Acute Abdomen + Physiology Flashcards
(182 cards)
1
Q
How is GI function regulated?
A
Integration of neural and hormonal signals Neurohormonal control: integration of neural + hormonal signals
2
Q
Outline the 3 neural stages of digestion.
A
a) Cephalic (30%): Sight, smell, thought or taste
• Stimuli ≈ neurogenic signals ≈ cerebral cortex ≈ medulla oblongata + appetite centres of amygdala and hypothalamus ≈ dorsal motor nuclei of vagus nerve ≈ vagus nerve to stomach = Meissner’s (Submucosal plexus) + Auerbach’s (myenteric) plexus ≈ ACh ≈ intramural gastric neurons ≈ ACh ≈ M3r of Parietal cells (fundus) ≈ HCl secretion + Motility (from submucosal and mucosal plexus)
b) Gastric (60%): Stretch (distension) + Raised pH
• Stimuli ≈ stretch receptors + chemoreceptors ≈ enteric NS + peptides and AAs ≈ ENS efferents and GRP neurone efferents ≈ ACh release + Gastrin ≈ Parietal cells to increase more HCl + ECL cell increase HA which increases parietal cell HCl + G cells to secrete more gastrin ≈ Increased acid secretion and motility
c) Intestinal (10%): Acid and semi-digested fats ≈ enterogastric reflex
• Stimuli ≈ inhibitory signals to the
i) Stomach by enteric NS
ii) Medulla by afferent neurones to inhibit vagal nuclei
iii) Chyme stimulates S and I cells of duodenum to release secretin and CCK which stimulate pancreas and gall bladder, acinar cells produce enzymes and suppress gastric secretion and motility
3
Q
Outline the Cephalic stage of digestion.
A
a) Cephalic (30%): Sight, smell, thought or taste
• Stimuli ≈ neurogenic signals ≈ cerebral cortex ≈ medulla oblongata + appetite centres of amygdala and hypothalamus ≈ dorsal motor nuclei of vagus nerve ≈ vagus nerve to stomach = Meissner’s (Submucosal plexus) + Auerbach’s (myenteric) plexus ≈ ACh ≈ intramural gastric neurons ≈ ACh ≈ M3r of Parietal cells (fundus) ≈ HCl secretion + Motility (from submucosal and mucosal plexus)
4
Q
Outline the Gastric phase of digestion.
A
b) Gastric (60%): Stretch (distension) + Raised pH
• Stimuli ≈ stretch receptors + chemoreceptors ≈ enteric NS + peptides and AAs ≈ ENS efferents and GRP neurone efferents ≈ ACh release + Gastrin ≈ Parietal cells to increase more HCl + ECL cell increase HA which increases parietal cell HCl + G cells to secrete more gastrin ≈ Increased acid secretion and motility
5
Q
Outline the Intestinal phase of digestion.
A
c) Intestinal (10%): Acid and semi-digested fats ≈ enterogastric reflex
• Stimuli ≈ inhibitory signals to the
i) Stomach by enteric NS
ii) Medulla by afferent neurones to inhibit vagal nuclei
iii) Chyme stimulates S and I cells of duodenum to release secretin and CCK which stimulate pancreas and gall bladder, acinar cells produce enzymes and suppress gastric secretion and motility
6
Q
List 3 main hormonal regulators of digestive function. State the specific site of production for each.
A
a) Gastrin: Enteroendocrine G cells in gastric mucosa (Pyloric Glands in Pyloric antrum)
b) Secretin: Enteroendocrine S cells in gastric mucosa (Duodenum)
c) CCK: Enteroendocrine I cells in duodenum releasing CCK in response to FAs and small peptides
d) GIP: Produced by enteroendocrine K cells in response to glucose in SI
7
Q
State the site of production and functions of Gastrin.
A
Gastrin: Enteroendocrine G cells in gastric mucosa (Pyloric Glands in Pyloric antrum)
• gastric acid secretion from parietal cells
• Peristalsis (GI motility via smooth muscle contraction)
• Relax pyloric sphincter (≈ gastric emptying
8
Q
State the site of production and functions of Secretin.
A
Secretin: Enteroendocrine S cells in gastric mucosa (Duodenum)
• [HCO3-] secretion by pancreas ≈ stabilise chyme pH
• Bile production by liver
• Reduced GI motility (reduced contraction of smooth muscle and GI mucosa)
9
Q
State the site of production and functions of CCK.
A
CCK: Enteroendocrine I cells in duodenum releasing CCK in response to FAs and small peptides
• [HCO3-] secretion by pancreas
• Secretion of pancreatic enzymes
• Contraction of gallbladder + relaxation of Sphincter of Oddi ≈ flow of bile into duodenum
• Inhibition of gastric emptying
• Growth of exocrine pancreas
10
Q
State the site of production and functions of GIP.
A
d) GIP: Produced by enteroendocrine K cells in response to glucose in SI
• Stimulates pancreas to release insulin
11
Q
Which hormone is responsible for the contraction of the gallbladder and relaxation of the Sphincter of Oddi?
A
CCK
12
Q
State two hormones which inhibit gastric emptying.
A
Secretin
CCK
13
Q
Are the timings of the three regulatory phases of GI function discrete?
A
No, there is considerable temporal overlap between the three regulatory phases of GI function
14
Q
What is salivary secretion?
A
Addition of substances (fluids, ions and enzymes) into lumen of GI tract from salivary glands
15
Q
State 3 substances which are present in salivary secretion. For each, give a factor which increases these or decreases.
A
Bicarbonate: PSNS (inc.) cf Sleep/Dehydration/Atropine (dec.)
K+: PSNS cf Sleep/Dehydration/Atropine
Amylase: SNS cf Sleep/Dehydration/Atropine
Lingual lipase: SNS cf Sleep/dehydration/atropine
16
Q
What is the process of HCl secretion from the parietal cell?
A
Stimuli (Gastrin, HA, ACh, distension and peptides) bind CSR (GPCR or L-AA transporter) ≈ rise in IC Ca++ or cAMP ≈ secretion mediated by proton pump P5 (Na/K ATPase) which transports cations in opposite directions under physiological function to create electrochemical gradient as K+ IN and H+ OUT. When stimulated, large changes occur and vesicles which possess p+ pumps become active and translocate from cytosol to apical membrane and fuse together to increase surface area
17
Q
What is the innervation of the exocrine component of the pancreas?
A
ANS follows Rest and Digest
- PSNS from vagus ≈ increased secretion
- SNS from Coeliac + SM ganglia ≈ reduced secretion
18
Q
Outline the duct system of the exocrine pancreas regarding its functioning.
A
The exocrine compartment of the pancreas is composed of a duct system with berry-like acinar cells connected by intercalated ducts that drain into intralobular collecting ducts and subsequently into the main pancreatic duct. The pancreatic duct runs the entire length of the pancreas and unites with the common bile duct at the Hepatopancreatic Ampulla of Vater, which drains into the duodenum at the major duodenal papilla
19
Q
What is the regulation of salivary secretion?
A
1) PSNS: Stimuli (+/-) —> chemo-/mechanoreceptors —> Afferent nerve impulses (+/- cerebral cortex prior to integration) —> Salivary centre in medulla —> CNVII and CN IX —> ACh —> M3 (Gaq) —> IP3, Ca++ ≈ secretion ≈ saliva ≈ large volume, watery + enzyme rich (serous; parotid)
2) SNS: Stimuli (+) —> chemo-/mechanoreceptors —> Afferent nerve impulses (+/- cerebral cortex prior to integration) —> salivary centre in medulla —> T1-T3 —> NE —> ß1 (Gas) —> cAMP ≈ secretion ≈ saliva which is mucous rich, small volume and thick (sublingual gland)
20
Q
What are salivation reflexes?
List two different types of salivation reflex and outline their pathway.
A
1) Simple (unconditioned): Food (stimulus) —> chemoreceptors/mechanoreceptors in mouth —> afferent nerves —> salivary centre in medulla —> impulses via autonomic nerves (SNS + PSNS stimulation) —> Salivary glands increase production
2) Acquired (conditioned): Sight/thought/smell —> Afferent impulses along afferent nerves —> Cerebral cortex —> Salivary centre in medulla —> impulses via autonomic nerves (SNS + PSNS stimulation) —> Salivary glands increase production
21
Q
What are the stages of salivation and where are these mediated?
A
1) Acini cells: 1º secretion which is isotonic
• Ions: Na+, Cl-, K+, HCO3-
• Enzymes: Amylase and mucin production
2) Myoepithelial cells: Eject saliva into ductal cells from acini cells
• Saliva into ducts
3) Duct cells: 2º secretion + modification
• Ions: Reabsorb Na+ and Cl-; add K+; Alter HCO3- according to flow rate (proportional association)
• High flow rate ≈ increased [HCO3-] ≈ osmotic gain drawing more water in
• Low flow rate ≈ reduced [HCO3-]
22
Q
List 5 substances secreted from the stomach.
A
HCl
Pepsinogen
Intrinsic factor
Mucous
Gastrin
Somatostatin
23
Q
Regarding HCl, what is its site of production, role and list 3 factors which increase and 3 which decrease its secretion from the stomach.
A
Parietal Cell in Oxyntic Gland
Protein degradation + Pepsinogen activation @ pH2
Increase: Thought/smell Distension ACh HA PSNS Gastrin
Decrease: Ghrelin Acidity (low pH) Chyme in duodenum SS Atropine Ranitidine Omeprazole
24
Q
Regarding Intrinsic Factor, what is its site of production, role and list 3 factors which increase and 3 which decrease its secretion from the stomach.
A
Parietal Cell (Oxyntic Gland)
Vitamin B12 absorption
Inc. Thought/smell Distension ACh HA PSNS
Dec. Ghrelin Acidity (low pH) Chyme in duodenum SS Atropine Ranitidine Omeprazole
25
Regarding pepsinogen, what is its site of production, role and list 3 factors which increase and 3 which decrease its secretion from the stomach.
Mucous Neck Cell (Oxyntic)
Chief Cells (Oxyntic)
Proenzyme cleaved to form pepsin
```
Inc.
Thought/smell
Distension
ACh
HA
PSNS
```
```
Dec.
Ghrelin
Acidity (low pH)
Chyme in duodenum
SS
Atropine
Ranitidine
Omeprazole
```
26
Regarding Mucous, what is its site of production, role and list 3 factors which increase and 3 which decrease its secretion from the stomach.
MNCs (Oxyntic)
Lubrication + barrier
```
Inc.
Thought/smell
Distension
ACh
HA
PSNS
```
```
Dec.
Ghrelin
Acidity (low pH)
Chyme in duodenum
SS
Atropine
Ranitidine
Omeprazole
```
27
Regarding Gastrin, what is its site of production, role and list 3 factors which increase and 3 which decrease its secretion from the stomach.
G cell (Pyloric)
Stimulate digestion via: HCl from parietal cells, pyloric sphincter relax and hepatic bile production
```
Inc.
Thought/smell
Distension
ACh
HA
PSNS
```
```
Dec.
Ghrelin
Acidity (low pH)
Chyme in duodenum
SS
Atropine
Opiates
```
28
Regarding Somatostatin, what is its site of production, role and list 3 factors which increase and 3 which decrease its secretion from the stomach.
D cells (Oxyntic + Pyloric)
Inhibit parietal cell acid secretion
Inc.
Acidity
Chyme in duodenum
VIP from Vagus
```
Dec.
Thought/smell
Distension
ACh
HA
PSNS
```
29
What is secreted from the pancreas?
High [HCO3-]
Enzymes: Pancreatic lipase, pancreatic amylase and pancreatic protease
30
List factors which increase or decrease pancreatic secretion.
Inc.
Secretin
CCK
PSNS
Dec.
Ghrelin
Opiates
31
What is the formation of pancreatic secretions regarding fluid and enzymes and how is this formed?
Stimulation by the physiological agonists CCK (I cells of duodenum) and ACh (Vagal nerve stimulation) cause an elevation of intracellular calcium which activates the calcium-activated chloride channel in the apical membrane, leading to fluid secretion
32
Outline the molecular mechanism of secretion by a pancreatic acinar and ductal cell.
i) (ACh): Vagal nerve efferents —> ACh —> M3r (GPCR) —> PLC —> IP3 —> IP3r2 and IP3r3 on ER —> Channel opens —> Ca++ elevation —>
a) Ductal cells: Open Cl- channel (TMEM16A) in apical membrane —> Na+ paracellular transport through tight junctions —> NaCl in lumen generates osmotic gradient —> water efflux via apical AQP5 water channels
b) Acinar cells: binds with synaptotagmin 2 (calcium sensor) for synchronised exocytosis (of vesicles containing enzymes)
ii) (CCK): Duodenal I cells —> CCK —> CCK1r —> indirectly open RyR on ER membrane —> Channel opens —> Ca++ elevation —>
a) Ductal cells: Open Cl- channel (TMEM16A) in apical membrane —> Na+ paracellular transport through tight junctions —> water efflux via apical AQP5 water channels
b) Acinar cells: binds with synaptotagmin 2 (calcium sensor) for synchronised exocytosis (of vesicles containing enzymes)
33
List 3 pancreatic enzymes.
* Pancreatic amylase
* Pancreatic lipase
* Pancreatic protease
34
List 5 components of bile. Give 3 stimuli for bile secretion.
Components:
Bile Salts
Bile Pigments (Bilirubin)
Cholesterol Esters
Phospholipids
HCO3-
Stimuli:
Secretin (production)
CCK (contraction of GB and relaxation of SOD)
Central and enteric neural input
35
What is bile?
Mixture of bile salts, bile pigments, cholesterol esters and bicarbonate which is produced by hepatocytes and stored in gallbladder, is not enzymatic, and emulsifies fats into micelles to prepare for digestion and solubilise products of digestion into micelles
36
What is the LI?
digestive organ which is partly intraperitoneal (transverse) and partly retroperitoneal (ascending and descending) which secretes alkaline mucous, protecting and lubricating the large bowel and responsive for absorption of vitamins
37
What is the secretory function of the LI?
Stimuli (distension, VIP and ACh increase secretion cf Adrenaline and SS reduce secretion)
1) Alkaline mucous ≈ protection + lubrication + neutralisation of H+ from gut bacteria
- High K+
- High HCO3-
38
List the sequence of mechanical digestion.
1) Mastication
2) Deglutition
3) Storage
4) Mechanica digestion
5) SI movements
6) Colon movements
39
Outline the chewing reflex.
Chewing reflex = Bolus of food in mouth —> inhibition of mastication ≈ jaw drops ≈ stretch reflex of jaw muscles —> afferent feedback —> Nuclei in brainstem —> CN V —> mastication ≈ rebound contraction
≈ incisors cut + molars grind to increase SA
40
Outline deglutition. Give the two stages.
Bolus at posterior of pharynx —> epithelial swallowing receptors —> afferent neurone CN V + CN IX —> medulla oblongata —> efferent motor impulses via CN V, CN IX + CN X—> elevation + retraction of velum (soft palate) ≈ velopharyngeal closure + palatopharyngeal folds medial (sagittal selection slit) —> larynx + epiglottis lifted upwards ≈ prevent choking/asphyxiation + upper oesophageal sphincter opens —> pharyngeal muscles contract ≈ 1º +/- 2º peristaltic wave (2º if vagus afferent fibres detect food —> MO —> CN IX + CN X ≈ 2º peristaltic contraction)
Stages:
• Oropharyngeal phase (Oral phase + Oral transmit phase + Pharyngeal phase)
• Oesophageal phase (1º and 2º peristaltic wave)
41
Outline the process of storage in the stomach.
Food enters stomach via upper oesophageal sphincter (cardiac sphincter) —> stretch/distension —> afferent feedback via CN X —> Medulla oblongata —> reduce tone in muscle wall ≈ rugae distend + increase volume (vasovagal reflex)
• Vasovagal reflex
42
Outline the process and 3 key areas of mechanical digestion.
Weak peristaltic mixing waves —> Constrictor rings of increasing intensity —> Retropulsion —> Chyme (food + stomach secretions)
Three stages
• Weak peristaltic mixing waves: Food in stomach —> distension —> vagal afferents; myenteric plexus —> MO; interneurone —> vagal efferents; myenteric plexus efferent —> weak peristaltic constrictor waves (mixing waves) in upper portion of stomach
• Retropulsion: Weak peristaltic constrictor (mixing) waves in upper portion of stomach —> increase intensity ≈ constrictor rings forcing antral contents under high pressure towards pylorus —> pylorus muscle contracts to prevent emptying via pylorus ≈ upstream squeezing ≈ retropulsion
• Pyloric pump: antral peristaltic contractions —> pyloric sphincter relaxes (modulated by nervous + hormonal signals) —> chyme passes into the duodenum
43
Outline the SI movements. State the main reflex of this stage.
(mixing contraction + propulsive contraction however less distinct as all movements cause a mixture of both contraction type)
• Segment contractions: Distended with chyme —> local concentric contractions along intestine —> segmentation of small intestine (spaced segments) with varied frequency of slow waves determined by intrinsic slow waves in smooth muscle + intrinsic ENS
• Peristaltic waves: Chyme propelled through SI by peristaltic waves with net movement
• Gastroileal reflex: Intensifies peristalsis in ileum forcing chyme through ileocaecal valve (ileocaecal valve controlled by SNS ganglia or myenteric plexus in gut wall)
• Reflex: Gastroileal reflex
44
Outline the key colon movements and reflexes.
Haustrations (circular + longitudinal muscle contractions) —> mass movements (modified peristalsis with constrictive ring at point of distension in colon then lose haustration and contract as unit propelling faecal material further down colon) —> Defaecation
• Haustrations: Circular muscle contract ≈ constrict lumen + longitudinal muscle contract (teniae coli) ≈ elongate lumen sagittally
• Mass movements: Modified peristalsis ≈ constrictive ring at point of distension + distal to constrictive ring loss of haustration ≈ propel faecal material down colon without interruption
• Gastrocolic + Duodenocolic reflexes: distension of stomach/duodenum —> enteric nervous system —> increase colonic motility + mass movements
• Defaecation: Defaecation reflex whereby facets enter rectum —> local enteric nervous system triggered (myenteric plexus in Submucosa) —> peristalsis in descending colon, sigmoid and rectum —> inhibitory signals from myenteric plexus (rest and digest) + PSNS augment intrinsic myenteric defaecation (increase motility + relax internal anal sphincter ≈ parasympathetic defaecation reflex) ≈ internal anal sphincter relaxed + external anal sphincter consciously relaxes
* Gastrocolic reflex
* Duodenocolic reflex
* Defaecation reflex
45
Give two inhibitory reflexes which are not directly from the GI tract and may cause inhibition and why does this occur?
1) Peritoneointestinal reflex: Peritoneum irritation strongly inhibiting excitatory enteric nerves ≈ intestinal paralysis due to peritonitis
2) Renointestinal/vesicointestinal reflexes: Kidney or Bladder irritation strongly inhibiting excitatory enteric nerves ≈ intestinal paralysis due to kidney or bladder infection
46
What factors modulate SI peristalsis and how?
```
Increase SI peristalsis:
- Duodenal distension
- Gastroenteric reflex (distension of stomach conducted via myenteric plexus along to SI)
- Gastrin
- CCK
- Insulin
- Serotonin
- Motilin
```
Decrease SI peristalsis:
- Secretin
- Glucagon
47
What factors alter gastric emptying?
Increase gastric emptying:
- Increased food volume in stomach: distension ≈ increase peristalsis (weak + constrictor rings) ≈ increase pyloric pump
- Gastrin: increase peristalsis, gastric acid secretion and relax pyloric sphincter ≈ gastric emptying
```
Decrease gastric emptying: Enterogastric reflex from duodenum via ENS, SNS (increase impulses) or PSNS (reduce impulses)
- Distension of duodenum
- Irritation of duodenum
- Acidity of duodenal chyme
- Breakdown products: FAs and Proteins
- CCK: block increased stomach motility
- GIP: reduce GI motility
- Secretin: reduce GI motility
```
48
List the factors which may contribute to the development of malnutrition in IBD?
1) Reduced dietary intake
2) Altered energy/nutrient metabolism
3) Increased GI nutrient losses
4) Drug-nutrient interactions
49
What are the manifestations of malnutrition in IBD?
1) Protein Energy Malnutrition (PEM)
- UC > CD
2) Altered body composition
- ∆ composition due to pro-inflammatory cascade + drugs e.g. steroids ≈ weight gain/adiposity + changed lifestyle such as reduced sport ≈ ∆ body composition
3) Micronutrient deficiencies
- Poor absorption + diarrhoea
- Vitamins A, B, C, D, E and Minerals Zn, Se, Cu, Ca++ \
4) Poor bone health
- Reduced bone mineralisation due to drugs (steroids), low activity (reduced PA) and reduced intake (low micronutrients) and metabolism (pro-inflammatory cytokines on bone formation, resorption and osteoblast maturation)
5) Reduced linear growth
- Shorter height due to poor bone growth and soft tissues
50
List the main micronutrient deficiencies a patient with IBD is vulnerable to.
- Fe
- Folic Acid
- Selenium
- Zinc
- Calcium
- Vitamin A
- Vitamin B12 (cobalamin)
- Vitamin B1 (thiamine)
- Vitamin B6 (pyridoxine)
- Vitamin D
- Vitamin K
51
Why may IBD patients have a higher risk of low bone density, osteoporosis and fractures?
1) Inflammation
2) Steroids
3) Reduced physical activity
4) Malabsorption
52
What are the calcium requirements for adult patients with IBD and how do they differ to the general adult population? State where this can come from.
1000mg per day for IBD patients cf adults require 700mg per day;
- Milk
- Cheese
- Yoghurt
- Custard
- Fortified juice
- Sardines
- Scampi
- Pitta bread/chapatti
53
Give a screening tool which can be used to assess nutrition in a patient with IBD.
Malnutrition Universal Screening Tool (MUST) is a validated screening tool comprising of 5 steps which is scored from 0-6.
Step 1: BMI calculation
0-2 (18.5-20 5 days
Step 4: Calculate
Step 5: Stratification
0 = low risk (repeat annually community or weekly hospital)
1 = medium risk (document intake for 3 days; hospital weekly and community 2-3 months)
2 = high risk (refer to dietitian, nutritional support team; set goals and monitor/review care plan weekly in hospital and monthly in community)
54
When is artificial nutrition support recommended for a patient?
Enteral tube feeding (delivery of nutritionally complete feed via tube into stomach, duodenum or jejunum)
Consider enteral tube feeding in patients who are at risk of malnutrition or malnourished and have inadequate/unsafe oral intake and functional, accessible GI tract
55
What may the benefit of enteral nutrition in Active CD be?
Exclusive enteral nutrition believed to promote mucosal healing in GI tract by positively altering intestinal microbiota, reducing intestinal permeability and promoting reduction in inflammatory cytokines
56
For which patient group is enteral nutrition often the primary therapy for inducing remission in active Crohn’s Disease and why?
Primary therapy for induing remission in active Crohn’s Disease supported in CD especially in children where adverse consequences f steroid therapy are proportionally greater, impacting nutrition, immune system and MSK growth
57
When might enteral nutrition be used in adults with active Crohn’s Disease to induce remission?
Acute active CD +/- may be susceptible to steroid treatment
58
Is enteral nutrition as a primary therapy for inducing remission in UC indicated?
Primary therapy using nutrition to treat IBD not supported in UC
59
What is a food-reintroduction diet?
Structured dietary protocols designed to slowly add food back to diet after period of exclusive enteral nutrition e.g. LOFFLEX ≈ exclude all foods which may cause food intolerance and followed for 2-4 weeks
60
What is Coeliac Disease?
Autoimmune disease associated with chronic inflammation of SI with malabsorption of glutens leading to malabsorption of micro and macronutrients increasing risk of complications
61
When should testing for Coeliac disease be considered in adults and children? Describe the recommended diagnostic process?
Serological tests should be offered to patients with:
- Persistent unexplained abdominal or GI symptoms
- Faltering growth
- Prolonged fatigue
- Unexpected weight loss
- Severe or persistent mouth ulcers
- Unexplained iron, vitamin B12 or folate deficiency
- Type 1 Diabetes
- Autoimmune thyroid disease
- Irritable Bowel Syndrome
- First degree relative with Coeliac Disease
62
List the foods that should be excluded from the diet by someone who has been diagnosed with Coeliac Disease and consider the implications of excluding gluten-containing foods from diet both practically and nutritionally?
```
Avoid gluten for life, gluten-free diet which can be found online (coeliac.org.uk)
- Barley
- Bulgar wheat
- Couscous
- Durum wheat
- Flours made from wheat, rye or barley
- Porridge oats, oat milk
- Biscuits and breads
- Muesli, wheat based breakfast cereals
- Canned and dried fresh wheat noodles and pasta
- Meat and poultry cooked in batter or breadcrumbs
- Beer, lager, stout
```
63
List foods that someone with Coeliac Disease can safely include in their diet and using Eatwell Guide consider how someone with Coeliac Disease can continue to consume a varied, balanced diet.
```
- Meat
- Fish
- Fruit and vegetables
- Rice
- Potatoes
- Lentils
- Fruit juice
- Flavoured water
- Fizzy drinks
- Cider
- Wine
- Sherry
- Spirits
- Port
```
64
Would a patient with Coeliac Disease need to take supplements? What are the RDI for calcium and vitamin D?
Take vitamin D and calcium supplements if dietary intake insufficient
Vitamin D: 10mcg
Calcium: 700mcg
65
What dermatological condition may accompany Coeliac Disease?
Dermatitis Herpetiformis, skin lesion which comprises of erythematous, pruritic excoriations consisting of urticarial plaques, papules with vesicles on the elbows, knees, buttocks, lower back and scalp appearing in older patients (50-69 years)
66
What is Irritable Bowel Syndrome?
Chronic, relapsing and remitting lifelong disorder featuring abdominal pain associated with defaecation and change in bowel habit
67
What first-line dietary advice would you give to a patient with IBS?
- Regular meals
- Avoid missing meals
- 8 cups of fluid
- Restrict caffeinated drinks to 3 per day
- Limit intake of high-fibre food
- Reduce intake of resistant starch
- Limit fruit to 3 portions per day
- Avoid Sorbitol (artificial sweetener) if diarrhoea (osmotic diarrhoea)
68
What lifestyle factors may be discussed with a newly diagnosed IBS patient?
```
Lifestyle
- Stress management
- Leisure time and relaxation time
- Physical activity
- Symptom targeted medication
```
69
List the complications of Coeliac Disease.
```
Osteoporosis
Ulcerative jejunitis
Malignancy
Functional hyposplenism
Vitamin D deficiency
Iron deficiency
```
70
What are the 4 major functions of the GI tract?
* Secretion (7L)
* Absorption (8.9L)
* Motility
* Digestion
71
Where are salivary secretions derived from/secreted by? How may these be classified?
1) Sublingual
• Floor of mouth
• Beneath tongue
• Mucous gland: Mucous-rich
2) Submandibular
• Inferior to mandibular lower edge
• Mixed glands: serous + mucous cells ≈ seromucous gland
3) Parotid
• Inferior to ear and over masseter (jaw muscle)
• Serous gland: Serous secretion ≈ aqueous fluid of water, ions and enzymes
72
What is oesophageal peristalsis?
1º peristaltic wave from beginning to end of oesophagus taking 4-10 seconds pushing food to stomach with circular fibres squeeze bolus down and longitudinal fibres shorten distance of travel
- Circular + Longitudinal muscle fibres
- Water travels faster
- Sticky food may get lodges ≈ 2º peristaltic wave + increased saliva production
- Food enters stomach through lower oesophageal sphincter (cardiac sphincter)
73
What is the structure of the stomach and its functional areas? What is secreted from each area?
```
1) Oxyntic:
• Parietal cells: HCl + IF
• Chief cells: Pepsinogen
• MNCs: Pepsinogen + Mucous
• EC cell: ANP
• ECLs: HA
• D cells: SS
```
2) Pyloric:
• MCN: pepsinogen + mucous
• G Cell: Gastrin
• EC Cell: ANP
74
Where is the specific location of Gastrin production?
G cells in Pyloric functional gland area
75
Which cells produce HCl and IF?
Parietal cells
76
Which cells produce Pepsinogen?
Chief cells and MNCs
77
Which cells produce Pepsinogen and Mucous?
MNCs
78
Which cells produce SS? State the location
D cells
79
Which cells produce ANP? State the location
EC cells in the oxyntic regions of the gastric pits.
80
What is the composition of the human body regarding cells and fluid compartments? How is this organised? What does this fluid estimation include?
• 60% body weight is water: 72kg x 0.6 = 42kg
* 70% ICF
* 30% ECF
```
Scenario: 72kg man
• 42L water
• 28L ICF
• 11L ISF
• 3L plasma
```
81
What is the major regulators of body fluid regarding output and input and their approximate amounts? What are the main compartments? What are their separating membranes?
```
Output:
• Kidneys (1.5L)
• Lungs (0.9L)
• Faeces (0.1L)
• Sweat (0.05L)
• Skin
```
Concept: Insensible water loss (feces, respiratory and skin) = difficult to measure
Input:
• Oral fluids
• Lymphatics
Compartments:
• Plasma = 3L
• ISF = 11L
• ICF = 14L
Membranes:
• Capillary membrane (plasma -> ISF)
• Cell membrane (ISF -> ICF)
82
How does fluid exchange occur across the capillary membrane? What factors determine the movement of water in and out of the capillaries?
• Starling Principle of Fluid Exchange: Result of Net Filtration Pressure (NFP)
Factors:
• Hydrostatic forces: Capillary hydrostatic pressure (Pc) vs tissue interstitial pressure (Pi)
• Oncotic forces: Capillary plasma oncotic pressure (πc) vs tissue interstitial oncotic pressure (πi)
• A: SA
• KF: Permeability of capillary barrier
83
What is the net driving force (NDF)?
net pressure gradient across determined by sum of individual hydrostatic (transendothelial) and oncotic pressures (plasma and subglycocalyx space) expressed in units of mmHg
84
When taking blood prior to prescribing fluids and electrolytes, what compartment is the fluid coming from a reflection of? Which ion is not as accurately reflected by the plasma concentration and why?
Plasma thus extracellular;
Potassium is lowest in extracellular (4-5 mM/L) cf intracellular is higher (140mM/L) thus IC K+ may act as a reserve and buffer the EC compartment, masking the true [K+]plasma
85
What are the 5Rs to prescribing IV fluids?
• Routine maintenance:
- Cannot meet enteral fluid requirement
- Adjust fluids to account for sources of fluid – IV drugs
- Adjust to body weight – e.g. malnourished or obese
- 30ml/kg/24 hours
- Concentration: 1mmol/kg/day: K+, Na+, Cl- and 50-100g/day
- Examples: NaCl (0.18%) in glucose (4%), 5% dextrose and 0.9% sodium chloride
• Replacement:
- Variable amount: Increase to replace ongoing external fluid losses
- Estimate losses and match
• Redistribution:
- Fluid adjustment for internal redistribution into ISF occurring in cardiac, renal or hepatic impairment
- Reduce maintenance fluids so possess not exacerbated
• Resuscitation:
- Shocked patient with no evidence of cardiogenic pulmonary oedema
- 0.5L of balanced crystalloid or 0.9% saline over 15 minutes; repeat to 4x
- Albumin solution 4-5% in severe sepsis
- Reassess using ABCDE approach and further boluses until 2L
- Patient still evidence of shock, request help urgently
• Reassess:
- Careful monitoring and reassessment for ASEs
86
What is routine maintenance fluid? Explain why it is given, the rate and the concentrations of nutrients. Give examples of IV fluid types which can be give.
• Routine maintenance:
- Cannot meet enteral fluid requirement
- Adjust fluids to account for sources of fluid – IV drugs
- Adjust to body weight – e.g. malnourished or obese
- 30ml/kg/24 hours
- Concentration: 1mmol/kg/day: K+, Na+, Cl- and 50-100g/day
- Examples: NaCl (0.18%) in glucose (4%), 5% dextrose and 0.9% sodium chloride
87
What is replacement fluid? How is it given?
• Replacement:
- Variable amount: Increase to replace ongoing external fluid losses
- Estimate losses and match
88
What is fluid resuscitation? Explain why it is given, the rate and the concentrations of nutrients. Give examples of IV fluid types which can be give.
• Resuscitation:
- Shocked patient with no evidence of cardiogenic pulmonary oedema
- 0.5L of balanced crystalloid or 0.9% saline over 15 minutes; repeat to 4x
- Albumin solution 4-5% in severe sepsis
- Reassess using ABCDE approach and further boluses until 2L
- Patient still evidence of shock, request help urgently
89
Why may oral fluids be preferred compared to IV? What must you be able to do to prescribe IV fluids?
Risks:
• Peripheral Vascular Catheter (PVC) required
• Fluid overload
• Prescribing errors
• Requires accessible site
Rx tip:
• Justification
• Access site
90
What are the general principles of fluid and electrolyte prescribing and monitoring?
* Patient fluid balance: Euvolemia/ Hypovolemia/Hypervolemia
* Need: History + O/E
* Volume: IV fluids
* Type: Crystalloids vs Colloids
* Follow-up: Assessment and monitoring plan reviewed daily
91
What are the signs and symptoms of hypovolemia?
* Hypotension (< 100mmHg)
* Tachycardia (> 90bpm)
* Slow capillary refill tine (> 2 seconds)
* Tachypnoea (> 20)
* Dehydration: dry mucous membranes, decreased skin turgor, response to passive leg raising (45º)
* Thirst
* Vomiting
* Diarrhoea
* Weight loss
* Dizziness
92
What are the signs and symptoms of hypervolaemia?
* Hypertension
* Raised JVP
* Oedema
* Inspiratory basal crackles
* Displaced apex beat
* Third heart sound (S3)
* Basal crepitations
* Peripheral + Sacral oedema
* Ascites
* Hepatomegaly
* Wheeze
* Dyspnoea
* Orthopnoea
* Weight gain
93
What radiographic signs may be seen on a CXR in a patient with pulmonary oedema? What aid-memoire can be used for signs of pulmonary oedema?
A = Alveolar shadowing (Batwing Shadowing)
B = Kerley B lines (reticular lines indicating oedema in interstitial tissues)
C = Cardiomegaly
D = Upper lobe diversion
E = Effusion with blunting of costophrenic angles
94
What are the electrolyte requirements for a human? Give the correct unit of measurement.
* Sodium: 1mmol/kg/24 hours
* Potassium: 1mmol/kg/24 hours
* Chloride: 1mmol/kg/24 hours
* Glucose: 50-100mg/day
95
List 3 types of crystalloid fluid.
Glucose (5% dextrose)
Sodium and Glucose (0.18% NaCl in 4% dextrose)
Isotonic Saline (0.9%)
96
List 2 types of colloid fluid.
Albumin (4.5%)
Hydrolysed gelatin in isotonic saline
97
Outline the key differences between crystalloid and colloid.
1) Crystalloids
- Aqueous solutions of water containing ions and sugars
- Balanced salt solutions are isosmotic with plasma and have similar sodium contents thus remain in ECF between plasma and ISF
- Large volumes of isotonic saline ≈ % of hyperchloraemic metabolic acidosis
- Large volumes of 5% Dextrose ≈ % of hyponatraemia thus reduce use of solutions containing saline and glucose or combinations of the two
2) Colloids
- Large Mw substances dissolved in crystalloid solution (e.g. isotonic saline)
- Do not cross capillary membrane ≈ resuscitation use
- Expensive
98
What is a fluid challenge and why would you consider it? How is it conducted?
Fluid challenge is rapid administration of fluid bolus found in critically ill, haemodynamically unstable patients who require rapid correction of hypovolemic state. Oliguria or hypotension and no signs of overload, consider a fluid challenge
- 500mL balanced
- Delivered quickly (< 15 minutes)
- Repeat up to 2000ml (2L) ≈ 4x
99
Which patient groups should you be cautious with IV fluid and electrolyte administration?
```
- Obese patients
- Elderly or frail
- Renal impairment
- Cardiac failure
- Malnourished or at risk of Refeeding Syndrome
```
100
What information should be documented on an IV fluid prescription?
- Type of fluid to be administered
| - Rate and volume of fluid to be administered
101
You are asked to review a 75 year old woman four hours after she underwent an uneventful Hartmann’s procedure for a diverticular abscess. The nurses are worried because her urine output has fallen to less than 0.5 mL/kg/h over the past two hours. You are asked to prescribe a fluid bolus and increase the rate of maintenance Hartmann’s solution.
On examination there is no clinical evidence of hypovolaemia (box 2) or abdominal distension, the urinary catheter is patent, and you note that her fluid balance is 4 L positive since her operation. Blood tests show haemoglobin 110 g/L (reference range 115-160), sodium 135 mmol/L (133-146), potassium 4.1 mmol/L (3.5-5.3), urea 6 mmol/L (2.5-7.8), creatinine 72 µmol/L (50-110), and venous lactate 1.5 mmol/L (0.5-2.2).
What would you do next?
You suggest to the nurse that—in the absence of hypovolaemia, a positive fluid balance, and reassuring blood tests—oliguria is probably a physiological response to surgery and that a fluid bolus is not immediately needed. However, you recognise that postoperative oliguria is commonly associated with acute kidney injury and you plan to reassess the patient in two hours.
102
A 50 year old, 70 kg man presents with circulatory shock secondary to a gastrointestinal bleed. His medical history includes alcoholic cirrhosis complicated by moderate ascites. He is usually compliant with a salt poor diet and takes spironolactone 100 mg daily. Blood tests show haemoglobin 70 g/L (reference range 135-180), sodium 130 mmol/L (133-146), potassium 3.5 mmol/L (3.5-5.3), urea 8 mmol/L (2.5-7.8), creatinine 110 µmol/L (60-120), and arterial lactate 2.5 mmol/L (0.5-1.6). His clotting screen is normal
What fluids would you prescribe?
This patient requires resuscitation, so you prescribe 500 mL of 0.9% sodium chloride to be given over 15 minutes, followed by a blood transfusion at a rate titrated to improvements in capillary refill, heart rate, and blood pressure. Haemodynamic stability is achieved after the administration of three units of blood over 60 minutes.
103
After resuscitation, endoscopy shows oesophageal varices, which are ligated. A ward nurse has asked for your review because the patient is nauseous and unable to tolerate oral fluids. On examination he has a normal circulation, moderate ascites, and ankle oedema. His urine output is 60 mL/h and repeat testing shows sodium 132 mmol/L (reference range 133-146), potassium 3.9 mmol/L (3.5-5.3), urea 10 mmol/L (2.5-7.8), and creatinine 120 µmol/L (60-120). Because you are reluctant to pass a nasogastric tube, for fear of dislodging his variceal bands, the nurse has asked you to prescribe intravenous maintenance fluids
You recognise that this is a complex fluid management problem, with clinical evidence of abnormal fluid redistribution (ascites and oedema), so you seek the advice of the consultant gastroenterologist. You are advised that the clinical picture is consistent with dilutional hyponatraemia, commonly seen in patients with cirrhosis, and that maintenance fluids are not currently indicated. You are asked to ensure that his fluid balance is carefully recorded and to discuss again if there is any evidence of circulatory instability, such as increasing heart rate, hypotension, or oliguria.
104
Four days after admission the patient develops profuse diarrhoea, thought to be related to his antibiotic prophylaxis. Although his maintenance fluids are being delivered enterally you suspect that intestinal absorption is reduced.
You recognise that this patient is at risk of excessive electrolyte loss including sodium, potassium, bicarbonate, and chloride. You prescribe intravenous Hartmann’s solution (1 L/day) because it contains all of these electrolytes (bicarbonate as lactate). You organise daily testing for urea and electrolytes, including magnesium, recognising that additional electrolyte supplementation, such as potassium, may be needed. You ensure that his fluid balance and requirements are reassessed twice daily.
105
What is inflammation? Where may inflammation occur in the GI tract?
Non-specific reaction (PRISH) via vasodilation, vascular permeability and cell infiltration which occurs due to injurious stimuli and may last < 6 weeks (acute); > 6 weeks (chronic) or be acute on chronic.
Any region
106
What is epithelial ulceration? Where may epithelial ulceration occur in the GI tract?
lesion or sore in skin or mucous membrane from erosion/gradual disintegration of surface epithelial tissue
- Superficial
- Deeper
107
What is an epithelial perforation?
hole in the wall (mucosa +/- submucosa +/- muscularis propria) often due to untreated ulcers which rupture or perforate
108
What is bacterial overgrowth and its major resultant histological effect in GI/SI?
Bacteria in the log + stationary phase > lag + dead phase which leads to colonisation of host mucosa ≈ imbalance of commensal vs opportunistic bacteria and subsequent increased epithelial permeability, pro-inflammatory cytokines and villous atrophy with impaired motility and stasis.
109
List the different categories of diarrhoeal pathogens.
- Bacteria
- Viruses
- Protozoa
- Helminths
110
What is diarrhoea? Types of diarrhoea? What diagnostic tool/aid can be used to compare the consistency of a stool? Main complication(s) of diarrhoea?
passage of three or more loose, watery stools per day or changed stool consistency (water > 75%) or stool quantity (200-250g per day)
- Acute (< 14 days)
- Persistent (> 14 days)
- Chronic diarrhoea (> 30 days)
```
Complications:
- Dehydration
- fluid and electrolytes
- Malabsorption
- poor nutrient absorption due to reduced digestion causing malnourishment potentially
```
111
What are the risk factors and disease transmission of diarrhoea and diarrhoeal pathogens?
- Direct contact + droplets
- Airborne
- Food/water (Traveler’s Diarrhoea)
- Animal exposure (zoonoses)
112
What are the classifications of diarrhoea according to pathophysiological mechanism?
- Exudative-Inflammatory diarrhoea: Damage to intestinal mucosa ≈ hyper secretion of cytokine-induced water, impaired absorption and disrupted water and electrolyte absorption
- Secretory diarrhoea: Active secretion of water
- Osmotic diarrhoea: Water drawn into intestinal lumen by poorly absorbed substances
- Motor diarrhoea: Rapid intestinal passage due to increased bowel movements
113
What are the main clinical features of diarrhoea?
- Fever
- Abdominal pain
- Haematochezia
- Nausea and vomiting
- Dehydration signs
- Malnutrition/failure to thrive
114
Why may investigations be indicated for diarrhoea? What are these investigations?
Indications: Diarrhoea > 4 days, High fever, Haematochezia, Suspicious IBD, Immunosuppression
Tests:
- FBC: anaemia or leukocytosis
- Stool samples + culture: leukocytes, ova and parasites
- Colonoscopy: chronic diarrhoea with no identifiable cause
- CT: Diverticulitis or IBD suspected
115
Give 3 common examples of ABX-associated diarrhoea.
ABX causing disruption of gut microbiota following ABX therapy which does not involve ingestion of a pathogen or toxin
- Vancomycin - resistance to vancomycin associated with C.difficile
- Clindamycin: suppresses gut microbiota and allows Clostridium/Costridioides difficile to multiply - overgrowth
- Tetracycline: colonisation by S.aureus and Candida spp.
116
What are the different resistance transmissions conferring antibiotic resistance? Give examples.
Transformation: Taking up DNA with ∆ affinity for the product.
E.g. S. pneumoniae; E.Coli
Conjugation: Transfer circular DNA plasmid via pili in horizontal/vertical gene transmission
E.g. MRSA; VRE
Transposons: Segments of DNA encoding Tpn elements allow mobile genome and genome plasticity providing resistance determinants
117
Give 3 mechanisms of ABX resistance and an example of ABX affected for each mechanism stated.
Enzyme inactivation: Production of beta-lactamase enzyme allowing hydrolysis of penicillin - Penicillins + Cephalosporins
Efflux: Pores in CSM ≈ extrude ABX - Tetracycline (bacteriostatic - inhibit tRNA and mRNA binding), Quinolones (inhibit DNA gyrase), Macrolides (inhibit translation via binding to 50s ribosomes)
Alternate pathway: Production of alternative pathway for survival e.g. MecA in S. aureus - Penicillin and Flucloxacillin
Alternate binding site: ∆ Protein structure of target - Rifampicin (inhibit RNA polymerase), Fluoroquinolones (inhibit DNA gyrase), Sulphonamides (inhibit folate synthesis)
Enzyme inactivation by addition: Covalent modification to ∆ structure - Aminoglycosides (X mRNA for protein translation)
118
How can you prevent protozoal infections in the GI tract?
- Improved hygiene and water supplies
- Eating fresh food + served hot
- Avoid salads and fruit which cannot be peeled
- Avoid tap water and ice cubes
119
List ways to stop the spread of highly infectious nosocomial infections.
- Recognise early symptoms
- Recognise risk groups: Elderly, Immunosuppressed, Babies, Pregnant Women
- Quarantine
- Hand hygiene
- PPE
- Aseptic technique
- Cleaning surfaces
- Safe disposal of occupational material
120
What are helminths? List the different types?
1) Nematodes
- Bisexual
- Cylindrical
2) Cestodes
- Elongated flatworms
- Segmented
- Hermaphrodite
3) Trematodes
- Leaf-shaped flatworms
- Hermaphrodites
- Rare in humans
121
What is the most common category of helminths to infect the GI tract?
Nematodes, often soil-transmitted with infection occurring by swallowing infective eggs (Ascaris lumbricoides, Trichuris Trichiura) or skin penetration and systemic migration through lung to intestine (Strongyloides stercoralis)
122
What is the purpose or Oral Rehydration Therapy (ORT)? What are the components of ORS?
Replacement of fluids and electrolytes lost in diarrhoeal illness
- Glucose = 13.6g/L
- Sodium chloride = 2.6g/L
- Potassium chloride = 1.5g/L
- Trisodium citrate dihydrate = 2.9g/L
123
What is an epithelial ulceration? Give two types.
lesion or sore in skin or mucous membrane from erosion/gradual disintegration of surface epithelial tissue
• Superficial
• Deeper
124
List 3 sites where an epithelial ulceration may occur.
* Mouth
* Oesophagus
* Stomach
* Duodenum
* Colon (SI + LI)
* Rectal ulcer
125
What is an epithelial perforation? What may it cause?
hole in the wall (mucosa +/- submucosa +/- muscularis propria) often due to untreated ulcers which rupture or perforate
• May cause leaking of luminal contents (e.g. food and gastric juices) to peritoneal or abdominal cavities
126
What is diarrhoea? Give the criteria for diarrhoea.
passage of three or more loose, watery stools per day or changed stool consistency (water > 75%) or stool quantity (200-250g per day)
Criteria:
• ≥ 3 loose, watery stools
• Changed consistency
• Stool quantity (200-250g)
127
Outline the categories of diarrhoea by chronicity.
* Acute (< 14 days)
* Persistent (> 14 days)
* Chronic diarrhoea (> 30 days)
128
Give two of the main complications of diarrhoea.
* Dehydration
| * Malabsorption
129
List 5 potential features of diarrhoea.
* Fever
* Abdominal pain
* Hematochezia
* Nausea and vomiting
* Dehydration signs
* Malnutrition/failure to thrive
130
List any reasonable tests you may order to investigate diarrhoea in a patient.
* FBC
* Stool samples + culture
* Colonoscopy
* CT
131
Outline the 4 main pathophysiological classifications of diarrhoea. Give an example of an associated disorder for each.
Exudative-Inflammatory: E.coli, Shigella, Salmonella, Campylobacter
Osmotic: Laxatives, lactose intolerance, malabsorption
Secretory: Cholera, E.coli, Drugs (colchicine)
Motor: Nervousness, anxiety, carcinoid syndrome, drugs (caffeine)
132
List 3 bacterial diarrhoeal pathogens. Give the shapes of each and their sources/transmission. Give common symptoms to each.
V. cholera: gram negative, comma-shaped, poor-irrigation/sewage (contaminated water source) thus faeco-oral
E. coli: gram negative, bacillus, contaminated food and soil
C. jejuni: gram negative, helical, undercooked meat
Salmonella: Gram negative, bacillus, undercooked meat/eggs/human 2º spread
L. monocytogenes: Gram positive, coccobacillus, congenital or food (cheese, pate, humous)
C. difficile: Gram positive, nosocomial + contaminated raw meat products
Common Sx:
- Diarrhoea
- Vomiting
- Dehydration
- Malabsorption
- Electrolyte imbalances
133
List 3 viruses which cause diarrhoea. Give the structure, its route of transmission and general symptoms.
Rotavirus: rota (wheel), faeco-oral/faeco-respiratory
Norovirus: Isocahedral, face-oral or shellfish or fomites; low numbers to infect
Adenovirus: Naked DNA
- Diarrhoea
- Dehydration
- Nausea and Vomiting
- Abdominal pain
- Myalgia
- Fever
- Malaise
134
Give an example of a protozoa which causes diarrhoea. Outline the route of transmission and general symptoms.
1) Giardia lamblia (Giardiasis)
• Traveller’s diarrhea
• Faeco-oral from water or person-person
• Infective: Low infective dose (10-25 cysts)
```
Signs and Sx:
• Diarrhoea
• Steatorrhea
• Fatigue and malaise
• Abdominal pain
• Gas or flatulence
• Nausea
• Weight loss
```
2) Cryptosporidium parvum
• Faeco-oral transmission or zoonosis
• Infective: Low infective doses
```
Signs and Sx:
• Diarrhoea
• Dehydration
• Anorexia
• Weight loss
• Abdominal pain
• Fever
• Nausea
• Vomiting
```
135
What type of helminth is strongyloides stercoralis? State the route of transmission.
Nematoda, cylindrical
Faecal, soil-transmitted
136
Outline the pathogenesis of strongyloides stercoralis.
• Penetration of skin ≈ migration in bloodstream to lungs ≈ migration into bronchial system to pharynx ≈ larvae mature into adult, egg-producing worms in intestine ≈ larvae excreted in faeces + ∆ intestinal mucosa, villus atrophy and loss of elasticity of intestinal wall
137
Give the signs and symptoms of a patient infected with strongyloides stercoralis.
* Diarrhoea
* Abdominal pain
* Anorexia
* Nausea
* Malabsorption
* Appendicitis
* Anal pruritus
* Dry cough
* Wheezing
* Swelling
* Erythema
* Maculopapular rash
* Serpiginous lesions
* Urticarial tracts
138
Outline the type of helminth an enterovirus vermicularis is. What is it's transmission.
Enterovirus vermicularis
• Threadworm
• Small cylindrical nematodes
• Faeco-oral transmission + digital-oral after scratching anal area
139
List the signs and symptoms a patient infected with enterovirus vermicularis may exhibit. Give the type of pathogen this is. Give a treatment for this.
2) Enterovirus vermicularis
• Threadworm
• Small cylindrical nematodes
• Faeco-oral transmission + digital-oral after scratching anal area
Pathogenesis:
• Ingestion of enterobius vermicularis
```
Signs and Sx:
• Anal pruritus
• Nausea
• Vomiting
• Diarrhoea
• Abdominal pain
```
Management:
• Anti-helminthic drugs: Bendazoles
140
A person eats some undercooked, contaminated pork. A patient presents asymptomatically to his routine GP appointment for his asthma but mentions he is struggling to gain weight despite going to the gym.
Suggest a pathogen he may have contracted. Give the route of transmission for this pathogen and the signs and symptoms. Suggest a treatment for this patient.
Taenia Solium (Taeniasis)
• Tapeworm (cestoda)
• Oral transmission from contaminated food
• Scolex: for attachment
Pathogenesis:
• Ingestion of larvae in raw or undercooked beef/pork
Signs and Sx:
• Asymptomatic
* Abdominal pain
* Anorexia
* Weight loss
* Nausea
* Vomiting
Management:
• Anti-helminthic drug: Praziquantel
141
List three helminths which can be ingested to give diarrhoeal symptoms. State the mnemonic used to remember these.
EATing makes you sick
Enterobius vermicularis,
Ascaris lumbricoides,
Taenia solium
142
What is acute abdomen?
Sudden onset of severe abdominal pain of less than 24 hours duration (< 5 days).
143
What two ways can the abdomen be divided into. Outline the lines which do these for each.
* 9 Region: transpyloric plane + transtubercular plane + midclavicular lines x2
* 4 Quadrants: transumbilical plane + median plane
144
List 5 conditions which may be located to the site of the RUQ.
```
Biliary:
• Cholelithiasis
• Choledolithiasis
• Cholecystitis
• Cholangitis
```
```
GI:
• Colitis
• Diverticulitis
Hepatic
• Abscess
• Hepatitis
• Mass
```
Pulmonary:
• Pneumonia
• Embolus
Renal:
• Nephrolithiasis
• Pyelonephritis
145
List 5 condition which may be located to the site of the epigastric region.
```
Biliary:
• Cholecystitis
• Choledolithiasis
• Cholelithiasis
• Cholangitis
```
Cardiac:
• MI
• Pericarditis
```
GI:
• Oesophagitis
• Gastritis
• Peptic ulcer
• Pancreatic Mass
• Pancreatitis
```
Vascular:
• Aortic dissection
• Mesenteric ischaemia
146
List 5 conditions which may be located to the site of the LUQ.
Cardiac:
• Angina
• MI
• Pericarditis
```
GI:
• Oesophagitis
• Gastritis
• Peptic ulcer
• Pancreatic Mass
• Pancreatitis
```
Renal:
• Nephrolithiasis
• Pyelonephritis
Vascular:
• Aortic dissection
• Mesenteric ischaemia
147
List 5 conditions which may be located to the periumbilical region.
```
GI:
• Oesophagitis
• Gastritis
• Peptic ulcer
• Small bowel mass/obstruction
• Early Appendicitis
```
Vascular:
• Aortic dissection
• Mesenteric ischaemia
148
Give 5 conditions which may have a site of pain at the RLQ.
```
GI:
• Appendicitis
• Colitis
• Diverticulitis
• IBD
• IBS
```
```
Gynaecological:
• Ectopic pregnancy
• Fibroids
• Ovarian mass
• Ovarian torsion
• PID
```
Renal:
• Nephrolithiasis
• Pyelonephritis
149
Give 5 conditions which may have a site of pain at the suprabic region.
```
GI:
• Appendicitis
• Colitis
• Diverticulitis
• IBD
• IBS
```
```
Gynaecological:
• Ectopic pregnancy
• Fibroids
• Ovarian mass
• Ovarian torsion
• PID
```
Renal:
• Cystitis
• Nephrolithiasis
• Pyelonephritis
150
Give 5 conditions which may have a site of pain at the LLQ.
```
GI:
• Colitis
• Diverticulitis
• IBD
• IBS
```
```
Gynaecological:
• Ectopic pregnancy
• Fibroids
• Ovarian mass
• Ovarian torsion
• PID
```
Renal:
• Nephrolithiasis
• Pyelonephritis
151
Give the aid-memoire for remembering pathological causes of acute abdomen.
* Vascular: Trauma/Emboli/Mesenteric ischaemia/Ruptured aneurysm/Colitis
* Infective: C.jejuni/ E.coli/ V. cholerae/ G. lamblia/ Adenovirus/ Rotavirus/ Norovirus
* Trauma: Stabbing/ Shooting/ Blunt trauma/ Falls
* Metabolic
* Inflammatory
* Neoplasm/Paraneoplastic
* Congenital
* Degenerative
* Endocrine
* Functional
152
Outline how you would conduct a physical examination to inspect the abdomen on a patient.
0. Hand Hygiene
1. Intro + ID
2. Consent
3. Manage set-up
4. General Inspection
5. Inspect Hands
6. Pulse
7. Eyes
8. Mouth
9. Lymph Node Palpation
10. Leg inspection
11. Manage set-up
12. Inspect abdomen
13. Palpate abdomen
14. Scooping - Organomegaly assessment
15. Percussion
16. Ascites Assessment
17. Auscultation
18. Hernia examination
19. Examine Testes
19. Thank patient + Discuss findings
20. Hand wash
153
Give the parameters for NEWS/FEWS. State the parameters and their cut-offs.
* SpO2
* Respiration
* Pulse
* BP
* Temperature
* Neuro (AVPU)
```
Score cut-offs:
• 1-4 = 4-6 hours
• 3 in one parameter = 1 hourly
• ≥ 5 = 1 hourly
• ≥ 7 = continuous monitoring
```
154
Give the investigations you may order in a patient with acute abdomen. Give the findings you may see.
1) Laboratory
```
FBC: Aneamia/Leukocytosis/Clotting factors/Leukopenia
U+E: eGFR reduced
CRP: Raised
Lipase, Amylase: Elevated or reduced
Lactate: Tissue hypoxia if raised
LFTs: Elevated transaminases and elevated bilirubin
Serum Glucose: Hypo or Hyper
Troponin: Elevated
ABG: Acidosis/Alkalosis
Coagulation studies: INR (PT)/APTT/TBT
Urinalysis: Haematuria/Protein/Leukocytes/Urinary crystals/ß-hCG
Cultures: Pathogen
```
```
2) Imaging
XR
- CXR
- AXR
CT
- CT-Chest
- CT-Abdomen
Ultrasound
Endoscopy
ECG
```
155
In a pneumoperitoneum on CXR, what feature would be identified.
crescent lucency (free air underneath diaphragm) under diaphragm
156
In a XR-Abdo of a patient with small bowel obstruction, what feature is seen.
Dilated small bowel due to small bowel obstruction as indicated by predominantly central dilated loops, valvular conniventes (plicae circulares seen in which is present in small bowel, not large bowel), dilated loops of small bowel proximal to obstruction
157
In a patient with large bowel obstruction, what may be observed on a CX-Abdomen.
Large bowel obstruction shows by colonic distension proximal to obstruction and collapse distally, apple core sign.
158
In a patient with RUQ pain radiating from loin to groin, what may a CX-Abdo show? Is there a scenario where the same pathology may be present but not seen.
Renal calculi as shown by discrete calculi of radiopacity in the patients left kidney
Yes, uric acid stones are radiolucent so may not be seen on a CT
159
Give 3 cardiovascular causes of acute abdomen. List the clinical features of each.
- AAA: Age (50+), sudden severe abdominal pain radiating to back, CAD and PMHx; hypotension, pulsatile mass, Grey Turner/Cullen Sign
- ACS: Heavy chest band pain, radiates to left shoulder + jaw, angor animi, anxiety and diaphoresis; pain may reduce with GTN spray
- Acute Mesenteric Ischaemia: Age (60+), embolic risk factors, severe diffuse abdominal pain and distension, melon and haematochezia
- Aortic Dissection: Sudden, sharp pain, tearing, radiating to back; hypotension, neurological symptoms, asymmetrical blood pressure
160
A 48 year old man presents with sudden onset of diffuse abdominal pain. He admits to experiencing constipation, nausea and vomiting. O/E, there is diffuse abdominal guarding, rigidity and rebound tenderness. On auscultation, there are absent bowel sounds and loss of liver dullness on percussion.
What investigation would you order? What would you expect to see? Give a differential.
- AXR: Pneumoperitoneum
- FBC
- Endoscopy
DDx: GI perforation
161
A 42 year old builder presents with colicky abdominal pain. He previously had abdominal surgery 9 years ago. O/E there is diffuse abdominal distension, with a tympanic abdomen on percussion. On auscultation, there were tinkling bowel sounds.
Give two investigations you may wish to order. What might they show?
Give a Ddx.
* AXR: Dilated bowel loops proximal to obstruction; Rectal air shadow absent; Multiple air-fluid levels
* CT-abdomen: transition point at site of obstruction (e.g. Apple Core Sign); dilated bowel loops, retail air shadow absent, multiple air-fluid levels
Mechanical Bowel Obstruction
162
A 21 year old male presents with acute abdominal pain. He says the pain is in the lower right abdomen (RIF), it is severe. At first the pain is felt in the umbilical region then migrated to the RIF. He mentions he has felt very hot and nauseous lately.
O/E there is guarding and rebound tenderness in the RLQ.
Give any investigations you may wish to order and what they may show.
Outline a DDx.
* Bloods: neutrophilic leukocytosis
* Abdominal CT scan: distended appendix, periappendiceal fat stranding
* Abdominal Ultrasound: non-compressible, aperistaltic, distended appendix, probe tenderness in RIF and Target sign (fluid-filled hypoechoic centre surrounded by echogenic mucosa and submucosa and hypo-echoic muscularis)
Acute Appendicitis
163
A 52 year old male presents with acute abdomen. He states the pain is in the central region, almost where his heart is, and is very concerned. He says the pain comes on following a meal (post-prandial) and is exacerbated by spicy foods. O/E he has no significant findings.
Suggest any investigations you may order for this patients and what you may see.
Would you suggest anything to manage to symptoms for the current symptoms?
Give a Ddx. Be specific and explain your answer.
* Laboratory: anaemia, FOBT (bleeding ulcer), Urea breath test for H.pylori
* Endoscopy (EGD): mucosal erosions+/-
Supportive:
- Avoid spicy foods and alcohol
- Try antacids
Peptic Ulcer Disease
- PPIs: Omeprazole or Lansoprazole
Gastric ulcer as pain exacerbated by food cf
164
A 68 year old presents with acute abdominal pain. She says she has previously had abdominal surgery but has been fine since. She reports a raised temperature and difficulty passing stools. O/E there is a tender mass in the LIF.
Suggest any investigations you may order for this patients and what you may see.
Give a Ddx. Be specific and explain your answer.
* Laboratory: Leukocytosis, CRP elevated
* CT-abdomen: Colonic diverticula with pericolic mesenteric fat stranding
Diverticulitis
- LIF thus sigmoid colon
165
A 32 year old regular party-goer who enjoys alcohol and recreational drugs presents with acute abdominal pain. He has a PMHx of gallstones and alcohol abuse. He also admits to feeling a bit feverish recently. The pain is described as severe, in the top of his tummy. O/E there is guarding and rigidity. On auscultation, there are hypoactive bowel sounds.
Suggest any investigations you may order for this patients and what you may see.
Give a Ddx. Be specific and explain your answer.
Identify the aetiological causes of the DDx given and suggest others.
* Laboratory: Elevated lipase and amylase; Hypocalcemia
* US-Abdomen: Pancreatic oedema, peripancreatic fluid, gallstones
* CT-Abdomen: Pancreatic oedema, peripancreatic fat stranding, gallstones
Acute Pancreatitis
- Drugs
- Alcohol
- Gallstones
```
Other causes:
Idiopathic
Gallstones
Ethanol
Trauma
Scorpion stings
Mumps
Autoimmune
Steroids
Hypertriglyceridemia
ERCP
Drugs
```
166
A 57 year old female presents with abdominal pain in her RUQ. The pain radiates to her right shoulder and begins mainly following a meal (post-prandial). She experience nausea and vomiting. O/E Normal.
Suggest investigations you would order.
Give a DDx should the investigation show gallstones.
* Laboratory: Normal
* Abdominal ultrasound: gallstones with posterior acoustic shadow
DDx: Symptomatic cholelithiasis
167
A 58 year old woman presents with abdominal pain in her RUQ. She previously visited a year ago for the same ailment/symptoms. She describes the appearance change, she seems to believe she is going yellow. She mentions she has had lighter stools and darker urine. O/E Normal
Suggest investigations you would order and what may you expect to see.
Give a DDx
* Laboratory: Elevated ALP, AST, ALT, total bilirubin
* US-Abdomen: Dilated CBD; Intrahpatic biliary dilatation; Echogenic structure within CBD with shadowing
* ERCP/MRCP: Filling defect in contrast-enhanced duct
Choledocholelithiasis
168
List the three Symptoms of Charcot's Triad. What disease are they suggestive of.
Ascending Cholangitis
RUQ/RH pain
Fever
Jaundice
169
A 58 year old female presents with severe RUQ/RH pain radiating to the right shoulder. She experiences fever and chills at night as well as nausea and vomiting. O/E there is a positive Murphy's Sign
Suggest investigations you would order and what may you expect to see.
Give a DDx
* Laboratory: Leukocytosis
* Ultrasound-abdomen: sonographic Murphy sign (tenderness from probe); pericholecystic fluid collection, gallbladder wall thickening +/- oedema (double-wall sign)
* Cholescintigraphy: Non-visualisation of gallbladder wait
Acute Cholecystitis
170
A 59 year old male presents with acute abdominal pain. He reports excruciating RH/RUQ pain and fever. He notes his wife saying he'd looked slightly tanned today however he has been bed-ridden and its winter.
O/E he has jaundice (icterus), hypotension, tachycardia and abdominal guarding.
Suggest investigations you would order and what may you expect to see.
Investigations come back showing hyperbilirubinemia, biliary dilatation, deranged LFTs and positive blood cultures
Give a DDx
* Laboratory: Leukocytosis, CRP elevation, Increased ALP, Increased AST, Increased ALT, Increased GGT, Increased total bilirubin, Positive blood cultures
* Ultrasound-Abdomen (RUQ): Biliary dilatation +/0 choledocholithiasis; thickening of bile duct walls
* MRCP/ECRP: Biliary dilation +/- thickening of bile duct walls
Acute Cholangitis
171
A 28 year old woman presents with acute abdominal pain. Her obstetric history is G1, P0. She is not a smoker but does enjoy drinking alcohol on a weekend (6 units?). She does not use any contraception and has been trying for a child but admits she has more than 1 sexual partner. She says the pain is predominantly lower abdominal. She reports PV bleeding.
O/E there is abdominal guarding and tenderness, cervical motion tenderness. Closed cervix and enlarged uterus.
Suggest investigations you would order and what may you expect to see.
Give a DDx.
* Laboratory: elevated ß-hCG
* US-Transabdominal/Transvaginal: Free fluid in Morison pouch+/-Pouch of Douglas; Empty uterine cavity; Thickened endometrial lining; Adnexal mass; Tubal ring sign
Ruptured Ectopic Pregnancy
172
71 years old male
Intermittent dull ache left iliac fossa for about a year
For past 6 months noticed increasing frequency and looseness of bowel motions but lately sometimes constipated
No weight loss
Now and again notices blood in the stools
FBC showed mild iron deficiency anaemia
Dr said he could feel something when he did a rectal examination.
Give the likely diagnosis.
Rectal carcinoma
173
53 y/o F
For 1 year been getting epigastric discomfort intermittently
Occasionally getting heartburn as well
No vomiting or weight loss
No alteration in bowel habit
Discomfort sometimes feels better after food
Drinking a glass of milk helps, as does Rennies
Feels tender in epigastrium
Blood tests normal
Dr said my stool test showed Helicobacter
Give the likely diagnosis
helicobacter pylori positive peptic ulcer disease
174
21 y/o M
Getting lots of noise from my tummy (Dr calls it borborygmi)
Often get cramps and loose motions (like rabbit droppings) several times a day
I notice it’s worse when I’m stressed, it’s really bad at exam times
No blood in motions, no weight loss
FBC normal
Faecal calprotectin negative, coeliac screen negative
Give the likely diagnosis
probable IBS
175
35 y/o F
Pain right lower abdomen
Intermittent 6 months or so
Sometimes gets severe cramp and diarrhoea no blood
Have had to have several days of work
Eating less as sometimes makes it worse and feel less hungry
Have lost half a stone in weight
Dr did bloods, said I was slightly anaemic with high CRP
Faecal calprotectin positive
Give the likely diagnosis
Likely Crohn's Disease (terminal ileum)
176
50 y/o M
Getting cramping left iliac fossa pain past 4 weeks
For last 2 weeks getting bloody diarrhoea
Feel ill with it
Dr checked stool spec. for infection but none seen
Said my FBC showed a raised WCC and I also have raised crp
Stool test showed raised faecal calprotectin
Give the likely diagnosis
Ulcerative Colitis
177
```
23 y/o F
Severe right iliac fossa pain
Came on over past 24 hours
Very tender in that area
noticed some spotting of blood PV yesterday and today
No fever
Feel faint
Pulse 110 bp 90/60
Beta HCG positive
```
Give the likely diagnosis
Ectopic pregnancy (ruptured?)
178
```
14 y/o M
Pain in abdomen
Started centrally, now right lower abdomen
Worse with movement
Off food (anorexia)
Tender to touch
Mild fever
```
Give the likely diagnosis
Appendicitis
179
```
39 y/o F
Right upper quadrant pain
Intermittent of last 6 months
Worse after eating – especially fatty foods
Usually lasts around half an hour
But today has been present for 6 hours and worsening
I have a fever
Extremely tender to touch
Pulse 110 bp 88/60 temp 39
```
Give the likely diagnosis
Acute cholecystitis
180
55 y/o M
Recurrent episodes of severe epigastric pain
Present last 3 years but getting steadily worse
No relieving factors
Sometimes worse after I’ve been drinking heavily ( I average 15 units a day)
My abdomen is tender in the epigastrium and centrally
My doctor says my blood glucose is up and my LFTs are raised
He checked my amylase – it’s high
Give the likely diagnosis
Chronic pancreatitis
181
28 y/o M
I have cramping abdominal pains intermittently all around my abdomen
I often feel bloated
I often have bouts of diarrhoea never seen any blood
When I think about it – it’s been happening for years
I’m worried as I can’t gain weight
I get really tired
My doctor says I have iron deficiency anaemia but I eat lots of red meat
He’s waiting for results of an IgAtTG and EMA test
Give the likely diagnosis
Coeliac Disease
182
71 y/o F
I have intermittent pain in my left lower abdom
I sometimes get constipated
I ‘ve never passed blood in my stools
My symptoms have been present for 2 years
It feels tender sometimes in this area
I haven’t lost weight
My Dr checked my blood tests and they are normal
My stool sample was sent for a Q-FIT test and it’s negative
Give the likely diagnosis
Diverticular disease/ constipation
