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MD3002 > WEEK 3 > Flashcards

WEEK 3 Flashcards

1
Q

Where are carbohydrates absorbed? What are they broken into?

A

The small intestine

  • glucose
  • galactose
  • fructose
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2
Q

What is the mechanism behind the production of (i) glucose (ii) galactose (iii) fructose from a carbohydrate?

A

(i) Sodium dependant cotransport
(ii) sodium dependent cotransport
(iii) facilitated diffusion

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3
Q

Describe how (i) secondary active transport (ii) facilitated diffusion work for carbohydrates?

A

(i) SGLT1 located on the apical membrane transports glucose and galactose
(ii) GLUT5 transports fructose across the apical membrane

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4
Q

Where does protein digestion (i) begin (ii) complete/end?

A

(i) in the stomach with pepsin

(ii) small intestine with pancreatic and brush-border proteases

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5
Q

What is the function of (i) endopeptidases (ii) exopeptidases?

A

(i) hydrolyse the interior peptide bonds of proteins

(ii) hydrolyse one amino acid at a time

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6
Q

Pancreatic proteases are secreted as inacitve precursors, what is the importance of tryspinogen?

A

It is converted to the active from trypsin, by the brush border enzyme enterokinase
- the trypsin catalyses the conversion of the other inactive precursors to active enzymes

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7
Q

Proteins are absorbed in the small intestine. What is the mechanism behind producing (i) amino acids (ii) dipeptides (iii) tripeptides?

A

(i) sodium dependent cotransport
(ii) H+ dipeptide cotransport
(iii) H+ tripeptide cotransport

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8
Q

What must happen to dietary lipids before digestion and absorption can occur? Why is this the case?

A

They must be solubilised because they are hydrophobic (insoluble in water)

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9
Q

Where does digestion of lipids begin? Where is it completed?

A

Begins in the stomach with the action of lingual and gastric lipases
- completed in the small intestine with the action of pancreatic enzymes

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10
Q

What is the key role of gastric lipase?

A

to slow the rate of gastric emptying so that pancreatic enzymes are able to digest lipid
- CCK secreted from I cells of duodenal and jejunal mucosa in response to the presence of monoglycerides and fatty acids and small peptides and amino acids

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11
Q

What emulsifies dietary lipids?

A

bile salts
lysolecithin
products of lipid digestion

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12
Q

What does emulsification of dietary lipids produce?

A

small droplets of lipids dispersed in an aqueous solution creating a large surface area for pancreatic enzyme digestion

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13
Q

What are secreted to complete the digestion of lipids?

A 
Pancreatic enzymes (pancreatic lipase, cholesterol ester hydrolase and phospholipase A2)
- Colipase (a protein)
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14
Q

What is the structure of a chylomicron?

A

100nm diameter

- have a core of triglycerides and cholesterol ester-phospholipids and apoproteins on the outside (80%/20%)

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15
Q

Where are chylomicrons found/stored? Where do they move?

A

Packaged into secretory vesicles on the golgi membrane and are exocytosed across the basolateral membrane
- they are too big to enter vascular capillaries but enter the lymphatic capillaries (lacteals) by moving between endothelial cells that line the lacteals

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16
Q

What does the lymphatic circulation do with chylomicrons?

A

They carry them to the thoracic duct

- where they are emptied into the blood stream

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17
Q

Lipids are absorbed in the small intestine. By which mechanism are fatty acids, monoglycerides and cholesterol produced?

A
  • bile salts form micelle
  • diffusion of products into intestinal cells
  • re-esterification within the cell to triglycerides and cholesterol
  • chylomicrons form in the cell and transfer to lymph
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18
Q

What are the tight junctions like in the (i) small intestine (ii) large intestine?

A

(i) leaky (permeable via the paracellular route)

ii) tight (impermeable via the paracellular route

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19
Q

What parts of the SMALL intestine are responsible for (i) absorption (ii) secretion?

A

(i) villi

(ii) crypts of Lieberkuhn

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20
Q

What parts of the LARGE intestine are responsible for (i) absorption (ii) secretion?

A

(i) surface epithelial cells

(ii) colonic glands

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21
Q

For an examination of the abdomen/GU, how should the patient be positioned?

A

Comfortably supine with head resting on 1 or 2 pillows

- have abdomen exposed from xiphisternum to symphysis pubis

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22
Q

What is involved in the general inspection of an abdominal and GU examination?

A
  1. Look AROUND pt
    - sick bowls
    - empty bottles/cans
  2. Look AT pt
    - do they look well? in pain?
    - nutritional state (cachectic or obese)
    - signs of liver disease e.g. bruising, spider naevi
    - oedema (cirrhosis, pelvic mass, nephrotic sydrome, renal failure)
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23
Q

What is involved in the close inspection of the hands and arms in an abdominal/GU examination?

A 
CLUBBING
- causes are MILC
- malabsorption (eg coeliac), IBD (UC and Crohn's), Lymphoma, Cirrhosis
ASTERIXIS
- coarse flapping tremor
- occurs with hepatic encephalopathy
RADIAL PULSE
BP/TEMP
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24
Q

What are you looking for at close inspection of the face?

A

Jaundice

Pull down eyelid to check for anaemia

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25
Q

What are you looking at/for during the mouth part of an abdominal/GU examination?

A

Mouth, Breath Lips, Tongue, Teeth, Gums
- stomatitis, glossitis, candidiasis, ulcers, pigmentation (Peutz-Jeghers Syndrome), telangiectasia, dentition, gingivitis and ‘mousy’ odour (fetor hepaticus)

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26
Q

When inspecting the chest and axillae, what are you looking for?

A

CHEST - spider naevi, gynaecomastia (in men)

AXILLAE - loss of axillary body hair

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27
Q

What are you looking for in the close inspection of the abdomen?

A

Movement, distension, scars, herniae, masses, striae, dilated veins ‘caput medusae’

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28
Q

What are the 5 reasons for distension of the abdomen? (HINT: the 5 F’s)

A 
Fat
Fluid
Faeces
Flatus
Foetus
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29
Q

During abdominal palpation you palpate all 9 regions both superficially and deep. What are you palpating for?

A

Tenderness (including guarding or re-bound tenderness)
Masses
Organomegaly (spleen, liver, kidneys)
Abdominal aorta

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30
Q

What are the causes of hepatomegaly?

A 
Hepatitis
Alcoholic Liver Disease
RHF
Fatty infiltration
Biliary tract obstruction
Malignancy (metastatic/primary)
Haematological disorders
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31
Q

How do you test for (i) Murphy’s sign (ii) Courvoisier’s sign?

A

(i) Feel for gall bladder tenderness (acute cholecystitis). The pt breathes in whilst you gently palpate RUQ in mid-clavicular line. On liver descent contact with inflamed bladder causes tenderness and sudden arrest of inspiration
(ii) Painless jaundice and a palpable gallbladder. Likely due to extrahepatic obstruction e.g. pancreatic cancer UNLIKELY to be gallstones

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32
Q

What are the causes of splenomegaly?

A
  1. Haematological - haemolytic anaemias, leukaemias, polycythaemia rubra vera, lymphoma, myeloproliferative diseases, myelofibrosis
  2. Infective - e.g. infectious mononucleosis, infective endocarditis, TB, malaria
  3. Rheumatological disorders - RA (Felty’s syndrome), SLE
  4. Rare causes - sarcoidosis, amyloidosis, glycogen storage diseases
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33
Q

What are the causes of renal enlargement?

A 
Hydronephrosis
Polycystic kidney disease
Renal cell carinoma
In CHILDREN, nephroblastoma (Wilm's tumour)
Solitary cysts
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34
Q

What is ascites? What are the causes?

A 
An abnormal collection of fluid in the peritoneal cavity
CAUSES:
- hepatic cirrhosis
- intra-abdominal malignancy
- nephrotic syndrome
- cardiac failure
- pancreatitis
- constrictive pericarditis
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35
Q

What is involved in auscultation using the diaphragm side of your stethoscope?

A
  1. Listen for normal bowel sound (up to 2 mins)
  2. Auscultate for abdominal aortic bruits
  3. Auscultate renal arteries
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36
Q

What 2 things are palpated for when examining the back?

A

Renal tenderness

Cervical lymph nodes

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37
Q

What are the 3 other areas offered in an abdominal/GU exam?

A

Offer to examine groin
Offer to examine genitalia
Requests to do digital rectal examination (DRE)

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38
Q

What are the indications for a rectal examination?

A

Rectal bleeding
Prostatic symptoms
Change in bowel habit
Possible spinal cord injury

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39
Q

How is a pelvic examination performed? What are the indications to perform?

A

Bi-manual - one hand palpates per vagina and other per abdomen
INDICATIONS:
- pelvic pain
- abnormal vaginal bleeding or discharge
- if considering a vaginal or uterine prolapse

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40
Q

What are the causes of (i) acute (ii) chronic oesophagitis?

A

(i) Infection in immunocompromised pts (HSV, candida, CMV)
Corrosives
(ii) SPECIFIC - TB, bullous pemphigoid and epidermolysis bullosa, Crohn’s disease
NON SPECIFIC - reflux oesophagitis

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41
Q

What happens to the body in reflux oesophagitis? What factors predispose GORD?

A 
Squamous epithelium damaged
- eosinophils epithelial infiltration
- basal cell hyperplasia
- chronic inflammation
GORD
- 'incompetent' GO junction: alcohol and tobacco, obesity, drugs (caffeine), hiatus hernia, motility disorders
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42
Q

What can severe reflux oesophagitis lead to?

A

Ulceration

- this may lead to healing by fibrosis (stricture or even obstruction)

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43
Q

What is Barrett’s Oesophagus?

A

Longstanding reflux
Normally aged 40-60, males more so than females
Lower oesophagus becomes lined by columnar epithelium
Premalignant and so a risk of adenocarcinoma of distal oesophagus 100 times more than general pop.

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44
Q

What is acute gastritis caused by?

A 
Usually due to chemical injury
- drugs e.g. NSAIDs
- Alcohol
Helicobacter pylori-associated 
- usually the transient phase but often becomes chronic
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45
Q

Describe the details of H pylori-associated Gastritis.

A

Gram -ve spiral-shaped or curved bacilli
Oral-oral, faecal-oral, environmental spread
It occupies the protected niche beneath mucus where the pH is approx. neutral
Doesn’t colonise intestinal type epithelium
Resolves with therapy

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46
Q

What therapy is used to resolve H pylori associated gastritis?

A

Double antibiotics and proton pump inhibitors

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47
Q

What are the 2 types of distribution patterns?

A
  1. Diffuse involvement of antrum and body
    - atrophy, fibrosis, intestinal metaplasia
    - associated with gastric ulcer and gastric cancer
  2. Antral but not body involvement
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48
Q

How is H pylori associated Gastritis detected?

A

Faecal bacteria
Urea breath test
Gastric biopsy rapid urease test (CLO test)

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49
Q

What is Chemical (reflux) Gastritis? What is it caused by?

A

Loss of epithelial cells with compensatory hyperplasia of gastric foveolae
- caused by regurgitation of bile and alkaline duodenal secretion
Associated with
- defective pylorus
- motility disorders

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50
Q

What is autoimmune chronic gastritis?

A

It is an autoimmune reaction to gastric parietal cells

  • loss of acid secretion
  • loss of intrinsic factors (vit B12 deficiency or macrocytic anaemia - pernicious)
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51
Q

With autoimmune chronic gastritis, what is there an increased risk of?

A

Of gastric cancer

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52
Q

What are the 4 major sites of peptic ulceration? Please put in descending order.

A

First part of duodenum
Junction of antral and body mucosa in stomach
Distal oesophagus
Gastro-enterostomy stoma

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53
Q

What is a peptic ulcer defined as?

A

A breach in mucosal lining of alimentary tract as a result of acid and pepsin attack

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54
Q

What factors can cause peptic ulceration? (HINT: there’s 7 factors)

A 
Hyperacidity 
H. pylori gastritis
Duodenal reflux
NSAIDs
Smoking 
Genetic factors
Zollinger-Ellison syndrome
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55
Q

What complications can arise as a result of peptic ulceration? (HINT there’s 6)

A 
Haemorrhage
Penetration of adjacent organs e.g. pancreas
Perforation
Anaemia
Obstruction
Malignancy
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56
Q

For gastric ulcers, what is the (i) relative incidence (ii) age (iii) social class (iv) blood group (v) acid levels (vi) helicobacter gastritis?

A

(i) 1
(ii) increases with age
(iii) higher in class V
(iv) A
(v) normal or low
(vi) about 70%

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57
Q

Where is the zone of cell proliferation found? How often does it replace villous cells?

A

In the base of the crypts

- every 48-96 hrs

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58
Q

What causes acute peptic ulcers? (HINT: there’s 3 causes)

A
  1. Related to acute gastritis
    - full thickness loss of epithelium, rather than just erosion
  2. Related to a stress response
    - e.g. curling’s ulcer following severe burns
  3. A result of extreme hyperacidity
    - e.g. gastrin secreting tumours
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59
Q

Where do chronic peptic ulcers tend to occur? What is their pathogenesis?

A 
They tend to occur at mucosal junctions
e.g. antrum -> body
PATHOGENESIS
- hyperacidity
- mucosal defence defects
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60
Q

What effect does a chronic gastric ulcer have on the body?

A 
Normal pH of gastric juice 1-2
Mucosal defences
- mucus-bicarbonate barrier
- surface epithelium (less important
Mucus-bicarbonate barrier
- dissolved by biliary reflux
Surface epithelium
- damaged by NSAIDs
- injured by H. pylori
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61
Q

WHERE does intestinal secretion occur?

A

In the epithelial cells lining the crypts of Lieberkuhn

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62
Q

What is the pathology of a chronic gastric or duodenal ulcer?

A 
They are usually small (less than 20mm)
- sharply 'punched out' with defined edges
Has a defined structure
- granulation tissue at base
- underlying inflammation and fibrosis 
- loss of muscularis propria
COMPLICATIONS
= bleed, burst or block. Penetration of adjacent organs (pancreas). Malignant change (rare in gastric and 'never' in duodenal ulcer
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63
Q

For duodenal ulcers, what is the (i) relative incidence (ii) age (iii) social class (iv) blood group (v) acid levels (vi) helicobacter gastritis?

A

(i) 3
(ii) increases up to 35 years
(iii) even distribution
(iv) O
(v) high or normal
(vi) 95-100%

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64
Q

What causes acute peptic ulcers? (HINT: there’s 3 causes)

A
  1. Related to acute gastritis
    - full thickness loss of epithelium, rather than just erosion
  2. Related to a stress response
    - e.g. curling’s ulcer following severe burns
  3. A result of extreme hyperacidity
    - e.g. gastrin secreting tumours
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65
Q

Where do chronic peptic ulcers tend to occur? What is their pathogenesis?

A 
They tend to occur at mucosal junctions
e.g. antrum -> body
PATHOGENESIS
- hyperacidity
- mucosal defence defects
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66
Q

Q ON CHRONIC GASTRIC ULCER???????

A
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67
Q

What 2 things cause the formation of a chronic duodenal ulcer?

A
  1. INCREASED ACID PRODUCTION
    - more important than for gastric ulcer
    - can be induced by H pylori
  2. REDUCED MUCOSAL RESISTANCE
    - gastric metaplasia occurs in response to hyperacidity
    - then colonised by H. pylori
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68
Q

What is the pathology of a chronic gastric or duodenal ulcer?

A 
They are usually small (less than 20mm)
- sharply 'punched out' with defined edges
Has a defined structure
- granulation tissue at base
- underlying inflammation and fibrosis 
- loss of muscularis propria
COMPLICATIONS
= bleed, burst or block. Penetration of adjacent organs (pancreas). Malignant change (rare in gastric and 'never' in duodenal ulcer
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69
Q

What are the ways that the GI tract can become damaged? (HINT: there’s 5 ways)

A
  1. Local Infammation
  2. Ulceration/perforation of mucosal epithelium
  3. Disruption of normal microbiota
  4. Pharmacological action of bacterial toxins
  5. Invasion to blood or lymphatics
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70
Q

How does epithelial perforation arise? What can it lead to? What is the current treatment?

A

The lining of the mucosa wall is perforated due to untreated ulcers

  • may result in leaking of food and gastric juices to peritoneal or abdominal cavities
  • treatment = surgery
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71
Q

What are the various bacterial diarrhoeal pathogens? Name them. (HINT: there’s 5/6)

A
  1. Vibrio cholerae
  2. Escherichia coli
  3. Campylobacter jejuni
  4. Salmonella spp.
  5. Shigella spp.
  6. Listeria monocytogenes
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72
Q

Where is the liver located?

A

Across the upper abdomen, under the diaphragm

- note it should not be palpable below the costal margin

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73
Q

Deep to the peritoneal covering, what is the liver surrounded by? Describe this surrounding.

A

By Glisson’s capsule

  • a thin connective tissue layer that sends extensions into the organ, in between the lobules
  • it isn’t really strong enough to hold sutures that may be required following trauma to the liver. Similarly, the interlobular connective tissue is hardly visible in a normal liver
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74
Q

What is the (i) arterial supply (ii) venous drainage of the liver?

A

(i) (hepatic) portal vein (divides into R and L terminal branches that enter porta hepatis behind arteries) bringing absorbed nutrients from the stomach and SI; and the hepatic artery (from coeliac trunk, divides into R and L terminal branches that enter porta hepatis) which supplies the hepatocytes with oxygen
(ii) hepatic veins emerge from posterior surface of liver and drain into the IVC

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75
Q

How is bile drained in the liver?

A

Via canaliculi that lie between the hepatocytes into bile ductules and eventually into bile ducts

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76
Q

What are the 4 functions of the liver?

A
  1. Synthesis and secretion of bile
  2. Storage of glucose, glycogen, proteins, vitamins and fats
  3. Detoxification of metabolic waste
  4. Synthesis of blood clotting & anticoagulant factors
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77
Q

What is the visceral surface of the liver covered by? Where is it NOT covered by this?

A

By peritoneum
- except at the fossa for the gall bladder and at the porta hepatis, which houses the portal triad (portal vein, hepatic artery, hepatic (biliary) ducts

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78
Q

What is the new surgical approach to describing sections of the liver? What are these sections related to?

A

Couinaud liver segments

- related to branches of the hepatic artery, portal vein and hepatic veins; the segments may be surgically removed

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79
Q

What are the 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

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80
Q

What is the lymphatic drainage of the liver?

A

The liver produces about one third to one half of all body lymph

  • the lymph vessels leave the liver and enter several lymph nodes in the porta hepatis
  • efferent vessels pass to coeliac nodes
  • a few vessels pass from the bare area of the lover through the diaphragm to the posterior mediastinal lymph nodes
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81
Q

What may a retrograde tumour spread from the coeliac nodes involve?

A

The hepatic nodes in the porta hepatis and obstruct the bile ducts to cause jaundice

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82
Q

What is the nerve supply of the liver?

A

Sympathetic nerves from the coeliac plexus

- the anterior vagal trunk gives rise to a large sympathetic hepatic branch, which passes directly to the liver

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83
Q

What are the various parts of the gallbladder?

A

A rounded fundus
A body that is its major part
A neck that narrows towards the cystic duct
- the cystic duct combines with common hepatic duct to form bile duct

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84
Q

What is the capacity of the gall bladder? What is the function of the gall bladder?

A

60ml

- sole function is to store and concentrate bile, both of which are non-essential

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85
Q

What is Hartmann’s pouch?

A

A dilatation at the neck of the gall bladder

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86
Q

Do the IVC and hilum of the right kidney lie anterior or posterior to the duodenum?

A

POSTERIOR

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87
Q

What is the spiral valve of Heister? What is its function?

A

The mucous membrane of the cystic duct is raised to form a spiral fold that’s continuous with a similar fold in the neck of the gall bladder
- function is to keep the lumen constantly open

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88
Q

What is the (i) arterial supply (ii) venous drainage of the gall bladder?

A

(i) cystic artery - a branch of right hepatic

(ii) cystic vein - drains directly to portal vein

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89
Q

What is the lymph drainage of the gall bladder?

A

To a cystic lymph node situated near the neck of gall bladder
- from here lymph passes to hepatic nodes along course of hepatic artery and then to coeliac nodes

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90
Q

What is the nerve supply of the gall bladder?

A

Sympathetic (T5-9) and parasympathetic vagal fibres from the coeliac plexus

91
Q

What does the gall bladder contract in response to?

A

The hormone CCK, which is produced by the mucous membrane of the duodenum on the arrival of fatty food from the stomach

92
Q

What is Calot’s cystohepatic triangle?

A

Bounded by the edge of the right lobe of the liver, the common hepatic and cystic duct

  • used to surgically locate the cystic artery
  • NOTE normal variations are very common in the location of the cystic artery
93
Q

Where is referred pain from the gall bladder to?

A

usually to the epigastrium (T7-9)
- but irritation of adjacent peritoneum may involve the phrenic nerve giving referred pain to the shoulder tip (via supraclavicular nerves)

94
Q

Describe the 4 parts of the course of the common bile duct.

A
  1. In the 1st part it lies in the free margin of the lesser omentum infront of the opening into the lesser sac. It lies in front of right margin of portal vein and to the right of the hepatic artery
  2. 2nd part its situated behind the 1st part of duodenum to right of gastroduodenal artery
  3. Lies in a groove on posterior surface of head of pancreas, where bile duct joins with main pancreatic duct
  4. Combined ducts open into duodenum at major duodenal papilla (ampulla of Vater)
95
Q

What structures lie on the transpyloric plane - L1 level (tips of 9th CC’s)? (HINT: there’s 9)

A
  1. Fundus of gall bladder
  2. Pylorus
  3. Neck of pancreas
  4. Formation of portal vein
  5. Hilum of kidney (right lower than left)
  6. Spinal cord ends at L1/2
  7. Aorta and origin of SMA
  8. IVC
  9. 2nd part duodenum
96
Q

What are the functions of the pancreas?

A

Has both exocrine and endocrine functions

  • digestive pro-enzymes secreted via pancreatic duct to 2nd part of duodenum
  • insulin and glucagon from islets of Langerhans
97
Q

Where is the pancreas located within the body?

A

Retroperitoneal

  • across epigastrium close to major BVs (=> difficult to access)
  • lies in the C shaped curve of the duodenum with a head, neck, body, tail and uncinate process
98
Q

Where does the pancreatic duct begin?

A

In the tail of the pancreas

- joins the bile duct at the hepatopancreatic ampulla (of Vater) which opens as the major duodenal papilla

99
Q

What are the 3 components of the Sphincter of Oddi?

A
  1. Around the end of the pancreatic duct (to control flow but prevent bile entering pancreas
  2. Around end of bile duct
  3. Around the combined ducts
100
Q

What is the arterial blood supply of the pancreas?

A
  1. COELIAC TRUNK
    - gives gastroduodenal which goes direct to pancreas but also divides to superior pancreaticoduodenal which gives off anterior and posterior branches
    - gives splenic which divides to greater and dorsal pancreatic branches
  2. SMA
    - gives inferior pancreaticoduodenal which gives anterior and posterior branches
101
Q

What is the venous supply of the pancreas?

A

same as arteries, all draining to portal vein

but the portal vein is the mirror image of the gastroduodenal artery

102
Q

What is the (i) lymphatic drainage (ii) nervous supply of the pancreas?

A

Nerve supply also comes with arteries and is vagus (parasympathetic) plus both T7 to 9 and T10 and 11

103
Q

Describe features of the bacteria Vibrio cholerae.

A

Gram -ve
Comma shaped rod, flagellated
- characterised by epidemics and pandemics
- human only pathogen
- it flourishes in communities with no clean drinking water/sewage disposal

104
Q

What are the (i) serotypes (ii) vaccines for Vibrio Cholerae?

A

(i) Based on O antigens
(ii) Parenteral vaccine - low protective efficiency
Oral vaccine - effective and suitable for travellers

105
Q

What is the pathogenesis of Vibrio Cholerae?

A

Only infective in large doses

  • many of the organisms are killed in the stomach
  • colonises the small intestine involving flagellar motion, mucinase, attachment to specific receptors
  • produces multicomponent toxin
  • there’s a loss of fluid and electrolytes without damage to enterocytes
106
Q

What is the make up of cholera toxin? What is it responsible for?

A

Oligomeric complex of 6 protein subunits that leads to an increase in cAMP
- 1 copy of A subunit (enzymatic)
- 5 copies of B subunit (receptor binding)
It is responsible for the characteristic watery cholera diarrhoea

107
Q

What are the consequences of Cholera infection? (HINT: there’s 5)

A
  1. Fluid loss of up to 1 lire/hr
  2. Electrolyte imbalance leading to dehydration, metabolic acidosis and hypokalaemia
  3. Hypovolaemic shock
  4. 40-60% mortality
  5. less than 1% mortality if given fluid/electrolytes (ORT)
108
Q

What is E.coli?

A

Gram neg bacillus

  • is a member of normal GI microbiota
  • some strains possess virulence factors enabling them to cause disease
109
Q

What are the 6 types of E.coli causing GI infections?

A
  1. EPEC (enteropathogenic) - sporadic cases and outbreaks of infection in under 5’s
  2. ETEC (enterotoxigenic) - ‘travellers’ diarrhoea
  3. VTEC (verocytotoxin-producing) - sporadic cases and outbreaks of gastroenteritis
  4. EHEC (enterohaemorrhagic)
  5. EIEC (enteroinvasive) - food-borne infection in areas of poor hygiene
  6. EAEC (enteroaggregative) - resource-poor countries
110
Q

What 2 enterotoxins does E.coli produce?

A

LT = heat-labile toxin (v. similar to cholera toxin) increase in cAMP
STa = heat stable toxin
leads to increase in cGMP

111
Q

What is C.jejuni?

A

Gram -ve helical bacillus with a large animal reservoir

  • causes food-associated diarrhoea and is the commonest case in the developed world
  • transmission through consumption of raw/undercooked meat, contaminated milk
  • mucosal inflammation and fluid secretion
112
Q

What is the histological appearance of C.jejuni?

A

Inflammation involves the entire mucosa

  • villous atrophy
  • necrotic debris in crypts
  • thickening of BM
113
Q

What is salmonella spp.?

A

Gram neg bacilli

  • causes food associated bacteria
  • transmission through consumption of raw/undercooked meat, contaminated eggs and milk
  • secondary spread can be human to human
114
Q

What are the 3 important species of salmonella?

A

S. typhi
S. paratyphi
S. enteritidis

115
Q

What is the pathogenesis of a salmonella infection?

A

Ingestion of large no. of bacteria

  • absorption to epithelial cells in terminal section of SI
  • penetration of cells and migration to lamina propria
  • multiplication in lymphoid follicles
  • inflammatory response mediates release of prostaglandins
  • stimulation of cAMP
  • release of fluid and electrolytes causing diarrhoea
116
Q

Describe the species S. typhi and S. paratyphi.

A

Cause enteric fevers - typhoid and parathyphoid

  • systemic infections initiated in GI tract
  • restricted to humans
  • multiply within, and are transported around the body, in macrophages
117
Q

Describe/ explain typhoid fever.

A

Pt can excrete S. typhi in faeces for several weeks after recovery

  • 1-3% become chronic carriers, most common in women and elderly
  • is a blanching rash
  • a notifiable disease (public health concern)
118
Q

Is there typhoid vaccines? If so, describe them. How effective are they and who are they recommended for?

A
  1. ORAL, live attenuated with a booster after 5 years
  2. PARENTERAL, capsular polysaccharide with a booster after 2 years

50-80% effective
- recommended for travellers to endemic areas

119
Q

What is shigella spp. ?

A

Bacillus that causes shigellosis

- is a human only species

120
Q

What are the 4 species of shigella?

A
  1. S. dysenteriae = most serious
  2. S. flexneri = severe
  3. S. boydii = severe
  4. S. sonnei = mild
121
Q

What is the pathogenesis of shigella infections?

A

Attaches to mucosal epithelium of distal ileum and colon

  • it causes inflammation and ulceration and is rarely invasive
  • produces shiga toxin and is usually self-limitiing
  • diarrhoea initially watery, but can contain blood and mucus in later stages
122
Q

What is listeria monocytogenes?

A

Coccobacillus that causes listeriosis

  • food borne pathogen associated with pate, soft cheese and unpasturised milk
  • usually presents as meningitis
123
Q

Who are the 3 populations at risk for listeriosis?

A

!. PREGNANT women

  1. IMMUNOSUPPRESSED individuals
  2. ELDERY
124
Q

What are the 6 diarrhoeal pathogens?

A
  1. Rotavirus
  2. Norovirus
  3. Enteric adenovirus
  4. Calicivirus
  5. Coronavirus
  6. Astrovirus
125
Q

What is rotavirus?

A

11 separate segments of double stranded RNA that infects many mammals

126
Q

What is the pathogenesis of a rotavirus infection?

A

Incubation period of 1-2 days

  • replication of virus in small intestinal epithelial cells at tips of villi, result in villous atrophy
  • damage caused to infected cells leaving immature cells with reduced absorptive capacity for sugar, water and electrolytes
  • onset of vomiting, diarrhoea for 4-7 dyas
127
Q

Who does rotavirus normally affect?

A

Children under 2 years old

128
Q

What is the occurence of rotavirus?

A

seasonal occurence as is more common in colder months

129
Q

What is the transmission of rotavirus?

A

Faceo-oral

but may also be faeco-resp

130
Q

What are the vaccines used for rotavirus?

A

RotaRix RotaTeq

  • orally administered (2-3 doses)
  • first dose @ 6-10 weeks of age
  • live, attenuated virus
131
Q

What is norovirus? How is it transmitted?

A

‘Winter vomiting disease’ accounts for most non-bacterial outbreaks worldwide
- past infection in 60% adults and is a human only pathogen
Transmission = faeco-oral, contaminated water/shellfish, fomites

132
Q

Is there a norovirus vaccine?

A

NO

133
Q

What is enteric adenovirus?

A

Accounts for 10% of community acquired diarrhoea’s in young children

  • no seasonal incidence
  • asymptomatic infections common
  • mild, but prolonged diarrhoea
134
Q

What is antibiotic-associated diarrhoea? How can it arise?

A

DOESN’T involve ingestion of pathogen/toxin

- can arise from the disruption of gut microbiota following antibiotic therapy

135
Q

What is C. difficile infection now associated with?

A

Resistance to vancomycin

136
Q

What does (i) tetracycline (ii) clindamycin allow?

A

(i) colonisation by staph aureus and candida spp.

(ii) suppresses gut microbiota and allows c. difficile to multiply

137
Q

What does C. difficile infection produce?

A

Spores for survival

- produces an enterotoxin and a cytotoxin

138
Q

What is largely responsible for the increase in cases of C. difficile diarrhoea?

A

Nosocomial infections

139
Q

What is the structure of Helicobacter pylori?

A

Gram neg spiral that is flagellated

  • microaerophilic
  • more than 80% individuals are asymptomatic
140
Q

What diseases can Helicobacter pylori cause? (HINT: there’s 4)

A

Duodenal ulcers
Gastric ulcers
GO reflux disease
Non-ulcer dyspepsia

141
Q

What are the key features of H. pylori? (HINT: there’s 5)

A
  1. ACID INHIBITING PROTEIN
    - allows for survival in stomach
  2. UREASE - neutralisation of acid pH
  3. ADHESINS - binding to gastric epithelium
  4. CYTOTOXIN - damage to gastric epithelium
  5. FLAGELLUM - movement through gastric mucus layer
142
Q

What is the treatment of H. pylori associated Gastritis?

A 
1 week triple therapy
EITHER:
PPI plus clarithromycin and amoxycillin
OR
PPI plus clarithromycin and metronidazole
143
Q

What is food poisoning?

A

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

144
Q

What are 3 examples of toxins that cause food poisoning?

A
  1. Emetic toxins of Bacillus cereus
  2. Enterotoxin of staph aureus
  3. Neurotoxin of Clostridium botulinum
145
Q

What is ORT? What does it involve?

A

Oral Rehydration Therapy

  • involves the replacement of fluids and electrolytes lost during diarrheal illness
  • 90 to 95% of acute watery diarrhoea can be successfully treated with an ORS
146
Q

What does ORS do?

A

Increases the resorption of fluids and salts into the intestinal wall

147
Q

What is can be used instead of ORS?

A

Fruit juices, coconut water and other indigenous solutions can be an alternative if unable to access ORS

148
Q

What is the food associated GI infection Clostridium perfringens?

A

Usually caused by type A strains from animal guts and soil

149
Q

How does Clostridium perfringens cause a food associated GI infection?

A

Contamination of raw meat products as the spores survive cooking and germination takes place

150
Q

What does Clostridium perfringens do to the body?

A

Multiplies in large intestine and produces spores and enterotoxin
- damages intestinal epithelium and causes diarrhoea

151
Q

What is the liver lobule?

A

Sheets of cells (hepatocytes) radiate outwards from the central vein which forms the central axis of the lobule

152
Q

Where do sinusoids lie? What do they do?

A

Lie between sheets and carry blood from hepatic artery and portal vein to the central vein

153
Q

What is the functional, vascular distribution of the liver?

A

Caudate and quadrate lobes are part of left lobe

- with the fossa for the gall bladder and IVC as the division between the right and left lobes

154
Q

What do infection levels of intestinal protozoa and helminths reflect?

A

Hygiene/sanitation standards

155
Q

How are intestinal protozoa and helminths acquired? What are the common symptoms?

A

Through ingestion of contaminated food or water

- symptoms usually present as acute to chronic diarrhoea and inflammation

156
Q

What are the types of protozoal infections of the (i) small intestine (ii) large intestine?

A

(i) Giardia lamblia
Cryptosporidium parvum
(ii) Entamoeba histolytica

157
Q

With regards to Giardia Lamblia; (i) what is it a frequent cause of? (ii) What is it detected in? (iii) how is it transmitted? (iv) How is it diagnosed?

A

(i) Travellers diarrhoea
(ii) Drinking and recreational water
(iii) Person to person
(iv) By microscopy of stool samples

158
Q

What are the 2 stages of a life cycle of G. lamblia? Describe them.

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
159
Q

Where is G. lamblia present? What is its pathogenesis?

A

In duodenum, jejunum and upper ileum

  • attaches to mucosa via ventral sucker but does not penetrate the surface
  • it causes damage to the mucosa and villous atrophy
  • leads to malabsorption of food, especially fats and fat soluble vitamins
  • may swim up the bile duct to the gall bladder
160
Q

What are the clinical manifestations of G. lamblia?

A

Mild infections are asymptomatic

  • diarrhoea is usually self-limiting (7 to 10 days)
  • chronic diarrhoea is present in immunocompromised pts
  • stools are characteristically loose, foul-smelling and fatty
161
Q

How is Cryptosporidium parvum transmitted? How large is an infective dose?

A

Transmitted through faecally-contaminated drinking water

Infective dose = as few as 10 oocysts

162
Q

What is the life cycle of C. parvum within the body?

A
  1. Asexual and sexual development within host
  2. Ingestion of resistant oocysts
  3. Release of infective sporozites in small intestine
  4. Invasion of intestinal epithelium
  5. Division to form merozoites with re-infect cells
  6. After the sexual phase, oocytes are released
163
Q

What is the pathogenesis of C. parvum?

A

Enters cells of the microvillus border of the SI
- it remains within a vacuole of an epithelial cell but it may multiply to give large no. of progeny, especially in immunocomropmised hosts

164
Q

How does C. parvum clinically manifest itself? What is the danger in certain HIV+ individuals?

A

Moderate-severe profuse diarrhoea

  • up to 25 litres of water faeces a day
  • usually self limiting
  • In HIV+ with CD4+ T cell counts of less than 100mm3 the diarrhoea is prolonged and may become irreversible and life-threatening
165
Q

With regards to Entamoeba histolytica; (i) where is it common? (ii) how is it transmitted? (iii) what do they do?

A

(i) in tropical and sub-tropical countries
(ii) Via ingestion of contaminated food or water, also through anal sexual activity
(iii) cysts pass through stomach and exist in SI, giving rise to progeny. they 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

166
Q

What is the pathogenesis of E. histolytica?

A

Adheres to epithelium and acute inflammatory cells

  • resists host humoral and cell mediated defence mechanisms
  • it produces hydrolytic enzymes, proteinases, collagenase and elastase
  • produces protein that lyses neutrophils, the contents of which are toxic to the host
167
Q

How does Entamoeba histolytica clinically manifest itself?

A

Small localised superficial ulcers leading to mild diarrhoea

- the entire colonic mucosa may become deeply ulcerated leading to severe amoebic dysentry

168
Q

What complications can arise from E. histolytica?

A

Intestinal perforation
Trophozoites may spread to the liver, and other organs
Rarely, abscesses spread to the overlying skin

169
Q

What is the difference between bacillary (Shigella) and Amoebic (Entamoeba) dysentry?

A 
BACILLARY
- many PMN in stool
- eosinophils absent
- many bacilli in stool
- blood/mucus present in stool
ENTAMOEBA
- few PMN in stool
- eosinophils present
- few amoebae in stool
- blood/mucus present in stool
170
Q

What is the treatment of protozoal infections of the GI tract, for (i) G. lamblia (ii) C. parvum (iii) E. histolytica?

A

(i) FOR G. LAMBLIA
- mepacrine hydrochloride
- metronidazole
- tinidazole
(ii) FOR C. PARVUM
- nitazoxanide
- spiramycin
(iii) FOR E. HISTOLYTICA
- metronidazole

171
Q

What is ORT? When is it used?

A

Involves the replacement of fluids and electrolytes lost during diarrhoeal illness
- 90-95% of cases of acute watery diarrhoea can be successfully treated with an oral rehydration solution (ORS) - which increases the reabsorption of fluids and salts into the intestinal wall

172
Q

What are 4 ways to prevent protozoal infections of the GI tract?

A
  1. Improved hygiene and water supplies
  2. Eating only freshly prepared food served hot
  3. Avoiding salads and fruits that can’t be peeled
  4. Avoiding tap water and ice cubes
173
Q

What are the 3 types of Helminths (worms)?

A
  1. ROUNDWORMS (Nematodes)
  2. TAPEWORMS (Cestodes)
  3. FLUKES (Trematodes)
174
Q

What are the 6 types of Helminthic infections of the GI tract?

A
  1. Stronglyloides stercoralis - pinworm/threadworn
  2. Trichuris trichiura - whipworm
  3. Ascaris lumbricoides - giant roundworm
  4. Enterobius vermicularis - pinworm/threadworm
  5. Ancylostoma duodenale - hookworm
  6. Taenia solium - tapeworm
175
Q

What are the most clinically important intestinal worms?

A

Nematodes

176
Q

How are nematodes transmitted? How does infection by them occur? How are they diagnosed?

A

Soil-transmitted
Infection occurs by one of the following:
1. Swalloing infective eggs
2. Active skin penetration by larvae and systemic migration through lung to intestine
Diagnosis by eye/sometimes stool microscopy

177
Q

What is Stronglyoides stercoralis?

A

A pinworm that causes disruption of the small intestinal mucosa causing villous atrophy and marked loss of elasticity of intestinal wall.

178
Q

How does stronglyoides stercoralis clinically manifest itself? (HINT: there’s 5 points)

A 
Dysentery (which is persistant in immunocompromised pts)
Dehydration
Malabsorption
Anal pruritis (itching)
Association with appendicitis
179
Q

What is T. trichiura? How is it acquired?

A

Whipworm that can live in the gut for greater than 3 years

  • acquired through ingesting eggs on vegetables
  • 10,000 eggs produced daily (by just one of them)
180
Q

What is A. lumbricoides?

A

A giant roundworm

  • large thick wide worm 20-30cm
  • females produce approx 20,000 eggs/day from 65 days after infection and adults live in the gut for 2 years
181
Q

How does Ascaris lumbricoides manifest itself clinically? (HINT: there’s 5 points)

A 
An allergic reaction in sensitised people
Digestive upsets
Protein/energy malnutrition
Intestinal blockages
Worm may invade mouth, nose etc.
182
Q

What is enterobius vermicularis? What symptoms arise as a result?

A

A threadworm

  • small cylindrical nematodes smaller than 1cm
  • females migrate to anus at night to lay approx. 10,000 eggs which may develop to infective stage within hours
  • cause intense itching - mild catarrhal inflammation and diarrhoea, slight eosinophilia
183
Q

What is Ancyclostoma duodenale? How is it picked up? What does it do? What does it cause?

A

A hookworm which is often picked up from walking bare foot in infected areas

  • attaches to SI, sucks blood and protein, often present in huge numbers
  • causes hypochromic anaemia
184
Q

What is taenia solium? How is it acquired? Where does it reside?

A

Tapeworm

  • acquired from ingesting worms or eggs in uncooked pork
  • resides in the large intestine and can grow up to 7m long
185
Q

Why do antiprotozoal and antihelminthic agents pose particular problems? (HINT: there’s 4 reasons)

A

Because of:

  1. Large variety of species
  2. Complexities of their life cycles
  3. Differences in their metabolic pathways
  4. Drugs active against protozoa are inactive against helminths
186
Q

What percentage of colorectal cancer pts have a familial history of it?

A

About 25%

- of those we only know the causative mutations in 5-6% of cases

187
Q

What does (i) FAP (ii) HNPCC stand for?

A

(i) familial adenomatous polyposis
- autosomal dominant
(ii) hereditary nonpolyposis colon cancer (Lynch syndrome)

188
Q

What are the features of FAP coli?

A

Autosomal dominant inheritance

  • Large number of polyps (100s or more) developing from adolescence onwards
  • 90% of patients also have pigmented lesions in retina (CHRPE)
189
Q

What is the gene defect in APC (adenomatous polyposis coli)? How do you test for the gene defect?

A

Chromosome 5 q21-22
- large gene
- mostly nonsense or frameshift mutations that result in a premature termination of the protein
Test for by protein truncation test or direct sequencing

190
Q

Why do defects in APC predispose to cancer?

A

If the first hit is a germline mutation, the second somatic mutation is more likely to enable cancer

191
Q

What 2 things does APC do?

A

Binds to beta catenin and microtubules

- the regions of binding match to the C terminus of the protein - in FAP pts this c terminus is often missing

192
Q

What is beta catenin? What does it do?

A
  1. Protein that can work as a transcription factor but is normally found in the cytoplasm where APC can bind to it and degrade the beta catenin, keeping its levels low
    - its levels can accumulate when not bound to APC and move into the nucleus where (with other transcription factors) it turns on genes to increase cell division.
  2. Also present in junctions which links actin cytoskeleton to the adherens junction
193
Q

What do defects in APC also cause?

A

Chromosome instability (CIN)

194
Q

Why is it the colon that cancer arises due to an APC gene defect?

A

Colon organised in v unusual way such that cell proliferation occurs at bottom of crypts due to there beings stem cells there constantly dividing
- if cells divide in wrong orientation they stay in crypts instead of moving out and so proliferate again whilst still in the crypts

195
Q

Where else is mutation of APC seen?

A

In sporadic tumours

- an APC mutation alone is not sufficient to cause cancer

196
Q

What is Gardner syndrome? Describe it.

A

A variant of FAP

  • rare
  • masses of benign tumours
  • jaw cysts and sebaceous cysts
  • osteomata (bone tumour)
  • pigmented lesions of the retina (CHRPE)
197
Q

What are the features of hereditary nonpolyposis coli (Lynch syndrome)?

A

1-5% of all colon cancers and is autosomal dominant

  • high risk of colon tumours
  • can be an underlying cause of other tumour types e.g. endometrium, ovarian, small intestine, stomach
  • low number of polyps
198
Q

What is the gene defect(s) in HNPCC (Lynch syndrome)? (HINT: there’s 3 defects)

A
  1. MSH2 2p21 (40% mutations)
  2. MLH1 3p21 (50% mutations)
  3. MSH6 2p16 (7-10%)
    DONT need to know actual genes but know they all have the same role/function - DNA MISMATCH REPAIR
199
Q

What do mismatch repair gene products do?

A

They exist to recognise when you have the WRONG pairs of bases paired together
- they attract machinery which can cut out the error and correct it

200
Q

What types of regions are more susceptible to errors? WHY is this the case?

A

Repetitive regions

- due to microsatelite instability

201
Q

How do you test for a mutation defect causing HNPCC?

A

Analysis of someone with stable microsatellites will have traces that loon the same for both normal and tumour cells but a patient with microsatellite instability will have different traced for normal and tumour cells
OR
Do biopsies of tumour and see which proteins are being expressed - use this as a code to figure out if there is any mutations

202
Q

Comparing both FAP and HNPCC, what is the difference in (i) number of polyps (ii) mutation rate (iii) risk of cancer?

A

(i) FAP = large no. of polyps
HNPCC = low no. polyps
(ii) FAP = high rate
HNPCC = low rate
(iii) FAP = high cancer risk bcoz high no. polyps
HNPCC = high cancer risk despite low no. polyps

203
Q

What is the average age of onset for both FAP and HNPCC?

A

Around 40

204
Q

What is the life-time risk (penetrance) for (i) FAP (ii) HNPCC?

A

(i) close to 100%

(ii) 80% approx

205
Q

What screening is currently done in Scotland for colon cancer?

A

Those over 50 are screened every 2 years for occult blood - if positive then colonoscopy
If known FAP/HNPCC then biannual colonoscopy from age of 25
Those classes as high to moderate risk have a colonoscopy every 5 years from age 50-75

206
Q

What is obesity? What BMI greater than is a pt then classed as obese?

A

Excess adiposity

- greater than or equal to 30 kg/m^2

207
Q

What is the score of BMI and risk of co-morbidities of (i) obesity class I (ii) obesity class II (iii) Obesity class III?

A

(i) 30.0 - 34.9 = moderate
(ii) 35.0 - 39.9 = severe
(iii) greater than 40 = v. severe

208
Q

What are some of the medical complications (co-morbidities) of obesity?

A

Stoke, Heart disease, diabetes, pancreatitis, lung disease, liver disease, gallstones, cancer, sleep apnea, arthritis, inflamed veins, gout and psychological problems (depression, body dysmorphia, anxiety)

209
Q

What does 1st degree kinship mean?

A

Would share 50% of your DNA with that individual

  • patent and child
  • siblings
210
Q

What protein is over-expressed often in sporadic colon cancer? What does this protein result in?

A

EGFR

  • increase proliferation
  • decrease apoptosis- increases invasion and metastasis
  • increases angiogenesis
211
Q

What drug is used to prevent over expression of EGFR?

A

Cetuximab

  • only used where wildtype Kras
  • antibody against EGFR and prevents ligand binding to EGFR
212
Q

Diet is another risk factor for colon cancer. What (i) reduces risk (ii) increases risk of colon cancer? WHY is this the case?

A

(i) high fibre and fish decrease risk
(ii) high intake of red and processed meats increase risk
WHY
- less time in bowel
- bile salts pass through quicker
- presence of anti-oxidants and folate in fruit and veg
- cooking methods

213
Q

How much does obesity increase the risk of colon cancer?

A

OVERWEIGHT men have a 25% increased risk

OBESE men have a 50% increased risk

214
Q

What risk does alcohol have on colon cancer?

A

40% increased risk if more than 5 units are consumed per day

215
Q

What is a preventative measure to colon cancer? WHY?

A

ASPIRIN

- inhibits COX-2 which is increased in the early stages of prostaglandin synthesis

216
Q

What is a drawback of using aspirin as a preventative measure to colon cancer?

A

Increased risk of CV problems as prostaglandins regulate BP

217
Q

What are the functions of COX-2? (HINT: there’s 3 functions)

A
  • increased prostaglandin synthesis
  • stimulates proliferation and angiogenesis
  • inhibits apoptosis
218
Q

Why is BMI a proxy measure?

A

Contains fat mass and fat free mass (e.g. muscle)

219
Q

How is obesity defined in children?

A

Tend to use arbitrary reference values
- but these vary worldwide and are difficult to compare

  • now the adult cut offs are linked to BMI centiles for children to provide child cut-offs
  • international cut offs reformulated to allow BMI to be expressed as a centile or SD score… very minor changes in existing cut-offs
220
Q

What are the centiles for (i) overweight (ii) obese in children?

A

(i) By sex, passing through a BMI of 25 kg.m^2 @ age 18

(ii) by sex, passing though BMI of 30kg/m^2 @ age 18

221
Q

What is the link between socioeconomic status and obesity?

A

Those with a lower income have a greater chance of being overweight/obese

222
Q

Are genes linked to obesity?

A

YES - but genes MODIFY they are not the sole reason for obesity

223
Q

Explain (i) monogenic (ii) polygenic forms of obesity.

A

(i) rare (less than 5%), single gene disorders

(ii) most common with complex interactions between genes and environments

224
Q

What is an example to show the importance of gene - environment interaction in the pathogenesis of obesity?

A

PIMA INDIANS

  • pima in Mexico have traditional methods of farming, cooking, fetching water and are largely unaffected by labour saving devices
  • pima in Arizona have a typical american lifestyle and diet
  • both have the same/similar genotypes yet those in Arizona on average have higher BMIs

MD3002 (14 decks)

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