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MD3002 Weeks 1-6 > Week 3 > Flashcards

Week 3 Flashcards

1
Q

Outline the regional variations in water and electrolyte uptake in the large intestine.
The anatomy behind this?

A

Structural difference:
– Tight junctional resistance increases towards the colon
– Tight junctions in the small intestine are ‘leaky’
(permeable via the paracellular route)
– Tight junctions in the colon are ‘tight’ (impermeable via the paracellular route

Regional variations in uptake mechanisms:

  • H2O (majority in the small intestine 6.5 litres)
  • Na+ in the jejunum, ileum and colon

Electrolyte uptake: Na+, Cl-, HCO3- and K+ are absorbed isosmotically with water by the villi (as in the renal proximal tubule)

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2
Q

Describe the mechanism of intestinal secretion from the crypts of Lieberkuhn

A

Zone of cell proliferation in the base of the crypts replaces the villous cells every 48 – 96 hours

Mechanism:
– Cl- enters the cell via the Na++K++2Cl- basal transporter
– Cl- diffuses across the apical membrane through apical Cl- channels (regulated by secretagogues)
– Na+ follows Cl- secretion passively via the paracellular pathway
– H2O follows NaCl secretion

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3
Q

e) List common secretagogues and briefly explain their mode of action

A

2 groups:

  1. Hormones/NTs: VIP, ACh, Bradykinin. Lead to release of second messenger e.g. cAMP, Ca2+
  2. Bacterial enterotoxins: Cholera, E coli leads to release of second messengers e.g. cAMP, Ca2+

Second messages increase anion secretion and inhibit NaCl absorption.

I.e. Secretagogues –> Bowel movement

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4
Q

Digestion and absorption of lipids

A
  1. Dietary lipids are hydrophobic (insoluble in water)
  2. They must be solubilised before digestion and absorption can occur
  3. Digestion begins the stomach with the action of lingual and gastric lipases
  4. Digestion is completed in the small intestine with the action of the pancreatic enzymes
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5
Q

Describe the digestion of lipids in the stomach

A

Stomach churns and mixes lipids to initiate enzymatic digestion
Lingual and gastric lipases hydrolyse 10% of ingested triglycerides to glycerol and free fatty acids

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6
Q

Key role of gastric lipase in lipid digestion in the stomach?

A

Slows the rate of gastric emptying so that pancreatic enzymes are able to digest lipid

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7
Q

What is secreted in the duodenal and jejunal mucosa in response to the presence of monoglycerides and fatty acids and small peptides and amino acids?

A

Cholecystokinin secreted from the I cells of the duodenal and jejunal mucosa

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8
Q

How are lipids digested in the SI?

A
  1. Bile salts, lysolecithin and products of lipid digestion emulsify dietary lipids.
  2. Emulsification produces small droplets of lipids dispersed in an aqueous solution creating a large surface area for pancreatic enzyme digestion
  3. Pancreatic enzymes (pancreatic lipase, cholesterol ester hydrolase and phospholipase A2) and the protein, colipase are secreted to complete digestion
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9
Q

Stages of digestion and absorption of lipids

A
  1. Bile salts from liver coat fat droplets
  2. Pancreatic lipase and colipase break down fats into monoglycerides and fatty acids stored in micelles
  3. Monoglycerides and fatty acids move out of micelles and enter cells via diffusion
  4. Cholesterol is transported into cells by a membrane transporter
  5. Absorbed fats combine with cholesterol and proteins in the intestinal cells to form chylomicrons
  6. Chylomicrons are released into the lymphatic system
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10
Q

Chylomicrons:
Structure?
Location?
Transport?

A

Structure: Chylomicrons (100 nm diameter) have a core of triglycerides and cholesterol ester - phospholipids and apoproteins on the outside (80%/20%)

Location: Chylomicrons are packaged into secretory vesicles on the Golgi membrane and are exocytosed across the basolateral membrane

Transport: The lymphatic circulation carries the chylomicrons to the thoracic duct which empties into the blood stream

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11
Q

What structures in the Si and LI are responsible for absorption and secretion?

A

Small intestine:
Villi – absorption
Crypts of Lieberkuhn – secretion

Large intestine:
Surface epithelial cells - absorption
Colonic glands – secretion

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12
Q

Effect of cholera toxin on intestinal secretion

A

Activates GCP in epithelial cells of the crypts. Leads to Cl- released into the lumen –> Diarrhoea

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13
Q

In the clinical examination of abdomen/ GU:

What is looked at during close inspection of the hands/arms?

A 
Finger clubbing: Due to Malabsorption, Inflammatory Bowen disease,lymphoma, cirrhosis
Asterixis (coarse flapping tremor): Due to hepatic encaphalopathy
Leuconychia: White deposits on nails
Koilongchia: Spoon shaped nails
Palmar erythema
Dupuytrens contracture
Spinal naevus
Purpura
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14
Q

GU/abdomen examination

A 
Intro
General inspection
Close inspection of the hands
Radial pulse
BP/temp (on charts)
Chest/axillae/ abdomen:
Close inspection of face
Close inspection chest/axillae
Palpation of chest/axillae
Palpate bladder
Palpate of kidneys 
Feel abdominal aorta
Percussion liver, spleen and bladder
Percussion for ascites 
Auscultation of the diaphragm

Back:
Inspect
Palpate for renal tenderness and cervical lymph nodes

Other areas:
• Offers to examine groin
• Offers to examine genitalia
• Requests to do digital rectal examination (DRE)

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15
Q

Conditions to look for during close inspection of the face in GU/abdomen of the face

A 
Jaundice
Mouth:
- Glossitis
- Oral candidiasis
- Angular stomatisis
- Peutz-jegers syndrome
- Telangiectasia
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16
Q

How to examine chest/ axillae during GU/abdomen exam?

A

Inspect chest for spider naevi, gynaecomastia in men, and both axillae for loss of axillary body hair.
Movement, distension, scars, hernia, masses etx.

Palpation:
-Superficial to deep
- Ask patient to point to painful area
-Palpate all 9 regions
- Watch patients face
Liver:
-Begin in right iliac fossa
-Ask patients to breath in and o§ut deeply
-Palpate upwards to right costal margin
- Feel for liver edge descending on inspiration. Shouldn't feel anything
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17
Q

What is Murphy’s Sign?

A

• Feel for gall bladder tenderness (e.g. acute cholecystitis)
• Patient breathes in whilst you gently palpate RUQ in mid-
clavicular line
• On liver descent contact with inflamed gallbladder causestenderness and sudden arrest of inspiration

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18
Q

What is Courvoisier’s Sign?

A
  • Painless jaundice and a palpable gallbladder

* Likely due to extrahepatic obstructionmE.g. Pancreatic cancer, UNLIKELY to be gallstones

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19
Q

What is the process to check for splenomegaly?

A
  1. Ask the patient to breathe in and out deeply
  2. Palpate upwards to left hypochondrium
  3. Feel for edge of an
    enlarged spleen as it descends on inspiration

Characteristic notch may be palpable
Move hand between each breath

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20
Q

Percussion of liver, spleen and bladder method

A

Percuss up to right costal margin for lower border of liver
Percuss downwards from just above right nipple for upper border of liver
Percuss towards left hypochondrium for lower border of spleen
Percuss from umbilicus down in midline for bladder

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21
Q

What is ascites?
Causes?
Method?

A

 Abnormal collection of fluid in peritoneal cavity

 Causes:
– Hepatic cirrhosis
– Intra-abdominal malignancy – Nephrotic syndrome
– Cardiac failure
– Pancreatitis
– Constrictive pericarditis etc.

Method:
 Start in mid-line
 Percuss towards flanks
 Shifting dullness and Fluid thrill

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22
Q

How is the diaphragm auscultated?

A

 Listen for normal bowel sounds (up to 2 min)
 Auscultate for abdominal aortic bruits
 Auscultate renal arteries

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23
Q

Why are the cervical lymph nodes examined?

A

 May indicate local disease
 May indicate more distant disease:
– Tumours of the upper gastrointestinal tract may metastasise to the lower part of the left posterior cervical triangle
– Virchow’s node / Troisier’s sign

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24
Q

Rectal examination:
Indications?
Key points?

A 
 Indications:
– Rectal bleeding
– Prostatic symptoms
– Change in bowel habit
– Possible spinal cord injury

Key points:
- Explain procedure
- Gain informed consent
- Offer a chaperone

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25
Q

How is the female reproductive system examined?
Indications?
Pathology?

A

 Pelvic examination
– Bi-manual = one hand palpates per vagina and other per abdomen

Indications:
 pelvic pain
 abnormal vaginal bleeding
 abnormal vaginal discharge
 if considering vaginal or uterine prolapse

Female pelvic pathology:
- Ovarian pathology E.g. Ovarian cyst, malignancy
- Uterine pathology E.g. Uterine prolapse, fibroids, cervical carcinoma,
carcinoma of body of uterus
- Vaginal pathology E.g. vaginitis , prolapse
- Pelvic infection (Pelvic inflammatory disease)
- Ectopic pregnancy - do a pregnancy test
- Always consider a pelvic ultrasound scan

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26
Q

How is the male reproductive system examined?

Pathology?

A 
Testicular exam
Pathology:
– Infection (epididymitis, orchitis, epididmyo- orchitis)
– Testicular torsion
– Epididymal cysts
– Testicular tumours
– Indirect inguinal hernia
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27
Q

Inflammatory disorders of the oesophagus?

A 
Acute:
Infection in immunocompromised patients. E.g. 
• Herpes simplex viruses
• Candida
• Cytomegalovirus(CMV)
– Corrosives 
Chronic:
Specific. E.g.
• Tuberculosis
• Bullous pemphigoid and Epidermolysis bullosa 
• Crohn’sdisease
Non-specific E.g.
• Reflux oesophagitis
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28
Q

What is GORD?

A

Gastro-oesophageal reflux disease

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29
Q

Causes for reflux oesophagitis (6)

Consequence? Leading to 3 pathologies?

A 
• Regurgitation of gastric contents
– Gastro-oesophageal reflux disease (GORD)
– ‘Incompetent’ GO junction
• Alcohol and tobacco
• Obesity
• Drugs e.g. caffeine!
• Hiatus hernia
• Motility disorders

Squamous epithelium damaged –>
– Eosinophils epithelial infiltration
– Basal cell hyperplasia
– Chronic inflammation

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30
Q

Consequences of reflux oesophagitis

A

Severe reflux leads to ulceration. Leading to fibrosis = stricture + obstruction.

Oesophagus narrower and more rigid

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31
Q

What is Barrett’s oesophagus?
Risk?
Diagnosis?

A

Longstanding reflex
Aged 40-60
Lower oesophagus becomes lined by columnar epithelium due to intestinal metaplasia

Risk? 100 times more likely to get adenocarcinoma of distal oesophagus

Diagnosis: Gastroscopy reveals red appearance of oesophagus

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32
Q

Two classifications of gastric inflammation?

A

Acute gastritis:

  • Usually due to chemical injury (e.g. drugs / alcohol)
  • H pylori- associated

Chronic gastritis:

  • Active chronic (H pylori associated)
  • Auto immume
  • Chemical (reflux)
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33
Q

H pylori-associate gastritis:

  • Bacteria shape?
  • Transmission?
  • Occupies?
  • Condition associated with?
  • Treatment?
  • Two distribution patterns?
  • Detections?
A

Bacteria shape?
-Gram negative spiral-shaped or curved bacilli

Transmission;
-Oral-oral, faecal-oral, environmental spread.

Occupies?

  • Occupies protected niche beneath mucus where pH approx 7
  • Does not colonise intestinal type eptithelium

Condition associated with?
-90% active chronic gastritis

Treatment?
-Resolves with therapy (double antibiotics + proton pump inhibitors)

Two distribution patterns:
1. Diffuse involvement of antrum and body
• Atrophy, fibrosis, intestinal metaplasia
• Associated with gastric ulcer and gastric cancer
2. Antral but not body involvement • Gastric acid secretion increased
• Associated with duodenal ulcer

Detection:
-Faecal bacterial, urea breath test, gastric biopsy rapid urease test

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34
Q

Chemical (reflux) gastritis:
Caused by?
Results in…
Associated with?

A

Caused by: Regurgitation of bile and alkaline duodenal secretion

Results in loss of epithelial cells with compensatory hyperplasia of gastric foveae

Associated with:

  • Defective pylorus
  • Motility disorders
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35
Q

Autoimmune chronic gastritis:
What is it? What happens?
Association?
Risk?

A

What is it? What happens?
Autoimmune reaction to gastric parietal cells. Serum antibodies to gastric patietal cells and intrinsic factor.
Loss of acid secretion (hypochlorhydria/achlorhydria)
Loss of intrinsic factor
–> Vit B12 deficiency
–>Macrocytic anaemia (pernicious anaemia)

Association?
With gastric atrophy and intestinal metaplasia

Risk?
Gastric cancer

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36
Q

What are the 3 causes for chronic gastritis?

A
  1. Autoimmune
  2. Bacterial infection (H pylori)
  3. Chemical injury
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37
Q

Peptic ulceration:
What is it? Caused by?
Major sites of ulceration?

A

What is it? Caused by?
Breach in mucosal lining of alimentary tract as a result of acid and pepsin attack

Major sites:
– First part of duodenum
– Junction of antral and body mucosa in stomach 
– Distal oesophagus
– Gastro-enterostomy stoma
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38
Q

Causes for peptic ulcers?

A 
– Hyperacidity
– H pylori gastritis 
– Duodenal reflux 
– NSAIDs
– Smoking
– Genetic factors
– Zollinger-Ellison syndrome
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39
Q

Complications of peptic ulceration?

A 
– Haemorrhage
– Penetration of adjacent organs e.g. pancreas
– Perforation
– Anaemia
– Obstruction
– Malignancy
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40
Q

Causes for acute peptic ulcers

A

Acute gastritis
Stress response
Extremem hyperacidity

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41
Q

Where to chronic peptic ulcers tend to occur?

A

At mucosal junctions e.g. Antrum- body

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42
Q

CHARACTERIC FEAUTRES OF ALL PEPTIC ULCERS

A
  1. Necrotic debris
  2. Nonspecific acute inflammation
  3. Granulation tissue
  4. Fibrosis
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43
Q

Causes of chronic duodenal ulcers?

A
  1. Increased acid production (can be induced by H pylori)
  2. Reduced mucosal resistance.
    - Gastric metaplasia occur in response to hyperacidity
    - Then colonised by H pylori
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44
Q

Risk of malignancy in ulcers?

A

Gastric: Rare
Duodenal: “Never”

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45
Q

Patholoigy of chronic duodenal ulcer

A

• Usually small (<20 mm)
• Sharply ‘Punched out’ with defined edges
• Defined structure:
-Granulation tissue at base
-Underlying inflammation and fibrosis
-Loss of muscular propria
-Complication such as “Bleed, burst or block”, Penetration of adjacent orange, malignancy

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46
Q

Patholoigy of chronic duodenal ulcer

A

• Usually small (<20 mm)
• Sharply ‘Punched out’ with defined edges
• Defined structure:
-Granulation tissue at base
-Underlying inflammation and fibrosis
-Loss of muscular propria
-Complication such as “Bleed, burst or block”, Penetration of adjacent orange, malignancy

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47
Q

What is intrinsic factor?

A

Intrinsic factor (IF), also known as gastric intrinsic factor (GIF), is a glycoprotein produced by the parietal cells of the stomach. It is necessary for the absorption of vitamin B12 (cobalamin) later on in the small intestine.

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48
Q

For chronic gastric caused by autoimmune, what is the mechanism + histology + clinical?

A

Mechanism:
Anti-parietal cell and intrinsic factor antibodies

Histology:

  • Glandular atrophy in gastric body
  • Intestinal metaplasia

Clinical:
Pernicious anaemia

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49
Q

For chronic gastric caused by bacterial infection of H pylori, what is the mechanism + histology + clinical?

A

Mechanism:
Anti-parietal cell and intrinsic factor antibodies

Histology:

  • Active chronic inflammation
  • Atrophy
  • Intestinal metaplasia

Clinical:

  • Peptic ulceration
  • ?Gastric cancer
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50
Q

For chronic gastric caused by chemical injury, what is the mechanism + histology + clinical?

A

Mechanism:

  • Direct injury
  • Disruption of mucus layer

Histology:

  • Foveolar hyperplasia
  • Few inflammatory cells

Clinical:

  • Gastric erosions
  • Gastric ulcer
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51
Q

What damage can be caused by GI pathogens?

A

Local inflammation
Ulceration / perforation of mucosal epithelium
Disruption of normal microbiota
Pharmacological action of bacterial toxins
Invasion to blood or lymphatics

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52
Q

Why is the lining of the epithelium perforated?

A

Due to untreated ulcers

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53
Q

Name 6 bacterial diarrhoea pathogens

A 
Gram neg:
• Vibrio cholerae
• Escherichia coli
• Campylobacter jejuni 
• Salmonella spp.
• Shigella spp.

Gram pos:
• Listeria monocytogenes

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54
Q 
V. cholerae:
Structure?
Characteristics?
Serotypes based on?
Vaccines?
A

Structure:
• Gram negative
• Comma-shaped rod
• Flagellated

Characteristics:
• Characterised by epidemics and pandemics
• Human-only pathogen
• Flourishes in communities with no clean drinking water / sewage disposal

Serotypes:
-Based on O antigens

Vaccines:

  • Parenteral vaccine: low protective efficiency
  • Oral vaccine: Effective and suitable for travellers
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55
Q 
Pathogenesis of V. cholerae:
Dosage?
Main barrier`?
Colonisation in SI requires?
Produces?
Results in?
A
  • Only infective in large doses
  • Many organisms killed in stomach
  • Colonisation of small intestine involving flagellar motion, mucinase, attachment to specific receptors
  • Production of multicomponent toxin
  • Loss of fluid and electrolytes without damage to enterocytes
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56
Q

What is the structure of the cholera toxin (CTx)?

What does it cause?

A

Structure of cholera toxin:
Oligomeric complex and 6 protein subunits.
- 1 x copy of A subunit (enzymatic)
- 5 x copies of B subunit (receptor binding)

Release of cAMP –> Lost of fluid and electrolytes.
Responsible for the characteristic, watery cholera diarrhoea. Acts as secretogogue.

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57
Q

5 potential consequences of cholera infection?

A
  1. Fluid loss of up to 1 litre/hour
  2. Electrolyte imbalance leading to dehydration, metabolic acidosis and hypokalemia
  3. Hypovolaemic shock
  4. 40-60% mortality
  5. <1% mortality if given fluid/electrolytes (ORT)
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58
Q

Structure of E.coli?

A

Gram neg
Bacillus
Normal GI microbiota, however, strains with virulence factors (e.g. toxins) enabling them to cause disease

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59
Q

Mode of action of E. coli enterotoxins

A

Enterotoxins secreted into the gut. E. coli has two of them, LT and STa
LT leads of cAMP ==> fluid loss
STa= leads to production of GMP

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60
Q

C. jejuni:
Structure?
Consequences?
Transmission?

A

Structure:

  • Gram neg
  • Helical bacillus

Consequences:

  • Food associated diarrhoea
  • Mucosal inflammation nd luid secretion

Transmission: Consumption of raw/undercooked meat, contaminated milk

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61
Q

Histological appearance of c. jejuni infection?

A
  1. Inflammation involves entire mucosa
  2. Villous atrophy
  3. Necrotic debris in crypts
  4. Thickening of basement membrane
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62
Q 
Salmonella spp.:
Structure?
Consequences?
Transmission?
Key species?
A

Structure:

  • Gram neg
  • Bacilli

Consequences: Food associated diarrhoea

Transmission: Consumption of raw / undercooked meat, contaminated eggs and milk

Key species:

  • S. typi
  • S. paratyphi
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63
Q

What are the stages of a Salmonella infection?

A
  1. Ingestion of large numbers of bacteria
  2. Absorption to epithelial cells in terminal section of small intestine
  3. Penetration of cells and migration to lamina propria
  4. Multiplication in lymphoid follicles
  5. Inflammatory response mediates release of prostaglandins
  6. Stimulation of cAMP
  7. Release of fluid and electrolytes causing diarrhoea
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64
Q

S. typhi and S. paratyphi: Cause which enteric fevers?

Role of macrophages?

A

Cause which enteric fevers? Typhoid and paratyphoid

Macrophages are the site of multiplication and transport around body

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65
Q

What are the two options for typhoid vaccine?

A

Oral: Live attenuated (booster after 5 years)

Parenteral: Capsular polysaccharide (Booster after 2 years)

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66
Q

Shigella spp.:
Structure?
Results in?
4 species?

A 
Structure: Bacillus
Causes shigellosis (bacillary dysentery)
4 species:
-S. dysenteriae (most serious)
-S. flexneri
-S. boydii
-S. sonnei
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67
Q

Stages of shigella infection?

A
  1. Attaches to mucosal epithelium of distal ileum
    and colon
  2. Causes inflammation and ulceration
  3. Rarely invasive
  4. Produces Shiga toxin
  5. Diarrhoea watery initially, later can contain blood and mucus
  6. Disease usually self-limiting
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68
Q

L. monocytogenes:

  • Structure?
  • Condition caused?
  • Population at risk?
  • Presents as?
A 
Structure: Coccobaccilus
Condition caused: Listeriosis
Population at risk:
-Pregnant women]
-Immunosuppressed individual
-The elderly
Presents as: Meningitis
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69
Q

3 viral diarrhoea pathogens?

A

Rotavirus
Norovirus
Enteric adenovirus

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70
Q

Rotavirus:
Structure?
Common patient?
Transmission?

A

Structure: Wheel, 11 separate segments of double-stranded RNA

Common: Children <2 years olds

Transmission: Faeco-oral, but may also be faeco-respiratory

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71
Q

Pathogenesis of rotavirus infection?

A
  1. Incubation period of 1-2 days
  2. Replication of virus in small intestinal epithelial cells at tips of villi
  3. Resultsinvillousatrophy
  4. Damage caused to infected cells leaving immature cells with reduced absorptive capacity for sugar, water and electrolytes
  5. Onset of vomiting, diarrhoea lasting 4 –7 days
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72
Q

What is the rotavirus vaccine?

A

RotaRix, RotaTeq

  • Oral administration
  • 2-3 doses
  • First dose at 6-10 weeks of age
  • Live,attenuated virus
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73
Q

Norovirus:
AKA?
Transmission?
Vaccine?

A

aka winter vomiting disease

Transmission: Faeco-oral, contaminated water / shellfish, fomites

No vaccine

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74
Q

Enteric adenovirus:

Presentation?

A

Presentation:

  • Asymptomatic infections common
  • Mild, but prolonged diarrhoea
75
Q

What is antibiotic associated diarrhoea?

Drugs involved?

A

Does not involve ingestion of pathogen or toxin
Can arise from disruption of gut microbiota following antibiotic therapy.

Drugs:
• Tetracycline-allows colonisation by Staphylococcus aureus & Candida sp.
• Clindamycin suppresses gut microbiota and allows Clostridium difficile to multiply
• C. difficile infection. is now associated with resistance to vancomycin

76
Q

Helicobacter pylori.:

  • Structure?
  • Assoication to disease?
A

Structure:

  • Gram neg
  • Spiral
  • Flagellated
  • Microaerophilic

Disease associations:

  • Duodenal ulcers
  • Gastric ulcers
  • Gastro-oesophageal reflux disease
  • Non-ulcer dyspepsia
77
Q

Key features of H. pylori?

A

• Acid-inhibiting protein: Survival in
stomach
• Urease – neutralisation of acid pH
• Adhesins – binding to gastric epithelium
• Cytotoxin – damage to gastric epithelium
• Flagellum – movement through gastric mucus layer

78
Q

Treatment of H. pylori associated Gastritis?

A

1 week triple therapy
Option 1. Proton pump inhibitor (PPI) + clarithromycin + amoxycillin
OR
Option 2: PPI + clarithromycin + metronidazole

79
Q

What is food poisoning?

A

Syndrome is restricted to diseases caused by toxins elaborated by contaminating bacteria in food before it is consumed

80
Q

4 ingredients in ORS?

A
  • Glucose (anhydrous)
  • Sodium chloride
  • Potassium chloride
  • Trisodium citrate dihydrate
81
Q

Characteristics of typhoid patients

A

Blanching rash
Rose spots
In faeces for several weeks after recovery\1-3% become chronic carriers
Public health concern

82
Q

Bile production vs storage location?

A

Bile production: Liver

Bile storage and concentration: Gall bladder

83
Q

What is Glisson’s capsule?

A

Deep to its peritoneal covering, the liver is completely surrounded by Glisson’s capsule, a thin connective tissue layer that sends extensions into the organ, in between the lobules

84
Q

Liver arterial supply?

Venous drainage?

A

The liver is supplied by the (hepatic) portal vein bringing absorbed nutrients from the stomach and intestine; and the hepatic artery which supplies the hepatocytes (liver cells) with oxygen.
Venous drainage is by hepatic veins that enter the inferior vena cava.

85
Q

Bile drainage from liver to gall bladder?

A

Bile is drained via canaliculi that lie between the hepatocytes into bile ductules and eventually into bile ducts.

86
Q

4 liver function?

A
  • Synthesis and secretion of bile.
  • Storage of glucose, glycogen, proteins, vitamins and fats.
  • Detoxification of metabolic waste.
  • Synthesis of blood clotting and anticoagulant factors (fibrinogen and prothrombin).
87
Q

Constituents of bile

A

Bile pigments (chiefly bilirubin), cholesterol, phospholipids (lecithin), fatty acids, water and electrolytes.

88
Q

Where do bile pigments derive from?

What is the role of KUPFFER CELLS?

A

Bile pigments are derived as the breakdown products of haemoglobin.
Kupffer cells play a role in their formation. Bile salts
are responsible for the detergent and emulsifying effect of bile on fats, they also increase the absorption of fats by the small intestine.

89
Q

What is the name of the liver functional unit?

A

Liver lobule

90
Q

What is the structure of a liver lobule?

A

Sheets of cells (hepatocytes) radiate outwards from the central vein, which forms the central axis of the lobule.
Sinusoids lie between the sheets and carry blood from the hepatic artery and portal vein (now mixed oxygenated and de-oxygenated blood) to the central vein.
Bile flow is in the opposite direction, in the canaliculi between the hepatocytes.

91
Q

The bare area of the liver is between which two ligaments?

A

The coronary and triangular “ligaments” on posterior liver surface

92
Q

What/where are the 4 lobes of the liver?

A

Anterior: Left, right (separated by falciform ligament, quadrate
Posterior: Caudate *next to IVC)

93
Q

What structure make up the portal triad>

A

Portal vein
Hepatic artery
Hepatic (biliary) ducts

94
Q

Liver divisions
Anatomically?
Functionally?

A

Anatomically:
-Right lobe (larger)
(Divided by the falciform ligament and lesser omentum)
-Left lobe

Functionally by vascular distribution:

  • Caudate and quadrate lobe are part of left
  • Divided by the fossa for the gall bladder and iVC
95
Q

What are the couinaud segments of the liver related to/

A

The functions of the liver segments

96
Q

What are liver ligaments?

A

Reflections of peritoneum that surround the bare area.
On the left, the coronary ligaments form the left triangular ligament, while on the right, they form the right triangular ligament

97
Q

Liver lymph drainage?

A

The lymph vessels leave the liver and enter several lymph nodes in the porta hepatis
The efferent vessels pass to the coeliac nodes
A few vessels pass from the bare area of the liver through the diaphragm to the posterior mediastinal lymph nodes.

98
Q

How is jaundice cause from lymph drainage of liver

A

Retrograde tumour spread from the coeliac nodes may involve the hepatic nodes in the porta hepatis and obstruct the bile ducts to cause jaundice

99
Q

Liver nerve supply?

A

Sympathetic nerves form the coeliac plexus (foregut, therefore greater splanchnic nerve, T 5 to 9)
The anterior vagal trunk gives rise to a large parasympathetic hepatic branch, which passes directly to the liver

100
Q

Structure of gall bladder?

A

Rounded fundus

Body that is its major part Neck that narrows towards the cystic duct

101
Q

How does bile reach GIT from gall bladder

A

`the cystic duct combines with the common hepatic duct to form the bile duct and enter the 2nd part of the duodenum with the pancreatic duct at the ampulla of Vater

102
Q

How is the cystic duct lumen held up?

A 
The mucous membrane of the 
cystic duct is raised to form a 
spiral fold that is continuous 
with a similar fold in the neck of 
the gallbladder
The fold is commonly known as the “spiral valve (of Heister)”, the function of which is to keep the lumen constantly open.
103
Q

Blood supply of gall bladder?

A

Arterial: Cystic artery, a branch of the right hepatic artery
Venous: Drains directly into the portal vein

104
Q

Lymph drainage of gall bladder?

A

To a cystic lymph node neck GB neck.

  • -> Hepatic nodes
  • -> Coeliac nodes
105
Q

Nerve supply of gallbladder?

A

Sympathetic:
-Foregut (T5-9)

Parasympathetic:
-Vagal fibres from the coeliac plexus.

106
Q

What is used to surgically locate the cystic artery?

Bounded by?

A 
The Calot's hystohepatic triangle
Bounded by:
-The edge of the right lobe of the liver
-The common hepatic duct
-The cystic duct
107
Q

Referred pain from gall bladder?

A

Referred pain from the gallbladder is usually to the epigastrium (T7 to 9), but irritation of adjacent peritoneum may involve the phrenic nerve (C3, 4, 5) giving referred pain to the right shoulder tip, via C3, 4 in the supraclavicular nerves

108
Q

Cause for painless, continues jaundice?

A

Carcinoma of the head of the pancreas may obstruct the bile duct causing painless, continuous jaundice

109
Q

Where does common bile duct enter duodenum?

A

At the major duodenal papilla

110
Q

What does the ERCP test stand for and identify?

A

Endoscopic, retrograde, cholangio pancreaticogram (ERCP) with stones in the gall bladder

111
Q

Where does the transpyloric place lie?

What structures lie on it?

A

The Transpyloric Plane at L1 is midway between the jugular notch and the pubic symphysis, and through the tips of the 9th costal cartilages

List of structures that lie on it:

  • Fundus of gall bladder
  • Pylorus
  • Neck of pancreas
  • Formation of portal vein
  • Hilum of kidney (right lower than left)
  • Spinal cord ends at L1/2
  • Aorta and origin of SMA
  • IVC
  • 2nd part of duodenum
112
Q

Functions of the pancreas?

A

Exocrine and endocrine functions: digestive pro-enzymes secreted via pancreatic duct to 2nd part of duodenum; insulin and glucagon from the islets of Langerhans

113
Q

Journey of pancreatic duct?

A

The pancreatic duct begins in the tail of the pancreas and joins the bile duct at the hepatopancreatic ampulla (of Vater), that opens as the major duodenal papilla

114
Q

What are the 3 sphincters that make up the sphincter of Oddi?

A

1 around the end of the pancreatic duct (to control flow but prevent bile entering the pancreas)
1 around the end of the bile duct
1 around the combined ducts

115
Q

Blood supply of the pancreas?

A
  1. Coeliac trunk FOREGUT
    - Gastroduodenal (direct to pancreas)
    - Superior pancreaticoduodenal (to Ant and Post branches)
    - Splenic –> Greater and Dorsal Pancreatic branches
  2. Superior mesenteric artery MIDGUT
    - Inferior pancreaticoduodenal (to Ant and Post branches)

Mirrored by veins. Draining to portal vein although the portal vein is the mirror of the gasproduodenal artery.

116
Q

Affect on gallbladder of cholecystokinin?

A

Contraction which is produced but he mucous membrane of the duodenum on arrival of fatty food from stomach.

117
Q

Lymph drainage of the pancreas?

A

Along arteries

Efferent vessels drain into the coeliac and superior mesenteric lymph nodes

118
Q

Nerve supply of the pancreas?

A

Comes with arteries and is vagus (PS) + T7-9 and T10-11

119
Q

What is the method of transmission of intestinal protozoa and helminths?

A

Faecal-derived materials

Acquired during ingestion of contaminated food or water

120
Q

Presentation of intestinal protozoa and helminths?

A

Acute to chronic diarrhoea and inflammation

121
Q

Name protozoal infection of the GIT, 2 in SI and 1 in colon?

A

SI: GIardia lambda, crytosporidium parvum

LI: Entamoeba histolytic

122
Q

Describe the 2 stages of the life cycle of G. lamblia?

A
  1. Trophozoite
    - Flagellated and bi-nucleated
    - Lives in upper part of SI
    - Adheres to brush border of epithelial cells
  2. Cyst
    - Formed when trophozoite forms resistant wall
    - Passes out in stools
    - Can survive for several weeks
123
Q

Pathogenesis of G. lamblia?

A

Present in duodenum, jejunum and upper ileum
Attaches to the mucosa via ventral sucker
Does not penetrate the surface
Causes damage to the mucosa and villous atrophy
Leads to malabsorption of food, esp. fats and fat soluble vitamins
May swim up bile duct to gall bladder

124
Q

Clinical presentation of G. lamblia?

A

Mild infections = asymptomatic
Chronic diarrhoea presents in immunocompromised patients
Stools are characteristically loose, foul-smelling and fatty

125
Q

C. parvum, transmission and reservoir?

A

Transmission: Faecally contaminated drinking water
Reservoir: Animals (usually cattle)

126
Q

Life cycle of C. parvum?

A

Asexual & sexual development
within host:
• Ingestion of resistant oocysts
• Release of infective sporozoites in small intestine
• Invasion of intestinal epithelium
• Division to form merozoites which re-infect cells
• After sexual phase, oocytes released

127
Q

Pathogenesis of C. parvum?

A
  • Enters cells of the microvillus border ofsmall intestine
  • Remains within vacuole of epithelial cell
  • May multiply to give large numbers of progeny, especially in immunocompromised hosts
128
Q

Presentation of C. parvum?

A
  • Moderate to severe profuse diarrhoea
  • Up to 25 litres of watery faeces / day
  • Usually self limiting disease
  • In HIV positive individuals with CD4+ T-cell counts of <100/mm3, diarrhoea is prolonged and may become irreversible and life- threatening
129
Q

E. histolytica:
Transmission?
Role of cysts?

A

Transmission: Ingestion of contaminated food/water, anal sexual activity

Role of cysts:
• Cysts pass through stomach and excyst (break open and release contents) in the small intestine giving rise to progeny
• These adhere to epithelial cells and cause damage mainly through cytolysis
• After mucosal invasion, cysts invade red blood cells giving rise to amoebic colitis
• Trophozoite stages live in large intestine and pass out as resistant, infective cysts

130
Q

Pathogenesis of E. histolytica?

A

• Adheres to epithelium and acute
inflammatory cells
• Resists host humoral and cell mediated immune defence mechanisms
• Produces hydrolytic enzymes, proteinases, collagenase, elastase
• Produces protein that lyses neutrophils, the contents of which are toxic to the host

131
Q

Clinical presentation fo E. histolytica?

A
  • Small localised superficial ulcers leading to mild diarrhoea
  • Entire colonic mucosa may become deeply ulcerated leading to severe amoebic dysentery
  • Complications include intestinal perforation
  • Trophozoites may spread to the liver, and other organs
  • Rarely, abscesses spread to overlying skin
132
Q

Difference between bacillary and amoebic dysentery?

A 
Shigella sp. (bacillary)
• Many PMN in stool
• Eosinophilsabsent
• Many bacilli in stool
• Blood/mucus present in stool
Entamoeba (amoebic)
• Few PMN in stool
• Eosinophils present
• Few amoebae in stool
• Blood/mucus present in stool
133
Q

Difference between the treatment of G. lamblia, C.parvum and E.histolytica?

A

G. lamblia
• Mepacrine hydrochloride
• Metronidazole
• Tinidazole

C.parvum
• Nitazoxanide
• Spiramycin

E.histolytica
• Metronidazole

ORT for all.

134
Q

Ways to prevent protozoal infections of the GIT?

A
  • Improved hygiene and water supplies
  • Eating only freshly prepared food served hot
  • Avoiding salads and fruit which cannot be peeled
  • Avoiding tap water and ice cubes
135
Q

What are the 3 categories of helminths?

A
  1. Roundworms (nematodes)
  2. Tapeworms (cestodes)
  3. Flukes (trematodes)
136
Q

5 examples of roundworms

1 example of a tapeworm

A 
Roundworm:
• Strongyloides stercoralis
• Trichuris trichiura
• Ascaris lumbricoides
• Enterobius vermicularis
• Ancylostoma duodenale

Tapeworm:
• Taenia solium

137
Q

Nematode intestinal infections:

  • Transmission?
  • Infection by?
  • Diagnosis?
A 
Transmission: Through soil
Infection by:
-Swallowing infective eggs
-Active skin penetration by larvae and systemic migration through lung to intestine  
Diagnosis: Stool microscopy
138
Q

Have 6 helminth infections of the GIT

A
  • Strongyloides stercoralis
  • Trichuris trichiura
  • Ascaris lumbricoides
  • Enterobius vermicularis
  • Ancylostoma duodenale

• Taenia solium

139
Q

S. stercoralis:
Class of helminth?
Result of infection?
Clinical presentation?

A

Class: Pinworm

Results in…

  • Disruption of SI mucosa
  • Villous atrophy
  • Marked loss of elasticity of intestinal wall

Clinical presentation:

  • Dysentery
  • Dehydration
  • Malabsorption syndrome
  • Anal pruritus
  • Associated with appendicitis
140
Q

T. trichiura:
Class of helminth?
Acquired by?

A

Class: Whipworm

Acquired by ingesting eggs on veg

141
Q

A. lumbricoides:
Class of helminth?
Clinical presentation?

A

Class: Giant roundworm

Clinical presentation:
• Allergic reaction in sensitised people 
• Digestive upsets
• Protein/energy malnutrition
• Intestinal blockages
• Worm may invade mouth nose etc.
142
Q

E. vermincularis:
Class of helminth?
Presentation?

A

Class: Threadworm

Presentation:
Intense itching
Secondary bacterial infection = Mild catarrhal inflammation and diarryhoea and slightly eosinophilia

143
Q 
A. duodenale:
Class of helminth?
Acquired by?
Pathogenesis?
Presentation?
A 
Class: Hookworm
Acquired by walking barefoot in infected
areas
Pathogenesis: Attaches to small intestine, suck blood and protein, often present in huge numbers
Presentation: Hypochromic anaemia
144
Q

Treatment and prevention of intestinal helminth infections

A

• Improved hygiene and sanitation are important in prevention of infection
• Specific drugs in lecture on “anti-helminthics”
– Mebendazole
– Praziquantel

145
Q

4 problems of antiprotozoal and antihelminthic agents

A
  • Large variety of species
  • Complexities of their life cycles
  • Differences in their metabolic pathways
  • Drugs active against protozoa are inactive against helminths
146
Q

Define the inheritance patterns of:

  1. Familial Adenomatous Polyposis coli, FAP

2. Hereditary non-polyposis coli, HNPCC (Lynch syndrome)

A
  1. FAP = Autosomal dominant

2. HNPCC= Autosomal dominant

147
Q

2 genetic tests for FAP and HNPCC?

A

FAP and HNPCC tests:

  • Protein truncation
  • Direct sequencing tumour support
148
Q

To describe the molecular mechanisms underlying FAP

A

In FAP, mutated APC leads to:

  • Distorted cytoskeletal network
  • Loss of polarity
  • Decreased cell-cell adhesion
  • Aberrant cell migration
  • -> Cancer initiation and progression
149
Q

To identify additional risk factors for colon cancer

A

Diet:

  • High fibre reduced risk
  • High intake of red and processed meats increases risk
  • Fish decreases risk

Obesity

Alcohol

150
Q

How aspirin may protect against colon cancer. Risk?

A

Aspirin and other NSAIDs inhibit COX-2.
Mechanism of inhibition? COX-2 increased in early stages of colorectal cancer
–> increase prostaglandin synthesis
–> Stimulates proliferation and angiogenesis
–> Inhibits apopotsis

Risk? Less prostaglandins, less bp regulation, increase CV risk

151
Q

What is beta- catenin?

A

Catenin beta-1, also known as β-catenin, is a protein that in humans is encoded by the CTNNB1 gene. β-catenin is a dual function protein, involved in regulation and coordination of cell–cell adhesion and gene transcription.

In cytoplasm B-catenin + APC –> B-catenin degradation

B-catenin – enter cell nucleus –> B-catenin + TCF –> Transcription and cell division

(TCF= T-cell factor)

152
Q

Role of b-catenin and APC in wnt signalling and cell proliferation?

A 
WITHOUT Ant SIGNAL
1. Inactive receptor
2. Inactive signalling protein
3. Active APC containing complex
4. Degradation of b-catenin
5. Inactive TCF complex
Wnt-responsive genes OFF
With WNT SIGNAL 
1. Wnt present and to receptor
2. Active receptor
3. Active signalling protein
4. Inactive APC containing complex
5. Stable b-catenin
6. Active TCF complex
Transcription of Wnt- responsive genes leading to proliferation of gut stem cells
153
Q

Why the colon?

A

Colon unusual organised means that there is a stem cell population in the centre of the colon, where the wnt pathway is active. Then areas of inactive pathway beyond it.
So areas of varying proliferation

154
Q

Mutation in APC is also seen in ______ tumours

Mutations of ____ alone is not sufficient to cause cancer

A

Mutation of APC is also seen in sporadic tumours
Mutation of APC alone is not
sufficient to cause cancer

155
Q

Which has higher risk of colon tumours, HNPCC or FAP?

A

Hereditary non-polyposis coli, HNPCC

156
Q

Repetitive regions of DNA are more susceptible to…

A

Errors

157
Q

Difference between FAP and HNPCC in number of polyps, mutation rate, risk of cancer, penetrance

A 
FAP
• Large number of Polyps
• Low mutation rate
• High cancer risk because of high number of polyps
• 100% penetrance
HNPCC
• Low number of polyps
• High mutation rate
• High cancer risk despite low number of polyps
• 80% penetrance
158
Q

What is the screening programme in Scotland for colon cancer?

A

> 50yrs screened every 2 years of occult blood and if positive then colonoscopy
If known FAP/HNPCC: bi annual colonoscopy from 25 years
If at high to moderate risk: Colonoscopy every 5 years from age 50-75

159
Q

What is classed as “high to moderate risk” of colon cancer?

A

People with 3+ affected relatives in a first degree kinship with each other
Two affected relatives less than 60 years old in a first degree kinship with each other

160
Q

What is the progression from polyp to carcinoma in HNPCC?

A

Intestinal epithelial lining – (APC signal)–> Adenoma (K-RAS –(p53, SMADs) –> Carcinoma

161
Q

Features of FAP?

A

Large number of polyps developing in adolescence onwards

90% of patients also have pigmented legions in retina (CHRPE)

162
Q

Why do defects in APC predispose to cancer?

A

Tumours suppressor gene. in normal, mutation by chance you are protected. by other working copy of gene. mutation in minority.
In patient who already have mutation, if you get mutation by chance. Patient is no longer protected. More at risk pattients.

163
Q

Name 4 other tissues affected by FAP

A
  • Gardner Syndrome
  • Rare
  • Variant of FAP
  • Masses of benign tumours
  • Jaw cysts
  • Sebaceous cysts
  • Osteomata
  • pigmented lesions of the retina (CHRPE)
164
Q

Features of HNPCC

A
  • High risk of colon tumours
  • Can be underlying cause of other tumour types eg endometrium, ovarian, small intestine, stomach
  • Low numbers of polyps
165
Q

3 gene defect in HNPCC?

A

MSH2
MLH1 **
MSH6

166
Q

What is the difference in the chromosomal instability of FAP and HNPCC?

A 
FAP= whole chromosome instabiloty
HNPCC= small segments of chromosome instability
167
Q

Define overweight and obesity in adults and children

A

Excess adiposity

In children:
Overweight= BMI of +25 at age 18
Obese= BMI 30+ at age 18

168
Q

Outline the components of energy balance and what factors cause excess weight gain

A

Energy balance = Energy intake and expenditure equal

Factors which lead to weight gain:

  • Lowered physical activity
  • Sedentary lifestyle
  • Large portion size
  • Variety of food options
  • Lower income background
169
Q

Understand the health implications of excess weight gain

A 
CV issues
Anxiety
Depression
Anorexia
Arthritis
Diabetes 
Cancer
170
Q

be able to describe modifiable behaviours in the treatment of childhood obesity

A

Leptin therapy to those with mutation in leptin gene

171
Q

What are the two main consequences of childhood obesity?

A

Endocrine: Insulin resistance/ impaired glucose tolerance: Type 2 diabetes
CVS: Hypertension, dyslipidaemia, fatty streaks, LV hypertrophy

172
Q

Genetic link to obesity

A

Evidence: familial, twin, family, functional

Monogenic forms of obesity

  • Rare
  • Single gene disorders

Polygenic/ common forms of obesity
-Complex interactions between genes and environment
• gene-gene
• gene-environment
[Individual variation in obese phenotype]

173
Q

Example of environment interaction in the pathogenesis of obesity

A

Pima in Arizona
• typical American lifestyle
• typical American diet

Pima in Sierra Madre Mountains of Mexico
• traditional methods of farming, cooking, fetching water
• largely unaffected by labour saving devices

174
Q

Candidate common gene variants predisposing to polygenic obesity

A
  • Peroxisome proliferator-activated receptor ( PPARG) (Pro12ala)
  • Uncoupling Proteins (UCPs)
  • Beta adrenergic receptors (B3-Trp64Arg)
  • FTO
  • MC4R…
  • NPY2R
  • Emerging evidence for gene variants involved in reward behaviour (e.g. DRD2 Taq1A)
  • Genes linked to variation in weight through taste (e.g. CD36)
175
Q

What does GWAS stand for?

A

Genome-wide association studies

176
Q

Use of GWAS

A

Identifies new obesity loci
Whole genome studies:
• systematic analysis of genome
• powered to detect small effects by testing in large populations

177
Q

Relevance of gene FTO in obesity

A

• Found on chromosome 16
• Encodes a protein with 2-oxoglutarate-dependent nucleic acid
demethylase activity
• Role in fatty acid metabolism, DNA repair, post-translational changes
• Expressed in brain, pancreatic islet, adipose tissue, adrenal glands
• Polymorphisms on FTO gene robustly linked to BMI & obesity in adults and children

FTO VARIEANTS PREDISPOSE TO OBESITY

  • Increases energy intake
  • Preference for fat intake
178
Q

Explain the difference between food allergy and food intolerance

A

Food allergy: An inappropriate reaction by the body’s immune system to the ingestion of a food that in the majority of individuals causes no adverse effects.

Food intolerance:
General term used to describe a range of adverse responses to food, including allergic reactions, adverse reactions resulting from enzyme deficiencies, pharmacological reactions and other non-defined responses

179
Q

List some conditions that result from food allergy

A

Anaphylactic shock

Delayed response

180
Q

Describe common examples of food intolerance

A 
Peanut allergy
Coeliac disease
Lactose intolerance
Hereditary fructose intolerance
Caffeine sensitivity
181
Q

Incidence definition?

A

The number of new cases in a population over a fixed period of time

182
Q

Period prevalence definition?

A

The total number of existing cases in a population over a fixed period of time

183
Q

Point prevalence definition?

A

The total number of existing cases in a population at a specific time

MD3002 Weeks 1-6 (5 decks)

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