Gastrointestinal Week 3 Flashcards
1
Q
Describe the gross anatomy of the duodenum:
A
- ~25cm long in total
- C shaped, 4 parts (superior 5cm, descending 7.5cm, inferior 10cm and ascending 2.5cm)
- extends from neck of GB to lower border of L3
- starts at pyloric sphincter
- diameter of 2.5-4cm
- superior part anterior to IVS and bile duct
- > connected to liver by hepatoduodenal ligament
- > last 2cm of superior part onwards = retroperitoneal
- descending part anterior to right kidney
- > curves around head of pancreas
- inferior part anterior to aorta and vena cava (superior mesenteric vessels pass anterior to intestine here)
- at end of ascending part is duodenal-jejunal flexure
- suspensory muscle of the duodenum is found at this flexure and alters the angle of the flexure to control movement of food into the jejunum
- Arteries from coeliac trunk and superior mesenteric artery.
- Above point of bile duct entrance = gastroduodenal artery - branch of coeliac trunk
- Below point of entry of bile duct = inferior pancreoduodenal artery - branch of SMA
- All duodenum veins follow arteries and drain into hepatic portal vein
- Para. supply from vagus
- Symp. supply from thoracic splanchnic nerves relayed through coeliac and superior mesenteric plexus’
- Drained by para-aortic nodes
2
Q
Describe the gross anatomy of the jejunum and ileum:
A
Attached to posterior abdominal wall by mesentery
- supplied by superior mesenteric artery and drained by superior mesenteric vein
Jejunum = 2.5m
Ileum = 3.6m
Jejunum:
- > upper L quadrant
- > red
- > long vasa recta (straight arteries) and few arcades
- > thick walled
Ileum:
- > lower R quadrant
- > pink
- > short vasa recta and many arcades
- > thin walled
3
Q
Describe the histology of the small intestine:
A
3 features to increase SA:
- > villi
- > microvilli (only seen with electron microscope)
- > plicae circulares (1cm tall circular folds, cause chyme to spiral as it moves through lumen, slows transit for more nutrient absorption)
General structure:
- villi and intestinal glands (Crypts of Lieberkühn)
- microvilli covered by protein coating called glycocalyx
- muscularis mucosa
- submucosa containing venules, arterioles and lymphatic vessels
- circular and longitudinal muscle layers with myenteric plexus inbetween
6 cell types:
- Absorptive enterocyte cells (cover the villi)
- Mucous secreting goblet cells (between enterocytes)
- Entero-endocrine cells (cover villi and produce secretin and CCK)
- Intestinal cells (line the glands and release juice)
- Stem cells (in glands for regeneration)
- Paneth cells (in glands, release lysosyme to destroy unwanted bacteria)
2 surface features of small intestine:
- Brunners glands: in submucosa of DUODENUM and secrete bicarbonate rich mucous
- Peyer’s patches: aggregates of lymphoid tissue
4
Q
Describe the gross anatomy of the pancreas:
A
- Head -> uncinate process -> neck -> body -> tail
- 15cm long, endocrine and exocrine function
- uncinate process acts as hook, passing behind superior mesenteric artery and vein
- tail of pancreas overlies hilum of L kidney
- duodenal-jejunal flexure of SI is tucked up below body of pancreas at left edge of uncinate process
- produced 1.5L pancreatic juice per day (pH8) to neutralise acidic chyme
- splenic vein runs behind body of pancreas to join superior mesenteric vein behind neck and they join forming hepatic portal vein
- contains part of biliary tree
- blood supply from splenic artery
- > head also supplied by branches of superior and inferior pancreoduodenal arteries
5
Q
Describe the histology of the pancreas:
A
- covered by thin fibrocartilaginous connective tissue capsule, with septa extending into the gland dividing it into lobules
- exocrine component made of cluster of acini cells
- acini contain RER and zymogen granules as they produce and contain manufactured digestive enzymes
- clusters of acini cells are connected by ducts:
intercalated ducts -> intralobular ducts -> main pancreatic duct
6
Q
How is the hepatic portal vein formed?
A
Superior mesenteric vein joins with splenic vein at the neck of the pancreas forming the hepatic portal vein
7
Q
What is the pathway of the biliary tree?
A
- R and L hepatic ducts from liver
- Join forming common hepatic duct
- Cystic duct joins common hepatic duct forming common bile duct
- Common BD enters pancreas and joins with main pancreatic duct at major duodenal papilla
- May be an accessory pancreatic duct which branches off the main duct and will open at minor duodenal papilla just a few cm proximally to the major papilla
8
Q
How are carbohydrates digested?
A
- salivary amylase breaks down small % of starch
- pancreatic amylase breaks down majority of starch
- brush border enzymes in intestines break disaccharides into monosaccharides
9
Q
How are carbohydrates absorbed?
A
[Glucose] low:
- SGLT moves glucose into cell
- GLUT2 moves glucose out of cell into bloodstream
[Glucose] high:
- SGLT transporters saturated so GLUT2 molecules are transported to the luminal border of enterocytes and take up glucose
- GLUT2 also transport the glucose out at basolateral side into the bloodstream
Fructose:
- GLUT5 moves fructose into cell
- GLUT2 moves fructose out into the bloodstream
10
Q
How are fats digested?
What are the contents of a micelle?
A
- Lipase (some lingual but mainly from stomach produced by chief cells) breaks TAG into fatty acids and monoglycerides
- Bile in intestine emulsifies TAG’s into micelles
- Micelles contain FA, MAG, cholesterol and fat-soluble vitamins and have hydrophilic outer and hydrophobic inner
11
Q
How are fats absorbed?
A
- Micelles diffuse into jejunal cells and bile left in gut lumen
- in enterocytes chylomicrons are formed (contain TAG’s, cholesterol, phospholipids….)
- chylomicrons are then absorbed by lymphatic system and released into the bloodstream
12
Q
How are proteins digested?
A
- pepsin in stomach digests ~20% proteins
- pancreatic enzymes released into duodenum to digest proteins
- trypsin and chymotrypsin: digest proteins -> small polypeptides
- carboxypeptidase: cleaves individual amino acids from carboxyl end of polypeptides
- elastase: digests elastin fibres that are found in meat
13
Q
How are proteins absorbed?
A
- all amino acids/dipeptides/tripeptides are carried into enterocytes by Na-dependent co-transporters
- enterocytes contain specific proteases to digest remaining peptide bonds
- single amino acids can then diffuse into the bloodstream
14
Q
What are the fat soluble vitamins and how are they absorbed?
A
Vitamins A, D, E and K
They are absorbed the same way as fats, by forming micelles
15
Q
How are pancreatic enzymes formed and secreted?
A
Glandular cells in acini produce the enzymes, the cells have lots of RER and zymogen granules. The epithelial cells lining the pancreatic ducts produce bicarbonate:
- the following reaction occurs in the epithelial cells lining the ducts
- CO2 + H2O H2CO3 H+ + HCO3-
- HCO3- is then secreted into the duct lumen
- zymogens are then activated in the duodenum by enterokinase which is produced by the duodenum, preventing autodigestion of the pancreas
16
Q
How is the production and release of pancreatic secretions regulated?
A
- increased acid production by stomach for digestion decreases the pH of chyme in the duodenum
- S cells in duodenum produce secretin to inhibit G cells releasing gastrin and to lower HCl production
- plasma levels of secretin increase
- increased bicarbonate production by the pancreas which flows into the SI
- this bicarbonate in the SI (along with digestive enzymes) helps to neutralise the acidic chyme
- also presence of lipids in duodenum causes I cells to release CCK: GB contracts, sphincter of oddi opens and bile is released to emulsify lipids
17
Q
Outline causes of chronic pancreatitis and clinical features:
A
- 60-80% of cases are alcohol related in developed countries
- other causes include CF, hereditary, idiopathic, trauma, hypercalcaemia, autoimmune conditions
- acute pancreatitis: self-limiting and reversible
- chronic: from multiple acute attacks, is not reversible
Features:
- diabetes
- jaundice
- dull epigastric pain radiating to the back
- anorexia (due to malabsorption)
- fear of eating (due to the pain)
- steatorrhoea
- pain after eating fatty foods
18
Q
What is the pathogenesis of chronic pancreatitis?
A
Two main hypothesis:
- increased/early activation of trypsinogen -> trypsin in the pancreas
- impaired activation/clearance of the activated enzymes from the pancreas = autodigestion
- prolonged intrapancretic enzyme activity leads to the formation of proteins in the duct lumens, plugs and calcifications form
- alcohol-related pancreatitis -> the alcohol impairs calcium regulation in the pancreas leading to increased calcium levels which promote increased trypsinogen activation
- various genes are also linked to trypsin activation which can be dysfunctional:
- > SPINK-1 gene (a trypsin inhibitor gene that if mutated can cause chronic pancreatitis development)
19
Q
How would you investigate/diagnose chronic pancreatitis?
A
1) serum amylase and lipase (levels elevated initially, but then low in severe disease once mass of pancreatic tissue has been lost)
2) faecal elastase - abnormal/reduced levels
3) transabdominal ultrasound scan - to look for duct irregularities or calcifications
4) CT scan and contrast - for detailed assessment of ducts and calcifications
5) MRI and MRCP - to define subtle abnormalities of the pancreatic ducts
20
Q
How would you treat chronic pancreatitis?
A
1) Lifestyle
- alcohol and smoking cessation
- enteral feeding to lower CCK levels
2) Diet - reduced fat and enzyme supplementation (especially lipase)
3) Medications
- opioid analgesics e.g. tramadol, for abdomen pain
- PPI’s to increase enzyme activity
4) Surgery
- relieve/remove any obstruction present
- insert a self-expandable metal stent for cholangitis
21
Q
What is pancreatic insufficiency?
A
Reduced digestive enzyme levels (therefore reduced effectiveness of digestion and absorption)
22
Q
What dietary advice would you give someone with chronic pancreatitis?
A
- avoid alcohol
- avoid high fat content meals (they can increase frequency and intensity of pain)
- monitor blood glucose to prevent hyperglycaemia
- supplementation of fat soluble vitamins
- take supplementary pancreatic enzymes with all meals (quantities adjusted according to quantity of food eaten and its fat content)
23
Q
What is patient adherence?
A
The extend to which a patient’s actions match the agreed recommendation
24
Q
What is unintentional non-adherence and causes of it?
A
- patient wants to follow medical advice but there are barriers out with their control preventing them
- > poor recall
- > difficulty understanding instructions
- > cost
- > memory issues
- > lack of education
- > controlling family/friends
25
What is intentional non-adherence and causes of it?
- patient deliberately/meaningfully decides not to follow the agreed treatment
- > beliefs
- > religion
- > previous bad experience
- > heard stigmas/rumours about the drug
- > media
26
Why is it important that patients adhere?
- so that they get the best medicinal benefits
- so that a patients health improves, not deteriorates
- to avoid costs of:
- > wasted medicines
- > knock-on costs from increased healthcare demands if the patients health deteriorates
27
What are strategies doctors can use to increase adherence?
- good explanations to remove stigmas
- address any patient concerns
- take 'no blame' approach so patient is comfortable with you and has faith in you to follow your advice
- identify potential barriers at the time of prescribing/at regular reviews
- get family and friends involved and educated (with patients permission) so that the patient has support
- make drug regimes are simple and straightforward and easy to understand as possible
28
What is coeliac disease and its aetiology?
- a gluten sensitive enteropathy
- genetically susceptible individuals get a T-cell mediated immune response
- genetically susceptible individuals get infected with adenovirus 12
- there are similar structures between a portion of the virus and peptides on alpha-gliadin and so CROSS REACTIVITY OCCURS
29
What is the pathophysiology of coeliac disease?
- stomach digests proteins including alpha-gliadin
- alpha gliadin passes into SI and binds to secretory IgA antibodies and this IgA-gliadin complex is normally targetted by the immune system and destroyed
- in coeliacs, the IgA-gliadin complex binds to Tf receptors on enterocytes and is transported into enterocyte
- then the enzyme TTG (tissue transglutaminase enzyme) deaminates the gliadin
- gliadin is the phagocytosed by macrophages and expressed on their MHCII receptors
- the HLA type that someone is determines what complex is expressed on their MHCII receptors
- in coeliac disease, HLA DQ2 and DQ8 cause this
- T helper (CD4) cells then recognise the gliadin and release pro-inflammatory factors e.g. TNF and IF-gamma
- these inflammatory factors destroy epithelial cells and the villi structure in the small intestine
30
What are clinical features of coeliac disease?
- vomiting
- impaired growth
- flatulence
- bloating
- diarrhoea
- unexplained increase in ALT and AST
31
Why do you get malabsorption in coeliac disease and what chemical imbalances occur?
Changes to the structure of the villi and mucosa in the duodenum and ileum cause reduced nutrient absorption in coeliac disease.
- loss of villi height
- short and broad villi
- mucosal inflammation and patchy mucosal damage
- NO CHANGE IN TOTAL MUCOSAL THICKNESS as the crypts of lieberkühn become elongated as the villi shorten
- increased number of intraepithelial lymphocytes and plasma cells
- electrolyte imbalances due to the malabsorption:
- > folate deficiency
- > calcium/vit D deficiency = osteoporosis
- > low vitamin K (coagulation issues)
- > low Mg
- > low vitamin B12
32
How does coeliac disease affect iron homeostasis is the body?
- makes individuals more prone to IDA (iron deficiency anaemia)
- in IDA various RBC changes are seen:
- > hypochromic cells (pale staining)
- > pencil shaped cells (elongated on smear)
- > microcytic cells (smaller and have a lower MCV)
33
How do you diagnose coeliac disease?
Endoscopy
- scalloped mucosal folds
- patchy mucosal damage
- damage is in mosaic pattern like cracked mud
- prominent sub-mucosal blood vessels
Serological tests
- look for 3 common antibodies: tTG, EMA, DGP (tissue transglutaminase antibodies, endomysial antibodies, deaminated gliadin peptide antibodies)
Biopsy - minimum of 4 taken from distal duodenum due to patchy mucosal damage
Marsh classification
34
What other diseases are associated with coeliac disease?
Associated with other autoimmune diseases:
- T1DM
- hyperthyroidism
- Addison's disease (adrenal insufficiency)
- dermatitis herpetiformis (itchy rash on extensor surfaces - occurs with 90% villous atrophy)
35
What are the different types of marsh classifications?
Marsh type No. intraepithelial lymphocytes per 100 enterocytes crypt hyperplasia villi
0 <40 normal normal
1 >40 normal normal
2 >40 increased increased
3a >40 increased mild atrophy
3b >40 increased marked atrophy
3c >40 increased absent villi
36
How do you treat coeliac disease?
- Gluten free diet (avoid wheat, barley, rye, oats are OK BUT RISK OF FACTORY CONTAMINATION)
37
What are complications of coeliac disease? (Name 6 and describe):
1 - Infection (coeliacs get defective spleen and poor immune responses)
2 - osteoporosis
3 - refractory coeliac disease where you have recurrent malabsorptive symptoms and villous atrophy after adherence to GFD for 6-12months.
-> type 1 = villous strophy and normal immunophenotype
-> type 2 = villous atrophy and ABNORMAL immunophenotype
4 - progression of type 2 RCD to EATL (enteropathy associated T-cell lymphoma)
- EATL = night sweats, itching, weight loss, thromboembolism, treat with chemotherapy or stem cell transplant
5 - small bowel adenocarcinoma
6 - oesophageal and colonic adenocarcinoma
38
Describe the anatomy of the gallbladder:
Fundus -> body -> neck -> cystic duct
Hartmann's pouch = an outpouching of the gallbladder wall forming a mucosal fold where stones commonly get stuck
Can hold 30-50ml bile
Concentrated bile removing H2O
Lies in the gallbladder fossa on the inferior surface of the livers right lobe
39
What does cholecystitis?
Inflammation of the GB
40
What does cholelithiasis?
Gallstone in GB
41
What does cholecystechtomy?
Removal of GB
42
What does choledocholithiasis mean?
Gallstone that passes out GB into bile duct
43
What does cholangitis mean?
Infection of the bile duct
44
How much bile is produced per day and where is it produced?
600ml (450ml by hepatocytes in liver and 150ml by epithelial cells lining the bile ducts)
45
Name the primary bile acids synthesised in the liver:
Cholic acid and chenodeoxycholic acid
46
How are secondary bile acids formed and name two?
Result from bacterial actions in the colon
| Deoxycholic acid and lithocholic acid
47
What is the enterohepatic circulation and why is it necessary?
Needed for recycling of bile salts.
Most reabsorption of bile salts occurs in the terminal ileum by ACTIVE TRANSPORT into the portal circulation --> eventually returning to liver sinusoids.
- 95% bile salts recycled and 5% excreted
- total pool of bile salts circulates 6-8x a day
- hydrophobic bile acids are bound to albumin in the blood to be carried back to the liver
48
Why are bile salts better at emulsification compared to bile acids?
Bile salts are ampipathic (they have hydrophobic and hydrophilic properties)
49
How is GB contraction regulated?
- S cells in duodenum produce secretin to inhibit G cells releasing gastrin and to lower HCl production
- plasma levels of secretin increase
- increased bicarbonate production by the pancreas which flows into the SI and increased bile secretion occur
- vagal stimulation causes weak GB contraction
- CCK released from duod in response to fat causing GB contraction and relaxation of sphincter of oddi
- Gut hormones like somatostatin and VIP (vasoactive intestinal polypeptide) can also cause GB relaxation and closure of the sphincter of oddi
50
How many times is bile concentrated in the GB?
Up to 15x times
51
What is the epidemiology and risk factors of gallstone development?
5 F's (female, forty, fair, fertile, fat)
Greater incidence in caucasians than non-caucasians
Increased risk with age and family history
80% of stones are asymptomatic and require no treatment
52
What are the three main types of gallstones?
1) cholesterol stone - solid, oval, up to 3cm diameter
2) bile pigment stone - smaller, multiple hard irregular stones
3) mixed stone - MOST COMMON (80%), multiple multi-faceted stones with LAMINATED STRUCTURE of cholesterol/bile pigment/Ca salts
53
What are the three steps involved in gallstone formation?
These three steps often all occur together:
1) cholesterol supersaturation (can occur when bile acid levels are low e.g. Crohn's, or when oestrogen levels are high e.g. pregnancy)
2) biliary stasis (during periods of fasting or starvation, lack of CCK release)
3) increased bilirubin secretion (when there is increased haemolysis or failure of hepatic conjugation)
54
What is biliary colic?
- stone impacted in neck or Hartmann's pouch of GB
- causes epigastric pain/right quadrant pain
* pain can radiate to back and the right shoulder as the PHRENIC NERVE consists of fibres from C4 and gives sensory innervation to the diaphragm and gallbladder as well as sensory supply to the shoulder
55
What is an empyema?
Collection of pus in the GB causing it to become an abscess
56
What is a mucocoele?
Gallstone acts as a one-way valve and GB fills with bile and becomes distended
57
What are causes of post-hepatic (obstructive) jaundice?
- gallstone in bile duct
- cancer of head of pancreas
- pancreatitis
- bile duct cancer
- benign bile duct stricture
58
What are clinical features of post-hepatic jaundice?
```
Pale stool, dark urine
Jaundice
Itching/scratch marks
Hepatomegaly
Abdominal tenderness
Palpable gallbladder
```
59
What LFT changes are seen in obstructive jaundice?
High ALP and GGT (suggest obstruction)
| Bilirubin will rise steadily
60
How can drugs enter the systemic circulation?
Directly (IV)
| Indirectly (topical, oral, absorption from SI)
61
What are the two stages of drug metabolism catalysed by the liver?
1) Polar metabolite formed
- > cytochrome P450 enzyme carries out oxidation, reduction and hydrolysis
2) Conjugation
- > the drug is converted into a more polar form by conjugating it with a compound like glycine/glutamine, or adding an acetyl/methyl group.
62
What is therapeutic range and why is it relevant in drug monitoring?
The DIFFERENCE IN CONCENTRATION between therapeutic effect and toxic effect of a drug.
Wide therapeutic range drugs -> need little monitoring
Narrow therapeutic range drugs -> need more monitoring and possible dosage changes
63
What is volume of distribution?
The apparent volume in which a drug must be distributed to obtain the measured plasma concentration.
64
What is the formula used to calculate volume of distribution?
V (L) = Dose (mg) / concentration (mg/L)
65
What will the volume of distribution of a drug be that is highly bound to:
a) plasma proteins?
b) tissue proteins?
a) Will have high distribution in the blood and low in tissues therefore VOD is low
b) Will have low distribution in the blood and high distribution in tissues therefore VOD is high
66
What is the VOD of
a) water soluble drugs?
b) lipid soluble drugs?
- water soluble drugs have a low VOD as the drug CANNOT easily cross cell membranes
- lipid soluble drugs have a high VOD as they CAN easily cross cell membranes
67
What is unusual about digoxin and its VOD?
It has a high VOD although it is not lipid soluble. However it binds to Na/KATPases in cardiac and skeletal muscle and makes the concentration of drug in the body that is present in the plasma LOW
68
What does the initial drug concentration achieved after administration (Co) depend on and what is the formula used to calculate it?
Co depends on volume of distribution and dose.
Co = Dose / volume of distribution
69
How do you calculate loading dose and when are they required?
= target concentration x volume of distribution
Loading doses are required for drugs with large volumes of distribution.
70
What is steady state concentration (Css) and what does it depend on?
Css = when the amount of drug entering the body in one dosage interval is equal to the amount of drug eliminated in that same interval.
It depends on input rate and output rate
71
How do you calculate output rate?
Serum concentration (mg/L) x clearance (L/h)
72
How do you calculate input (infusion rate)?
target concentration x clearance
73
What is clearance and what does it depend on?
Volume of plasma cleared of drug per unit time
- depends on rate of drug delivery (i.e. rate of blood flow) to the liver and the extraction ratio of drug removed by the liver
74
What patient characteristics alter clearance and therefore maintenance dose requirements?
age
weight
pregnancy
- patients who are sick often require lower doses of drugs than less-ill patients as they will have lower clearance rates
75
How is average steady state concentration calculated?
The average concentration from a graph between the steady state PEAKS and the steady state TROUGHS
76
How do you calculate dosing rate?
= dose / dosing interval (wiggly t)
77
How can you calculate the average steady state concentration?
= (F x dose) / (Cl x Dosing interval [wiggly t])
78
What is bioavailability (F)?
the fraction of an oral administered drug that reaches the systemic circulation
79
What is the elimination rate constant (k) and how can it be calculated?
The amount of drug that is eliminated from the body per unit time
k = CL/V
High k values mean high clearances and low volumes of distribution
80
What is elimination half life (t1/2) and how is it calculated?
The time taken for the concentration of a drug to fall by half
- drug decline is always exponential, so natural logarithms are used:
t = (-ln0.5) / k
81
How many half lives does it take for a drug to reach steady state concentration?
4-5 half lives
82
What is extraction ratio and how is it related to bioavailability?
The proportion of a drug that is eliminated from the body, and the remaining amount is bioavailability
E.g. is extraction ratio = 0.9, only 10% of drug is bioavailable
83
How can hepatic disease affect clearance, VOD, half life and drug dose requirements?
- clearance of a drug depends on rate of blood flow to the liver
- factors that reduce this blood flow (e.g. cardiac failure) will reduce drug clearance meaning that increased drug dosage requirements are necessary
84
Does the small intestine lie in the supra or infracolic compartment?
Infracolic compartment
85
Describe the blood supply to the large intestine:
See Week 3 lecture revision page 17
86
Name 4 ways in which the large and small intestines differ:
Large intestine has no plicae circulares
Large intestine has no microvilli
Large intestine has more muscularis externa
Large intestine has more glands and goblet cells
87
Describe lymphatic drainage of the large intestine:
- ascending and transverse colons -> superior mesenteric nodes
- descending and sigmoid colons -> inferior mesenteric nodes
- lymph from both these groups of nodes then passes into intestinal trunks, into the cisterna chyli (dilated sac at lower end of thoracic trunk) and through the thoracic duct to the junction of the left subclavian and internal jugular veins
88
What is the definition of diarrhoea?
Liquid that conforms to the shape of the container it is in, 3+ loose, watery stool movements per day
89
What are the common bacterial/viral/parasitic causes of diarrhoea?
Bacterial = campylobacter, salmonella, e.coli, shigella
Viral = norovirus, adenovirus, rotovirus
Parasites = giardia, cryptosporidium
90
What is gastroenteritis and its clinical signs?
Inflammation of the stomach and intestines resulting from a bacterial or viral infection
Signs/symptoms:
- vomiting (if onset is within 6-12hrs of food ingestion the toxin is preformed)
- diarrhoea
- non-intestinal manifestations: botulism
91
What is botulism?
Toxins produced by C.botulinum bacteria that attack the nervous system causing muscle paralysis
92
Describe large intestinal diarrhoea:
- frequent
- small volume
- fever
- blood common
93
Describe small intestinal diarrhoea:
- watery and large volume
- cramps
- blood rare
94
What should you include when taking a history from someone with suspected infectious diarrhoea?
onset, occupation, recent travel, diet, antibiotics, pets
95
How should you treat diarrhoea?
1) oral rehydration therapy / IV if severe
2) antibiotics only used if risk of sepsis as they can actually worsen the diarrhoea by killing off more gut flora
3) symptomatic treatment not generally advised (immodium) as they just make the infection last longer as the diarrhoea is trying to rid the infection from your body
4) other treatments e.g. probiotics/dietary modifications
96
Outline the campylobacter infection:
```
undercooked chicken
9000 organisms for infecting dose
1-7 day incubation period
nausea, fever and abdominal pain
COMPLICATIONS: reactive arthritis and güillain barre syndrome - immune system damages PNS
```
97
Outline the salmonella infection:
reduced cases since chickens had vaccinations in 90's
can spread human to human
10,000 organism infective dise
COMPLICATIONS: bacteraemia (bacteria in the blood) and endocarditis (infection of inner lining of heart)
98
Outline the E.coli infection:
undercooked meat, especially burgers at BBQ
~10 organism infectious dose
- 2-4 day incubation period
bloody diarrhoea and abdominal tenderness
COMPLICATION: HUS
99
What is HUS?
Haemolytic uraemic syndrome
Where a toxin enters the blood stream and small clots form around the body, especially in the kidneys and patient required dialysis
100
Outline the C.diff infection:
common causes are antibiotic use, PPI use and old age
there is reduced colonic colonisation of healthy bacteria and bad bacteria can flourish
associated with fever
101
Outline the norovirus infection:
faecal -> oral transmission
10-100 organisms for infectious dose
- clings to hard surfaces and very stable (60 degree heat and bleach cannot destroy it)
- extremely common in care homes and the elderly and dehydration is a common COMPLICATION
