LO's (Non-Clic) Flashcards
(90 cards)
1
Q
Name the roles of acid in our body.
A
- Digestion of food
- Iron absorption
- Killing pathogens
2
Q
Explain how the body has adapted to stomach acid.
A
▪ Mucous secreting cells
○ Trap bicarbonate ions ( creating an alkaline environment )
○ Creates gel like barrier which is an important protective layer
▪ Prostaglandins locally produced
○ Stimulate secretion of mucus and bicarbonate
○ Dilate mucosal blood vessel
○ Cytoprotective effect (this is where chemical compounds protect cells from harmful agents)
3
Q
Name the cells that produce HCL.
A
▪ Parietal cells
4
Q
What do parietal cells produce?
A
- HCL
- Intrinsic Factor
5
Q
Name the cells that produce pepsinogen.
A
Chief / Peptic cells
6
Q
What is another name for proton pump?
A
▪ K+H+ATPase
7
Q
Describe the process of HCL secretion by the parietal cells.
A
- Water and carbon dioxide combine to form carbonic acid
- Carbonic Anhydrase breaks down the carbonic acid into its constituents (CO2, OH-, H+)
- H+ is pumped out into lumen of canaliculus, and K+ is pumped into the cell by the proton pump
- Bicarbonate from the carbonic acid constituents is then pumped out into interstitial fluid and chloride is pumped into the cell by Antiport
- Cl- then transported into the lumen by channels
- H+ and Cl- combine to form HCL
8
Q
Name three endogenous secretagogues in the stomach.
A
▪ Gastrin (Polypeptide Hormone)
▪ Acetylcholine
- Histamine
9
Q
a) What cells secrete gastrin?
b) Where are they found?
A
A) G Cells
B) Gastric antrum, duodenum
10
Q
Describe the role of gastrin in acid production and digestion.
A
▪ Released into the blood
▪ Stimulates secretion of acid by parietal cells through the PP
▪ Increases pepsinogen secretion
▪ Stimulates blood flow and increases gastric motility
11
Q
Describe the role of acetylcholine in acid secretion.
A
▪ Released from neurons
Stimulates muscarinic receptor on surface of parietal cells and histamine containing cells
12
Q
Describe the role of histamine in acid secretion.
A
▪ Mast cells lying close to parietal cell release histamine
▪ Histamine release increased by gastrin and acetylcholine
▪ Acts on parietal cell H2 receptors
13
Q
What percentage of the world population are infected with H.Pylori?
A
50%
14
Q
A) H.Pylori is a causative factor in….
B) H.Pylori is a risk factor for…
C) H.Pylori has a strong link with….
A
A) Gastric and duodenal ulcers
B) Gastric cancer (adenocarcinoma)C) MALT Lymphoma
15
Q
Other than peptic ulcers, name 4 conditions associated with Pylori.
A
▪ Dyspepsia
▪ Atrophic gastritis (gastritis leading to scarring and loss of glandular cells)
▪ Iron deficiency anaemia
▪ Idiopathic Thrombocytopenia Purpura
16
Q
Describe the pathogenesis of a Helicobacter Pylori Infection.
A
1- Flagella acts as a corkscrew allowing it to invade the protective layers and cause damage directly
2- Produces urease enzyme which produces ammonia from water and urea which neutralises gastric acid
3- Ammonia itself has a local damaging effect
4- Neutral environment (increased pH) allows the Pylori to colonise and proliferate so more ammonia
5- Leads to damage of the protective mechanisms of the mucosa
6- Increases susceptibility of damaged mucosa to the acidic environment where there is inflammation (neutrophils and inflammatory cells, with marked persistent lymphocyte penetration) and cell death
17
Q
List the symptoms of an acute infection of H.Pylori (usually when this occurs the symptoms are associated with something else like gastritis etc… - but this is where the damage is being caused and where it may lead to chronic infection).
A
▪ Nausea
▪ Dyspepsia
▪ Malaise
▪ Halitosis
18
Q
Name three factors that make it more likely to develop H.Pylori chronic infection.
A
▪ Smoking
▪ Heavy alcohol drinking
▪ Older
▪ Male
19
Q
Name three pieces of lifestyle advice you may give a patient with GORD/Dyspepsia.
A
▪ Healthy eating (lower bmi is better) ▪ Weight reduction ▪ Smoking cessation ▪ Lift the head of the bed ▪ Eat within 3-4 hours before bed, and eat small frequent meals
20
Q
Name 4 precipitants of GORD/dyspepsia.
A
▪ Alcohol
▪ Coffee
▪ Chocolate
▪ Fatty foods
21
Q
A patient presents with GORD/Dyspepsia. Part of the management you advice the patient regarding lifestyle changes which he informs you they have tried yet the symptoms persisted. Describe other management options at this point.
A
▪ Stop NSAID’s if possible
▪ Over counter remedies:
▪ Antacids (directly neutralise acid + inhibit activity of peptic enzymes - constitute salts of magnesium and aluminium) - Example: Maalox
▪ Alignates - taken in combo with antacid (usually have antacids in them), increase viscosity and adherence of mucus to oesophageal mucosa and forms a gel layer on the top of the stomach contents which prevents constituents from irritating the oesophagus - Example: Gaviscon
▪ Simeticone - antifoaming agent (helps bloating, flatulence) - Example: Infacol
▪ Consider H.Pylori testing
22
Q
What are the possible tests for H.Pylori?
A
▪ Urea breath test - tests for the bacteria, and can tell if it has been eardicated (give labelled urea in capsule, if there is urease then the urea will break down to ammonia and CO2 which are also labelled, the CO2 will travel through blood and be exhaled in the breath test)
▪ Stool antigen
▪ Rapid urease test (biopsy based diagnostic test, done when an endoscopy is needed)
23
Q
A) Describe first-line treatment of Patients who are H.Pylori positive following testing.
B) What if allergic to penicillin?
C) If they had previous exposure to clarithromycin? (just because the more you use it the higher the risk of resistance developing)
A
A) 7-day twice daily course of treatment with PPI + Amoxicillin and either clarithromycin or metronidazole
B) PPI + clarithromycin + metronidazole
C) PPI + Bismuth + metronidazole + tetracycline
24
Q
Name 3 PPI’s.
A
▪ Omeprazole
▪ Lansoprazole
▪ Esomeprazole
25
List the conditions where PPI's are used.
▪ Ulcer disease
▪ Reflux oesophagitis
▪ One component of H.Pylori eradication
▪ Zollinger-Ellison Syndrome (tumours called gastrinomas in the duodenum and pancreas lead to increased secretion of gastrin which leads to the increased secretion of acid)
26
Describe the mechanism of action of PPI's.
▪ Block the K+H+ATPase (proton pump) of gastric parietal cells
▪ Reduces gastric acid secretion
▪ Example: omeprazole irreversibly inhibits the PP
▪ Usually oral administration
27
A) Name 3 side effects of PPIs. (they are rare which is why people stay on these drugs for long time which risks masking other serious conditions).
B) What is the danger of staying on PPI's for a long time if they don’t usually cause harm?
A)
▪ GI symptoms (diarrhea, constipation, abdo pain)
▪ Headaches
▪ Rashes
B)
▪ May mask the symptoms of gastric cancer
▪ May increase GI infections
28
Describe the pathophysiology of Peptic ulcers.
▪ Can be associated with infection of mucosa with H.Pylori
▪ Due to imbalance between mucosal damaging factors (acid, pepsin) and mucosal protecting factors (mucus, bicarbonate, prostaglandins, nitric oxide)
29
List the symptoms of peptic ulcer disease.
▪ Burning gastric pain which may be partially relieved by antacids and related to meal times
▪ DU pain - worse a night and when hungry
▪ Nausea
▪ Heartburn
▪ Flatulence
▪ Perforation/haemorrhage/bleeding
30
A) Once you confirmed that there is a peptic ulcer due to symptoms and endoscopy, what do you do next?
B) What if the peptic ulcer disease is NSAID associated?
C) What if the patient is Pylori negative, and no NSAID association?
A)
▪ PPI or H receptor antagonist therapy; or
▪ H.Pylori testing and eradication if the patient is positive
▪ (offer endscopy and H.pylori re-testing 6-8 weeks after initiating treatment)
B)
▪ Stop NSAIDs if possible
▪ Offer full dose of PPI or H2RA for 8 weeks
▪ If Pylori present, subsequently offer eradication therapy
C)
▪ PPI OR H2RA For 4-8 weeks
31
A) What is Histamine H2 receptor antagonists used for?
B) Descrine H2RA MoA.
C) Give examples of H2RA.
D)
A)
▪ Peptic ulcers
Reflux oesophagitis
B)
▪ Competitive inhibition of H2 receptors
▪ Inhibits histamine, gastrin, and acetylcholine stimulated acid production
Pepsin secretion falls -> reduced volume of gastric juice
C)
▪ Ranitidine
▪ Cimetidine
(oral, low dose available over counter)
D)
▪ Diarrhoea
▪ Constipation
- Dizziness
32
Name possible complications of cimetidine.
▪ Interacts with androgen receptors leading to gynaecomastia in men and decreased sexual function
▪ Inhibits cytochrome P450 slowing down the metabolism of a range of drugs including anticoaglulatns and tricyclics
Can cause confusion in the elderly
33
List 4 potential causes of an unhealed ulcer.
▪ Non-adherence to treatment plan
▪ Malignancy
▪ Inadvertent NSAID use
Failure to detect H.Pylori
34
List 4 potential causes of an unhealed ulcer.
▪ Non-adherence to treatment plan
▪ Malignancy
▪ Inadvertent NSAID use
Failure to detect H.Pylori
35
Describe the different views on whose job is it to ensure that we lead healthy lives (legislation and policy regarding health)?
- View spectrum
- Libertarian view = authority should be limited to ensure that members of populations enjoy natural rights - this views that the role of the state is not population welfare
- Collectivist views = utilitarian view - maximisation of utility for the population as whole should be achieved by achieving the greatest collective benefit so the well fare of some may be sacrificed if it is in the benefit of the collective
- Liberal = many states have this view now, certain individual rights should be held but also care for the individual well fare (People argue this is very paternalistic)
36
A) What is hiatus hernia?
B) List risk factors for hiatus hernia.
C) Describe treatment of hiatus hernia.
A) Part of the stomach pushes/slides through the hole in the diaphragm in the lower part of the chest -> compression of stomach -> acid comes up the sphincter
B) over 50, obesity, smoking
C) Symptomatic as it usually requires no intervention, weight loss, smaller meals, surgery if really bad with food coming back up and dysphagia
37
A) Describe barret's oesophagus.
B) What are the symptoms?
C) What is the management?
A)
- Caused by repeated damage to the oesophagus lining by stomach acid
- Metaplasia (change from one type to another which is usually an adaptive response - by it self is not premalignant) - change from squamous to glandular epithelium
- Metaplasia may be gastric in type or intestinal (intestinal is further away from the stomach)
- Risk of dysplasia - that is features in epithelium of disordered maturation and proliferation
- Then you have progressive risk of developing adenocarcinoma (gland forming) where as usual oesophageal carcinoma is squamous in cell type
(GORD is a risk factor)
B) Recurrent Chronic Heat Burn
C)
- Annual endoscopy
38
Immunosuppression can cause heartburn through a number of routes, particularly infection. Name two types of infection in an immunosuppressed patient that may cause heart burn.
Candida - erosive oesophagitis (acute, can be dangerous to the patient)
CMV
39
A) List main causes of acute gastritis. (Neutrophils, acute inflammation and ulceration)
B) Why is it difficult for an ulcer to heal itself without intervention.
A) ▪ NSAID e.g. aspirin
▪ Alcohol
▪ Tobacco
▪ Infection - H.pylori (lymphocytic)
B)
▪ Acid remains in contact with the underlying tissue
▪ Continuing inflammation
▪ Leads to chronic inflammation which leads to fibrosis and scarring
▪ Or can lead to perforation
40
A) What is atrophic gastritis?
B) What type of condition is AG?
C) What cells are attacked in AG?
D) Based on the cells that are affected/attacked by the immune system in Atrophic Gastritis, what condition may develop as a result and why?
A) (Chronic ill-defined indigestion associated with anaemia)
B) Autoimmune
C) Parietal
D)
- Pernicious Anemia
- Destruction of parietal cells -> lack of acid and intrinsic factor
- > vitamin B12 deficiency and malabsorption
41
List risk factors for stomach ulceration.
- H.Pylori
- Age 35-65
- M>F
- Hyperacidity
- Smoking
42
List functions of small intestine.
Digestion
Fat Absorption
Sugar and amino acid absorption
43
A) Describe the pathophysiology underlining Gluten Enteropathy (coeliac disease.)
B) Based on the pathology , what sort of symptoms/clinical signs do you get
A)
▪ Gluten is absorbed - particularly gliadin (this is a protein found in gluten)
▪ Gluten is recognised wrongly as a pathogen by antigen presenting cells who present it to CD4+ T cell which then present it to B cells
▪ B cell producing anti-gliadin antibodies which attack and damage the cells of the mucosa
▪ Vilus atrophy (main defining feature)
▪ Reduced surface area for absorption and for digestion -> Malabsorption
B)
▪ Malabsorption -> dietary insufficiency
▪ Presence of undigested/unabsorbed food in lumen -> risk of super infection
▪ Retaining water by osmotic pressure -> cramps, bloating, diahrrea
- Pain and discomfort
- weight loss
- Risk of lymphoma is not controlled by a gluten free diet
- Skin - dermatitis herpetiform
44
List three causes of malabsorption.
- Infection - especially giardia
- Coeliac disease
Lactose intolerance
45
Name the criteria used to identify FGIDs, and the definition used.
▪ Criteria: Rome IV (used for categorizing and recognizing disorders)
▪ Definition:
• They are disorders of gut-brain interaction
• Disorders classified by GI Symptoms with a combination of symptoms such as motility disturbance, visceral hypersensitivity, altered mucosal and immune function, altered gut micropia
(essentially biological/genetic and environmental/social factors have an effect on psychosocial (stressful life events or factors which along side with biological have an effect on physiological state of someone)
46
List 4 examples of FGIDs.
▪ Reflux hypersensitivity (in patients presenting with heartburn yet they have normal upper endoscopy and esophageal biopsies and normal esophageal pH)
▪ Functional Dyspepsia
▪ IBS
▪ Functional Constipation
47
A) Describe the prevalence and occurence of IBS.
B) List symptoms.
C) Describe diagnostic criteria
D) Describe management.
A)
▪ 20-30 years old
▪ F > M
11% of population
B)
- Stomach pain or cramps (worse after eating and better after a poo)
- Bloating (full and swollen uncomfortable tummy)
- Diarrhoea
- Constipation
C)
▪ Recurrent Abdominal Pain at least 1 day a week associated with two or more of:
• Related defecation
• Associated with a change in frequency of stool
• Associated with a change in form (appearance of stool)
▪ But in the UK also need two additional symptoms of:
• Change in how you pass stools (urgency, not emptied bowels)
• Bloating, hardness or tension in abdomen
• Symptoms worse after eating
• Passing mucus form rectum
▪ In the last 3 months
▪ But symptoms onset at least 6 months prior to diagnosis
▪ (Extra: carry out blood tests to rule out other conditions such as coeliac, and stool sample to rule out other condition like IBD - check for calprotectin)
D)
- Lifestyle changes - food diary to see if there is triggers like fizzy drinks or caffeine)
- Drug treatment (Antidiarrheal - loperamide, laxatives - not lactulose, anti depressants TCA then SSRI if TCA don't work)
- Psychological approach
- Complementary therapies approach
48
A) Define Acute Liver Failure
B) Name causes of ALF.
C) List the categories of AFL.
A)
Definition: A rare syndrome defined by rapid decline in hepatic function characterized by jaundice, coagulopathy (INR >1.5) and hepatic encephalopathy in patients with no evidence of previous liver disease.
B)
- Acute Hepatitis
- Paracetamol Overdose
C)
The ALF can be viewed in terms of time interval between jaundice and hepatic encephalopathy:
▪ 7 days from Jaundice to encephalopathy = hyper-acute AFL
▪ 8-28 Days = acute
▪ >21 and <26 weeks = sub-acute
49
Categories the causes of acute liver failure and give examples of each
```
Viruses
▪ HAV, HBV
▪ Cytomegalovirus
Drugs
▪ Paracetamol
▪ Antibiotics (doxycycline, ciprofloxacin)
Toxins
▪ Amanita Phalloides mushroom toxin
▪ Yellow Phosphorus
Hepatic Failure In Pregnancy
▪ HELLP (Haemolysis, elevated liver enzymes, low platelets)
▪ Acute Fatty Liver of pregnancy
Vascular Causes
▪ Ischaemic Hepatitis
▪ Portal Vein Thrombosis
Metabolic Causes
▪ Alpha1-Antitrypsin deficiency
▪ Wilson's Disease
Malignancies
▪ Primary (HCC)
▪ Secondary (Extensive hepatic Metastases)
```
50
Describe the examination findings seen in acute liver failure.
```
Clinical Features:
→ Jaundice with small liver
→ Signs of hepatic Encephalopathy
• Drowsiness
• Confusion
• Disorientation (Grade I and II)
• Unresponsive Coma (Grade IV)
→ Fetor Hepaticus (sour, musty dour in the breath due to substances that are formed in the stool by bacteria and normally removed by liver, but in this case they are not)
```
51
Describe the abnormalities in blood tests seen in acute liver failure and appreciate the link between certain variables and prognosis.
Blood results abnormalities in AFL:
▪ Hyperbilirubinemia
▪ High Serum ALT
▪ Low levels of coagulation (so higher INR)
Other tests: EEG, USS
52
• Describe the mechanism of hepatotoxicity in paracetamol overdose
1. Paracetamol is usually metabolised by the sulphate conjugation pathway (it is conjugated with glucuronide and sulphate then excreted)
2. Some paracetamol will by metabolised by oxidation pathway -> produces NAPQI (a highly toxic and reactive compound -> NAPQI quickly deactivated and conjugated with glutathione and excreted
3. In OVERDOSE = too much paracetamol --> a lot metabolised by oxidation as sulphate conjugation pathway is saturated -> too much NAPQI but glutathione is depleted -> cannot deactivate NAPQI -> liver toxicity
53
Outline the principles of treatment of paracetamol overdose
▪ Acetylcysteine within 8-10 hours of ingestion of the overdose
▪ Replenishes the glutathione stores
54
There are 4 main types of vomit. List them.
○ 'Normal' vomit (you see on side of the road)
§ Common causes= drinking too much alcohol, viral gastroenteritis, or being generally unwell
§ Other causes= (pre-pyloric) pyloric stenosis, large gastric malignancy
○ Coffee Ground Vomit
§ Most caused by people who are generally unwell and have gastric stasis and have non-specific gastritis
§ Common cause is young diabetic patient with DKA
§ Rarely indicates serious bleed
- upper GI
○ Haematemesis (fresh blood in the vomit)
§ Causes such as oesophageal or gastric varices (due to blockage of blood flow to the liver for example due a clot or scarring), duodenal or gastric ulcer, or Mallory Weiss tear (between oesophagus and the stomach)
○ Bilious vomiting
§ Causes are post-pyloric obstruction after the ampulla due to small bowel obstruction etc
§ Important to check for bowel sounds and check bloods as electrolyte imbalances can cause this
55
What is Russell's sign ?
Russell's sign on the back of hands and knuckles indicates an eating disorder - scarring scratching etc
56
Describe examination/investigations for patient presenting with vomiting.
```
▪ Teeth? (if someone vomiting all the time they lose enamel on teeth such as those who are bulimic) Hand? (Russell's sign on the back of hands and knuckles indicates an eating disorder - scarring scratching etc)
▪ Abdominal exam
○ Abdominal pain?
○ Bowel sounds present?
○ Never forget to do a PR (rectal exam - to check for constipation for example or obstruction)
▪ Bloods
○ All standard bloods + venous gas
▪ Pregnancy test
▪ Urinalysis
▪ CXR
▪ CT abdomen (only if really necessary)
```
57
Describe management of vomiting presentation.
- Underlying cause
- Ensure well hydrated and electrolytes
- If Upper GI bleed = Fluid Resus, Blood products, discussion with surgeons
- Anti-emetics
○ Prochlorperazine - can be sedating
○ Metoclopramide (consider using it as a second line due to the secondary effects)
§ Aids gastric motility
§ Extra-pyramidal side effect
§ Oculogyric crisis in young women - dystonic reaction characterised by prolonged involuntary upward deviation of the eyes
○ Ondansetron
§ Acts centrally
§ Delays gastric emptying
§ Good in chemotherapy
○ Cyclizine
Can give a high
58
What is dyspepsia?
```
▪ A collection of symptoms
▪ Dyspepsia is not GORD
▪ Characteristics include:
○ Retrosternal discomfort
○ Bloating/Borboygmi (gurgling sound due to movement of fluids and gases)
○ Heaviness
```
59
What is the difference between organic dyspepsia and functional dyspepsia?
```
--- Organic
▪ Duodenal or gastric ulcer
▪ Oesophagitis/Duodenitis
▪ Gastric Cancer
▪ H.Pylori
Treatment:Underlying cause
High dose PPI
```
--- Functional ▪ Ulcer type = epigastric pain
▪ Dysmotility = early satiety, distention, nausea
▪ Reflux type = retrosternal discomfort
Functional Dyspepsia:
Lifestyle modification
Weight (they may have added weight on recently), alcohol, smoking, coffee
Consider acid suppression
60
List the red flag symptoms of dyspepsia.
```
▪ Weight loss
▪ Dysphagia
▪ Iron deficiency anaemia
▪ Recurrent vomiting
Worrying medications (steroids, NSAIDs)
```
61
What is GORD?
▪ Retrosternal pain related to eating, and lying down
▪ Regurgitation of acid/bile
▪ Water brash (excess salivation, often acidic - when you are about to be sick you get taste in your mouth, this is water brash)
Nocturnal cough/wheeze
62
Describe the management of GORD.
▪ Trial of acid suppression
▪ Endoscopy
○ Assess for oesophagitis/hiatus hernia (hiatus hernia when part of the stomach moves up the hiatus into the chest area)
○ Assess for Barret's (change in the type tissue that line the oesophagus from squamous to columnar - increases risk of cancer)
▪ Consider oesophageal manometry pH impedance (specialist work)
63
What is one important aspect that should always be explored if a patient presents with what maybe GORD?
▪ Myocardial Infarction as it mimics GORD
| ▪ Oesophageal spasm presents in similar type of pain however very rare! Always check MI first
64
What is dysphagia?
Difficulty swallowing - the action of swallowing is difficult (not painful swallowing or chokcing or something stuck in the back of throat)
65
What are the 4 questions you should ask when someone presents with dysphagia?
▪ Interval
○ Is the difficulty in initiating swallowing? (probably oropharyngeal - refer to ENT)
○ Repeated attempts to 'get food over'
○ Dysphagia immediately after swallowing
▪ PMH that probably represents oropharyngeal dysphagia
○ Previous stroke
○ MND (motor neuron disease)
○ Pharyngeal pouch
○ Parkinson's disease
▪ Ask about the type of food
○ Struggling to swallow liquids - mostly oropharyngeal causes
○ Struggling to swallow solids? - probably oesophageal cause
○ Both? - likely oesophageal dysmotility
▪ Pattern
○ Intermittent? - probably oesophageal dysmotility or atypical cause
○ Progressive? - E.g couldn’t swallow solids then liquids, then probably an organic oesophageal cause and need to eliminate carcinoma
66
Associated features of Dysphagia that should raise concern:
▪ Weight loss
▪ Heart burn
▪ Odynophagia
▪ Systemic Disease??
○ Astham - (Eosinophilic esophagitis (EoE) is a chronic, allergic inflammatory disease of the esophagus (the tube connecting the mouth to the stomach). It occurs when a type of white blood cell, the eosinophil, accumulates in the esophagus.)
○ Scleroderma - autoimmune condition where connective tissue is attacked under the skin and around the organ
67
List differential diagnosis for Dysphagia .
1- Oesophageal Stricture (Peptic with long standing reflux oesophagitis, radiotherapy (particularly breast/lung), corrosives such as bleach)
2- Oesophageal Carcinoma (Progressive, Weightloss)
3- Achalasia - this iw where the lower oseophageal sphincter fails to open leading to build up of food in the oesophagus (Absent peristalsis, increases LOS pressure, regurgitation of solid food stuffs)
4- Eosinophillic oesophagitis (Intermittent food bolus obstruction, history of asthma/eczema/atopy, really painful, need antibiotics/steroids)
5- Candidiasis (steroid use, immunosuppressed, odynophagia)
68
List causes of abdominal bloating.
Causes: (6 F's)
▪ Foetus - pregnancy
▪ Flatulence
▪ Faeces
▪ Fluids (Ascites) - decompensated lung disease, cirrhosis or heart failure
▪ Fat - when there is bloating over a long period of time and the person doesn’t realise they just added on weight
Intraabdominal mass - acute hepatitis, disseminated colorectal cancer
69
What types of diarrhoea are acute on the Bristol Scale?
6 and 7
70
What are the two types of diarrhea?
Osmotic (poorly/malabsorbed osmotic substance which draws out water, this can be fixed with fasting)
Secretory (Often stimulant by toxins e.g. bacteria or peptide)
71
What is a likely diagnosis of vomiting first thing in the morning and diarrhoea first thing in the morning?
Alcohol cause
72
List risk factors for C.Diff diarrhoea.
- PPI
- Antibiotics use
- over 65's
- Immunocompromised
73
what is coeliac?
Autoimmune condition where you cannot process gluten found in bread, pasta, cereal - causes abdominal pain, bloating, flatulence
74
What does blood in stool signify?
Colonic cause - should do a colonoscopy
75
What does a stool that cannot be flushed signify?
Steatorrhea -> malabsorption problem
76
What are the features of organic pathology, rather than functional, relating to diarrrhea.
- <3 months and continuous
- weight loss
- nocturnal
77
How do you investigate a patient presenting with diarrhoea?
▪ Stool
○ Stool culture
○ Faecal Elastase (someone with chronic pancreatitis)
○ Faecal calprotectin - protein produced by the gut in response to inflammation
§ Could be an indicator of IBD
§ But if someone has acute episode of diarrhoea they still produce this
§ If acute episode wait until patient over the episode then test for this
▪ PR
○ Constipated - it maybe over flow diarrhoea
○ Rectal mass - might be over flow due to a mass
▪ Bloods
○ FBC
○ U+E''s, CRP
○ Thyroid function - thyrotoxicosis /hyperthyroidism causes diarrhoea
○ Anti-tTG (assess for coeliac - tTG is an IgA), and immunoglobulins (to check if there is general immunoglobulin deficiency coz then the tTG would be useless)
○ 7-Alpha-cholestanone - bile acid malabsorption (happens to people who get diarrhoea after a cholecystectomy)
▪ Colonoscopy
○ All change in bowel habit >50
○ Rectal Bleeding (spotting is hamo
○ Weight Loss
○ Strong family history
78
Name two dietary potential causes of IBS.
▪ Gluten hypersensitivity
| ▪ Lactose intolerance
79
List the commonest causes of constipation.
```
▪ Drug
○ Opiates
○ Anticholinergics
○ Iron
▪ Diet
○ Poor fibre intake
▪ IBS
▪ Anorectal disease
○ Strictures
○ Fissures
```
80
What is one important exam you should never forget to do with constipation?
PR!@!!!@!@!
81
Describe the management of constipation.
▪ Correct the correctable
○ Change analgesia
○ Rehydrate
○ Treat infection
○ Manage their diet
▪ Laxatives
○ Osmotic laxatives - example: lactulose/laxido
§ Unabsorbable peptides which draw water into gut
§ Do not lose effect over long periods
○ Stimulant laxatives - Example: Senna/Bisacodyl
§ They lose their long term effect
§ Don’t give them for too long as they lead to sluggish bowels
○ Faecal softeners
§ Glycerin suppositories
§ Docusate sodium
82
A) List causes of Upper GI Bleed.
B) Describe features.
C) Investigations?
- Peptic Ulcer
- Gastritis
- Oesophagitis
- Varices
- Mallory Weis tear
- Vascular malformation
- Malignancy
B)
- Iron deficiency anaemia
- malaena
- Haematemesis +/- malena
- Coffee ground vomiting
- FOB +ve
C)
- Oesopago-gastro-duodenoscopy (OGD)
- CT Mesenteric angiogram
83
A) List causes of Lower GI bleed.
B) List features.
C) Investigations?
```
a)
Diverticulosis + anorectal
- IBD
- Coagulopathy
- Angiodysplasia
- Unknown
```
B)
- Iron deficiency anaemia
- Malaena
- Blood mixed with stools
- PR bleeding (Gush in pan)
- Bright blood on toilet paper
```
C)
- OGD + Colonoscopy
- CT Mesenteric angiogram
- Formal angiogram + embolisation
(You do not do a colonscopy in acute bleeds - do ct)
```
84
How do you treat varices?
OGD
- Band ligation
- Stenting
- TIPS (a shunt)
85
How do you treat Ulcers?
- Clips
- Thermal coagulation + adrenaline
- Thermal coagulation + Fibrin
86
A) List potential underlying causes of Heart Burn.
▪ GORD
▪ Oesophagitis
▪ Gastric Cancers
▪ Functional Dyspepsia - if no detectable cause
87
How might the patients lifestyle impact his health in this situation?
```
▪ Overweight
▪ Smoking
▪ Binge drinking
▪ Sedentary Lifestyle
▪ Stress at work
▪ Travelling and diet
```
88
How do you manage Functional Dyspepsia:
▪ Lifestyle advice
▪ Prokinetic Agents (they help control acid reflux and help strengthen the lower oesophageal sphincter) (E.g. cisapride)
▪ H2-RECEPTOR ANTAGONIST (e.g. ranitidine)
89
Describe pharmacological tx of heart burn.
1- Antacid - neutralise HCL, while alginates create acid gel physically reducing reflux
2- H2 Receptor - prevent action of histamine on parietal cells
3- PPI - block the parietal cells independent of neurohormonal control
90
Describe how you would test for H.Pylori.
▪ Stool Sample Test
▪ Test for stool antigen for H.Pylori
▪ Should have stopped PPI or bismuth for at least two weeks
▪ Should have stopped antibiotics for 4 weeks
H2 receptor antagonists should have been stopped at least 2 days before
