GIM Flashcards
(253 cards)
1
Q
What is the superior abdominal boundary
A
Diaphragm
2
Q
What is the inferior abdominal boundary
A
Pelvic inlet (continuous with the pelvis)
3
Q
What is the anterolateral abdominal boundary
A
Musculo-aponeurotic abdominal wall
4
Q
What is the posterior abdominal boundary
A
Lumbar vertebrae
5
Q
What are the planes of the quadrants of the abdomen
A
Median plane (vertical) and transumbilical plane (horizontal)
6
Q
4 quadrants of the abdomen
A
RUQ, LUQ, RLQ, LLQ
7
Q
Clinical significance of the quadrants
A
Locate abdominal organs
Locate sites of pain
Allow accurate history to be taken
8
Q
What are the horizontal planes of the regions of the abdomen
A
Transtubercular plane
Subcostal plane
9
Q
What is the transtubercular plane
A
Iliac tubercles and body of L5
10
Q
What is the subcostal Plane
A
Inferior border of the 10th cc and body of L3
11
Q
What are the vertical planes (regions)
A
Midclavicular planes (halfway along clavicle and mid inguinal point)
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
13
Q
What lymph nodes are superior to umbilicus
A
Axillary lymph nodes
14
Q
What lymph nodes are inferior to umbilicus
A
Superficial inguinal lymph nodes
15
Q
Clinical significance of lymphatic drainage
A
Diagnosis, prognosis and treatment of cancer
16
Q
Where are melanomas in men
A
Most often thorax, abdomen or back
17
Q
Where are melanomas in women
A
Most often lower legs
18
Q
What dermatome supplies skin superior to umbilicus
A
T7-9
19
Q
What dermatome supplies umbilicus
A
T10
20
Q
What dermatome supplies iliohypogastric (L1) and ilioinguinal (L1) supply skin below umbilicus
A
T11-12
21
Q
What dermatome supplies suprapubic region
A
L1
22
Q
Clinical significance of dermatome
A
Referred pain
Dermatome using sensory testing if spinal nerve / cord functioning normally
23
Q
What is the peritoneum
A
Smooth transparent serous membrane
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)
25
What does serous mean
Fluid secreting
26
What are the layers of the peritoneum
Parietal peritoneum - covers body wall
| Visceral peritoneum - covers organs (continuous)
27
What is the peritoneal cavity
Potential space with small amount of peritoneal fluid (no organs)
28
What is peritoneal fluid
Water, electrolytes, leukocytes and antibodies
29
Importance of peritoneal fluid
Lubrication
Free movement of abdominal viscera
Immunity
30
What are the intraperitoneal organs
Stomach (covered with visceral peritoneum)
31
What are the retroperitoneal organs
Kidneys (behind peritoneum)
32
What is peritonitis
Inflammation of peritoneum
Eg by trauma, penetration
Release of serum / pus into cavity -> pain, tenderness, nausea
33
What is ascites
Accumulation of fluid in peritoneal cavity
34
What viscera is in the right hypochondriac region
Pylorus of stomach, part of right lobe of liver, gall bladder, right kidney
35
What viscera is in the epigastric region
Liver, stomach, duodenum, pancreas
36
What viscera is in the left hypochondriac region
Stomach, left kidney, spleen
37
What viscera is in the right lumbar (lateral) region
Ascending Colon, small intestines
38
What viscera is in the umbilical region
Small intestines
39
What viscera is in the left lumbar (lateral) region
Descending colon, small intestines
40
What viscera is in the right inguinal (groin) region
Caecum, appendix
41
What viscera is in the hypogastric (pubic) region
Sigmoid colon
42
What viscera is in the left inguinal (groin) region
Descending colon
43
2 subdivisions of the peritoneal cavity
```
Greater sac
Lesser sac (omental bursa)
```
44
Where is the lesser sac
Posterior to the stomach and lesser omentum
45
Where is the communication between the greater and lesser sac
Epiploic (omental) foramen of Winslow
46
Where is the greater omentum
4 layers of visceral peritoneum
| Connects the stomach and proximal part of the duodenum to the transverse colon
47
What are omenta
Sheets of visceral peritoneum which extend from the stomach and the proximal part of the duodenum to other abdominal organs
48
What are the parts of the greater omentum
```
Gastrophrenic ligament ( greater curvature of stomach)
Gastrosplenic ligament (side of stomach near spleen)
Gastrocolic ligament ( on the sheet of the omenta)
```
49
What is the lesser omentum
Double layer of visceral peritoneum
| Connects lesser curvature of the stomach and proximal duodenum to the liver
50
2 parts of the lesser omentum
Hepatogastric ligament
| Hepatoduodenal ligament
51
What is a mesentery
Double layer of peritoneum b/c invagination of peritoneum by organ eg small intestine mesentery
52
What is the peritoneal ligament
Double layer of peritoneum that connects an organ with another organ to the abdominal wall
53
What is the falciform ligament
Attaches liver to anterior abdominal wall
54
Where is the linea alba
Runs from xiphoid process to pubic symphysis
55
What is the supracolic compartment
Above transverse mesocolon stomach, liver, spleen
56
What is the infracolic compartment
Below transverse mesocolon small intestine, ascending and descending colon
57
What are the paracolic gutters
Space between the ascending and descending colon and the posterolateral abdominal wall
58
What is gastrulation
Formation of 3 germ laters (ectoderm, mesoderm, endoderm) week 3
59
What is embryonic folding
Converting a flat germ disc into a 3D structure (parts of yolk sac become incorporated into embryo) week 4
60
Which germ layer is the GI tract derived from
Endoderm
61
What is gut tube formation
Midline fusion transforms flat endoderm into a gut tube
62
What is fore, mid and hind gut formation
- cranial and caudal blind ended tubes (foregut and hindgut)
Midgut remains temporarily open to the yolk sac
63
What GI tract organs are derived from the foregut
Oesophagus
Stomach
Duodenum - whole of the superior part and upper half of descending part
- liver and extra hepatic biliary system
- pancreas
64
What GI tract organs are derived from the midgut
Duodenum- descending distal to major papilla, horizontal and ascending parts
- jejunum
- ileum
- caecum and appendix
- ascending colon
- proximal 2/3 of transverse colon
65
What GI tract organs are derived from the hindgut
Distal 1/3 of the transverse colon
Descending colon
Sigmoid colon - rectum
Upper part of anal canal
66
What is the blood supply of the foregut
Coeliac trunk
67
Where is the blood supply of the midgut from
Superior mesenteric aa
68
What is the blood supply of the hindgut
Inferior mesenteric aa
69
Explain stomach rotation and growth in an embryo
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
70
What happens to the vagus nerve in the abdomen
Left vagus -> anterior a gal trunk
Right vagus -> posterior vagal trunk
B/c stomach rotation
71
Examples of congenital abnormalities of the GI tract
Atresias and stenosis
Abnormal rotations
Anterior abdominal wall defects
72
How does the omental bursa form
Rapid expansion of the liver forms a sac region behind the stomach
73
Why do the greater and lesser curvatures of the stomach form
Because the walls grow at different rates
74
What is the midgut
Suspended from the dorsal abdominal wall
Communicates with yolk sac by vitelline duct
Rapid elongation forms primary intestinal loop
75
What is the rotation fo the midgut
270 anticlockwise rotation around the superior mesenteric aa
Elongation of small intestine loop = jejunum and ileum coiled loops
76
Where can atresis and stenosis occur
Anywhere along the developing intestinal loop
77
What is an atresia
Complete absence of a lumen
78
What is a stenosis
Narrowing of the lumen
79
Define nutrition
The provision of nourishment to cells, tissues, organs, systems and the body as a whole = how food influences out body function and health
80
What is clinical nutrition
Feeding patients
| Dietetics - diet as therapy / prevention of disease
81
What are the core concepts of nutrition
- nutrient balance
- nutrient turnover
- nutrient flux
- metabolic pools
- adaptation to altered nutrient supply
82
What is nutrient balance
Intake - output = change in body stores -> buffering effect of body stores
83
What is nutrient turnover
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
84
What is nutrient flux
A measure of the activity of the pathway
| Not necessarily related to the size of the metabolic pool
85
What is a functional pool
Direct involvement in body functions
86
What is a storage pool
Provides buffering effect ie can be made available to the functional pool when and as
87
What is a precursor pool
Provides the substrate for nutrient / metabolite synthesis
88
What is adaptation to altered nutrient supply
Minimises the consequences of such alterations
| The greater the capacity to respond to adverse nutritional states the greater the capacity to survive those states
89
Role of GI tract
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
90
Layers of the GI tract
1) mucosa (inner lining)
2) submucosa (support)
3) muscularis externa / propria (muscle)
4) serosa / adventitia (outer wrapping)
91
What makes up mucosa
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
92
What makes up submucosa
Connective tissue, blood vessels, lymphatics and nerves
| Some of the glands
93
What is the submucosal plexus
Supplies glands and muscularis mucosa
94
What makes up muscularis externa/ propria
Smooth muscle: inner circular and outer longitudinal. Responsible for peristalsis
95
What is myenteric (auerbach’s) plexus
Between muscle layers
Modulates peristalsis
Modulated by autonomic nervous system
96
What is peristalsis
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
97
What is the adventitia
The outer wall of the gut tube
| Thin later of connective tissue
98
What is the serosa
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
99
What is protective epithelium
Stratified squamous non keratinising
100
Where would you need protective (stratified squamous) epithelium
Oesophagus, anal canal, oral cavity, pharynx
101
What is secretory / absorptive epithelium
Columnar (microvilli)
102
Where would you need secretory / absorptive (columnar) epithelium
Stomach, small intestine, colon, pancreas
103
What is stretchy epithelium
Transitional
104
Where would you need stretchy (transitional) epithelium
Urinary tract (bladder, urethra)
105
What is facilitating diffusion epithelium
Simple squamous
106
Where would you need facilitating diffusion (simple squamous) epithelium
Capillaries
107
What are sphincters
Thickening of smooth muscle, close off lumen
108
What is the oesophageogatric sphincter
Prevents reflux of stomach contents into oesophagus
109
What is the pyloric sphincter
Between stomach duodenum: controlled release to food to allow for max absorption and not too much acidic release after meal eaten into duodenum
110
What is the ileocaecal sphincter
Between small and large intestine
111
What is the internal anal sphincter
Upper anal canal: retains faeces
112
What is GALT (gut associated lymphoid tissue)
In lamina propria
| Lymphocytes (T&B)
113
What are the layers of the oral cavity and pharynx
Only 2: mucosa and submucosa
114
What is the mucosa of the oral cavity and pharynx
Stratified squamous non keratinising
Lamina propria
No muscularis mucosa
115
What is the submucosa of the oral cavity and pharynx
Small salivary glands (origin of adenocarcinoma)
116
What are the lips
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
What is the common hepatic artery
A branch of the coeliac trunk
| Branches: hepatic artery proper, gastroduodenal artery
118
What is the portal triad
Hepatic artery
Portal vein
Bile duct
(In free edge of lesser omentum)
119
What is the hepatic artery proper
A branch of the common hepatic artery
| Branches: left and right hepatic arteries, right gastric artery
120
What is the pyloric sphincter
Circular muscle that keeps food in the intestines
121
What is the pyloric antrum
Large part of the funnel leading to the pyloric canal
122
What is the first part of the duodenum
- associated with greater and lesser omentum
| - from pylorus
123
What is plicae circularis
- folds of mucosa
- contain villi and microvilli to increase SA
- most absorption at the beginning therefore jejunum has more than distal ileum.
124
Which structures pass through the diaphragm with the oesophagus
T10
- vagal trunks
- left gastric artery
125
What are arterial arcades
The arteries that unite to form loops of arches which give rise to straight arteries called vasa recta
- supply small intestine
126
Blood supply to the duodenum
Gastroduodenal aa (from common hepatic aa)
Superior pancreaticoduodenal aa (from gastroduodenal aa)
Inferior pancreaticoduodenal aa (from SMA)
127
What are rugae
Folds in the stomach (gastric folds)
128
What is the pylorus
Part of the stomach that attaches to the duodenum
129
Which organ lies posterior to the descending part of the duodenum
Right kidney
130
Rugae
Gastric folds
131
What is saliva
Solution with electrolytes
| Derived from plasma
132
What are the main pairs of branched glands that produce saliva
Parotid (cheek)
Submandibular (under chin)
Sublingual (under tongue)
133
What are acinar cells
Produce primary secretion that is isotonic with plasma
| Some salivary proteins are secreted
134
What are duct cells
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
What happens to the concentration of saliva as the flow rate increases
Less time to reabsorb / secrete
- Na+ increases
- Cl- increases
- K+ decreases
- HCO3- increases
136
What does saliva contain
Mucous
Proteins (IgA)
Enzymes (amylase, lysozyme)
137
What happens with sympathetic stimulation of acinar cells
Small volume of thick saliva rich in mucous
138
Functions of saliva
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
How does deglutition (swallowing) work
Initiated when food bolus forced by tongue to rear of mouth to pharynx
2 phases: oropharyngeal and oesophageal
140
What is the oropharyngeal phase of deglutition
Food bolus directed into the oesophagus therefore seals off nasal passages (by uvula)
Trachea (by epiglottis)
141
What is the oesophageal phase of deglutition
Oesophagus protected from damage caused by passing food bolus by mucous secretion
- movement by peristalsis (+gravity)
142
Functions of the stomach
Storage of food
Initiation of digestion of proteins
Kill ingested bacteria (via acid)
Formation of chyme (before transfer to small intestine)
143
How does storage of food in the stomach work
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
What are parietal cells
Produce hydrochloride acid and intrinsic factor
| Important for VitB12 absorption
145
What cells secrete mucous into the stomach
Surface epithelial cells and mucous neck cells
146
What is carbonic anhydrase
Enzyme that catalyses reaction CO2 + H2O -> h2co3 (carbonic acid)
In parietal cells
147
What is the epithelial change at the gastro-oesophageal junction
Lining changes from squamous epithelium to columnar epithelium (glandular)
148
What is Barrett’s oesophagus
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
What types of cels line the surface of the stomach
Mucous producing columnar epithelial cells - protects stomach lining from HCL
150
What are the muscle layers of the stomach
```
Middle circular
Outer longitudinal
Inner oblique (for churning)
```
151
What cell types are in the gastric pits and glands
Mucous cells
Parietal cells
Chief (peptic / zymogenic) cells
Enteroendocrine cells
152
What are mucous cells
At surface
Produce mucous and bicarbonate (protects surface from acid and digestion)
153
What are the parietal (oxyntic) cells
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
What are the chief (peptic or zymogenic) cells
Produce enzymes
| Eg Pepsinogen: converted to pepsin in acidic env
155
What are enteroendocrine cells
Produce hormones
| Eg gastric, serotonin, somatostatin (SS), vasoactive intestinal peptide
156
How to prevent acid secretion
PPI (protein pump inhibitor) because HCL produced by active transport
157
What is a gastric ulcer
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
How do you fix a gastric ulcer
Stop stomach acid to allow the cells to repair and produce mucous : PPIs
- antibiotics to kill H pylori
159
How can helicobacter pylori survive in the stomach
```
Produces ammonia (alkaline) to protect from acid
Helical structure with flagella -> like a drill through mucous
```
160
What are brunners glands
In submucosa of duodenum
Secrete alkaline mucous
Neutralise HCL
161
What are villi
Lined with simple columnar epithelium
- continues into crypts which extend to muscularis mucosa
- lamina propria extends between crypts and core of villus
162
What are the cell types of the villus
- enterocytes (migrate upwards)
- goblet cells
- neuroendocrine cells
- stem cells
- intraepithelial lymphocytes
- paneth cells
163
What are enterocytes
Absorptive cells
| Migrate from base of the crypts (where formed) to villus tip
164
What is digestion
Luminal digestion:
- chyme and pancreatic secretions mix to break down food into component parts
Membrane digestion:
- brush border enzymes
165
What is malabsorption
Inability to absorb nutrients despite eating the right food
166
What causes malabsorption
Insufficient pancreatic enzymes (eg CF)
Insufficient bile
Loss of small intestinal SA (coeliac)
Lack of mucosal brush border enzymes
167
What are the manifestations of malabsorption
Diarrhoea and steatorrhoea (fatty stool)
- haemopoietic
- anameia
- bleeding (vit K deficiency)
- skeletal
- endocrine: impotency, infertility, amenorrhoea
168
What is coeliac disease
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
How does coeliac disease present
Failure to thrive, diarrhoea, abdo distension, malnutrition
170
Risk factors of coeliac disease
T1 diabetes
Autoimmune conditions
Familial tendency
171
How to diagnose coeliac disease
Serology for IgA
- anti EMA
- endoscopy + biopsy of small bowel mucosa
- nutritional disorders
172
Treatment of coeliac disease
Complete removal of gluten from diet -> complete recovery
If diet isn’t adhered to, cancer risk for non Hodgkin’s lymphoma
173
What is meckel diverticulum
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
What causes obstruction of the small bowel
Pain, absolute constipation, abdo distension, vomiting
175
What can obstruction of the small bowel lead to
```
Distension
Loss of fluids / electrolytes
Interruption of blood flow
Necrosis
Rapid bacterial growth
Gangrene
Perforation
```
176
What is cystic fibrosis
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
Function of large intestine
Absorb water and salt to produce more solid waste product
178
What type of cells are in the large intestine
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
What is the appendix
Outgrowth of caecum containing lymphoid material
180
What muscle types in the colon
Longitudinal, circular and taenia coli mm
181
What causes a slower transit rate through the colon
Constipation because dehydration / lack of fibre can cause diverticulosis
182
What causes a faster transit rate through the colon
IBS
| Diarrhoea
183
What causes a blockage in the colon
Obstruction
184
What causes ischaemia of the Bowel
Caused by a range of factors
Can cause necrosis
V good anastomoses in bowel
185
Types of ischaemia of the bowel
Thrombosis
Embolism
Spasm
Atheroma
186
What is diverticulosis
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
2 main inflammatory bowel diseases
Crohn’s disease
| Ulcerative colitis
188
What is IBS
Idiopathic and chronic relapsing
Abnormal local immune response to normal gut flora / self antigens
- more common in white pts in developed nations
189
What is Crohn’s disease
Inflammation (granulomatous) of the entire GI wall thickness
190
What happens in Crohn’s disease
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
Symptoms of Crohn’s disease
Diarrhoea, cramps, fever
192
What is UC
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
Risk factors for colorectal tumours
```
Age
Race
Obesity
Lack of exercise
High fat low fibre diet
Smoking
Alcohol
Diabetes
Personal or family history
Previous abdominal radiation therapy
IBS
```
194
Symptoms of colorectal tumours
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
How to prevent colorectal cancer
Screening
Fecal occult blood test-> traces of blood in stool for all over 60s
Lifestyle factors
196
What is the anal canal
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
What are the anal sphincters
Internal: smooth mm thickening at end of rectum (involuntary control)
- external: skeletal mm (voluntary control)
198
What are food borne outbreaks
Often local
Exposure to contaminated food
Need to recognise and track
Pathogens: E. coli, salmonella, shigella
199
What is gut microbiota-mediated colonisation resistance
Gut microbiota produces products with antimicrobial effects including SCFA, 2nd bile acids, bacteriocins
Each contributes to resistance against microbes
200
How do you test C. difficile
Enz. Immunoassay for simultaneous detection of antigen GDH and toxins A &B in stool
- rapid membrane test for rotavirus antigen in stool
201
What is viral gastroenteritis
```
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
What is E. coli
Enterotoxigenic (foodborne/ waterborne)
Enteroinvasive (foodborne / waterborne )
Enteropathogenic (foodborne / person to person / waterborne)
Entherohaemorrhagic (foodborne)
Lab identified from food
Short incubation
Tx - oral rehydration
203
What is campylobacter
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
What is (non typhoid) salmonella enteritidis
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
What is (typhoid) salmonella typhoid and paratyphi
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
What is shigella
```
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
What are parasites
Waterborne from faecally contaminated water supplies
Often travel related
Incubation 7-10 days
Detection by stool microscopy
208
What is clostridioides difficile
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
What is the histology of C. difficile
Psuedomembranous colitis (inflammation of colon w elevated yellow - white plaques on mucosa that coalesce to form pseudomembranes)
210
How to diagnose C. difficile
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
How to treat c diff
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
What is toxic megacolon
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
What is helicobacter pylori
```
Bacterial infection
Chronic gastritis
Gastric ulcer (70-80%)
Duodenal ulcer disease (95%)
Inflammatory response
Associated with gastric adenocarcinoma and MALT lymphoma
```
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How to diagnose H pylori
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
How to treat H pylori
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
What is dyspepsia
Indigestion
| - gastro-oesophageal reflux disease (GORD) -> heartburn
217
What is zollinger Ellison syndrome
Rare gastric secreting tumour of D - and / or G cells of the pancreas -> results in lots of gastrin release
218
Signs and symptoms of peptic ulceration
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
What is peptic ulceration
Caused by H pylori (mostly) or NSAIDs
| - infection can lead to chronic inflammation and gastric damage (gastritis) -> ulceration
220
Recognised complication of peptic ulceration
Iron deficiency anaemia
221
How to diagnose peptic ulceration
Urea breath test (C13)
Biopsy for urease activity
H pylori antigens / antibodies in specimens
222
How does the urea breath test (C13 urea) work
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
Systems that increase acid secretion
Histamine (H2 receptors)
Gastrin (CCK2 receptors)
ACh (M receptors, M3 on parietal cells)
224
Systems that decrease acid secretion
Prostaglandins
| Cytoprotective via bicarbonate and mucous release
225
What role do prostaglandin receptors have
(Local regulation)
COX releases prostanoids -> stimulate prostaglandin receptors which switch PP off -> also stimulate release of mucous and HCO3-
226
What are antacids
```
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
What are Latinate
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
What are the different preparations of drugs
Suspension
Tablets
Capsules
229
What is absorbed fastest and has the lowest risk of bioavailability problems
Aqueous solutions
Syrups
Elixirs
230
What had mediums absorption and risk of bioavailability problems
```
Suspensions
Chewed tablets
Granules
Capsules
Conventional tablet
```
231
What is absorbed the slowest and has the highest risk of bioavailability problems
Compressed tablets
Enteric coated tablets
Complex forms
232
What is bioequivalence
Comparable bioavailability between drugs (identical rate and extent of absorption)
233
What is bioequivalence assessed by
Time to peak plasma level (tmax)
Peak plasma level (cmax)
Bioavailability (F)
234
Why are some medicines taken at night
Because highest plasma conc (cmax) will be at night so less likely to feel side effects if asleep
235
What is sustained release (SR)
Has many layers of protective coating, slows down release of drug and smooths it out
236
What is morphine
Opioid analgesic
T1/2 - 2-3 hours
- oramorph (rapid relief)
- oral suspension for immediate pain relief
237
What is nifedipine
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
How is omeprazole (PPI) prepared
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
What are depot injections
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
What is the ampulla of vater (hepatopancreatic ampulla)
Common bile duct and pancreatic duct
241
What is the porta hepatis
Site where vessels / nerves / ducts leave / enter liver in between caudate and quadrate lobes
242
What parts of the large intestine have a mesentery (membrane that attaches intestine to abdominal wall and holds it in place)
Appendix
Transverse colon
Sigmoid colon
243
What is the superior mesenteric vein
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
What is the common bile duct
Common hepatic duct and cystic duct
245
What does CCK do after a meal
Relaxes sphincter of oddi
Contracts gall bladder
Allows bile to pass to duodenum
246
What is jaundice
Bilirubin accumulation in plasma
Sx: yellowing of skin, sclera, mucous membranes
- may produce kernicterus (deposits of pigment in brain)
247
What is first pass metabolism
Drugs are absorbed from small intestine
| Taken to liver via portal circulation -> some drugs metabolised before reaching systemic circulation
248
What is absorbed in the small intestine
Most weak acids and bases because high levels of uncharged drugs
(PH 5.3)
Long residence time
249
What are acid labile drugs
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
What are acid stable drugs
Taken on a full stomach so it spends longer in the stomach so slows down the rate of absorption (tmax is decreased)
251
What does a change in absorption cause a change in
AUC, tmax, F
252
What does a change in distribution cause a change in
V, t1/2
253
What does a change in elimination cause a change in
AUC, CL, t1/2
