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Med 3 > GIM > Flashcards

GIM Flashcards

1
Q

What is the superior abdominal boundary

A

Diaphragm

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2
Q

What is the inferior abdominal boundary

A

Pelvic inlet (continuous with the pelvis)

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3
Q

What is the anterolateral abdominal boundary

A

Musculo-aponeurotic abdominal wall

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4
Q

What is the posterior abdominal boundary

A

Lumbar vertebrae

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5
Q

What are the planes of the quadrants of the abdomen

A

Median plane (vertical) and transumbilical plane (horizontal)

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6
Q

4 quadrants of the abdomen

A

RUQ, LUQ, RLQ, LLQ

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7
Q

Clinical significance of the quadrants

A

Locate abdominal organs
Locate sites of pain
Allow accurate history to be taken

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8
Q

What are the horizontal planes of the regions of the abdomen

A

Transtubercular plane

Subcostal plane

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9
Q

What is the transtubercular plane

A

Iliac tubercles and body of L5

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10
Q

What is the subcostal Plane

A

Inferior border of the 10th cc and body of L3

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11
Q

What are the vertical planes (regions)

A

Midclavicular planes (halfway along clavicle and mid inguinal point)

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12
Q

What are the 9 regions of the abdomen

A

Right hypochondriac, epigastric, left hypochondriac, right lumbar (lateral), umbilical, left lumbar (lateral), right inguinal, hypogastric, left inguinal

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13
Q

What lymph nodes are superior to umbilicus

A

Axillary lymph nodes

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14
Q

What lymph nodes are inferior to umbilicus

A

Superficial inguinal lymph nodes

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15
Q

Clinical significance of lymphatic drainage

A

Diagnosis, prognosis and treatment of cancer

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16
Q

Where are melanomas in men

A

Most often thorax, abdomen or back

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17
Q

Where are melanomas in women

A

Most often lower legs

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18
Q

What dermatome supplies skin superior to umbilicus

A

T7-9

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19
Q

What dermatome supplies umbilicus

A

T10

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20
Q

What dermatome supplies iliohypogastric (L1) and ilioinguinal (L1) supply skin below umbilicus

A

T11-12

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21
Q

What dermatome supplies suprapubic region

A

L1

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22
Q

Clinical significance of dermatome

A

Referred pain

Dermatome using sensory testing if spinal nerve / cord functioning normally

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23
Q

What is the peritoneum

A

Smooth transparent serous membrane

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24
Q

What is the importance of the peritoneum

A

Holds organs within cavity

Reduce friction to allow organs to slide against each other during movement (esp in a very active GI tract)

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25
Q

What does serous mean

A

Fluid secreting

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26
Q

What are the layers of the peritoneum

A

Parietal peritoneum - covers body wall

Visceral peritoneum - covers organs (continuous)

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27
Q

What is the peritoneal cavity

A

Potential space with small amount of peritoneal fluid (no organs)

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28
Q

What is peritoneal fluid

A

Water, electrolytes, leukocytes and antibodies

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29
Q

Importance of peritoneal fluid

A

Lubrication
Free movement of abdominal viscera
Immunity

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30
Q

What are the intraperitoneal organs

A

Stomach (covered with visceral peritoneum)

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31
Q

What are the retroperitoneal organs

A

Kidneys (behind peritoneum)

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32
Q

What is peritonitis

A

Inflammation of peritoneum
Eg by trauma, penetration
Release of serum / pus into cavity -> pain, tenderness, nausea

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33
Q

What is ascites

A

Accumulation of fluid in peritoneal cavity

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34
Q

What viscera is in the right hypochondriac region

A

Pylorus of stomach, part of right lobe of liver, gall bladder, right kidney

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35
Q

What viscera is in the epigastric region

A

Liver, stomach, duodenum, pancreas

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36
Q

What viscera is in the left hypochondriac region

A

Stomach, left kidney, spleen

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37
Q

What viscera is in the right lumbar (lateral) region

A

Ascending Colon, small intestines

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38
Q

What viscera is in the umbilical region

A

Small intestines

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39
Q

What viscera is in the left lumbar (lateral) region

A

Descending colon, small intestines

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40
Q

What viscera is in the right inguinal (groin) region

A

Caecum, appendix

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41
Q

What viscera is in the hypogastric (pubic) region

A

Sigmoid colon

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42
Q

What viscera is in the left inguinal (groin) region

A

Descending colon

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43
Q

2 subdivisions of the peritoneal cavity

A 
Greater sac 
Lesser sac (omental bursa)
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44
Q

Where is the lesser sac

A

Posterior to the stomach and lesser omentum

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45
Q

Where is the communication between the greater and lesser sac

A

Epiploic (omental) foramen of Winslow

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46
Q

Where is the greater omentum

A

4 layers of visceral peritoneum

Connects the stomach and proximal part of the duodenum to the transverse colon

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47
Q

What are omenta

A

Sheets of visceral peritoneum which extend from the stomach and the proximal part of the duodenum to other abdominal organs

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48
Q

What are the parts of the greater omentum

A 
Gastrophrenic ligament ( greater curvature of stomach) 
Gastrosplenic ligament (side of stomach near spleen) 
Gastrocolic ligament ( on the sheet of the omenta)
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49
Q

What is the lesser omentum

A

Double layer of visceral peritoneum

Connects lesser curvature of the stomach and proximal duodenum to the liver

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50
Q

2 parts of the lesser omentum

A

Hepatogastric ligament

Hepatoduodenal ligament

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51
Q

What is a mesentery

A

Double layer of peritoneum b/c invagination of peritoneum by organ eg small intestine mesentery

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52
Q

What is the peritoneal ligament

A

Double layer of peritoneum that connects an organ with another organ to the abdominal wall

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53
Q

What is the falciform ligament

A

Attaches liver to anterior abdominal wall

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54
Q

Where is the linea alba

A

Runs from xiphoid process to pubic symphysis

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55
Q

What is the supracolic compartment

A

Above transverse mesocolon stomach, liver, spleen

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56
Q

What is the infracolic compartment

A

Below transverse mesocolon small intestine, ascending and descending colon

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57
Q

What are the paracolic gutters

A

Space between the ascending and descending colon and the posterolateral abdominal wall

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58
Q

What is gastrulation

A

Formation of 3 germ laters (ectoderm, mesoderm, endoderm) week 3

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59
Q

What is embryonic folding

A

Converting a flat germ disc into a 3D structure (parts of yolk sac become incorporated into embryo) week 4

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60
Q

Which germ layer is the GI tract derived from

A

Endoderm

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61
Q

What is gut tube formation

A

Midline fusion transforms flat endoderm into a gut tube

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62
Q

What is fore, mid and hind gut formation

A
  • cranial and caudal blind ended tubes (foregut and hindgut)
    Midgut remains temporarily open to the yolk sac
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63
Q

What GI tract organs are derived from the foregut

A

Oesophagus
Stomach
Duodenum - whole of the superior part and upper half of descending part
- liver and extra hepatic biliary system
- pancreas

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64
Q

What GI tract organs are derived from the midgut

A

Duodenum- descending distal to major papilla, horizontal and ascending parts

  • jejunum
  • ileum
  • caecum and appendix
  • ascending colon
  • proximal 2/3 of transverse colon
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65
Q

What GI tract organs are derived from the hindgut

A

Distal 1/3 of the transverse colon
Descending colon
Sigmoid colon - rectum
Upper part of anal canal

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66
Q

What is the blood supply of the foregut

A

Coeliac trunk

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67
Q

Where is the blood supply of the midgut from

A

Superior mesenteric aa

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68
Q

What is the blood supply of the hindgut

A

Inferior mesenteric aa

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69
Q

Explain stomach rotation and growth in an embryo

A

Begins to form in week 4 (fusiform shape)
Rotates 90 clockwise along longitudinal axis
Rotates on AP axis, pylorus moves up, duodenum becomes c shaped

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70
Q

What happens to the vagus nerve in the abdomen

A

Left vagus -> anterior a gal trunk
Right vagus -> posterior vagal trunk
B/c stomach rotation

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71
Q

Examples of congenital abnormalities of the GI tract

A

Atresias and stenosis
Abnormal rotations
Anterior abdominal wall defects

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72
Q

How does the omental bursa form

A

Rapid expansion of the liver forms a sac region behind the stomach

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73
Q

Why do the greater and lesser curvatures of the stomach form

A

Because the walls grow at different rates

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74
Q

What is the midgut

A

Suspended from the dorsal abdominal wall
Communicates with yolk sac by vitelline duct
Rapid elongation forms primary intestinal loop

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75
Q

What is the rotation fo the midgut

A

270 anticlockwise rotation around the superior mesenteric aa
Elongation of small intestine loop = jejunum and ileum coiled loops

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76
Q

Where can atresis and stenosis occur

A

Anywhere along the developing intestinal loop

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77
Q

What is an atresia

A

Complete absence of a lumen

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78
Q

What is a stenosis

A

Narrowing of the lumen

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79
Q

Define nutrition

A

The provision of nourishment to cells, tissues, organs, systems and the body as a whole = how food influences out body function and health

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80
Q

What is clinical nutrition

A

Feeding patients

Dietetics - diet as therapy / prevention of disease

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81
Q

What are the core concepts of nutrition

A
  • nutrient balance
  • nutrient turnover
  • nutrient flux
  • metabolic pools
  • adaptation to altered nutrient supply
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82
Q

What is nutrient balance

A

Intake - output = change in body stores -> buffering effect of body stores

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83
Q

What is nutrient turnover

A

Metabolic substrates are continually being utilised and replaced. Allows for rapid adjustments to changes in metabolic state
Potential for dysfunction if rates of utilisation and synthesis are mismatched

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84
Q

What is nutrient flux

A

A measure of the activity of the pathway

Not necessarily related to the size of the metabolic pool

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85
Q

What is a functional pool

A

Direct involvement in body functions

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86
Q

What is a storage pool

A

Provides buffering effect ie can be made available to the functional pool when and as

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87
Q

What is a precursor pool

A

Provides the substrate for nutrient / metabolite synthesis

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88
Q

What is adaptation to altered nutrient supply

A

Minimises the consequences of such alterations

The greater the capacity to respond to adverse nutritional states the greater the capacity to survive those states

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89
Q

Role of GI tract

A

Ingest food, break it down mechanically and enzymatically into molecules that can be absorbed into the blood and taken to the liver to be used to synthesise proteins, carbohydrates and lipids needed for cellular functions

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90
Q

Layers of the GI tract

A

1) mucosa (inner lining)
2) submucosa (support)
3) muscularis externa / propria (muscle)
4) serosa / adventitia (outer wrapping)

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91
Q

What makes up mucosa

A

Epithelium - changes throughout the tube in relation to function
Basement membrane
Lamina propria - supports the epithelium (structurally and nutritionally)
Muscularis mucosa - causes the lining to be visibly folded

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92
Q

What makes up submucosa

A

Connective tissue, blood vessels, lymphatics and nerves

Some of the glands

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93
Q

What is the submucosal plexus

A

Supplies glands and muscularis mucosa

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94
Q

What makes up muscularis externa/ propria

A

Smooth muscle: inner circular and outer longitudinal. Responsible for peristalsis

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95
Q

What is myenteric (auerbach’s) plexus

A

Between muscle layers
Modulates peristalsis
Modulated by autonomic nervous system

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96
Q

What is peristalsis

A

The involuntary constriction and relaxation of the muscles of the intestine or another canal, creating wavelike movements that push the contents of the canal forward

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97
Q

What is the adventitia

A

The outer wall of the gut tube

Thin later of connective tissue

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98
Q

What is the serosa

A

Where covered by a serous membrane
Serous membrane = squamous epithelial cells secreting a small amount of fluid to allow the organs to glide over each other (peritoneum in the abdomen) = visceral peritoneum

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99
Q

What is protective epithelium

A

Stratified squamous non keratinising

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100
Q

Where would you need protective (stratified squamous) epithelium

A

Oesophagus, anal canal, oral cavity, pharynx

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101
Q

What is secretory / absorptive epithelium

A

Columnar (microvilli)

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102
Q

Where would you need secretory / absorptive (columnar) epithelium

A

Stomach, small intestine, colon, pancreas

103
Q

What is stretchy epithelium

A

Transitional

104
Q

Where would you need stretchy (transitional) epithelium

A

Urinary tract (bladder, urethra)

105
Q

What is facilitating diffusion epithelium

A

Simple squamous

106
Q

Where would you need facilitating diffusion (simple squamous) epithelium

A

Capillaries

107
Q

What are sphincters

A

Thickening of smooth muscle, close off lumen

108
Q

What is the oesophageogatric sphincter

A

Prevents reflux of stomach contents into oesophagus

109
Q

What is the pyloric sphincter

A

Between stomach duodenum: controlled release to food to allow for max absorption and not too much acidic release after meal eaten into duodenum

110
Q

What is the ileocaecal sphincter

A

Between small and large intestine

111
Q

What is the internal anal sphincter

A

Upper anal canal: retains faeces

112
Q

What is GALT (gut associated lymphoid tissue)

A

In lamina propria

Lymphocytes (T&B)

113
Q

What are the layers of the oral cavity and pharynx

A

Only 2: mucosa and submucosa

114
Q

What is the mucosa of the oral cavity and pharynx

A

Stratified squamous non keratinising
Lamina propria
No muscularis mucosa

115
Q

What is the submucosa of the oral cavity and pharynx

A

Small salivary glands (origin of adenocarcinoma)

116
Q

What are the lips

A

Folds of skeletal muscle (orbicularis oris) covered by keratinised squamous w/o adnexal strucyures (absence of glands gives dry feeling) thick stratum lucidum and high dermal papillae with rich capillaries

117
Q

What is the common hepatic artery

A

A branch of the coeliac trunk

Branches: hepatic artery proper, gastroduodenal artery

118
Q

What is the portal triad

A

Hepatic artery
Portal vein
Bile duct
(In free edge of lesser omentum)

119
Q

What is the hepatic artery proper

A

A branch of the common hepatic artery

Branches: left and right hepatic arteries, right gastric artery

120
Q

What is the pyloric sphincter

A

Circular muscle that keeps food in the intestines

121
Q

What is the pyloric antrum

A

Large part of the funnel leading to the pyloric canal

122
Q

What is the first part of the duodenum

A
  • associated with greater and lesser omentum

- from pylorus

123
Q

What is plicae circularis

A
  • folds of mucosa
  • contain villi and microvilli to increase SA
  • most absorption at the beginning therefore jejunum has more than distal ileum.
124
Q

Which structures pass through the diaphragm with the oesophagus

A

T10

  • vagal trunks
  • left gastric artery
125
Q

What are arterial arcades

A

The arteries that unite to form loops of arches which give rise to straight arteries called vasa recta
- supply small intestine

126
Q

Blood supply to the duodenum

A

Gastroduodenal aa (from common hepatic aa)
Superior pancreaticoduodenal aa (from gastroduodenal aa)
Inferior pancreaticoduodenal aa (from SMA)

127
Q

What are rugae

A

Folds in the stomach (gastric folds)

128
Q

What is the pylorus

A

Part of the stomach that attaches to the duodenum

129
Q

Which organ lies posterior to the descending part of the duodenum

A

Right kidney

130
Q

Rugae

A

Gastric folds

131
Q

What is saliva

A

Solution with electrolytes

Derived from plasma

132
Q

What are the main pairs of branched glands that produce saliva

A

Parotid (cheek)
Submandibular (under chin)
Sublingual (under tongue)

133
Q

What are acinar cells

A

Produce primary secretion that is isotonic with plasma

Some salivary proteins are secreted

134
Q

What are duct cells

A

Actively reabsorption Na+ and Cl-
Secrete K+ and HCO3-
Impermeable to H2O therefore excess absorption -> saliva hypotonic relative to plasma
- rate of flow determines how much is reabsorbed / secreted

135
Q

What happens to the concentration of saliva as the flow rate increases

A

Less time to reabsorb / secrete

  • Na+ increases
  • Cl- increases
  • K+ decreases
  • HCO3- increases
136
Q

What does saliva contain

A

Mucous
Proteins (IgA)
Enzymes (amylase, lysozyme)

137
Q

What happens with sympathetic stimulation of acinar cells

A

Small volume of thick saliva rich in mucous

138
Q

Functions of saliva

A

Contains salivary amylase (breakdown of polysaccharides)

  • produces mucous (for swallowing)
  • protective function (secretes lysozyme antibacterial IgA)
  • acts as a solvent to stimulate taste
  • moisturiser (aids speech)
  • promotes oral hygiene
139
Q

How does deglutition (swallowing) work

A

Initiated when food bolus forced by tongue to rear of mouth to pharynx
2 phases: oropharyngeal and oesophageal

140
Q

What is the oropharyngeal phase of deglutition

A

Food bolus directed into the oesophagus therefore seals off nasal passages (by uvula)
Trachea (by epiglottis)

141
Q

What is the oesophageal phase of deglutition

A

Oesophagus protected from damage caused by passing food bolus by mucous secretion
- movement by peristalsis (+gravity)

142
Q

Functions of the stomach

A

Storage of food
Initiation of digestion of proteins
Kill ingested bacteria (via acid)
Formation of chyme (before transfer to small intestine)

143
Q

How does storage of food in the stomach work

A

Intragastric pressure doesn’t increase because distension of stomach wall and reflex (vagal) inhibition of smooth muscle tone
- important because delivers digested food to small intestine at a good rate for optimal digestion and absorption -> ingestion takes minutes, digestion / absorption takes hours

144
Q

What are parietal cells

A

Produce hydrochloride acid and intrinsic factor

Important for VitB12 absorption

145
Q

What cells secrete mucous into the stomach

A

Surface epithelial cells and mucous neck cells

146
Q

What is carbonic anhydrase

A

Enzyme that catalyses reaction CO2 + H2O -> h2co3 (carbonic acid)
In parietal cells

147
Q

What is the epithelial change at the gastro-oesophageal junction

A

Lining changes from squamous epithelium to columnar epithelium (glandular)

148
Q

What is Barrett’s oesophagus

A

Pathology - metaplasia - change of epithelium from stratified squamous to gastric due to repeated damage from gastric reflux
- risk of adenocarcinoma (glandular) from metaplastic cells

149
Q

What types of cels line the surface of the stomach

A

Mucous producing columnar epithelial cells - protects stomach lining from HCL

150
Q

What are the muscle layers of the stomach

A 
Middle circular 
Outer longitudinal 
Inner oblique (for churning)
151
Q

What cell types are in the gastric pits and glands

A

Mucous cells
Parietal cells
Chief (peptic / zymogenic) cells
Enteroendocrine cells

152
Q

What are mucous cells

A

At surface

Produce mucous and bicarbonate (protects surface from acid and digestion)

153
Q

What are the parietal (oxyntic) cells

A

Produce HCL (by active transport of H+ and passive transport of Cl-)
And intrinsic factor
- invaginate apical surface with microvilli
- stimulated by gastrin, ACh, histamine

154
Q

What are the chief (peptic or zymogenic) cells

A

Produce enzymes

Eg Pepsinogen: converted to pepsin in acidic env

155
Q

What are enteroendocrine cells

A

Produce hormones

Eg gastric, serotonin, somatostatin (SS), vasoactive intestinal peptide

156
Q

How to prevent acid secretion

A

PPI (protein pump inhibitor) because HCL produced by active transport

157
Q

What is a gastric ulcer

A

Caused by H pylori infection
- breaks down mucous cells lining stomach therefore damages stomach wall epithelium -> ulcer -> deep chronic ulcer
- damage and repair occurring simultaneously -> chronic inflammation
If left, would perforate through peritoneum -> peritonitis

158
Q

How do you fix a gastric ulcer

A

Stop stomach acid to allow the cells to repair and produce mucous : PPIs
- antibiotics to kill H pylori

159
Q

How can helicobacter pylori survive in the stomach

A 
Produces ammonia (alkaline) to protect from acid 
Helical structure with flagella -> like a drill through mucous
160
Q

What are brunners glands

A

In submucosa of duodenum
Secrete alkaline mucous
Neutralise HCL

161
Q

What are villi

A

Lined with simple columnar epithelium

  • continues into crypts which extend to muscularis mucosa
  • lamina propria extends between crypts and core of villus
162
Q

What are the cell types of the villus

A
  • enterocytes (migrate upwards)
  • goblet cells
  • neuroendocrine cells
  • stem cells
  • intraepithelial lymphocytes
  • paneth cells
163
Q

What are enterocytes

A

Absorptive cells

Migrate from base of the crypts (where formed) to villus tip

164
Q

What is digestion

A

Luminal digestion:
- chyme and pancreatic secretions mix to break down food into component parts
Membrane digestion:
- brush border enzymes

165
Q

What is malabsorption

A

Inability to absorb nutrients despite eating the right food

166
Q

What causes malabsorption

A

Insufficient pancreatic enzymes (eg CF)
Insufficient bile
Loss of small intestinal SA (coeliac)
Lack of mucosal brush border enzymes

167
Q

What are the manifestations of malabsorption

A

Diarrhoea and steatorrhoea (fatty stool)

  • haemopoietic
  • anameia
  • bleeding (vit K deficiency)
  • skeletal
  • endocrine: impotency, infertility, amenorrhoea
168
Q

What is coeliac disease

A

Most common cause of SI malabsorption

  • sensitive to gluten -> immune response (T cell) to gliadin (in wheat, barley, rye)
  • most severe in proximal duodenum (max exposure)
  • loss of villi bc inflammation
  • lymphocytic infiltration of mucosa and lamina propria
169
Q

How does coeliac disease present

A

Failure to thrive, diarrhoea, abdo distension, malnutrition

170
Q

Risk factors of coeliac disease

A

T1 diabetes
Autoimmune conditions
Familial tendency

171
Q

How to diagnose coeliac disease

A

Serology for IgA

  • anti EMA
  • endoscopy + biopsy of small bowel mucosa
  • nutritional disorders
172
Q

Treatment of coeliac disease

A

Complete removal of gluten from diet -> complete recovery

If diet isn’t adhered to, cancer risk for non Hodgkin’s lymphoma

173
Q

What is meckel diverticulum

A

Congenital outpouching of SI
Bc of incomplete reabsorption fo the vitalline duct
Often no symptoms or treatment needed
Surgical removal if it causes bleeding /obstruction

174
Q

What causes obstruction of the small bowel

A

Pain, absolute constipation, abdo distension, vomiting

175
Q

What can obstruction of the small bowel lead to

A 
Distension 
Loss of fluids / electrolytes 
Interruption of blood flow 
Necrosis 
Rapid bacterial growth 
Gangrene 
Perforation
176
Q

What is cystic fibrosis

A

Genetic disease (autosomal recessive)
Affects secretion of exocrine glands in epithelium
Main affects in resp and GI
Sticky and thick secretions : get stuck and cant be secreted out through ducts -> malabsorption

177
Q

Function of large intestine

A

Absorb water and salt to produce more solid waste product

178
Q

What type of cells are in the large intestine

A

Goblet cells (lubrication)
Enterocytes (absorption -> active membrane transport but no digestion)
- some enteroendocrine and stem cells
- arranged as tubular glands but no villi because large SA not needed
- tall columnar absorptive cells (w microvilli)

179
Q

What is the appendix

A

Outgrowth of caecum containing lymphoid material

180
Q

What muscle types in the colon

A

Longitudinal, circular and taenia coli mm

181
Q

What causes a slower transit rate through the colon

A

Constipation because dehydration / lack of fibre can cause diverticulosis

182
Q

What causes a faster transit rate through the colon

A

IBS

Diarrhoea

183
Q

What causes a blockage in the colon

A

Obstruction

184
Q

What causes ischaemia of the Bowel

A

Caused by a range of factors
Can cause necrosis
V good anastomoses in bowel

185
Q

Types of ischaemia of the bowel

A

Thrombosis
Embolism
Spasm
Atheroma

186
Q

What is diverticulosis

A

Caused by lack of fibre, ageing, poor bowel habits
- often asymptomatic
Treat: increasing bulk to decrease intraluminal pressure
- outpouches of sigmoid colon: mucosa herniates through muscularis

187
Q

2 main inflammatory bowel diseases

A

Crohn’s disease

Ulcerative colitis

188
Q

What is IBS

A

Idiopathic and chronic relapsing
Abnormal local immune response to normal gut flora / self antigens
- more common in white pts in developed nations

189
Q

What is Crohn’s disease

A

Inflammation (granulomatous) of the entire GI wall thickness

190
Q

What happens in Crohn’s disease

A

Can be anywhere from oesophagus to anus (common: ileum)
- granulomatous inflammation ulcerated mucosa and submucosa
Areas between ulcers are ok
Cobblestone appearance
Deep fissure can form in wall to serosa
Thickened GI wall due to inflammation: oedema, fibrous MM hypertrophy -> narrow lumen

191
Q

Symptoms of Crohn’s disease

A

Diarrhoea, cramps, fever

192
Q

What is UC

A

Starts at rectum, is continuous and can affect whole colon
- superficial damage of mucosa
- replacement of straight glands with branched short glands,, recovering ulcers protrude into lumen as pseudopolyps
Lack of absorption -> watery stools (w blood)
- high risk of bowel cancer because high cell turnover

193
Q

Risk factors for colorectal tumours

A 
Age 
Race 
Obesity 
Lack of exercise 
High fat low fibre diet 
Smoking 
Alcohol 
Diabetes 
Personal or family history 
Previous abdominal radiation therapy 
IBS
194
Q

Symptoms of colorectal tumours

A

Persistent change in bowel habit (eg diarrhoea or constipation), rectal bleeding or blood in stool, persistent abdominal discomfort, incomplete voiding, fatigue, unexplained weight loss

195
Q

How to prevent colorectal cancer

A

Screening
Fecal occult blood test-> traces of blood in stool for all over 60s
Lifestyle factors

196
Q

What is the anal canal

A

Muscular, controlled by 2 sphincters

  • columnar epithelium of rectum -> stratified squamous epithelium (squamocolumnar junction) -> keratinised when meets skin
  • glands lubricate passage of faeces
  • venous supply -> haemorrhoidal plexi -> if distended b/c congestion: piles
197
Q

What are the anal sphincters

A

Internal: smooth mm thickening at end of rectum (involuntary control)
- external: skeletal mm (voluntary control)

198
Q

What are food borne outbreaks

A

Often local
Exposure to contaminated food
Need to recognise and track
Pathogens: E. coli, salmonella, shigella

199
Q

What is gut microbiota-mediated colonisation resistance

A

Gut microbiota produces products with antimicrobial effects including SCFA, 2nd bile acids, bacteriocins
Each contributes to resistance against microbes

200
Q

How do you test C. difficile

A

Enz. Immunoassay for simultaneous detection of antigen GDH and toxins A &B in stool
- rapid membrane test for rotavirus antigen in stool

201
Q

What is viral gastroenteritis

A 
Faecal - oral spread 
Sx: explosive diarrhoea, colicky abdo pain with nausea or vomiting, fever 
Incubation: 24-48 hours 
- rotavirus, norovirus, adenovirus 
- detected by PCR or antigen testing 
- supportive management eg rehydration 
- vaccines
202
Q

What is E. coli

A

Enterotoxigenic (foodborne/ waterborne)
Enteroinvasive (foodborne / waterborne )
Enteropathogenic (foodborne / person to person / waterborne)
Entherohaemorrhagic (foodborne)
Lab identified from food
Short incubation
Tx - oral rehydration

203
Q

What is campylobacter

A

Peaks late spring / summer

  • foodborne transmission
  • incubation 2-5 days
  • sx: diarrhoea, abdo pain, fever, vomiting
  • complications: guillain-barre, reactive arthritis, HUS
  • culture w/ selective agar under reduced O2 conditions
  • Tx: clarithromycin
204
Q

What is (non typhoid) salmonella enteritidis

A

Foodborne transmission ; person to person contact with infected animals
Incubation 12-48 hours
- watery and sometimes bloody diarrhoea, abdo pain, headache, nausea and vomiting, fever
- symptoms can persist for days
- usually resolve without treatment.

205
Q

What is (typhoid) salmonella typhoid and paratyphi

A

Cause typhoid or paratyphoid fever - severe systemic illness

  • transmission: consumption of contaminated water or food
  • higher risk of infection in low and middle income countries
  • abdo pain, headache, rise in fever over several days; abdo rash; diarrhoea behind in 2nd or 3rd week and may progress to severe GI bleeding
  • can be grown from blood cultures
  • give antibiotics (IV ceftriaxone)
206
Q

What is shigella

A 
Faecal - oral and sexual transmission (men who have sex with men MSM) 
- incubation 12 hrs - 4 days 
Symptoms vary 
- cultured with selective agar 
- supportive treatment
207
Q

What are parasites

A

Waterborne from faecally contaminated water supplies
Often travel related
Incubation 7-10 days
Detection by stool microscopy

208
Q

What is clostridioides difficile

A

Anaerobe spore former

  • spores germinate in small bowel
  • vegetative cells produce toxins
  • can colonise without causing disease
  • main risk factors: antibiotics, increased age, PPIs, cytotoxic agents
  • person to person spread
  • disease varies from diarrhoea to toxic megacolon and perforation
209
Q

What is the histology of C. difficile

A

Psuedomembranous colitis (inflammation of colon w elevated yellow - white plaques on mucosa that coalesce to form pseudomembranes)

210
Q

How to diagnose C. difficile

A

Samples sent from hospital patients with diarrhoea
Can check if colonised with C diff by detection of antigen glutamate dehydrogenase (GDH) and toxins via enzyme immunoassay or PCR (C diff / toxins genes)
Lateral flow tests available that can simultaneously detect C diff GDH and its toxins

211
Q

How to treat c diff

A

Depends on severity
Usually oral vancomycin for 10 days
In severe disease, add IV metro, consider IVIG or proceed to anti toxin monoclonal antibodies or fecal mictobiota transplant

212
Q

What is toxic megacolon

A

Total or segmental non obstructive colonic dilatation that occurs in context of systemic toxicity
Can rarely complicate severe c diff infection, ischaemic bowel, IBD or any infectious and inflammatory cause of bowel
- risk of bowel perforation, peritonitis and death
- management coordinated between medical and surgical teams

213
Q

What is helicobacter pylori

A 
Bacterial infection 
Chronic gastritis 
Gastric ulcer (70-80%) 
Duodenal ulcer disease (95%) 
Inflammatory response 
Associated with gastric adenocarcinoma and MALT lymphoma
214
Q

How to diagnose H pylori

A

Serology (antibody testing: doesn’t distinguish between active and past infection)

  • urease breath test
  • stool antigen test
  • endoscopy and gastric biopsy (rapid urease testing, bacterial culture especially useful in refractory cases)
215
Q

How to treat H pylori

A

Triple therapy regime comprising a proton pump inhibitor + 2 antibacterial:

  • amoxicillin
  • clarithromycin
  • metronidazole
  • tetracycline

In treatment failure offer 2nd and 3rd line regimes

May need to undertake endoscopic biopsy culture and susceptibility testing in treatment resistant cases

216
Q

What is dyspepsia

A

Indigestion

- gastro-oesophageal reflux disease (GORD) -> heartburn

217
Q

What is zollinger Ellison syndrome

A

Rare gastric secreting tumour of D - and / or G cells of the pancreas -> results in lots of gastrin release

218
Q

Signs and symptoms of peptic ulceration

A

Epigastric pain (may be located by patient pointing)

  • pain variable in relation to food
  • night pain (relieved by food, milk, antacids)
  • water rash
  • nausea and less freq vomiting
  • vomiting blood
219
Q

What is peptic ulceration

A

Caused by H pylori (mostly) or NSAIDs

- infection can lead to chronic inflammation and gastric damage (gastritis) -> ulceration

220
Q

Recognised complication of peptic ulceration

A

Iron deficiency anaemia

221
Q

How to diagnose peptic ulceration

A

Urea breath test (C13)
Biopsy for urease activity
H pylori antigens / antibodies in specimens

222
Q

How does the urea breath test (C13 urea) work

A

H pylori produces enz. Urease to protect it from HCL
- urease produces NH3 to neutralise HCL which makes breath small
C13 urea given to pt, if urease in stomach 13-CO2 exhaled which can be detected by sampling breath and using mass spec

223
Q

Systems that increase acid secretion

A

Histamine (H2 receptors)
Gastrin (CCK2 receptors)
ACh (M receptors, M3 on parietal cells)

224
Q

Systems that decrease acid secretion

A

Prostaglandins

Cytoprotective via bicarbonate and mucous release

225
Q

What role do prostaglandin receptors have

A

(Local regulation)
COX releases prostanoids -> stimulate prostaglandin receptors which switch PP off -> also stimulate release of mucous and HCO3-

226
Q

What are antacids

A 
Raise pH, OTC 
Provide rapid relief, not cure 
- sodium bicarbonate (antacid) 
- Na+ drugs bad for CVD 
- Mg(OH)2 also used 
- Mg2+ side effect: diarrhoea
227
Q

What are Latinate

A

Can be combined with antacids eg gaviscon / peptac
- alginic acid when combines with saliva -> viscous foam
- floats on gastric contents forming a raft that protects oesophagus during reflux
V safe (good for pregnancy)
- OTC

228
Q

What are the different preparations of drugs

A

Suspension
Tablets
Capsules

229
Q

What is absorbed fastest and has the lowest risk of bioavailability problems

A

Aqueous solutions
Syrups
Elixirs

230
Q

What had mediums absorption and risk of bioavailability problems

A 
Suspensions 
Chewed tablets 
Granules 
Capsules 
Conventional tablet
231
Q

What is absorbed the slowest and has the highest risk of bioavailability problems

A

Compressed tablets
Enteric coated tablets
Complex forms

232
Q

What is bioequivalence

A

Comparable bioavailability between drugs (identical rate and extent of absorption)

233
Q

What is bioequivalence assessed by

A

Time to peak plasma level (tmax)
Peak plasma level (cmax)
Bioavailability (F)

234
Q

Why are some medicines taken at night

A

Because highest plasma conc (cmax) will be at night so less likely to feel side effects if asleep

235
Q

What is sustained release (SR)

A

Has many layers of protective coating, slows down release of drug and smooths it out

236
Q

What is morphine

A

Opioid analgesic
T1/2 - 2-3 hours
- oramorph (rapid relief)
- oral suspension for immediate pain relief

237
Q

What is nifedipine

A

DHP Ca channel inhibitor
Used in hypertension and angina
T1/2 - 2 hours

  • immediate release prep associated w more cardiac events bc peaks and troughs in BP
    Should be used as adalat LA prescribed o.d
238
Q

How is omeprazole (PPI) prepared

A

Acid labile (broken down by acid)

  • given as enteric coated capsule -> prevents it being broken down in stomach
  • breaks down in duodenum -> released and absorbed in duodenum
  • goes to parietal cells and activated by acidic pH because of its pKA
239
Q

What are depot injections

A

Used to aid compliance with weekly / monthly injections
Absorption by use of thick oils to slow down rate of diffusion from injection site
- avoid first pass metabolism: be careful of bioequivalence

240
Q

What is the ampulla of vater (hepatopancreatic ampulla)

A

Common bile duct and pancreatic duct

241
Q

What is the porta hepatis

A

Site where vessels / nerves / ducts leave / enter liver in between caudate and quadrate lobes

242
Q

What parts of the large intestine have a mesentery (membrane that attaches intestine to abdominal wall and holds it in place)

A

Appendix
Transverse colon
Sigmoid colon

243
Q

What is the superior mesenteric vein

A

Drains the small intestine, caecum, ascending colon, transverse colon
- begins in right iliac fossa
- convergence of vv draining terminal ileum, caecum, appendix
Ascends within mesentery of small intestine -> travels posteriorly to neck of pancreas -> joins splenic vv

244
Q

What is the common bile duct

A

Common hepatic duct and cystic duct

245
Q

What does CCK do after a meal

A

Relaxes sphincter of oddi
Contracts gall bladder
Allows bile to pass to duodenum

246
Q

What is jaundice

A

Bilirubin accumulation in plasma
Sx: yellowing of skin, sclera, mucous membranes
- may produce kernicterus (deposits of pigment in brain)

247
Q

What is first pass metabolism

A

Drugs are absorbed from small intestine

Taken to liver via portal circulation -> some drugs metabolised before reaching systemic circulation

248
Q

What is absorbed in the small intestine

A

Most weak acids and bases because high levels of uncharged drugs
(PH 5.3)
Long residence time

249
Q

What are acid labile drugs

A

Easily destroyed in acidic env
Take w/o food so passes through stomach
Quicker otherwise would be broken by HCl and wouldn’t have an effect eg PPIs

250
Q

What are acid stable drugs

A

Taken on a full stomach so it spends longer in the stomach so slows down the rate of absorption (tmax is decreased)

251
Q

What does a change in absorption cause a change in

A

AUC, tmax, F

252
Q

What does a change in distribution cause a change in

A

V, t1/2

253
Q

What does a change in elimination cause a change in

A

AUC, CL, t1/2

Med 3 (10 decks)

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