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Medicine Year 1 > Week 101 Diarrhoea > Flashcards

Week 101 Diarrhoea Flashcards

1
Q

What are the 4 layers of the gut?

Histology

A

Mucosa
Sub-mucosa
MUSCULARIS PROPRIA
SEROSA (Peritoneum)

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2
Q

What are the two type of muscle in the oesophagus?

Histology

A

inner circular muscularis propria

outer longitudinal muscle

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3
Q

What is at the base of the mucosa?

Histology

A

A thin double layer of muscle- the muscular mucosal which may massage the glands/crypts

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4
Q

What type of cells line the oral cavity, pharynx and oesophagus?
(Histology)

A

squamous

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5
Q

What kind of cells line the stomach?

Histology

A

flat columnar

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6
Q

What kind of cells line the duodenum, jejunum and ileum?

Histology

A

Villous columnar

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7
Q

What kind of cells line the colon and rectum?

Histology

A

Flat columnar

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8
Q

Describe the squamous epithelium

Histology

A

Squamous epithelium- only the basal layer attached to the basement membrane. Skin, mouth, pharynx, oesophagus anus. Gives rise to squamous cell carcinoma

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9
Q

Describe the columnar epithelium

Histology

A

Columnar epithelium – all cells attached to basement membrane. Stomach, intestines, colon, rectum. Gives rise to adenocarcinoma.

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10
Q

Describe parts of the stomach

Histology

A

As the oesophagus meets the stomach, it’s called the gastro-oesophageal junction and this is where the cardia/Z-line is. The upper portion of the stomach is the funds, followed by the body and antrum- ending with the pyloric sphincter.

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11
Q

What two mucosa are similar?

Histology

A

Cardiac mucosa and astral mucosa

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12
Q

Describe the surface mucous cells in the body and funds of the stomach
(Histology)

A

Much longer compared to the antrum/pre-pylorus mucous cells. They have a neck (stem cell region), parietal cells and chief cells.

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13
Q

Describe the surface mucous cells of the antrum/pre-pylorus

Histology

A

Shorter than the body and fundus mucous cells. They have stem cells and mucous cells.

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14
Q

In the body of the stomach, what can the stem cells become?

Histology

A

They can move up to become mucous cells or move down to produce parietal, chief and endocrine cells

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15
Q

In the Antrum of the stomach, what can the stem cells become?
(Histology)

A

They can move up to become mucous cells or down to also become mucous cells or endocrine cells

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16
Q

What is the purpose of the parietal cells in the stomach?

Histology

A

Secrete Hal and intrinsic factor (Vit B12)

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17
Q

What is the purpose of the chief cells in the stomach?

Histology

A

To produce digestive enzyme

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18
Q

What are the endocrine cells in the stomach?

Histology

A

Gastrin

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19
Q

Describe how the stem cells in the small intestine can differentiate
(Histology)

A

Stem cell compartment:

  • move up to form brush-bordered enterocytes/goblet cells/endocrine cells
  • move down to form paneth cells
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20
Q

What do the stem cells in the colon/rectum differentiate into ?
(Histology)

A

Stem cells:

  • up to form brush-bordered colonocytes/goblet cells/endocrine cells
  • move down to form paneth cells in the right side of the colon only
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21
Q

What do the connective tissue and fat contain in the sub-mucosa?
(Histology)

A 
Connective tissue and fat containing
• Superficial nerve plexus
• Peripheralnerves
• Bloodvesselsandlymphatics
• Sub-mucosal glands:
-in oesophagus
-in duodenum (Brunner’s glands)
• Peyer’spatches–macroscopicallyvisiblelymphoid tissue in terminal ileum.
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22
Q

What is the omentum known as?

Histology

A

The abdominal police

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23
Q

Describe how the muscularis propria of the gut changes throughout the GI tract
(Histology)

A

Smooth muscle (involuntary)
• Inner circular muscle
• Deep nerve plexus
• Outer longitudinal muscle

• In oesophagus, upper third is voluntary skeletal muscle

• In stomach, as well as circular and longitudinal layers an oblique
layer is present

• In colon, the outer longitudinal layer bunches up into three bands – the taenia coli – running from caecum (tri-radiate point) to the end of the sigmoid colon

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24
Q

What is the serosa?

Histology

A

Serosal (peritoneal) surface – lining of flat mesothelial cells covers stomach, small intestine and colon

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25
Q

Where is the peritoneal surface absent?

Histology

A

oesophagus and rectum, which are intra-thoracic and pelvic structures respectively

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26
Q

What are the layers of the oesophagus?

Histology

A 
Squamous epithelium
• Basement membrane
• Lamina propria
• Muscularis mucosae
• Submucosa , superficial nerve plexus, glands
• Muscularis propria
Inner circular muscle Myenteric nerve plexus Outer longitudinal muscle
• Adventitia (fat)
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27
Q

What are the layers of the body of the stomach?

Histology

A 
Surface mucous cells
• Neck or foveolar region
• Parietal cells and chief cells in glands surrounded by lamina propria
• Muscularis mucosae
• Sub-mucosa
• Muscularis propria
circular, oblique nerve nerve plexus
longitudinal
• Serosa
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28
Q

What are the layers of the Antrum?

Histology

A 
• Surface mucous cells
• Mucous glands in lamina propria • Muscularismucosae
• Submucosa
• Muscularis propria
Inner circular muscle nerve plexus
Outer circular muscle
• Serosa
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29
Q

What are the layers of the small intestine?

Histology

A
  • Villi covered by columnar epithelium
  • Crypts/glands
  • Lamina propria surrounds glands and fills villi
  • Muscularis mucosae
  • Submucosa
  • Muscularis propria (inner circular, nerve plexus, outer longitudinal)
  • Serosa
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30
Q

What are the layers of the colon and rectum?

Histology

A 
Lamina propria and crypts/glands 
• Muscularis mucosae
• Submucosa
• Muscularis propria (inner circular, nerve plexus, outer longitudinal) 
• Serosa
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31
Q

What 4 densities do plain x-ray film show?

Anatomy

A

Metal; bone, calcium
Soft tissue; fluid, liver
Fat
Gas

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32
Q

What abnormalities can you detect on an abdominal radiograph?

(Radiography)

A 
Foreign bodies
Kidney stones
Abdominal masses (e.g. right renal mass)
Bowel obstruction (e.g. dilated small bowel)
Perforation (e.g. triangles of free gas)
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33
Q

What can you see in an abdominal ultrasound and under what health conditions?

(Radiography)

A

Good:
- Liver, spleen, kidneys, bladder, gallbladder

Bad:
- Bowel, bone

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34
Q

What abnormalities can you see on ultrasound?

Radiography

A

Gallstones

Masses

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35
Q

What can you see on CT (computed tomography)?

Radiography

A 
Bone +700
Liver  +30
Water   0
Fat      -50
Gas.    -700

(and kidney/spleen/aorta/large bowl/small bowl/bladder/rectum)

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36
Q

How does MRI work?

Radiography

A

Images based on how much water is in the tissues.

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37
Q

What method of imaging has the best tissue contrast?

Radiography

A

MRI

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38
Q

What are the 2 types of MRI?

Radiography

A

T2 weighted- bright water

T1 weighted- bright fat

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39
Q

What abnormalities can you see on MRI?

Radiography

A

Cirrhosis
Liver metastasis
Polycystic kidneys
Enlarged prostate

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40
Q

Name types of viruses that can cause acute diarrhoea

A

Rotavirus
Norovirus
Astrovirus
Enteric adenovirus

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41
Q

Describe the features of rotavirus causing acute diarrhoea

A

- Leading cause of gastroenteritis worldwide

- Infects nearly all children throughout the world during early childhood; peak
incidence of infection ages 6-24 months

  •  Causes up to 40% of all cases of severe diarrhoea in infants
  •  In the USA, rotavirus is the leading cause of hospital admissions for AD

- Infection occurs during the winter months in temperate climates, but
perennially in tropical countries

- >7 antigenic groups (A – G) with group A being the most common worldwide;
multiple different serotypes within each group (important for vaccine
development)

- Shed in high titers in stools (therefore infectious to contacts) for up to 21
days after onset of symptoms

- Transmission via fomites (toys, hard surfaces) increases disease spread within
families and institutions

- Vaccine available and used in some countries

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42
Q

Describe features of norovirus in AD

A

- Second most common cause of severe AD in children in industrialized
countries

- Most common cause of outbreaks of AD, typically during winter months and in closed communities such as restaurants, schools, day care centers,
hospitals, and cruise ships

- Highly contagious

- Transmission is by direct person-to-person spread, through contaminated
food and also through vomit

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43
Q

Describe features of astroviruses in AD

A
  •  Cause sporadic AD, mainly in young children
  •  More common in winter months
  •  Cause outbreaks in institutions

- May be shed in the stool for several weeks after the illness, and longer in
immunocompromised children

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44
Q

Describe features of enteric adenovirus in AD

A

Causes AD throughout the year, primarily in younger children

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45
Q

Name types of bacteria that can cause AD

A
  • Campylobacter
  • Salmonella
  • Diarrhoeagenic
  • Escherichia coli (E. coli)
  • Cholera
  • Shigellosis
  • Typhoid (Salmonella typhi and S. paratyphi; “enteric fever”)
  • Clostridium difficile
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46
Q

Describe features of campylobacter causing AD

A
  •  Present in the gastrointestinal tract of wild and domestic birds and animals (therefore, faeces of these animals are a source of infection)
  •  Transmission by contaminated water, undercooked poultry, unpasteurized milk, direct person-to-person
  •  Faecal shedding of bacteria persists for 2-3 weeks

- Second most common cause of travelers’ diarrhoea, after enterotoxigenic E.
coli (ETEC)

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47
Q

Describe features of salmonella causing AD

A
  •  Highest infection rates in infants and young children
  •  Present in the gastrointestinal tract of animals and reptiles, including pets

- Transmission mainly via contaminated animal foods (poultry, eggs, dairy
products, beef, fish)

- Faecal shedding persists for several weeks, especially in younger children,
and can be prolonged by antibiotic therapy; 1% cases become chronic carries (faecal shedding > 1 year)

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48
Q

Describe features of Diarrhoeagenic Escherichia coli (E. coli) causing AD

A

- Five main strains of E. coli cause diarrhoea: Enterotoxigen (ETEC),
Enterohemorrhagic (EHEC), Enetropathogenic (EPEC), Enteroinvasive (EIEC)
and Enteroaggerative E. coli (EAEC)

- Transmission is from contamination of food (especially undercooked meat
and unpasteurized milk) and water with human or animal faeces, or direct
contact with an infected case or carrier

- EHEC
o Most common cause of diarrhoea in U.S., especially E. coli O157:H7 which is highly contagious
o Shed in cattle faeces
o Occurs sporadically and in outbreaks
o Associated with haemolytic-uraemic syndrome (HUS)
ETEC
- Causes hundreds of millions of cases of AD and tens of thousands of
deaths of infants and younger children in developing countries every
year
 - The major cause of diarrhoea in travelers to countries with poor
sanitation

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49
Q

Describe features of cholera causing AD

A

- Endemic in many countries with poor sanitation and lack of safe water in
Africa, Asia, and South and Central America

- Occurs in outbreaks, especially following contamination of water supplies
during natural disasters, wars and civil unrest

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50
Q

Describe features of Shigellosis causing AD

A
  •  Four species: Shigella (S.) sonnei, S. flexneri, S. boydii and S. dysenteriae
  •  Endemic in countries with poor sanitation

- Causes severe dysentery (blood and mucus in the stools) mainly in children
under age 5

  •  also infects travelers
  •  highly infectious

- Humans are the reservoir of infection, and transmission is through direct
person-to-person contact (including sexual contact), fomites, and
contaminated food and water

  •  Houseflies may also transmit after feeding on infected faeces
  •  Faecal shedding persists for a few weeks; chronic carriage is rare
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51
Q

Describe features of Typhoid (Salmonella typhi and S. paratyphi; “enteric fever”) causing AD

A

Endemic in South and South-East Asia, Africa, South America and Eastern
Europe

52
Q

Describe features of

Clostridium difficile causing AD

A
  • Present in the soil and common in the environment

- Commensal organism in the gut of up to 50% of healthy infants but <5% of
older children and adults

- Diarrhoea associated with secretion of toxins A and B which may be life
threatening, especially in the elderly

- Outbreaks occur within health care institutions – major cause of health-care
acquired diarrhea (along with norovirus)
  •  3 major risk factors: recent antibiotic use, admission to hospital and age >65
    years. Use of PPIs is also likely to be a risk factor – through compromised gastric acid barrier
53
Q

Name types of parasites that cause AD

A

Giardiasis
Cryptopsoridium parvum
Entamoeba histolytica causes diarrhoea and dysentery in developing countries

54
Q

Describe features of Giardiasis causing AD

A

 Occurs worldwide
 Most common cause of parasitic diarrhoea in developed countries
 Humans are the main reservoir but infection also occurs in dogs, cats, and
other animals
 Transmission is through direct person-to-person contact or ingestion of
resistant cysts in contaminated water and food
 Excretion of cysts in faeces may persist for several months

55
Q

Describe features of Cryptopsoridium parvum causing AD

A

- Occurs worldwide

- Carried by mammals, birds, and reptiles
 Transmission occurs from livestock, zoo animals, and pets

  •  Extensive outbreaks occur following contamination of water supplies
  •  Outbreaks in nurseries associated with high attack rates
  •  Common cause of traveler’s diarrhoea
56
Q

History: What is PC

A

Presenting complain

What is the main problem?

57
Q

History: HPC?

A

History of presenting complaint

Detailed description of the problem

58
Q

History: DQ?§

A

Direct questions

Responses to specific questions relevant to the PC

Important positive and negative information

59
Q

History: functional enquiry?

A

Important symptoms in each of the major

systems (cardiovascular, respiratory, etc.)

60
Q

History: PMH

A

Past medical history

What illnesses and hospital admissions have occurred in the past? Concurrent illnesses.

61
Q

History: DH?

A

Drug history: Recent and current treatment

62
Q

History: allergies?

A

Known allergies e.g. latex/drugs

63
Q

History- what end things should you ask?

A

Developmental milestones- Developmental milestones

Immunisations

Family history

Social history and employment

Smoking/alcohol

Travel history

64
Q

What should you include in a clinical examination?

A 
General appearance
Systems 
Summary of problem
Working diagnosis
Differential diagnosis
Management plan
Name, sign, date, GMC number
65
Q

What is the definition of diarrhoea?

A

WHO* definition of diarrhoea:
– 3 or more loose or watery stools (taking the shape of the container) in a 24-hour period
– Acute: <14 days duration
– Persistent: ≥14 days duration

66
Q

What are features of dysentery?

A

small volume, bloody, mucoid stools + abdominal pain / toxicity

67
Q

What do you need to ask a pt regarding diarrhoea?

A

– Stool frequency

– Stool consistency; ± blood, mucus

68
Q

What are signs of dehydration?

A
  • sunken eyes
69
Q

What are the types of diarrhoea?

A
  • Osmotic
  • Secretory
  • Inflammatory
70
Q

What are the features of Osmotic diarrhoea?

A

Stool volume: moderately increased

Response to fasting: diarrhoea stops

Stool osmolality: Normal to increased

Ion gap: > 100 mOsm/kg

71
Q

What are the features of secretory diarrhoea?

A

Stool volume: very large

Response to fasting: diarrhoea continues

Stool osmolality: normal

Ion gap: < 100 mOsm/kg

72
Q

Describe features of inflammatory diarrhoea:

A
  • Disordered structure and function
  • Damage to the SI mucosa (digestion and absorption)
  • Symptoms: – Pain
    – Bloody, mucoid stools – Weight loss
    Main Causes:
    • Infection – esp. bacterial pathogens
    • Auto-immune disease – inflammatory bowel disease
    • Food sensitivity (Coeliac, CMP)
    • Other – e.g. radiation
73
Q

Describe causes of loose stools via increased intestinal fluid secretion (secretory diarrhoea)

A

Infection caused by e.g. cholera, rotavirus, ETEC

74
Q

Describe causes of loose stools via osmotically active substances (osmotic diarrhoea)

A

Malabsorption: CHO/protein- lactose intolerance

Rapid gut transit- IBS, toddler diarrhoea, stimulant laxative

Osmotic laxative- lactulose, PEG

75
Q

Describe the causes of steatorrhoea

A

Malabsorption of fat- e.g. pancreatic disease or coeliac disease

76
Q

Describe causes of inflammatory diarrhoea

A

Inflammatory bowl disease e.g. Crohn’s, UC

Dysentery e.g. shigella, campylobacter

Other- radiation enteritis

77
Q

What are the consequences of secretory diarrhoea?

A

– Excess loss of fluid → dehydration

– Loss of electrolytes → disordered physiology

78
Q

What are the consequences of osmotic diarrhoea/malabsorption?

A

– Loss of nutrients → malnutrition if prolonged

79
Q

What are the consequences of inflammatory diarrhoea?

A

– Excess loss of fluid → dehydration
– Loss of electrolytes → disordered physiology
– Loss of nutrients → malnutrition if prolonged
– Energy consumption
– Mucosal damage: GIT haemorrhage, perforation, gut derived sepsis

80
Q

What is the likely cause of:

  • Woman aged 28 years
  • Episodes of abdominal pain, bloating and watery diarrhoea (BO x 3-6/day) lasting 1-2 days for past 6 months
  • No blood/mucus
  • Episodes occur about every 1-2 weeks
  • Otherwise well; entirely well between episodes
A

IBS:

“Spastic colon” or “functional diarrhoea” - increased gut motility

Management:
- reassurance
• anti-spasmodics
• anti-diarrhoeals

caused by osmotic, neuronal, possible low-grade inflammation

81
Q

What is the likely cause of:

UK toddler with sudden onset watery, large volume stools; no blood
• BO more than x 10 in last 24 hours
• Some vomiting and mild fever
• Thirsty; some dehydration
• Other children in playgroup have also had diarrhoea recently
• ? Likely diagnosis

A

Rotavirus diarrhoea

RNA virus; multiple diarrhoea mechanisms

Diagnosis: stool virology

Management: ORF (self- limiting after 4-5 days)

82
Q

What is the likely cause of:

  • 19 year old gap-year student just back from India
    • Pale, foul-smelling, greasy stools that float + difficult to flush
    • x 3-5/day for 3 weeks
    • Maybe“explosive”
    • Lost a lot of weight – “two clothes sizes”
    • Feels generally unwell, nauseous and very tired
A

Giardiasis

Steatorrhoea

Diagnosis: microscopy of x3 fresh stool specimens

Management: tinidazole or metronidazole

83
Q

What is the likely cause of:

  • 40 year old UK businesswoman attending conference in Belarus
  • 2 days of very frequent, large volume watery stools
  • Abdominal cramps
  • “Unable to leave the bathroom”
  • Very thirsty
A

Traveller’s diarrhoea

Enterotoxigenic
Escherichia coli (ETEC)
• Attaches to mucosa and
produces toxins
• Severe but usually self limiting
• Clinical diagnosis
84
Q

What is the likely cause of:

  • Man aged 75 years discharged from hospital 3 weeks ago; treated for pneumonia
  • 2/7 frequent, bloody, mucoid stools • Severe abdominal pains
  • Unwell; can not get out of bed
A

Clostridium difficile

• Gram positive, spore forming bacillus
• Enterotoxins A and B
• Typically older in-patients exposed to antibiotics in last 8 weeks
• Highly infectious: barrier nursing
• Wide spectrum of disease from self-limiting to severe colitis
Most severe form:
– pseudomembranous colitis
– multiple elevated yellow/white plaques up to 20 mm across
Diagnosis: faecal toxin; sigmoidoscopy
Treatment: metronidazole / vancomycin; faecal enema

85
Q

In an emergency, what do you initially assess?

A 
Airways
Breathing
Circulation- hydration status
Disability
Don't forget glucose
86
Q

In the child case, what fluids are appropriate to use?

A

Enteral (oral; NGT) rather than parenteral fluids - much safer

87
Q

When should you use parenteral fluid?

A

if
• suspected or confirmed shock
• deterioration despite ORS solution
• persistent vomiting of ORS solution given orally or via a nasogastric tube

88
Q

What is the treatment for immediate shock? (Step 1)

A

Administer O2
• Establish IV (or IO) line
• Give rapid IV infusion of 20 mls/kg body weight of 0.9% sodium chloride*
• Frequent monitoring of clinical response
• Repeat if signs of shock persist but also consider causes of shock other than dehydration (e.g. sepsis)

89
Q

How can you administer fluid if you can’t access veins due to severe dehydration?

A

Intra-osseous line inserted into e.g. tibia

90
Q

What is the most appropriate parenteral fluid for fluid replacement?

A

Normal saline because high salt and high chloride but no potassium

91
Q

During fluid replacement, what must you beware of?

A 
Overhydration:
• Increasing heart rate
• Respiratory distress / cough
• “Crackles” in the lung fields
• Hepatomegaly (enlargement of the liver)
• Oedema (e.g. peri-orbital swelling)

Hypernatreamic dehydration
• Serum Na+ >150 mmol/L • Suspectif
– jittery movements
– increased muscle tone
– increased reflexes (hyperreflexia)
– convulsions
– drowsiness/coma
Fluid management is as described above, but
•replace the fluid deficit more slowly – over 48 rather than 24 hrs
•Reduce serum Na+ slowly (aim for <0.5 mmol/L/hour)
•Measure serum Na+ frequently to guide management

92
Q

What are the signs of clinical dehydration?

A
  • appears unwell/deteriorating
  • altered responsiveness (e.g. irritable, lethargic)
  • decreased urine output
  • skin colour unchanged
  • warm extremities
  • sunken eyes
  • dry mucous membranes (except for mouth breather)
  • tachycardia
  • tachypnoea
  • normal peripheral pulses
  • normal capillary refill time
  • reduced skin turgor
  • normal blood pressure
93
Q

What are the signs of clinical shock? (highest severity of dehydration)

A
  • decreased level of consciousness
  • pale or mottled skin
  • cold extremities
  • tachycardia
  • tachypnoea
  • weak peripheral pulses
  • prolonged capillary refill time (normally 2 secs)
  • hypotension (decompensated shock)
94
Q

What is the 2nd step of dehydration treatment?

A

• After rapid fluid infusion for shock, add 100 mL/kg/day for fluid deficit replacement to maintenance IV fluid requirement
• If treatment of shock was not required, add 50 mL/kg/day for fluid deficit replacement to maintenance fluid requirement
• Use 0.9% saline or 0.9% saline with 5% dextrose
• Measure plasma Na+, K+, urea, creatinine and glucose regularly and adjust fluid therapy accordingly
• Add K+ to parenteral fluids if serum level is low
• Attempt to introduce ORS solution early and gradually. Stop parenteral
fluids once ORS solution tolerated
• Frequent monitoring of clinical response

95
Q

How do you prevent dehydration? (Step 3)

A

• Continue breastfeeding and other milk feeds
• Encourage fluid intake
• Avoid fruit juices and carbonated drinks
• Offer ORS solution as supplemental fluid to those at increased risk of dehydration*
• Use low-osmolarity ORS solution (240–250 mOsm/l)
*Infants and children at increased risk of developing dehydration
• age <1 year, esp. <6 months
• infants who were low birth weight
• > 5 loose stools in past 24 hours
• vomited > twice in past 24 hours
• additional fluids either not offered or not tolerated
• infants who have stopped breastfeeding during the illness
• signs of malnutrition

96
Q

How can you nutritionally manage AD?

A

During rehydration therapy
• continue breastfeeding / give full-strength milk
• do not give solid foods
After dehydration corrected
• reintroduce the child’s usual solid food
• avoid fruit juices and carbonated drinks until the diarrhea has stopped

97
Q

How can we manage AD in children of developing countries?

A

Compared with industrialised countries, the epidemiology and context of acute diarrhoea in children in poorer countries is characterised by:
•more frequent episodes of diarrhoea - up to 6-7 episodes/child/year
•more severe diarrhoea (greater electrolyte loss) and greater frequency of bacterial diarrhoea
•increased host susceptibility – especially malnutrition, vitamin A and zinc deficiencies and HIV infection
•management is usually by non-doctor, first-level staff and occurs with few resources (therefore, simplified guidelines)
Although the principles of management are the same, WHO recommendations for management differ to account for these differences.

98
Q

What is SAM?

A

Severe acute malnutrition:

Muscle wasting and reduced subcutaneous fat
• Angular stomatitis
• Tongue - smooth
• Conjunctival and palmar pallor
• Skin: hypo- and hyper- pigmentation
99
Q

How can you measure SAM?

A

Anthropometry

100
Q

What are 2 specific features of SAM?

A
  • Clinical signs of shock and dehydration unreliable

* Parenteral fluids can cause severe deterioration

101
Q

What are features of SAM but NOT dehydration?

A

SAM: sunken eyes, but moist conjunctivae and hypersalivation (sore mouth)
→ NOT dehydrated
(Note angular stomatitis + perineal ulcertion

102
Q

What happens to the Na/K pump in SAM?

A

The pump fails and results in increased total body [Na]. Also K+ lost in diarrhoea.

103
Q

How is fluid management modified for SAM?

A

Risks
•Total body Na+ high
•Reduced cardiac reserve to cope with fluid bolus
•Impaired endothelia – fluid leaks from circulation

Danger! Parenteral fluids may cause heart failure and death

• Oral fluids preferred to parenteral
• If required, IV fluids administered cautiously
• Use lower Na+ concentration (e.g. 0.45% saline)
• Switch ASAP to reduced osmolarity ORS solution
(ReSoMal: 37.5 mmol/L Na; 40 mmol/L K)

104
Q

Name the order of stomach to anus

A

fundus–> body–> antrum–> pyloric sphincter–>duodenum–> jejunum (leaky, mech: Na-nutrient/Na-H) –> ileum (moderately leaky, mech: Na-Cl, Na-nutrient, Na) –> cecum (moderately tight)–> proximal colon–> distal colon (obviously it’s not completely this)

105
Q

Describe the functional design of the small intestine

A

Anatomy designed to amplify the surface area in order to expand the interface of luminal contents with enterocytes.

•The microvillus membrane has a surface area 600-fold larger than a simple cylinder with the diameter of the small intestine

Duodenum:

  • very leaky
  • absorbs 8L (saliva/bile/pancreatic secretions/gastric secretion/diet)
  • absorbs calcium and iron

Jejunum:

  • loses 7L
  • very leaky
  • darker than ileum

ileum:

  • loses 1.5L and 1L to colon
  • moderately leaky
  • absorbs bile salts and vit b12
106
Q

Describe parts of the duodenum

A

superior, descending (where bile duct and pancreatic ducts drain into), inferior, ascending

107
Q

Where is more than 95% macronutrients rapidly absorbed?

A

Jejunum

108
Q

What does intestinal chyme in the ileum consist of?

A

indigestible carbohydrates (fibre), bile acids, vitamin B12·IF, water, and electrolytes

109
Q

Where are tile acids and B12-IF absorbed?

A

in the ileum by specialized transport systems

110
Q

What happens to nutrients that escaped absorption in the jejunum?

A

They are absorbed in the ileum

111
Q

What types of cells are in the small intestine?

A
  • goblet cells
  • absorptive cells
  • crypt cells
  • paneth cells
  • M cells
  • endocrine, caveolated and cup cells
112
Q

Describe goblet cells

A

Goblet cells contain clear mucin granules. Mucus secretion serves a protective role. Denser in the proximal intestine, and sparser on the villus tip.

113
Q

describe absorptive cells

A

have well-developed microvilli

114
Q

Describe crypt cells

A

smaller, with fewer, less-developed microvilli and narrow apices

115
Q

describe paneth cells

A

found in the base of the crypt. Contain eosinophilic secretory granules. More common in the ileum than in the jejunum. Probably involved in intestinal barrier function

116
Q

Describe M Cells

A

found over Peyer’s patches. Rapidly transport luminal macromolecules and some microorganisms by transcytosis. Probably important for processing and presenting antigen to mucosal immune system.

117
Q

Describe epithelial cell turnover

A

Rapid, continuous, and coordinated process.

Anchored stem cells give rise to proliferative cells of the crypt. As the cells migrate from the crypt to the villus, they stop dividing and become more differentiated.

Exfoliation occurs as mature cells are shed into the intestinal lumen.

Apoptosis, or programmed cell death, is integral to maintaining the cellular balance in the crypt:villus unit. Apoptosis may also serve to remove genetically abnormal cells early in the course of differentiation.

In the small intestine, apoptosis has been demonstrated in the area adjacent to the stem cell. By contrast, in the colon, apoptosis occurs more distantly from the stem cells, at the surface, some abnormal cells escape apoptotic control.

118
Q

Describe the barrier function

A

•Barriers separating hostile, variable environment of the intestinal lumen from carefully controlled subepithelial space.
•Mucus - viscous hydrated gel, binds bacteria.
•Secreted immunoglobulin A - binds bacterial antigens.
•Bicarbonate - neutralizes luminal acid. Together make the unstirred layer -
functional diffusion barrier.
•Apical membrane of the epithelial cells is the greatest barrier. Lipid bilayer of the plasma membrane is a barrier to hydrophilic solutes, but allows diffusion of hydrophobic molecules.
•Membrane proteins are necessary for entry of hydrophilic solutes into the cell.
•Paracellular pathway provides a low electrical resistance shunt around cells and blocks the movement of macromolecules around cells

119
Q

Describe the large intestine

A

Role in carbohydrate digestion and absorption.
Indigestible carbohydrates partially broken down by enzymes in colonic bacteria to short-chain fatty acids (acetate, propionate, and butyrate), absorbed by the colonic mucosa.
Short-chain fatty acids are important substrates for mucosal cells in the colon.
Colon may serve in carbohydrate salvage in patients with carbohydrate malabsorption (eg, short- bowel syndrome with retained colon). About 80 g of nondigested or nonabsorbed carbohydrate can be converted to short-chain fatty acids by bacteria and absorbed by the colon

120
Q

Describe features of the human rectal columnar epithelial cell

A

Many fewer microvilli than in small intestine
Prominent glycoprotein overlies microvilli
stops bacteria attaching e.g. e.coli

121
Q

describe the movement of Na K and Cl in the large intestine

A

Chloride is transported into the cell via the concerted actions of the Na+, K+, Cl- exchanger (A) and the Na+, K+- ATPase.
Active chloride secretion is stimulated by cyclic AMP (cAMP) or increases in intracellular calcium, which then serve to normalize intracellular Cl-

122
Q

What happens to the osmotic gap in secretory diarrhoea?

A

In secretory diarrhoea, electrolyte absorption lower, so that sodium, potassium, and their counterions account for most of the osmoles in stool water.

123
Q

What happens to the osmotic gap in osmotic diarrhoea?

A

In osmotic diarrhoea, electrolyte absorption is normal - measured ions account for only a fraction of the osmoles in stool water

124
Q

What is the sum of concentrations of ions and small molecules?

A

Sum of the concentrations of ions and small molecules must equal plasma osmolality, usually 290 mOsm/kg

125
Q

Describe intestinal flora

A

The colonic lumen has a luxuriant flora - assists in fermentation of the faecal material, suppresses overgrowth of pathogens, affects hydration status and weight of the individual, alters stool pH, and degrades intestinal mucins.
In the colon there is a gradient in numbers of organisms ranging from 106/mL in the caecum to 1012/mL in the rectum.

126
Q

GO OVER DRUGS!

A

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Medicine Year 1 (13 decks)

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