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GEM > Module 5 Alimentary System > Flashcards

Module 5 Alimentary System Flashcards

1
Q

The peritoneum coverings

A

The peritoneum is a double-layered membranous sheet

Parietal peritoneum: lines abdominal wall

Visceral peritoneum: covers suspended organs

Serous fluid -> friction-free movement in organs

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2
Q

Intraperitoneal organs:

A

Stomach, Appendix, Liver & gallbladder, Transverse colon, Duodenum (1st part), Small intestines (jejunum & ileum), Pancreas (only tail), Rectum (upper 1/3), Spleen, Sigmoid colon

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3
Q

Extraperitoneal organs:

A

Retro-peritoneal (i.e. kidneys & ureters, aorta)

Sub- or infra-peritoneal (i.e. urinary bladder)

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4
Q

Peritoneal cavity divided into:

A

Greater sac
Lesser sac (omental bursa)

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5
Q

Peritoneal formations:

A

Mesenteries

Omenta (greater omentum & lesser omentum)

Peritoneal ligaments

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6
Q

The 4 quadrants pattern

A

Median plane:
Xiphoid -> pubic symphysis

Transumbilical plane: Horizontal plane through umbilicus

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7
Q

4 quadrants contents

A

Right upper quadrant:
(Right lobe) liver
Gallbladder
Stomach (pylorus)
Duodenum (parts 1-3)
Pancreas (head)
Right kidney & adrenal gland
Right colic flexure
Transverse colon (right ½)
Ascending colon (superior part)

Left upper quadrant:
(Left lobe) liver
Spleen
Stomach
Jejunum + prox ileum
Pancreas (body & tail)
Left kidney & adrenal gland
Left colic flexure
Transverse colon (left ½)
Descending colon (superior part)

Right lower quadrant:
Caecum, (most of) ileum & appendix
Ascending colon (inferior part)
Right ureter
Right ovary & uterine tube/ right spermatic cord
Uterus (if enlarged)
Urinary bladder (if full)

Left lower quadrant:
Sigmoid colon
Descending colon (inferior part)
Left ureter
Left ovary & uterine tube/ left spermatic cord
Uterus (if enlarged)
Urinary bladder (if full)

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8
Q

The 9 regions pattern

A

Subcostal plane

Midclavicular planes

Intertubercular plane: Horizontal line between iliac tubercles

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9
Q

The transpyloric plane

A

The transpyloric plane is usually found at vertebral level L1

Important structures lie at this level:
Pylorus of the stomach
Origin of superior mesenteric artery (SMA)
Splenic vein joins superior mesenteric vein  portal vein
Hilum of left kidney
Origin of renal arteries
Fundus of gallbladder

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10
Q

The supracristal plane

A

The supracristal plane is usually found at vertebral level L4/5

Significance:

Landmark for lumbar puncture

Level of bifurcation of aorta

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11
Q

The anterolateral abdominal wall structure layers

A

Superficial fascia:

Fatty layer (Camper’s fascia)

Fibrous/membranous layer (Scarpa’s fascia)

Extends into perineum, labia majora/scrotum & penis (link to module 7)

Muscles:

Anteriorly: Rectus abdominis & pyramidalis

Laterally:

External oblique
Internal oblique
Transversus abdominis

Transversalis fascia

Extraperitoneal fascia -> parietal peritoneum

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12
Q

Cross-sectional anatomy of the abdominal wall

A

Aponeuroses from lateral muscles blend to form rectus sheath

External oblique + Internal oblique  anterior rectus sheath

Internal oblique + Transversus abdominis  posterior rectus sheath

Connective tissues of both sides fuse and form the linea alba medially

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13
Q

The posterior abdominal wall

A

The posterior abdominal wall is continuous with:

Posterior thoracic wall (superiorly)

Posterior wall of the pelvis (inferiorly)

Anterolateral abdominal wall (laterally)

It provides support for retroperitoneal structures

Muscles:

Respiratory diaphragm

Iliacus

Quadratus lumborum

Psoas major

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14
Q

Abdominal wall muscles innervation

A

External Oblique (anterior rami T7-T12)
Internal Oblique (anterior rami T7-T12 and ilioinguinal and iliohypogastric nerves L1)
Transversus Abdominis (anterior rami T7-T12 and ilioinguinal and iliohypogastric nerves L1)

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15
Q

Nerve supply to abdominal wall & peritoneum

A

Skin and deep muscles of the back are supplied by posterior rami of spinal nerves

Muscles of the anterolateral abdominal wall are supplied by anterior rami of spinal nerves T7-L1

Anterior rami T7-T11  intercostal nerves
Anterior ramus T12  subcostal nerve

The skin has a dermatomal innervation from thoracic spinal nerves (and L1)

Parietal peritoneum: somatic afferent (sensory) fibres from branches of associated spinal nerves  well-localised pain

Visceral peritoneum: visceral afferent fibres  referred and poorly localised pain

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16
Q

lower Abdominal wall innervation

A

Some of the nerves from the lumbar plexus provide sensory and motor supply to the lower abdominal wall and groin areas

Subcostal (T12)
Iliohypogastric (L1)
Ilioinguinal (L1)
Genitofemoral (L1-2)

Sensation to the lower abdominal wall and groin
Motor supply to skeletal muscles of the abdominal wall

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17
Q

Blood supply to the abdominal wall

A

Upper abdominal wall:

Aorta  subclavian artery internal thoracic artery musculophrenic artery, superior epigastric, & 10-11th intercostal arteries + subcostal artery (laterally)

Lower abdominal wall:

Aorta  common iliac artery  external iliac artery  femoral artery  superficial epigastric artery & superficial circumflex iliac artery

Aorta  common iliac artery  external iliac artery  inferior epigastric artery & deep circumflex iliac artery

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18
Q

Venous drainage of the abdominal wall

A

Superficial veins:

Subcutaneous plexus

Tributaries of superior and inferior epigastric veins

Tributaries of intercostal, subcostal, lumbar & deep circumflex iliac veins

(inguinal region) Superficial epigastric & superficial circumflex iliac  femoral vein

Deep veins:

Upper abdomen:
Superior epigastric vein
Musculophrenic vein

Lower abdomen:
Inferior epigastric vein
Deep circumflex iliac vein
Intercostal & subcostal veins
Lumbar veins

Ultimately drain into axillary or femoral vein  systemic circulation

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19
Q

Indirect Inguinal Hernia

A

An indirect hernia is:
More common than direct herniae
More common in males than females
Is ‘congenital’ because:
Some part or all of the processus vaginalis remains patent
The peritoneal sac protrudes through the deep inguinal ring
In larger defects the sac may exit the superficial inguinal ring and end up in the scrotum (males) or labia majora (females)

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20
Q

Direct Inguinal Hernia

A

A direct hernia is ‘acquired’:

It develops when abdominal muscles become weak
The peritoneal sac protrudes through a weakened posterior wall (Hesselbach’s triangle) of the inguinal canal (where the conjoint tendon lies)
Less common than indirect herniae
Is more common in ‘mature’ males!

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21
Q

Oral cavity structures

A

Hard palate; (maxilla + palatine bones)
Soft palate
Uvula
Palatoglossal arch (palatoglossus)
Palatine tonsil
Palatopharyngeal arch (palatopharyngeus)

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22
Q

Primary dentition

A

Each side (left or right) of mandible and maxilla has:
2 incisors
1 canine
2 molars x4 = 20 primary (“baby”) teeth by age 3 years

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23
Q

Secondary dentition

A

Each side (left or right) of mandible and maxilla has:
2 incisors
1 canine (cuspid)
2 premolars
3 molars

x4 = 32 teeth by age 21

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24
Q

Muscles of mastication (chewing)

A

Temporalis
Masseter
Medial and lateral pterygoids

Mainly elevate mandible but lateral pterygoid helps to depress mandible
Temporomandibular joint (TMJ) disorders e.g. bruxism

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25
Q

Tongue and lingual papillae

A

Tongue comprised of extrinsic and intrinsic muscles

Filiform lingual papillae - no taste bud (CN V trigeminal nerve)

Fungiform (CN VII facial nerve chorda tympani)

Vallate (CN IX glossopharyngeal nerve) – often called circumvallate

Foliate (CN IX glossopharyngeal nerve) – not many on human tongue

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26
Q

Salivary glands

A

Three pairs of major salivary glands in humans – parotid, submandibular and sublingual
Plus minor salivary glands in mucosa of lips, tongue, palate and buccal (cheek) surfaces

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27
Q

Parotid gland and duct

A

Overlies mandibular ramus and secretes serous saliva – 25% of salivary volume.

Surrounded by parotid fascia

Parasympathetic innervation from CN IX glossopharyngeal nerve
Increased saliva production

NO facial nerve innervation – CN VII fibres only run through parotid to reach muscles of facial expression

Parotid duct pierces cheek wall and opens into oral vestibule opposite second upper molar

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28
Q

Submandibular gland

A

Located deep to mandible in floor of mouth

Saliva produced is mixed serous and mucous in composition – ~70% of salivary volume

Saliva drains into submandibular duct

CN VII facial nerve parasympathetic preganglionic nerve fibres travel via chorda tympani

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29
Q

Sublingual gland

A

Smallest of the major salivary glands – located deep to tongue and supplies ~5% of saliva

Secretion is mostly mucous – contributes to dental pellicle
Also main source of lipase

Similar innervation to submandibular gland (CNVII)

Submandibular and sublingual glands both drain into submandibular duct – opens at sublingual caruncle, just lateral to frenulum of tongue

Xerostomia: dry mouth due to insufficient salivary production

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30
Q

Pharynx STRUCTURES

A

Pharyngeal tonsil (lymphoid tissue)
Other tonsillar tissue present e.g. palatine tonsils, lingual tonsils
Waldeyer’s ring

Nasopharynx = nasal choanae  soft palate
Oropharynx = soft palate  epiglottis
Laryngopharynx = epiglottis  oesophagus

Epiglottis separates pharynx from larynx e.g. during swallowing

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31
Q

Swallowing (deglutition)

A

Oral phase: food pushed by tongue to back of mouth after chewing (mastication)
Voluntary tongue movements – under conscious control

Pharyngeal phase: reflex response by trigeminal, glossopharyngeal and vagus nerves induces swallowing
Soft palate elevates to prevent food from entering nasopharynx and nasal cavities
Epiglottis prevents food from entering larynx and trachea
Involuntary pharyngeal peristalsis

Oesophageal phase: upper oesophageal sphincter (cricopharyngeus muscle) relaxes to allow food to enter oesophagus
Peristaltic wave pushes bolus of food past the sphincter and down towards the stomach
Lower oesophageal sphincter relaxes to allow bolus to enter stomach

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32
Q

How can the swallowing mechanism be visualised?

A

Barium swallow used as part of an upper GI series to visualise stomach and duodenum

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33
Q

Oesophagus

A

Muscular tube around 25cm long
Upper 1/3 = skeletal muscle, lower 2/3 = smooth muscle

Three regions: cervical, thoracic and abdominal

Starts at C6 vertebral level – inferior border of cricoid cartilage

Thoracic oesophagus descends through superior and posterior mediastinum to oesophageal hiatus of diaphragm (T10 vertebral level)

Abdominal oesophagus is ~1.5cm long and ends at oesophagogastric junction (T11 vertebral level)

Anterior and posterior trunks of vagus nerve run along external surface

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34
Q

Oesophagus supply

A

Arterial supply: oesophageal branches of the thoracic aorta, bronchial arteries, left gastric artery (from the coeliac trunk) and the left inferior phrenic artery (from the abdominal aorta)

Venous drainage: to the azygos vein, hemiazygos vein, and the left gastric vein in the abdomen

Innervation: oesophageal plexus (parasympathetics from vagus nerve, sympathetics e.g. from T6 – T9 spinal nerves for distal oesophagus)

Lymphatic drainage: mainly to the posterior mediastinal and coeliac group of pre-aortic lymph nodes

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35
Q

Anatomical relations of oesophagus

A

Posteriorly: thoracic duct, thoracic aorta (near the diaphragm – to the left of oesophagus more proximally)

Anteriorly: Aortic arch, trachea and tracheal bifurcation. Right pulmonary artery and the left main bronchus (below level of tracheal bifurcation). Left atrium and pericardium.

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36
Q

Oesophagus may be compressed or narrowed by:

A

The junction of the oesophagus with the pharynx
The arch of the aorta in superior mediastinum
The left main bronchus in the posterior mediastinum
The oesophageal hiatus of the diaphragm

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37
Q

Stomach structures

A

Production of gastric acid, enzymes e.g. pepsin
1000 – 1500ml max capacity in adults

Cardia – next to upper oesophageal sphincter
Fundus
Body
Antrum (pyloric antrum)
Pylorus

Greater and lesser curvatures

Rugae – internal gastric folds (increased surface area)

Intraperitoneal organ

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38
Q

Lower oesophageal (cardiac) sphincter

A

Most inferior part of oesophagus with slight thickening of circular smooth muscle to help prevent gastric reflux.

Also reinforced by other structures:
Cardial/cardiac notch: angle created when oesophagus enters stomach. Narrows as stomach fills
Oesophageal hiatus: oesophagus surrounded by muscle fibres of diaphragm and fat pads in-between
Phrenico-oesophageal ligament: connects oesophagus to diaphragm
Combination of anatomical and ‘physiological’ factors to help close the sphincter

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39
Q

Pyloric sphincter

A

Anatomical sphincter – distinct enlargement of circular smooth muscle in the muscularis externa.
Sphincter is palpably thicker than stomach and duodenum
Controls diameter of pyloric orifice and passage of chyme (digested food + stomach acid) into the duodenum

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40
Q

Hiatus hernias

A

Herniation of the abdominal oesophagus, cardia and/or other parts of the stomach through oesophageal hiatus
Common – genetic, increased prevalence with age and body mass index
Gastrooesophageal reflux disease (GORD) is main symptom – dyspepsia, heartburn

Three types: sliding, paraoesophageal or mixed

Sliding (type I, 90% of cases): abdominal oesophagus and cardia displaced into thoracic cavity

Paraoesophageal (type II): phrenico-oesophageal ligament intact, proximal stomach displaced. Other organs may herniate through diaphragm e.g. spleen

Mixed (type III): combination

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41
Q

Blood supply of stomach

A

Branches from the coeliac trunk (abdominal aorta)
Left and right gastric, left and right gastro-omental, short gastric arteries

Venous:
To the hepatic portal vein via tributaries draining into the splenic and superior mesenteric veins

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42
Q

Lymphatic drainage of stomach

A

Most lymph from stomach will ultimately drain to the coeliac group of pre-aortic lymph nodes (via other groups of lymph nodes e.g. left gastric nodes)
Coeliac nodes drain directly into cisterna chyli + thoracic duct

Virchow’s node: enlarged left supraclavicular node, potential sign of gastric cancer

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43
Q

Types of epithelium and location in GI

A

Protective:
Oral cavity and pharynx, oesophagus, anal canal
Stratified squamous non-keratinising

Secretory:
Stomach
Simple/branched tubular glands for acid secretion.

Absorptive:
Small intestine
Projections (villi) and glands (crypts), lined by columnar cells (enterocytes) specialised for absorption (microvilli).
Goblet cells produce mucus for lubrication and protection

Absorptive/protective:
Large intestine
Lots of goblet cells for lubrication of faeces.
Enterocytes absorb water.

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44
Q

Mucosal layer

A
  1. Epithelium (various types)
    Site of absorption and/or secretion
    Exocrine glands
  2. Lamina propria (LP)
    Blood & lymph
  3. Muscularis mucosae (MM)
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45
Q

Submucosal & Muscularis layers

A

Submucosa (SM)
Connective tissue, blood vessels, lymphatics & nerves

Submucosal (Meissner’s) plexus – supplies glands and muscularis mucosae

Myenteric (Auerbach’s) plexus - autonomic nerves between muscle layers modulates peristalsis

Muscularis externa/ propria (MP)
Inner circular & outer longitudinal muscle coats help propel food

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46
Q

Gut associated lymphoid tissue E.G. A feature of the ileum of the small intestine:

A

A feature of the ileum of the small intestine: ‘Peyer’s patches’ overlain by antigen sampling cuboidal cells

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47
Q

Oesophagus histology

A

Normally closed (highly folded mucosa), stretches on swallowing food bolus
Lined by stratified squamous epithelium – resists friction
Submucosa: blood vessels, lymphatics, nerves, lymphoid tissue and mucus glands
Muscularis externa layer: skeletal in first third (voluntary), smooth in last third (involuntary), mixed in middle third
Outer layer is mostly adventitia - fixed to adjacent structures by connective tissue.
Last part beyond the diaphragm covered with serosa

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48
Q

Gastro-oesophageal junction

A

Final 1-1.5cm of oesophagus (below the diaphragm)
Lining changes from squamous to columnar epithelium (glandular)

Barratt’s oesophagus - change of epithelium from stratified squamous to gastric due to repeated damage from gastric reflux (exposure to acid and digestive enzymes)

Scarring as a result of healed ulcers can narrow the lumen (oesophageal stricture) – impeding swallowing

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49
Q

Gastric pit

A

Mucous cells (surface & neck): secrete mucus & bicarbonate
Parietal cells: secrete gastric acid (HCl) & intrinsic factor (required for vit B12 absorption in ileum)
Stem cells – present in small numbers, increase with epithelium damage
Chief (peptic) cells: near base, secrete pepsinogen & gastric lipase
Endocrine cells: hormone-producing e.g. gastrin (G cells), somatostatin, cholecystokinin (CCK)

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50
Q

Small intestine histology features

A

Mucosa and submucosa are thrown into folds: plicae circularis
Mucosa is folded to form finger like projections: villi
Villi are lined with several cell types-the most numerous is the enterocyte: apical surface has a brush border of microvilli.
Crypts are tubular glands at the base of villi

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51
Q

Small intestine wall

A

Villi
Fingerlike projections extending into lumen of small intestine
Increase surface area x600
Continues into crypts of Lieberkuhn: short glands between villi extending to muscularis mucosa.

Brush border
Collective name for microvilli
Enzymes – maltase, sucrase, lactase, Aminopeptidase

Lacteal
Single blind ended lymphatic vessel at centre of each intestinal villus
Involved in fat absorption

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52
Q

Sections of small intestine

A

Duodenum
Receives digestive secretions from the gall bladder & pancreas through the ‘hepatopancreatic ampulla’
Brunner’s glands neutralise gastric acid i.e. balance the stomach acid and allow the pH to be at the correct level for pancreatic secretions to work.
Absorptive site for iron

Jejunum
Main absorptive site (amino acids, monosaccharides, fatty acids)
Well developed plicae and prominent finger-like villi

Ileum
Peyer’s patches
Villi and crypts smaller and more poorly developed
By the terminal ileum, no plicae circulares

Absorbs bile salts
Vitamin B12 (intrinsic factor)
Water
Electrolytes

Majority of chyme is digested & absorbed in 1st ¼ of small intestine – duodenum & jejunum – implications for resection surgery

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53
Q

Segmentation

A

Rhythmical contraction & relaxation
Produces continuous division & subdivision of intestinal contents
Major role = MIXING

Rhythm varies along length of intestine
Duodenum – 12 contractions/min
Ileum – 9 contractions/min

Will push contents in both directions, unlike peristalsis which forces in only one direction

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54
Q

Large Intestine features

A

Specialised for water & salt absorption
Arranged as tubular glands i.e. Has crypts but no villi
Large surface area not necessary
Tall columnar absorptive cells

Large numbers of mucous cells - more friction = needs more mucus
Circular & teniae coli muscle

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55
Q

Large intestine motility

A

Mixing
Haustration/Segmentation
Contraction of the circular muscle in each haustra to mix contents and increase mucosal contact

Propulsion
Mass peristalsis
Intense contraction 1-3 times a day
Contents propelled 20cm+ towards anus

56
Q

Anal canal

A

Columnar epithelium of rectum gives way to stratified squamous epithelium (squamocolumnar junction). This becomes keratinised when it meets the skin
Anal glands lubricate the passage of faeces
Venous supply is the haemorrhoidal plexi which can become distended: haemorrhoids
Muscular canal controlled by 2 sphincters (internal & external)

57
Q

Gastric Mucosal Protection

A

Gastric acid
Mucus and HCO3 – ‘pre-epithelial defence’
Epithelial layer
Prostaglandins

58
Q

Gastric Juice makeup

A

HCl
Mucus
Enzymes
Pepsinogen
Early hydrolysis of proteins
Liberates B12 from proteins
At least 8 types
Lipase
Early hydrolysis of triglycerides
Intrinsic factor

59
Q

How does the stomach reduce acidity on its surface

A

Secretes a large amount of Bicarbonate

60
Q

Helicobacter pylori characteristics and mechanism of degrading mucosal barrier

A

Gram negative
Microaerophilic
Flagellated and highly motile
High affinity urease
20% adhere to gastric epithelium
Vacuolating cytotoxin
Phospholipase A2
Mucinases

61
Q

H pylori associated diseases

A

Duodenal ulcer
Gastric ulcer
Gastric adenocarcinoma
MALT lymphoma
Chronic gastritis
Possible associations
Non-ulcer dyspepsia
Iron deficiency anaemia

62
Q

Aspirin and NSAID gastric effects

A

Membrane destabilisation
Reduced HCO3
Reduced mucus
Tight junction loosening

63
Q

What is dyspepsia

A

‘pain or discomfort related to eating or drinking that can be attributed to the upper gastro-intestinal tract’

64
Q

Causes of dyspepsia

A

Gastro-oesophageal reflux (GORD)
Gastric ulceration (GU)
NSAID, H pylori
Duodenal ulceration (DU)
H pylori, NSAID
Biliary colic
Chronic pancreatitis
Upper GI cancer
Functional (non-ulcer dyspepsia)
Rare
ischaemia

65
Q

Drugs that cause dyspepsia

A

NSAIDS
Bisphosphonates
Steroids

Metformin

Calcium antagonists
Theophyllines
Nitrates

66
Q

Treatment of GORD

A

Lifestyle advice
Acid Inhibition
Antacids
H2 receptor antagonists
Cimetidine, Ranitidine, Nizatidine
Proton Pump Inhibitors (PPI)
Omeprazole, Lansoprazole, Pantoprazole, Rabeprazole
Surgery
Laparoscopic
Open
Endoscopic

67
Q

H. pylori treatment

A

Omeprazole 20 mg bd
+
Clarithromycin 500 mg bd
+
Metronidazole 400 mg bd

68
Q

GP management of dyspepsia

A

Consider referral to a specialist service for people:
- of any age with gastro-oesophageal symptoms that are non- responsive to treatment or unexplained
- with suspected gastro-oesophageal reflux disease who are thinking about surgery
- with H. pylori and persistent symptoms that have not responded to second-line eradication therapy

In people needing referral, suspend NSAID use.

If people have had a previous endoscopy and do not have any new alarm signs, consider continuing management according to previous endoscopic findings.

69
Q

Megaloblastic Anaemia

A

Macrocytic anaemia
Morphological changes in bone marrow
Inhibition of DNA synthesis in marrow
Commonly due to:
B12 deficiency
Folate deficiency
Rarely due to :
Myelodysplasia
Inherited defects of DNA synthesis
Drugs (e.g. methotrexate)

70
Q

Causes of B12 Deficiency

A

Diet
Vegans
Malabsorption
Pernicious anaemia
Gastrectomy
Pancreatic insufficiency
Coeliac Disease
Ileal surgery
Crohn’s disease
Bacterial overgrowth*

71
Q

When turning vegan without supplements, when are you likely to develop a b12 deficiency?

A

B12 deficiency may take 5 years to develop

72
Q

Clinical Features of B12 Deficiency

A

Lemon-yellow skin
Glossitis
Hepatosplenomegaly
Bruising, bleeding
Neurological signs
Peripheral paraesthesia
Loss of proprioception
Loss of vibration sense
Weakness
Ataxia

73
Q

Management of B12 Deficency

A

Investigation
B12 levels (<160-180 ng/L)
Intrinsic factor, Parietal cell antibodies
Coeliac serology
Hydrogen breath test
Small bowel radiology
Treatment
i.m. hydroxycobalamin 1mg daily for 5 days
Repeat injection every 2-3 months

74
Q

Why should you take care when transfusing a b12 deficient patient

A

Blood transfusion of patients with anaemia secondary to B12 deficiency can precipitate subacute combined degeneration of the cord and render the patient disabled.

75
Q

Causes of Folate Deficiency

A

Nutritional Deficiency
Old age
Alcoholism
Deprivation
Anorexia (cancer, GI disease)
Pregnancy and lactation
Haematological disease
Haemolysis
Malignancy
Dialysis
Malabsorption (rare)
Antifolate drugs
Phenytoin, methotrexate, trimethoprim

76
Q

Intraperitoneal versus retroperitoneal

A

Retroperitoneal organ e.g. kidney, between posterior body wall and peritoneum

Intraperitoneal organ e.g. small intestine or transverse colon, suspended in peritoneal sac via mesentery

77
Q

Greater omentum

A

Large apron-like fold of peritoneum with lots of fat
Contains leucocytes e.g. macrophages
Protects viscera and can wrap around damaged or infected bowel

Attaches to greater curvature of stomach and first part of duodenum
Drapes over transverse colon, jejunum and ileum
Turns to adhere to the transverse colon and transverse mesocolon before attaching to posterior abdominal wall

Gastrophrenic, gastrosplenic and gastrocolic ligaments

78
Q

Lesser omentum

A

Hepatogastric ligament
Hepatoduodenal ligament

Free edge of lesser omentum contains portal triad:
Proper hepatic artery
Common bile duct
Hepatic portal vein

Pringle manouevre: clamping the portal triad at the hepatoduodenal ligament during liver surgery to control bleeding

79
Q

Supracolic and infracolic compartments

A

Supracolic compartment, containing the stomach, liver, and spleen

Infracolic compartment, containing the small intestine and ascending and descending colon. This compartment lies posterior to the greater omentum

80
Q

Paracolic gutters

A

Lateral to the ascending colon and descending colon

Allow for communication between the supracolic and infracolic compartments e.g. movement of peritoneal fluid, blood, metastases, infection

81
Q

Subphrenic and subhepatic recesses

A

Part of supracolic compartment

Subphrenic recess separates the diaphragmatic surface of the liver from the diaphragm
Divided into right and left subphrenic spaces by the falciform ligament

Subhepatic (hepatorenal) recess lies inferior to the liver, adjacent to stomach and right kidney

Infections and metastases in the peritoneal cavity can spread into these spaces via the right paracolic gutter and cause abscesses e.g. peritonitis due to a ruptured appendix

82
Q

Arterial and lymphatic supply to GI tract

A

Foregut
Oesophagus to duodenum (D2)
Arterial supply = coeliac trunk
Lymphatics = coeliac (group of pre-aortic) nodes

Midgut
Duodenum (D2) to distal 1/3 transverse colon.
Arterial supply = superior mesenteric artery
Lymphatics = superior mesenteric nodes

Hindgut
Distal 1/3 transverse colon to mid anal canal.
Arterial supply = inferior mesenteric artery
Lymphatics = inferior mesenteric nodes

83
Q

Biliary tree and gallbladder; clinical relavance

A

Bile produced in liver enters left and right hepatic ducts
Form common hepatic duct

Bile stored in gallbladder
Enters via cystic duct
Gallbladder has a neck, body and fundus

Bile duct joins main pancreatic duct to form hepatopancreatic ampulla (ampulla of Vater)
controlled by hepatopancreatic sphincter (sphincter of Oddi)

Gallstones: blockage of biliary tree causes colic pain in right hypochondrium

84
Q

Spleen

A

Intraperitoneal organ derived from embryonic mesoderm (not embryonic foregut)

Inferior to diaphragm, deep to ribs 9 and 10 on the left. LUQ / left hypochondrium

Gastrosplenic ligament (contains short gastric and gastro-omental vessels)
Splenorenal ligament (contains splenic vessels)

Splenomegaly – spleen can enlarge in an anterior, medial and inferior direction

85
Q

Anal canal: superior to pectinate line

A

Arterial supply = superior rectal artery
Venous drainage = internal rectal venous plexus  superior rectal vein (inferior mesenteric vein)
Lymphatic drainage = internal iliac lymph nodes

86
Q

Anal canal: inferior to pectinate line

A

Arterial supply = inferior rectal artery
Venous drainage = internal rectal venous plexus  inferior rectal vein (internal iliac vein)
Lymphatic drainage = superficial inguinal lymph nodes (for perineum)

87
Q

Intestinal obstruction

A

Usually small intestine. Due to mechanical obstruction or impairment of peristalsis (due to nerve or muscle damage e.g. after abdominal surgery)

Results in distension and loss of fluids and electrolytes.
Can lead to interruption of blood flow (strangulation due to increased pressure), necrosis and rapid bacterial growth, gangrene and perforation
Symptoms: pain, absolute constipation, abdominal distension and vomiting

88
Q

Crohn’s disease and Ulcerative colitis
Features common to both diseases:

A

Idiopathic and chronic relapsing inflammatory diseases
Abnormal local immune response to normal gut flora/self antigens
Both more common in white population in developed nations and rising in incidence
Both have systemic effects

89
Q

Crohn’s Disease features

A

Can affect anywhere from oesophagus to anus but commonly terminal ileum
Granulomatous inflammation ulcerates mucosa and deep into submucosa – entire wall thickness

Symptoms: diarrhoea, crampy pain, fever

Skip lesions – lengths of diseased bowel separated by apparently normal tissue
Fissures – deep ulcers that involve the full wall thickness
Thickened GI wall due to inflammation: oedema, fibrosis, muscle hypertrophy. Leads to a narrow lumen – strictures
Cobblestoning – appearance of oedematous (fluid-filled) mucosal folds and fissures

Sequelae:
Strictures may lead to obstruction
Fistulae may lead to adhesions of bowel loops or to other abdominal structures
Fistulae may lead to perforation and abscess/peritonitis

Sufferers have remission and relapses of inflammation, punctuated by complications
Surgery is often required to relieve intestinal obstruction & repair fistulas
No cure, but treatment improves the symptoms and maintains remission

90
Q

Ulcerative colitis

A

A disease of the large intestine
Starts at the rectum and is continuous and can affect the whole colon
Extensive inflammatory damage to the mucosa (and submucosa) - ulceration

Watery stools are common (may contain blood)

Severe damage causes replacement of the straight glands with branched short glands
Recovering ulcers protrude into lumen as pseudopolyps
Lack of absorptive = watery stools (may contain blood)
High risk of bowel cancer

91
Q

Malabsorption causes (4)

A

Insufficient pancreatic enzymes (CF)
Insufficient bile (gallstones)
Loss of small intestinal surface area (coeliac)
Lack of mucosal brush border enzymes

92
Q

Manifestations of malabsorption

A

Diarrhoea and steatorrhoea
Haemopoietic:
Anaemia due to deficiency in iron, folate and B12
Bleeding due to vitamin K deficiency (fat soluble)
Skeletal:
Osteopenia due to Ca, Mg, vit D and protein deficiency
Endocrine:
Impotence, infertility, amenorrhea, due to malnutrition
Hyperparathyroidism due to low Ca and Vit D
Skin: oedema (protein deficiency) and dermatitis (vitamin A)
Nervous system: peripheral neuropathy (Vits A and B12)

93
Q

Coeliac disease

A

Diagnosis: serology for IgAs: anti-TtG (tissue transglutaminase) and anti EMA (endomyseal antibody); endoscopy + biopsy of small bowel mucosa; check for nutritional disorders e.g. iron deficiency anaemia

Sensitivity to gluten- immune response (T cell) to gliadin, a protein in gluten (from wheat, barley and rye-not oats)
Treatment: complete removal of gluten from the diet. Leads to recovery

Infant symptoms: failure to thrive, diarrhoea, abdominal distension and malnutrition. Less obvious in adults
Adult symptoms (less obvious): anaemia, constipation (dermatitis herpetiformis)

Most severe in proximal small intestine (maximal exposure to gluten)
Loss of villous architecture (blunting or flattening) due to inflammation
Lymphocytic infiltration of mucosa and lamina propria
Various stages dependant on extent of loss of surface area and number of lymphocytes
Increased cancer risk for non-Hodgkin’s lymphoma

94
Q

Diverticulosis

A

Affects 5-10% of over-45s in western society
Seen in 80% of over 85yrs.
Lack of fibre, aging and poor bowel habit. Often asymptomatic. Treat by increasing bulk to decrease intraluminal pressure
Outpouches of the sigmoid colon: mucosa herniates through muscularis - due to arrangement of wall of colon-teniae coli x3

Diverticulitis: inflammation/perforation of diverticulae. Lower left quadrant pain and tenderness, bloody stool, and mild fever. Treat with antibiotics and liquid food.

95
Q

Carbohydrate digestion

A

Salivary α-amylase begins break down of CHO in the mouth.

Pancreatic amylase continues digestion in the small intestine (SI).

Brush border enzymes dextrinase and glucoamylase continue to digest compounds of 3+ simple sugars.

Brush border enzymes maltase, sucrase, and lactase break down maltose, sucrose, and lactose into monosaccharides.

96
Q

Glucose, galactose, fructose uptake in the SI

A

Glucose entry is via a coupled transport process.
Sodium-Glucose cotransporter (SLGT1) provides entry at the apical membrane (2 molecules of Na+ per 1 molecule of glucose).
Na+ moves down a concentration and electrochemical gradient.
Na+,K+ ATPase pumps Na+ out of the basolateral membrane, coupled to K+ transport in to maintain the gradient. Secondary active transport.
Fructose movement via facilitated diffusion.

97
Q

Maladsorption of carbohydrates

A

Glucose-galactose malabsorption (GGM) syndrome (rare), autosomal recessive, mutations in the SGLT1 transporter.
Characterized by severe diarrhoea and dehydration as early as Day 1 of life due to the effect of glucose and galactose that draw water out of the body into the intestinal lumen, resulting in diarrhoea.
Symptoms (diarrhoea) controlled by removing lactose, sucrose, and glucose from diet. Infants can still will thrive on a fructose-based replacement formula.
Pancreatic insufficiency: Cystic fibrosis or Shwachman-Diamond syndrome both result in reduced pancreatic amylase.

98
Q

Protein digestion by pancreatic enzymes

A

Acinar cells grouped to form lobules and a ductal system that flows into the main pancreatic duct.
Pancreatic zymogens produced to prevent autodigestion.
Zymogen definition: an inactive substance which is converted into an enzyme when activated by another enzyme.
Pancreas receives neural and peptide stimulation e.g secretin, gastrin, cholecystokinin (CCK).

99
Q

Amino acid transport

A

Free amino acids transported into enterocytes by 4 active, carrier-mediated Na+-dependent mechanisms. Carriers for:
Neutral amino acids
Basic amino acids and cystine
Acidic amino acids
Glycine and imino acids

100
Q

Maladsorption of proteins and amino acids

A

Cystic Fibrosis or Shwachman-Diamond syndrome, patients with limited pancreatic proteases.
Enterokinase Deficiency (very rare), results in protein malabsorption, poor growth and development.
Hartnup disease, autosomal recessive, lack of transport of neutral amino acids, results in a range of physical, neuronal, emotional/mood changes. Treatment: high protein content (+supplements).

101
Q

Fat digestion

A

emulsification of fats and then digestion

102
Q

Embryology midgut

A

From week 5, the midgut and dorsal mesentery undergo rapid elongation to form the primary intestinal loop which communicates with the yolk sac through the vitelline duct

The primary intestinal loop has cranial and caudal limbs
The cranial limb will form: distal duodenum, jejunum and proximal ileum
The caudal limb will form: distal ileum, caecum, appendix, ascending colon and proximal 2/3 transverse colon

From week 6, there is rapid elongation of the midgut and growth of the liver

Not enough room in the abdominal cavity
Primary intestinal loop herniates into the umbilical cord

As herniation occurs, the midgut also rotates 90° anti-clockwise bringing the cranial limb to the right and the caudal limb to the left

Jejuno-ileal loops form

From week 10, the midgut returns to the abdomen and rotates a further 180° anti-clockwise

This brings the proximal jejunal loops to the left side and the caecum lies inferior to the liver

The caecum develops a wormlike diverticulum: vermiform appendix

The vitelline duct is also obliterated during this process

The midgut has re-entered the abdominal cavity by week 11 and has undergone 270° anti-clockwise rotation in total

Once the midgut has returned, the caecum descends from the liver to the right iliac fossa

This pulls the ascending and transverse colon into place resulting in the final arrangement of the midgut

The dorsal mesentery of the ascending and descending colon now shortens and degenerates pulling them against the posterior abdominal wall: secondarily retroperitoneal

103
Q

Meckel’s (ileal) diverticulum

A

A remnant of the vitelline duct (vitellointestinal duct) that creates an outpouching of the ileal wall

Most common gastrointestinal malformation
affects approx. 2% population

Often asymptomatic but may contain ectopic pancreatic or gastric tissue, causing inflammation, ulceration and bleeding

Rule of 2s:
Affects 2% population
2 times more common in males
2 feet (50 cm) from ileocaecal junction
2 inches (3-6 cm) long
Symptomatic in 2% cases

104
Q

Omphalocoele

A

Failed midgut retraction – midgut does not fully return to the abdominal cavity

Associated with an increased risk of mortality and other malformation e.g. cardiac or neural tube defects

Diagnosed prenatally using ultrasound

Varies in size - may only contain intestines or may include other organs e.g. liver

105
Q

Abnormal rotation of midgut and volvulus

A

Abnormal rotation of the midgut can cause parts that would normally be retroperitoneal (e.g. duodenum) to remain suspended by dorsal mesentery

This can lead to volvulus (twisting) of the midgut

Volvulus causes acute obstruction of the bowel and bilious vomiting

Volvulus may also constrict arterial supply to the gut causing ischaemia

106
Q

Ventral and dorsal mesenteries Embryology

A

Caudal foregut has both ventral and dorsal mesenteries
Ventral mesentery critical for development of liver and pancreas

Midgut and hindgut have a dorsal mesentery – not all of it persists into later development
Retroperitoneal structures e.g. ascending/descending colon

Dorsal mesentery permits development of neurovascular structures associated with gut

Dorsal mesentery: from distal/abdominal oesophagus to cloaca

Ventral mesentery: from distal/abdominal oesophagus to first part of duodenum (D1)
Forms lesser omentum and falciform ligament (umbilical vein)

Mesenteries carry blood supply, lymphatics and nerve supply to and from organs

107
Q

Development of the stomach

A

The stomach appears in week 4 as a dilation of the foregut

It is suspended in the abdomen by the dorsal and ventral mesenteries

Differential growth in week 5 forms greater curvature (the dorsal wall grows faster)

In weeks 4 – 8, the stomach undergoes rotation around 2 axes
90° clockwise rotation around the craniocaudal (longitudinal) axis causes the lesser curvature to move to the right
The greater curvature moves from dorsal position to the left
The vagus nerves are initially on left and right sides of the gut tube but also rotate so the left vagus trunk becomes anterior and the right becomes posterior

There is also some rotation around the ventrodorsal (anteroposterior) axis so that:
the greater curvature faces caudally (inferior)
the lesser curvature cranially (superior)

108
Q

Formation of the lesser sac

A

As the stomach rotates around the craniocaudal axis, it creates a space behind it
The lesser sac (omental bursa)
The rest of the peritoneal cavity is now the greater sac
The epiploic foramen is the narrow opening that connects greater and lesser sacs

109
Q

Formation of hindgut

A

The hindgut forms distal 1/3 of transverse colon, descending colon, sigmoid colon, rectum and proximal 2/3 of anal canal

The distal end of the hindgut enters the dorsal part of the cloaca – anorectal canal
The ventral part of the cloaca (urogenital sinus) will form some pelvic organs e.g. bladder

During weeks 4 – 6 a layer of mesoderm extends caudally to separate the urogenital sinus and anorectal canal
Urorectal septum

The urorectal septum approaches near to the cloacal membrane (ectoderm derivative)

Week 7: cloacal membrane ruptures
Creates the anal opening and a ventral opening for the urogenital sinus

The tip of the urorectal septum lies between them and forms the perineal body

110
Q

Formation of the anal canal

A

The upper 2/3 is derived from hindgut (endoderm)

The lower 1/3 is derived from proctodeum / anal pit (ectoderm)

Join together when cloacal (anal) membrane degenerates

Junction between endoderm and ectoderm derivatives is marked in adult by the pectinate line

Different epithelial linings, lymphatic drainage and blood supply

111
Q

Congenital rectourethral and rectovaginal fistulae

A

Uncommon: affects 1 in 5,000 births

Caused by abnormal cloaca e.g. too small or failure of urorectal septum to extend caudally

Opening of hindgut is shifted ventrally to the urethra in males and the vagina in females

112
Q

Imperforate anus

A

Failure of anal membrane to degenerate
Skin covers site of anal opening

Usually requires immediate surgery to allow evacuation of faeces

Good long term prognosis in the majority of cases

113
Q

The classification of jaundice.

A

PRE-HEPATIC
Excess production of bilirubin
Examples: haemolysis, sickle cell, thalassaemia, hereditary spherocytosis, elliptocytosis, autoimmune hereditary haemolysis.

HEPATIC
Liver (conjugation) failure (usually due to inflammation)
Examples: hepatitis, sepsis, drugs, pregnancy, primary biliary cirrhosis, sclerosing cholangitis, hereditary.

POST-HEPATIC
Biliary obstruction
Examples: calculus (gallstone), tumour, chronic pancreatitis.

114
Q

The metabolism of bilirubin.

A

Bilirubin: a product mainly of catabolism of the haem moiety of haemoglobin from effete rbcs.
Haem, oxidised via microsomal haem-oxygenase to biliverdin.
Biliverdin reduced to bilirubin by cytosolic reductase.
Plasma bilirubin associated with albumin, termed unconjugated.

Bilirubin taken up by hepatocyte as protein ‘bound’ to albumin.
Bilirubin then undergoes conjugation and is water soluble, and enters bile canaliculi.
Enters gut via duodenal papilla.
Bacteria form urobilinogen, absorbed into urine and colours stools brown.

115
Q

Liver cells

A

Cords of cells separated by sinusoids as leaky ‘capillaries’ lined by endothelial cells and Kupffer cells.
Kupffer cells: phagocytic cells (recticulo-endothelial system) - capture and breakdown of bacteria and aged/damaged rbcs) – filtering action.
Stellate cells within the Space of Disse, store vitamin A in lipid droplets. Myofibroblasts participate in collagen production and repair and fibrosis.

116
Q

Major liver functions

A

Metabolism: carbohydrate, protein, lipid, nucleic acid.
Vitamin storage (A, D, E, K, B12), and copper and iron.
Bile synthesis and secretion.

Detoxification: conjugation and elimination of metabolites and toxins: Phase I – eg CytP450 catalysed hydrolysis/Ox and then Phase II conjugation to make more water soluble for excretion.

Carbohydrate metabolism - Glycogen storage and release as glucose on requirement (glycogenolysis) including overnight fasting.
‘Surplus’ glucose utilisation for glycerol production with fatty acids for TG production and storage.
Starvation: initiation of gluconeogenesis.

Protein metabolism - Synthesis:
albumin (required for maintenance of colloid osmotic pressure and major transport protein for endogenous proteins and exogenous drugs).
globulins, clotting factors, fibrinogen, plasminogen, prothrombin etc.
non-essential amino acid production via transamination.
innate immunity proteins e.g. complement proteins, CRP, and proteins for the acute phase response.

Degradation:
Transamination: removal of an amino group from amino acids to make non-essential amino acids and C-skeletons used for gluconeogenesis.
Deamination: removal of an amino group making ketoacids and ammonia, which is toxic and so is rapidly converted to urea via the urea cycle.

117
Q

Major liver functions

A

Metabolism: carbohydrate, protein, lipid, nucleic acid.
Vitamin storage (A, D, E, K, B12), and copper and iron.
Bile synthesis and secretion.

Detoxification: conjugation and elimination of metabolites and toxins: Phase I – eg CytP450 catalysed hydrolysis/Ox and then Phase II conjugation to make more water soluble for excretion.

Carbohydrate metabolism - Glycogen storage and release as glucose on requirement (glycogenolysis) including overnight fasting.
‘Surplus’ glucose utilisation for glycerol production with fatty acids for TG production and storage.
Starvation: initiation of gluconeogenesis.

Protein metabolism - Synthesis:
albumin (required for maintenance of colloid osmotic pressure and major transport protein for endogenous proteins and exogenous drugs).
globulins, clotting factors, fibrinogen, plasminogen, prothrombin etc.
non-essential amino acid production via transamination.
innate immunity proteins e.g. complement proteins, CRP, and proteins for the acute phase response.

Degradation:
Transamination: removal of an amino group from amino acids to make non-essential amino acids and C-skeletons used for gluconeogenesis.
Deamination: removal of an amino group making ketoacids and ammonia, which is toxic and so is rapidly converted to urea via the urea cycle.

Lipid metabolism - Main site of lipogenesis (cholesterol, phospholipid, and lipoprotein production).
Free fatty acids can be oxidised to ketones as an energy source, particularly utilized during starvation.
Trigyceride production as a fat storage product.

118
Q

Cholesterol production

A

Stored in the liver and exported with majority (~80%) converted to produce bile salts.
Biosynthesis of cholesterol is limited by the enzyme HMG-CoA reductase, which is a target for statins.

119
Q

Bile production and storage

A

Hepatocytes make bile (~1 L/day) which flows via bile canaliculi, through bile ductules into portal tracts and then into the common hepatic duct.
Gall bladder (GB) is a site of concentrated bile (~50 mL). Muscular-walled sac, pear-shaped, under surface of RL of liver.
Epithelium adapted for salt and water absorption, highly folded with microvilli, Na+/K+ ATPase pumps out Na+ and Cl-.
Concentrated bile exits the GB via the cystic duct into the common bile duct and then into the duodenum

120
Q

Release of bile

A

Essential for fat digestion via emulsification and absorption of fats (via micelles).
Contains water, bile salts (Na+, Cl-, K+ and HCO3-), bilirubin (colour) and cholesterol.
Released into the duodenum via the CBD, majority absorbed in the intestine, passes through the portal system and recycled up to 20x and then excreted in the faeces.
Duodenal release (FAs stimulate) cholecystokinin (CCK) release that stimulates contraction of GB & relaxation of sphincter of Oddi at the Ampulla of Vater.

121
Q

Liver function tests (LFTs)

A

Alkaline phosphatase (ALP)
Mainly in cell membrane between canaliculi and hepatocyte (also cells lining bile ducts) – often increased in disorders affecting bile duct (biliary system).
But, also used as a marker of bone turnover/metabolism/damage.

Gamma glutamyl transpeptidase (GGT)
Involved in transport of amino acids and peptides to the liver. Transport increases with recent alcohol exposure. Sensitive to hepatobiliary disease, if changes mirror ALP, often indicates biliary system damage.

Albumin – blood levels measured.
Blood clotting time measured as prothrombin time (PT) (typically 10-14 sec) also considered as International Normalization Ratio (INR).
Reduced liver synthetic function results in reduced production of clotting factors and increased PT time.

Transaminases within the hepatocytes – released due to cell injury e.g. ischaemia/hypoxia/hepatitis/toxic drugs/xenobiotic exposures.
AST (aspartate transaminase) – blood levels quantified.
ALT (alanine aminotransferase) – blood levels quantified.
high AST:ALT ratio sometimes used, indicative of cirrhotic liver damage typically in alcoholism.
Lactate dehydrogenase (LDH) measures hepatocyte integrity/death since it is released after a loss of cell membrane integrity.

122
Q

Hep A

A

+ve single stranded RNA genome, like the enteroviruses
Faecal-oral route of transmission
Entry via contaminated food or water
Excreted in faeces

Asymptomatic infection
Acute icteric hepatitis
Fulminant hepatitis (rare)

Prevention of hepatitis A:
Avoidance of uncooked foods, unboiled water, when travelling
Passive immunisation – normal human immunoglobulin – contains IgG anti-HAV
Active immunisation – HAV vaccine – killed whole virus vaccine

123
Q

Hepatitis B Virus (HBV)

A

Hepadnavirus (DNA)
Perinatal (mother to baby – at birth)
Sexual
Parenteral (unsafe injections and transfusion)

Chronic if:
Defined as persistence of HBsAg for > 6 months
(i) HBeAg positive
High infectivity eg needlestick
Increased risk of inflammatory liver disease
(ii) Anti-HBe positive
Lower infectivity
Lower risk of inflammatory liver disease

Prevention of HBV infection:
Simple precautions and education of carriers
Passive immunisation – HBIg
Active immunisation
Sub-unit vaccine
HBsAg, induces anti-HBs response

124
Q

Hepatitis E virus; Summary

A

RNA virus classified as hepeviridae
Faecal-oral spread
No chronic sequelae in immunocompetent host
Higher mortality than HAV – espec in pregnancy
Usually associated with travel abroad, but endogenous infection increasingly recognised
In UK, zoonosis – genotype 3 virus found in pigs

125
Q

Hep C

A

+ve ss RNA
Bloodborne
75% chronic

126
Q

Haem

A

Heam is a complex organic molecule that contains Iron at the center of a porphyrin ring. It contains a single ferrous (Fe2+) or ferric (Fe3+) ion, able to bond with diatomic oxygen and transport it around the body.

127
Q

Biosynthesis of haem

A

Haem has a very complex biosynthesis pathway and can be generated in most tissues. However, the main types are erythroid cells (immature red blood cells) in the bone marrow and hepatocytes, in the liver.

a) most cells: cytochrome C (oxidative phosphorylation)

b) liver: cytochrome P450 (steroid / drug metabolism)

c) bone marrow: haemoglobin (transport oxygen)

128
Q

Where do Succinyl CoA and Glycine come from?

A

The first step involves the enzyme aminolevulinic acid (ALA) synthase that catalyses the condensation of glycine with succinyl-CoA to form ALAin the mitochondrial matrix.

129
Q

What nutritional problems could stop us from making Haem?

A

General nutritional deficit
Reduced Succinyl-CoA from TCA cycle

Iron poor diet
Haem needs Iron to form the core

Vitamin deficiency, especially the vitamin B group cofactors, can also impair the production of haem. These include but is not exhaustive:

B6 Pyridoxine B9 Folic acid
B2 Riboflavin B12 Cyanocobalamin
B3 Niacin
B5 Pantothenic acid

These either work directly as cofactors, as in vitamin B6 affecting the first step in the synthesis pathway, or indirectly by disrupting erythroid progenitor cells

130
Q

Types of porphyria’s

A

There are two general categories of porphyria:
The acute porphyria’s which mainly affect the nervous system (also called acute hepatic porphyria’s – AHP)

The cutaneous porphyria’s, which mainly affect the skin.

There are two types of porphyria that have both acute and skin symptoms
Variegate Porphyria (VP) and Hereditary Coproporphyria (HCP)

Acute porphyrias:
Acute Intermittent Porphyria (AIP)
Variegate Porphyria (VP)
Hereditary Coproporphyria (HCP)
Aminolevulinate Dehydratase (ALAD) Deficiency Porphyria (ADP)

Cutaneous (skin) porphyrias:
Porphyria Cutanea Tarda (PCT)
Erythropoietic Protoporphyria (EPP)
X-linked Dominant Erythropoietic Protoporphyria (XLDPP)
Congenital Erythropoietic Porphyria (CEp)

For some of the most common Porphyria
Hepatic and Erythropoietic
Uroporphyrin accumulates in Urine
Red-Brown in natural light
Photosensitivity

131
Q

Colonic Polyps

A

A polyp is a macroscopic protrusion of the colonic mucosa into the bowel lumen.
Colonic polyps can be classified according to their malignant potential. Neoplastic polyps can become malignant while non-neoplastic polyps cannot.
Certain characteristics are associated with higher cancer risk. These include:
Multiple adenomas
Size > 1.0 cm
Advanced histology (villous, tubulovillous, high grade dysplasia)
Proximal location of adenoma
Older age at diagnosis of adenoma(s)
Family history of colon cancer in a parent

132
Q

Lynch Syndrome (HNPCC)
(Hereditary Non-Polyposis Colorectal Cancer)

A

HNPCC is an autosomal dominant syndrome caused by a germline mutation in one of the DNA mismatch repair (MMR) genes.

It is associated with 2% - 3% of all colon cancer cases. The lifetime risk of a developing colon cancer can be as high as 70%.

In recent report, median age of colon cancer diagnosis in patients with Lynch Syndrome (HNPCC) was 54 years in men and 70 years in women.

This syndrome is also associated with tumors of other organs such as the uterus, ovaries, stomach, pancreas, ureters, kidneys, small bowel, biliary tract, and brain.

133
Q

Familial Adenomatous Polyposis

A

FAP is an autosomal dominant syndrome caused by germline mutation in the APC gene.
It accounts for < 1% of all colon cancer cases. Approximately 50% of affected patients develop adenomatous polyps by age 15 and 95% by age 35.
The average age at diagnosis of colon cancer is about 35-40 years. The lifetime risk of developing colon cancer in a patient with FAP approaches 100%.

134
Q

Right–sided colorectal cancers:

A

Tend to be polypoid or fungating or ulcerating
Unlikely to obstruct
Tends to present with weakness & anemia
May have melena.
Advanced lesions can cause change in bowel habits and bowel obstruction

135
Q

Left–sided colorectal cancers:

A

Tend to be annular or constricting lesions
Likely to obstruct
Produce an “apple-core”
Or “napkin-ring” appearance on Ba enema
Tends to present with change in bowel habits & Gross bleeding

136
Q

RECTAL CANCER

A

Most common symptom of rectal cancer is hematochezia
Unfortunately, this is often attributed to hemorrhoids (by patient & physician), hence correct diagnosis is consequently delayed until the cancer has reached an advanced stage.

Other symptoms include:
– mucus discharge
– tenesmus
– change in bowel habit
– pain (usually with locally advanced rectal cancer

137
Q

Stages of Bowel Cancer

A

Stage 0 or CIS=early stage of bowel cancer. Cancer cells in the bowel lining (completely contained). There islittle risk of any cancer cells having spread.
Stage 1 - cancer has grown through the inner lining of the bowel, or into the muscle wall, but no further.
Stage 2 - 2A means that the cancer has grown into the outer covering of the bowel , 2B - plus into the tissues and organs next to it.
Stage 3 - + LN involvement ; Stage 4 - + Metastasised to other parts of the body

GEM (18 decks)

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