or chronic diarrhoea,

or if the stools contain excess mucus.

o Hypomagnesemia after prolonged diarrhoea may cause

tetany.


DiarrhoeaFurther considerations:-

o Avoidance of foods that contribute to colonic residue –

high fibre, resistant starch, fructose and sugar alcohols –

these retain fluids in the colon and contribute to osmotic

diarrhoea.

o Milk and dairy products may worsen diarrhoea if lactose

tolerance is an issue.

o Fatty meals can aggravate diarrhoea.

o Poorly digested or absorbed carbohydrates can increase

stomach distension and cause discomfort.

o Caffeine should be avoided as this will reduce water

reabsorption (Rolfes, Pinna & Whitney 2012, p732)


Diarrhoea

Prebiotics & Probiotics

o Probiotics & prebiotics was shown to reduce diarrhoea

from various causes (infections, HIV, antibiotics & IBS).

Probiotic strains should be present at 109 to be effective

o Prophylactic prebiotics have been found to result in less

severe diarrhoea in travellers. Dose 10-15g/day.

(Braun & Cohen, 2010, 751, 1046)

o Inulin, oligofructose with L. plantarum & B. bifidum was

found inhibit pathogenic strains that cause diarrhoea

(de Vrese & Marteau 2007)


Diarrhoea

Bovine Colostrum

o Benefits infectious diarrhoea caused by rotavirus,

shingella & HIV (300mg - 10g/day)

Zinc

o A systematic review of zinc supplementation

demonstrated consistent decreases in acute or

persistent pediatric diarrhoea (dose 10mg/day).

(Braun & Cohen, 2010. p. 360, 1046)


Diarrhoea


Bifidobacterium

bifidus

10-40

bill org

Recolonise bacteria. Anaerobic pleomorphic rods

(club shaped organisms) that have the role in

breaking down dietary CH2O & interact directly with

the host metabolism.

Glucosamine 1500-

3,000mg

Precursor to the ground substance/gap junctions for

epithelial cells

Soluble fibre 1tsp/bd Mucosal support/repair, Bulking agent.

Mucopolysaccharide

Glutamine 500-

3,000mg

Tissue repair, Restores gut wall integrity & normal

intestinal flora colonisation (great with probiotics &

zinc)

Bromelain 150-

400mg

Anti-inflammatory, Proteolytic enzyme, COX – 2

(Osiecki 7th ed, p. 91, 171, 187, 196; Osiecki 2000, p 273)


Diarrhoea


Amylase Carbohydrate Digestion

Lipase Fat Digestion

Betaine

Hydrochloride

100-400mg /

Meal

Raises stomach acid, Substrate for HCL

production

Glutamic Acid 500-3000mg Raises stomach acid, Substrate for HCL

production

(Gropper, Smith & Groff 4th ed, Osiecki 7th ed, p91, 170; Mahan & Escott-Stump 2012, p2)


Diarrhoea


Adsorbents:

Kaolin &

Pectin

Coats the mucous

membranes, binds to the

toxins and excretes via

the stool

Constipation Interfere with the

absorption of other

drugs.

Can alter water and

electrolyte levels

Adsorbents:

Aluminium

hydroxide

As above Increased risk of

aluminium toxicity –

renal failure

Can alter water and

electrolyte levels

Opioid Anti-

diarrhoeals:

Loperamide,

Diphenoxylate

Codeine

Narcotic analgesics

activate opioid receptors

in GIT lining reducing

peristalsis and increasing

the mixing action

Constipation.

Loperamide =

nausea, vomiting

and abdominal

cramping

Adverse reactions

with alcohol

(Katzung 8thed, p1071Bryant et al 2007, p766)


Haemorrhoids


Haemorrhoids

o Arise from congestion of the venous plexuses (internal & external)

around the anal canal

o Can be classified as external, internal or internal-external

hemorrhoids; also as first, second and third degree

o Factors increasing venous congestion in perianal region can induce

hemorrhoid formation

• increasing intra-abdominal pressure (inducing straining on

defecation)

• low fibre diet

• Pregnancy – there’s generally slower return of blood from the

lower half of your body, which increases the pressure on the

veins below your uterus and causes them to become more

dilated or swollen. Constipation also a contributing factor.

(Boon, Colledge & Walker, 2006, p. 933)


Haemorrhoids

Nutritional Considerations:

1. Assess fibre intake

o A high fibre diet and fibre supplements are the

cornerstone of nutritional management

o Fibre attracts water and forms a gelatinous mass to

ensure stools are soft and pass without straining

o Psyllium (Plantago ovata) is less irritating than other

fibres, and has been shown in trials to reduce

haemorrhoid symptoms

(Pizzorno & Murray, 2006, p. 2070-2071)


Haemorrhoids

2. Maintain regular eating patterns.

Breakfast

o Skipping breakfast leads to a 7.5 fold increased risk of

haemorrhoids

3. Ensure adequate bioflavonoids

o The strengthening effect of flavonoids on venous tissues

makes them useful in both presentation and treatment

(Pizzorno & Murray, 2006, p. 2070-2071)


Haemorrhoids


Vitamin A 10000–

50000IU

Assist in the maintenance of the gut integrity + Antioxidant.

Mucous Membrane, Assist in the maintenance of the

epithelial integrity, ability to stimulate specific and non-

specific immune functions, Antioxidant.

Vitamin C 250-

10000mg

Collagen Synthesis + Immune system + Antioxidant.

Facilitates & regulates immune function including increasing

levels of macrophage activity, lymphocyte production &

antibodies (IgA, IgG, IgM). Modulates prostaglandin

synthesis. Heals & rebuilds damaged tissue.

Vitamin E 100-

1000iu

Antioxidant - Enhances Cell Membrane Stability

(Osiecki 7thedn, p4, 44-54)


Haemorrhoids


Bioflavonoids 600mg – 3

gm

Collagen synthesis, antioxidant functions & ascorbic

acid can protect flavonoids from oxidative

degradation.

Zinc 10-100mg Collagen Synthesis (Ulcer) + Immune system.

Protein, fats & cholesterol synthesis.

Dietary Fibre

Fruit and

vegetable

12-20gm Bulking agent. Fuel source for bacteria, provides

structure and form, protective barrier for mucous

membranes, Provides an aqueous matrix for diffusion

of nutrients and electrolytes

(Osiecki 7thed, p34, 162,185)


Haemorrhoids


Rectinol

Ointment

Local aesthetic - relieve pain.

Steroids - reduce

inflammation, swelling and

itching.

Antiseptic agents – infection.

Astringents – tighten tissue

and reduce swelling.

Vasoconstrictors – reduce

venous swelling (Bullock et

al 2007)

Local aesthetic –

sensitise the anus.

Steroids – can

irritate infections

and cause skin

thinning

None listed

(Bullock et al 2007)


Helpful links

o Royal Australian College of General Practitioners 2014.

Helicobacter pylori eradication – an update on the latest

therapies, available at:

http://www.racgp.org.au/afp/2014/may/helicobacter-

pylori-eradication/

o National Prescribing Service (NPS) information on drugs

and drug interactions for health professionals, available

at: http://www.nps.org.au/

o Therapeutic Goods Administration (TGA). Adverse event

reporting, available at: https://www.tga.gov.au/

http://www.racgp.org.au/afp/2014/may/helicobacter-pylori-eradication/

http://www.nps.org.au/

https://www.tga.gov.au/


Patient Reported Outcome

Measures (PROMs)

o In your own time, you may find this clip a useful resource

on PROM’s to asssit with your tutorial activities and case

study assignments.

o https://www.youtube.com/watch?v=KlBXLVd25gQ&featur

e=youtu.be [13.53 minutes]

https://www.youtube.com/watch?v=KlBXLVd25gQ&feature=youtu.be

https://www.youtube.com/watch?v=KlBXLVd25gQ&feature=youtu.be


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Boon, N., Colledge, N., & Walker, B. (Eds.). (2006). Davidson’s principles and practice of

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Braun, L., & Cohen, M. (2015). Herbs & natural supplements: An evidence-based guide

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Communication & Referral

Networks


Communication & Referral

Networks

o Optimal care = effective communication between different

practitioners managing the same patient.

o This potentially reduces side effects or unsafe outcomes

o Research has suggested that around 70% of medical practitioners

are interested in collaborative teamwork with CAM practitioners

o The referral process between medical practitioners and CAM

practitioners can be made effective with the use of formalised

referral letters

(Ben-Arye, et al. 2007; Braun & Cohen, 2010, p.76)


Interaction Reporting




o Two types of adverse drug reactions

Type A – predictable

Type B – idiosyncratic

o Reporting of any negative or suspected interaction is

vital for patient safety and is required from a professional

stand point.

o Reporting is to the Therapeutic Goods Administration.

(Braun & Cohen, 2010, p. 81-92)

nmdc221 session 2: gastrointestinal & alimentary disease ......drug action side effects...

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