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Applied Clinical Physiology > Gastro & Hepatic Systems > Flashcards

Gastro & Hepatic Systems Flashcards

1
Q

What is function of mouth?

A
  • To prepare food for swallowing

- Mixes food with amylase in the saliva to break down starch into sugars.

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2
Q

What are salivary glands called?

A

Submandibular
Parotid
Sublingual

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3
Q

How much saliva is produced daily in adults?

A

500ml

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4
Q

What is oesophagus wall made of?

A

Mucosa,
submucosa
muscularis mucosa

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5
Q

What is GOJ?

A

Gastro-oesphageal junction

physiological barrier which reduces reflux of gastric contents.

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6
Q

What is at base of oesophagus?

A

Intrinsic lower oesophageal sphincter

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7
Q

What causes food to move down oesophagus?

A

Peristalsis

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8
Q

What is peristalsis regulated by?

A

Smooth muscles controlled by:

Enteric Nervous System
Peptide Hormones
Inherent timing of monocytes

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9
Q

What does the stomach secrete to aid digestion?

A

Hydrochloric acid
Lipase
Pepsin

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10
Q

What regulates stomach fluid secretions?

A

Central and enteric nervous system

Neuroendocrine cell networks

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11
Q

How does mechanics of stomach work?

A

Very coordinated antropyloroduodenal contractions to titrate solid food

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12
Q

What is titration of food?

A

Breaking it down

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13
Q

What is purpose of gastric antrum?

A

Sieves liquid chyme through remaining solid matter in stomach and delivers slow rate of gastric contents into the duodenum.

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14
Q

What is function of small intestine?

A

To absorb water, electrolytes and nutrients

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15
Q

What is approximate length of duodenum?

A

30cm

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16
Q

What is length of jejunum

A

2.5metres

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17
Q

What is length of ileum?

A

4 metres

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18
Q

Where does common bile duct enter small intestine?

A

Duodenum - about half way down.

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19
Q

What is chyme?

A

Acidy pulpy fluid that passes from stomach to small intestine

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20
Q

What happens as food passes from stomach to small intestine?

A

Chyme passes into small intestine which stimulates release of hormones secretin & CCK (cholecystokinin).

The stimulates release of bicarbonate and pancreatic enzymes and causes gallbladder to release bile.

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21
Q

Where is CCK produced?

A

Cholecystokinin - produced in I cells in lining of duodenum

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22
Q

What foods are broken down into different things in the small intestine?

A

Proteins/peptides - amino acids
Lips - fatty acids and glycerol
Triglycerides - free fatty acids and monoglycerides
Carbs - oligosaccharides

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23
Q

What is water uptake driven by in s.intestine?

A

Absorption of Na and K

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24
Q

How much fluid passes through small bowel each day?

A

9litres. Mixture of water and secretions

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25
Q

What is function of large bowel?

A
  1. Propulsion of colonic contents towards rectum for expulsion
  2. Absorption of water and electrolytes from remaining chyme
  3. Absorption of short-chain fatty acids produced from microbiota
  4. Defacation
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26
Q

What is function of short chain fatty acids the large bowel?

A

To keep microbiota of gut wall healthy

To help with remaining absorption of sodium

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27
Q

How long is typical transit of chyme in adult?

A

12-30 hours

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28
Q

What does wall of colon do?

A

Has role in production of vit k, vit b7 and B3

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29
Q

What does the stomach absorb?

A

Alcohol

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30
Q

What does duodenum absorb?

A

Cl, SO4, Iron, calcium, magnesium

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31
Q

What does Jejunum/ileum absorb?

A 
glucose
vit c
thiamin
ribolfavin
folic acid
prtein
fat
cholesterol
Vit A & D
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32
Q

What does colon absorb?

A

Na
K
Vit K
H20

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33
Q

What is peristalsis?

A

Contraction and relaxation above and below a bolus of food to push food through gut

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34
Q

How does peristalsis work?

A

Pre bolus: circular contracts
longitudinal muscle relaxes,

Post bolus: circular muscle relaxes
longitudinal muscle contracts

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35
Q

How many lobes are in the liver?

A

2 main lobes with 4 lobes within that, and 8 segments altogether

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36
Q

which ligament divides the liver?

A

falciform ligament

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37
Q

How much weight does the liver contribute in adults and infants?

A

2.5% in adults

5% in infants

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38
Q

What is blood supply of liver?

A

25% hepatic artery

75% portal vein

39
Q

Describe a liver lobule

A

Roughly hexagonal
Central vein with plates of hepatocytes radiating around
At the 6 corners there are branches of hepatic artery, hepatic portal vein and biles duct (the portal triad)

The hepatocytes are in close contact with blood filled sinusoids and are next to canaliculi that bile is secreted into.

Blood flows out the sinusoids into the central vein and is transported out of liver by hepatic vein.

40
Q

What are sinusoids in the liver lined with?

A
  1. endothelial cells
  2. phagocytic Kupfer cells
  3. hepatic stellate cells
41
Q

What is function of kupfer cells in liver?

A

eradicate bacteria from the gut

42
Q

What is function of hepatic stellate cells in the liver?

A

store fat and vitamin A

43
Q

How many functions does the liver perform?

A

Over 400

44
Q

Name the main functions of the liver

A
  1. Secretory
    Synthesis and excretion of bile
  2. Storage:
    of glycogen, iron, vitamins A, D, E, K and B12, blood
  3. Metabolism
    - of fat protein and carbs
    - synthesis of blood-clotting factors and inhibitors
    - synthesis of albumin
    - detoxification of hormones, drugs and other substances like ammonia
45
Q

What is albumin?

A

Main plasma protein - maintains oncotic pressure and transportation of substances in blood

46
Q

What is bile made of?

A

Excretory pathway for bilirubin - breakdown product of haemoglobin.

Also contains bile salts, cholesterol, electrolytes, copper, water, lecithin, mucus

47
Q

Describe bilrubin metabolism

A

Erthrocyte
120 days
macrophages engulf
releases Hb
broken into: globin - the protein, further broken down into amino acids and reused by body
and haem - broken into Fe2+ which is reused
and unconugated bilirubin (LIPID soluble)
carried by albumin to the liver
CONJUGATION by combining with gluceronic acid
is now CONJUGATED BILIRUBIN (water soluble)
excreted in bile to s.intestine via common bile duct
in terminal ileum/early colon
bacteria remove glucoronic acid
makes urobilinogen
90% of it oxyidised by bacteria
makes stercobilinogen - comes out in faeces. has brown colour

10% is absorbed back to liver by portal vein - 5% desecrated, 5% to kidney, converted to yellow urogilngen = yellow urine colour.

48
Q

What is role of bile acids?

A

emulsify fats

49
Q

What is an imperforate anus?

A

Absence of normal anal opening - can range from full rectal atresia to recto-bladder neck fistula.

Congenital abnormality

50
Q

What is occurrence of imperforate anus?

A

1 in 5000 births. cause unknown

50% of children born with T21 will have anal defect at birth.

51
Q

What happens if imperforate anus noted on newborn physical exam?

A

Ultrasound to rule out cardiac or urological defects

Observe for 18-24 hours to see if pas meconium

May need colostomy surgery

52
Q

What is duodenal atresia?

A

The duodenum is closed off. Nothing can pass as it is disconnected from rest of intestine

53
Q

When in foetal growth does duodenal atresia occur?

A

About 6 weeks embryo stomach starts to rotate.

Then atresia happens between 6-10 weeks for no known reason

54
Q

What is oeosphageal atresia?

A

Short section at top of oesophagus not formed properly and so is not connected to stomach.

55
Q

When in embryo growth does oesophageal atresia occur?

A

Within first 6 weeks

56
Q

How do they repair oesophageal atresia?

A

Depends on the distance between the ends of the oesophagus. There are 5 broad types of OA including TOF-OA with oesophagus connected to airway.

57
Q

What is Hirschsprungs?

A

The failure of parasympathetic ganglion cells to form in all or lower part of large intestine.

This causes lack of nerve innervation and therefore the absence or alteration of peristalsis.

Means waste cannot pass through colon and normal colon swells with blocked still

58
Q

What is incidence of Hirschsprungs and cause?

A

Has genetic component

1 in 5000 live births

59
Q

What is gastroschisis?

A

Abdomen wall does not form completely so intestines develop outside body and are open to air.

60
Q

What is difference between omphalocele and gastroschisis?

A

Omphalocele = SEAL = intestines outside but in protective sac

Gastroschisis = completely out - no sac

61
Q

When is gastroschisis identified?

A

12 weeks scan - see bowel loops in amniotic fluid

62
Q

Are there any occurrence links for gastroschisis?

A

Interesting higher occurrence link between premature births and young mothers.

63
Q

What is intussusception?

A

Telescoping of the bowel wall in itself. Can be fatal as blood supply can block off and cause necrosis.

64
Q

Where is most common site for intussusception to occur?

A

Ileocaecal valve

65
Q

What is common age and presenting factors for intussusception?

A

6 months - 3 years
Boys > girls
Children with CF

66
Q

What is treatment of intussusception?

A

Hydrostatic reduction. If fails then has to have theatre.

67
Q

What is volvulus?

A

When part of the intestine becomes twisted at least 180 degrees and cuts off blood supply resulting in gut ischaemia

68
Q

What is presentation of volvulus?

A

Bilious vomiting
Abdominal pain
Distended Abdo
Absent Bowel Sounds

69
Q

What is treatment of volvulus?

A

Surgery:

Untwisting in viable
Resection and end to end anastomosis if bowel nectrotic

70
Q

What is pyloric stenosis?

A

Increased mass size of circular muscle of pylorus. Narrows the pyloric canal and prevents stomach from emptying properly..

71
Q

What is presentation of pyloric stenosis?

A

Projectile vomiting
Poor weight
Palpitation reveals olive shaped bulge below right costal margin and distended upper abdo
Derranged blood electrolytes

72
Q

What is treatment of pyloric stenosis?

A

NBM
NG on free drainage
IV’s to correct electrolytes
Surgery - pyloromyotomy

73
Q

What is inflammatory bowel disease?

A

Importantly NOT irritable bowel syndrome

IBD includes Crohns, Ulcerative colitis and indeterminiate colitis.

74
Q

What is Crohn’s disease?

A

Inflammation of mucosa in any part of digestive tract from mouth to anus.

Can affect all layers of the bowel, and result in granulomas

75
Q

What is ulcerative colitis?

A

inflammation of mucosa affecting only the colon, and only the inner lining of the bowel.

76
Q

What is indeterminate colitis?

A

Histologically shows characteristics of both crowns and UC so cannot be categorised.

77
Q

What is jaundice?

A

Raised level of bilirubin in the blood

78
Q

What is bilirubin?

A

By product of break down of haemoglobin.

79
Q

What is life span of RBC?

A

Children & adults = 120 days
Neonate 60-80 days
Preterms maybe only 20-30 days

80
Q

How are RBCs removed from system?

A

The reticuloendothelial system removes them through phagocytosis

81
Q

What is reticuloendothelial system?

A

Heterogenous population of phagocytic cells that are fixed in tissues that play important role in clearance of particles and substances

82
Q

What is presentation of Crohn’s diease?

A 
Abdo pain that pain relief won't help
Nausea/vomiting
Loss of appetite
Diarrhoea
Constipation
Nocturnal bowel movemets
Weight loss (due to small bowel involvement)
PR bleeding/mucus
Peri-anal disease like fissures, fistulas, skin tags or abscesses
Lethargy
Mouth ulcers
Arthrtitis (joint pains) 
Uveitis (inflamed eyes) 
Erythema nodosom (fatty lumps under skin) 
Pyoderma gangrenous (painful pustules)
83
Q

What is presentation of ulcerative colitis?

A 
Abdo pain
PR bleeding (bright red) 
Diarrhoea
Painful bowel motion
Poor appetite
Lethargy
84
Q

How many babies have jaundice?

A

30-50% of term neonates have jaundice after birth. More in pre-term neonates

85
Q

Why do babies have jaundice?

A

Normal factors such as liver take up to 2 weeks to become efficient in conjugating bilirubin

86
Q

What is baby jaundice called?

A

Physiological jaundice “normal”.

87
Q

What are symptoms of prolonged jaundice?

A 
Pale chalky stool
Dark urine that stains nappy
Measure conjugated bilirubin
Need full blood count and urine culture
Need routine metabolic screening
88
Q

What are most common causes of unconjugated hyperbilirubinaemia?

A

Physiological
Breast milk jaundice
haemolysis
congenital defects of conjugation or Gilbert syndrome

89
Q

What is biliary atresia?

A

End result of destructive idiopathic inflammatory process.

Affects both intra and extra hepatic bile ducts
Leads to fibrosis and obliteration of biliary tract
Eventually leads to biliary cirrhosis

Most common surgically correctable liver disorder in infancy. Most common cause for liver transplant in children.

90
Q

What happens if biliary atresia is left untreated?

A

symptoms of chronic liver disease

Death by 2 years of age

91
Q

What is incidence of biliary atresia?

A

In Northern Europe - 1 in 20,000

In Taiwan 1 in 5000

92
Q

What is cause of biliary atresia?

A

Definitive unknown but thought to be 4 main types:

Syndromic
Cystic
CMV associated
Isolated

93
Q

What is presentation of biliary atresia?

A 
Conjugated jaundice
Pale chalky stools
Dark urine
Hepatomegaly/splenomegaly
Signs of liver failure: 
Hypoglycaemia
Ascites
Acid-Base imbalance
Coagulopathy

Applied Clinical Physiology (14 decks)

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