Gastrointestinal conditions and drugs Flashcards
1
Q
What can cause high or low albumin levels?
A
Lower albumin my be caused by:
Malnutrition
Liver disease
Kidney disease
Inflammatory disease.
Higher albumin levels may be caused by:
Acute infections
Burns
Stress from surgery or a heart attack.
2
Q
How can inflammation cause hypoalbuminaemia?
A
Inflammation increases capillary permeability and escape of serum albumin, leading to expansion of interstitial space and increasing the distribution volume of albumin and therefore lower concentrations in the blood.
3
Q
What is an abdominal migraine and what are the symptoms?
A
A neurological condition originating in the brain causing abdominal pain receptors being stimulated resulting in intermittent bouts of generalised severe abdominal pain with associated nausea and vomiting, without a headache migraine. 7/10 sufferers have had previous head migraines
4
Q
What is cholecystitis and its symptoms?
A
Inflammation of the gall bladder.
Causes severe upper right quadrant abdominal pain often with referred right shoulder tip pain. Pain is worse on inspiration and palpation (Murphy’s sign is useful tool) and comes with associated nausea, vomiting, pyrexia with a history of intolerance of fatty foods (pain and vomiting)
5
Q
What symptoms other than pain can accompany appendicitis?
A
Nausea
Vomiting
Loss of appetite
Constipation
Low grade temperature
Diarrhoea
Facial flushing
Dry tongue
Halitosis
6
Q
What are possible complications of appendicitis and their symptoms?
A
Perforation
- Tachycardia and sudden temporary relief or decrease in pain
Peritonitis
- Blumberg’s sign
7
Q
What is Crohn’s disease?
A
Crohn’s Disease is an inflammatory bowel disease (IBD) of the GI tract that causes inflammation & ulceration.
8
Q
What portion of the bowel does Crohn’s disease affect?
A
Can be in one area or multiple segments (this can be anywhere in the digestive tract from the mouth to the anus) but most usually found in the end of the ileum and the ascending colon
9
Q
Which layers of the bowel does Crohn’s disease affect?
A
All of them through to the serosa
10
Q
What is the internal appearance of Crohn’s?
A
Bumps of inflamed mucosa give a ‘Cobblestone’ or ‘Skip lesion’ appearance
11
Q
What is the cause of Crohn’s disease?
A
No known cause at present but research has shown in many cases it is linked to a faulty immune system. Research also suggests that a persons diet, dairy intake, stress, smoking, a viral or bacterial illness changes the gut flora. Research has also shown that it tends to run in families so it may be genetic.
All of these are scientists best informed opinion at the moment.
12
Q
How is Crohn’s diagnosed?
A
A GP would ask for a food diary along with a symptom diary as Crohn’s tends to present with flare ups of symptoms.
A blood test to check for inflammatory markers.
A faecal calprotectin test which tests for inflammation in the bowel (it specifically tests for neutrophil degranulation). - This would tell your clinician that you have inflammatory bowel disease.
You would then likely be referred to a gastroenterologist.
Possibly sent for colonoscopy or biopsy or an MRI/CT scan with contrast dye.
13
Q
What is the normal age of presentation of Crohn’s disease?
A
Crohn’s disease presents most commonly in adolescence and early adulthood, but it may occur at any age.
About 20–30% of cases present before the age of 20 years.
The median age at diagnosis is about 30years.
It occurs in men and women at approximately equal rates.
14
Q
What are the symptoms of Crohn’s disease?
A
Abdominal pain
Diarrhoea (w/ associated dehydration)
Extra intestinal symptoms
Fatigue & weight loss
Flare up and remission
15
Q
What is the most common presentation of Crohn’s disease pain?
A
Lower/mid right side, typically 1-2 hours after eating.
16
Q
Why does Crohn’s disease cause diorrhea?
A
1) If the ileum is affected then a patient will have difficulty absorbing fats - this is where diet will play a huge part in symptom control, some patients will find that wheat or dairy cause diarrhoea (this is why the GP will encourage the pt to keep a food diary).
2) If the pt has had part of their ileum removed then they are unable to reabsorb bile salts produced in the liver, these are usually reabsorbed in the ileum and do not enter the colon. If these bile salts do enter the colon this draws fluid into the colon causing watery diarrhoea.
3) Some of the medications given to treat the symptoms of crohns cause diarrhoea.
17
Q
What extra-intestinal symptoms can be present with Crohn’s disease?
A
Joint pain
Enteropathic arthritis
Enthesitis
Tenosynovitis
Dactylitis
Mouth ulcers
Angular cheilitis
Crohn’s disease in an inflammatory disease so inflammatory conditions in other body sites are commonly associated with it
18
Q
How does Crohn’s disease cause joint pain?
A
The actual relationship is not fully understood but, a protein called tumour necrosis factor that get’s overproduced and it is thought that this amongst other proteins may be the cause
19
Q
How does Crohn’s disease cause fatigue and weight loss?
A
Malabsorption associated with GI inflammation/damage - the small intestine is responsible for exchange of nutrients so with increased scar tissue this cannot happen. Malabsorption and malnutrition can also cause anaemia which exacerbates these symptoms
20
Q
How can Crohn’s disease lead to bowel perforation?
A
Repeated patches of Crohns can cause damage and scar tissue. This leads to strictures, bowel obstruction and perforation.
21
Q
What are some common treatments for Crohn’s disease?
A
Corticosteroids (prednisolone)
Immunosuppressive drugs (thiopurines, methotrexate)
Biologic therapy (anti-tumour necrosis factor e.g. infliximab, adalimumab)
Amino salicylates
Enteral nutritional supplementation
Loperamide (slows gastric transit)
Mebeverine (anti-spasmodic)
Colestyramine (bile salt binder)
22
Q
When are coticosteroids prescribed to Crohn’s disease patients, for how long are they given?
A
Prednisolone may be prescribed to manage a flare up, they should not be prescribed long term to prevent flare up. Long term use of corticosteroids causes problems for the patient so they are only used as a short term management option.
23
Q
When are Aminosalicylates used for patients with Crohn’s disease?
A
When a patient can no longer tolerate steroid treatments
24
Q
When may you see some specialist nutritional supplements prescribed for patients with Crohn’s disease?
A
These are usually in children where they cannot have steroids for various reasons.
25
What holistic treatment is given for Crohn's disease, can it be cured?
There is no cure for Crohn's disease, focus is on:
Diet, medication, lifestyle changes, smoking cessation, referral to gastroenterologist, symptom management.
Surgery may be offered
26
What surgeries are used to treat Crohn's disease?
Small-bowel resection (major surgery so only under set circumstances after a while)
Endoscopic balloon dilation (the established endoscopic treatment)
Strictureplasty,
Stents (Fully covered self-expandable metal stents (FCSEMS) have been used for endoscopic treatment of patients for whom EBD was unsuccessful)
27
What is Ulcerative Colitis?
Ulcerative colitis is an inflammatory bowel disease (IBD) of the colon and rectum. Inflammation damages the bowel wall and areas of ulceration form. These areas bleed, produce more mucus & pus.
28
What are the main differences between ulcerative colitis and Crohn's disease?
**Crohn’s:**
Affects whole intestine
Can affect all layers of bowel wall
Usually begins in the ilium
Found in patches in the bowel wall
**Ulcerative colitis:**
Affects large intestine
Affects inner lining of colon
Starts in the rectum and migrates back
Affects the bowel wall in a “sheet”
29
What are the 4 forms of ulcerative colitis?
**Ulcerative proctitis** – this is limited to the rectum and the most mild type.
**Proctosigmoiditis** – affects the rectum and the sigmoid
**Left sided or distal colitis** – affects rectum, sigmoid and descending colon, this being the left side or the most distal part of the colon before the sigmoid.
**Pancolitis or total colitis** - the whole colon, this is the most severe case.
30
What are the symptoms of ulcerative colitis?
Abdo pain and cramps
Fever
Anaemia
Urgent and frequent bowel movements (the colon is irritated and therefore wants to empty frequently in an attempt to dispel the irritation)
Watery diarrhoea w blood/mucus/pus (from ulcers)
Dehydration & electrolyte imbalances (colon usually absorbs most of the bodies water)
Weight loss/fatigue
Low appetite
31
What does the mnemonic – ULCERS stand for?
U-rgent bowel movements
L-oss of weight & Low RBC
C-ramps in abdo
E-lectrolyte imbalance & Elevated temperature
R-ectal bleeding
S-evere diarrhoea (w blood/mucus/pus)
32
What causes ulcerative colitis?
No known cause at present but research has shown in many cases it is linked to a faulty immune system i.e. an over-reaction to substances.
Research suggests that a persons diet, dairy intake, stress, smoking, a viral or bacterial illness changing the gut flora may all be responsible for flare ups in the condition.
33
How are patients diagnosed with ulcerative colitis?
Patients will be asked to keep a food diary, tested for anaemia & inflammatory markers, and tested for blood in stools
Colonoscopy - easier to access with a camera and track backwards through the colon just as the condition does, can usually see how far it has progressed
Barium enema – contrast dye enema & xray
**It is a long process**
34
What treatment and symptom control is used for patients with ulcerative colitis?
Steroids
Amino salicylates
Immune suppressants/immunomodulators
Antibiotics
Surgery – proctocolectomy (the removal of the colon & rectum, this would then require a permanent ileostomy)
Symptom control:
Anti diarrhoea meds
Pain relief (**no NSAIDs** - can cause flare up and increase ulcers)
Nutritional supplements
Specific diet (no nuts/seeds/fibre things that are difficult to digest. High fat/spicy foods/dairy to avoid)
35
How many people in the UK live with ulcerative colitis or Crohn's disease?
500,000
36
Is ulcerative colitis a young or old onset disease?
Generally, a young onset disease
37
What is pancreatitis and how is it categorised?
Inflammation of the pancreas for any reason. It can be categorised as;
Acute
Chronic
Hereditary
Calcifying
Necrotising
Haemorrhagic
**Not mutually exclusive, overlap is common**
Bile/pancreatic duct are closed/narrowied, pancreatic enzymes build up and cause damage
38
What are the causes and risk factors for acute pancreatitis?
I GET SMASHED
Idiopathic
Gall stones (number one cause for acute)
Ethanol (number one for chronic, two for acute)
Trauma
Steroids
Mumps/Malignancy
Autoimmune
Scorpion stings
Hypercholesteremia/hypercalcemia
ERCP
Drugs
39
Why can pregnancy cause gallstones and pancreatitis?
Gallstones leading to pancreatitis can be common in pregnancy due to weight gain and hormonal changes - internal organs also getting compressed
40
How does ethanol (alcohol) cause pancreatitis?
Exact mechanism not known. However it is known that alcohol stimulates pancreatic secretions and may also induce oedema and spasm of the pancreatic sphincter around the end of the duct.
This leads to high intraductal pressure which causes duct necrosis and escape of pancreatic enzymes into the tissue. The enzymes cause widespread damage and therefore inflammation to the pancreas.
41
What is the epidiemiology for acute and chronic pancreatitis?
**Acute**
Gall stones approx. 50% of cases
Chronic alcohol consumption approx. 25%
Other factors account for the remaining 25%
**Chronic**
Chronic alcohol consumption approx. 70-80%
The male to female ratio is 7:1
average age of onset is between 36 and 55 years
Significant increase in risk in pancreatic CA
42
What are the symptoms of acute pancreatitis?
Sudden severe epigastric pain
Post prandial pain
Pain increases over time – radiates across back
Nausea/vomiting
Indigestion
Pyrexia of 38°c or more
Jaundice in sclera/skin
Abdo tenderness on palpation
Tachycardia/tachypnoea
43
What treatment is given for acute pancreatitis?
Treatment is supportive in nature, patients usually feel better after 48hrs with treament:
Analgesia
Fluids
Treatment for an infection (can cause necrosis and sepsis)
Treatment of cause if possible (gall stones, toxins etc.)
Lifestyle advice
Worsening care advice on discharge
44
What are the symptoms of chronic pancreatitis?
Same as acute symptoms, especially during flare ups, however usually more gradual and/or intermittent
Other symptoms will develop as the damage to the pancreas progresses and ther is more difficulty breaking down fats & some proteins:
Weight loss
Loss of appetite
Jaundice
Diabetes
Grey turners sign and Cullen's sign (can be caused by severe acute necrotizing pancreatitis, but really the research has shown it is non-specific and may be present with almost any condition causing intra-abdominal or retroperitoneal bleeding - present in about 1% of pancreatitis cases)
45
What is the treatment for chronic pancreatitis?
Supportive in nature:
Analgesia
Fluids
Lifestyle advice
Long term steroids
Enzyme supplements
Endoscopic surgery (Endoscopic Retrograde Cholangio pancreas tography (ERCP), may remove gallstones or debris blocking the duct, drainage of any area of strictures, drainage of any cysts that may have formed.)
Pancreas resection/Total pancreatectomy (drastic measure usually only done for CA and in trauma, long term consequences)
46
What is liver cirrhosis?
Cirrhosis is a disorder in which the liver demonstrates extensive diffuse fibrosis and loss of lobular organization.
The liver can regenerate itself however if the liver is being damaged faster than it can replace itself then damaged tissue is just replaced with fibrous scar tissue, this degeneration is cirrhosis.
47
How does liver cirrhosis affect the size of the liver and what can it lead to?
Initially the liver is enlarged but it becomes small and shrunken as fibrosis occurs.
Leads to portal hypertension and end stage liver disease
If the primary cause is removed further damage may still occur because fibrosis interferes with the blood supply to the liver tissues.
48
What is the most common cause of liver cirrhosis?
Alcoholic liver disease
49
How can liver disease or cirrhosis lead to nervous sytem dysfunction?
Liver dysfunction and collateral vein formation can cause altered blood chemistry and the build up of excessive ammonia (which can cross the BBB) or other toxic substances. These travel around the central circulation and can affect the central nervous system and brain leading to hepatic encephalopathy.
50
How does liver cirrhosis affect its cell function?
Decreased removal and conjugation of bilirubin
Decreased production of bile
Decreased removal of toxins such as drugs
Decreased production of blood clotting factors and plasma proteins
Impaired digestion and absorption of nutrients particularly fats
51
How can liver cirrhosis affect its blood and bile flow function?
**Reduction in the amount of bile entering intestine**
–digestion and absorption impairment.
**Back up of bile in liver**
-elevated bilirubin levels in the blood causes jaundice.
**Congestion of bile in the spleen**
-leading to Splenomegaly
**Blockage of blood to the liver**
-leading to portal hypertension
**Development of ascites and oesophageal varices**
-Portal hypertension causes an increase in the pressure of blood in the gastric veins which can lead to the formation of oesophageal varices which can haemorrhage and be life threatening.
52
How does alcohol intake lead to end stage cirrhosis and cancer?
1) **Fatty Liver** – Accumulation of fat in the liver cells. Other than enlargement of the liver (hepatomegaly) this stage is asymptomatic and can be reversible if alcohol intake is reduced.
2) **Alcoholic Hepatitis** – Inflammation and necrosis occur and fibrous tissue forms which is irreversible. This may be asymptomatic or manifest with mild symtoms such as anorexia, nausea and liver tenderness.
3) **End stage cirrhosis** – When fibrous tissue replaces so much of the normal liver tissue that the basic structure of the liver is significantly altered and little function remains. Cancer can develop
53
What causes portal hypertension?
Resistance before, within or after the liver. Most commonly within - by cirrhosis or schistosomiasis (parasitic flatworm infection. But also portal vien thrombosis or a tumour causing compression.
54
What are the most common causes of liver cirrhosis?
Alcohol abuse
Chronic Viral Hepatitis (HCV)
Fatty liver
55
What are the signs and symptoms of portal hypertension?
Enlarged liver and spleen.
Enlarged veins (varices) of the esophagus and stomach and formation ofcollateral vessels (these can cause abnormal bleeding - can be life threatening)
Internal hemorrhoids.
Weight loss from malnutrition.
Fluid buildup in the belly (ascites)
Kidney malfunction.
Low platelets.
Fluid on the lungs.
56
What treatment is given for liver cirrhosis and portal hypertension?
Supportive in nature to allow liver repair/regeneration:
Prevention and management of varices and bleeding
Medication
Livestyle changes
Surgery (Portosystemic shunting, liver transplant)
57
How does portal hypertension lead to ascites?
Portal hypertension increases the hydrostatic pressure in the veins and lymphatics causing a fluid shift into the abdominal cavity.
The increase in aldosterone levels in the blood serum result in increased sodium ion and water in the extracellular compartment
58
What complications can follow ascites?
Upward pressure on the diaphragm which can impair respiration.
Increased risk of peritonitis
Impaired digestion and absorption
59
How does portal hypertension cause oesophageal varices?
Portal hypertension causes the veins at the junction between the portal and systemic venus systems to become distended and distorted causing what we call varices.
60
Where do oesophageal and GI varices form?
Varices tend to be in the distal oesophagus and/or the proximal stomach but isolated varices may be found in the distal stomach, large and small intestine.
61
How can varices haemorrhage and what are the risk factors for it?
Varices can very easily haemorrhage even just by food passing down the oesophagus, other risk factors include infections, NSAID’S, Excessive alcohol intake, smoking (all risk factors for portal htn too). Bleeding is characteristically severe and may be life-threatening.
Majority of patients with variceal bleeding have chronic liver disease.
62
What determines the size of oesophageal/GI varices?
The size of the varices and their tendency to bleed are directly related to the portal pressure, which is usually directly related to the severity of underlying liver disease.
63
What are the signs and symptoms of oesophageal varices?
**Symptoms**
Haematemesis (most commonly), melaena
Abdominal pain
Features of liver disease and specific underlying condition
Dysphagia/odynophagia (pain on swallowing; uncommon)
Confusion secondary to encephalopathy (even coma)
**Signs**
Peripherally shut down
Pallor
Hypotension and tachycardia (i.e. shock)
Reduced urine output
Melaena
Signs of chronic liver disease
Reduced Glasgow Coma Scale
Signs of sepsis may also commonly be present
64
How does infection affect oesophageal varices?
Infection occurs in up to 50% of patients and is associated with a worse outcome. It is thought that bacteria release endotoxins that enhance portal pressure and impair coagulation
65
What is the diagnosis and treatment process for oesophageal varices?
**Urgently requires endoscopy and surgery (band litigation) and Vasopressin drugs as well as prophylactic antibiotics.**
All patients with newly diagnosed cirrhosis should have screening endoscopy, looking for oesophageal varices.
Presence of moderate or large varices requires beta-blockers in the first instance (indefinite treatment).
If there are contra-indications to beta-blockers, the varices should be banded or sclerosed.
In the long term, repeated endoscopic screening is usually required - e.g. every 2-3 years in cases of small varices.
Patients who have survived an oesophageal variceal bleed should receive beta-blockers, ± nitrates and endoscopic screening and treatment.
66
What are peptic ulcers?
A Peptic ulcer is an erosion in a segment of the gastrointestinal mucosa called the muscularis mucosa, typically in the stomach (gastric ulcer) or the first few centimeters of the duodenum (duodenal ulcer), Ulcers may range in size from several millimeters to several centimeters.
67
What causes pain and haemorrhaging of peptic ulcers?
Irritants such as bacteria (specifically h.pylori), stomach acid or NSAIDs can cause wounds which may progress deeper and form ulcers.
Inflammatory mediators released to aid tissue repair can cause pain in the area.
Consistent irritation by medications or irritating foods can aggravate the condition and lead to perforation or hemorrhage.
The presence of perforation may lead to peritonitis and may become life-threatening because of sepsis and profuse bleeding.
Haematemesis or melaena are associated with erosion of a large blood vessel and significant haemorrhage.
**Urgent admission to hospital is required.**
68
What are the most common sites for peptic ulcers?
Stomach and Duodenum
69
What are the causes of peptic ulcers?
Irritants such as bacteria specifically h.pylori, stomach acid or nsaids can cause wounds which may progress deeper and form ulcers.
-H. pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) disrupt normal mucosal defense and repair, making the mucosa more susceptible to acid.
Other causes include:
Smoking (Smoking also impairs ulcer healing and increases the incidence of recurrence)
Alcohol
Steroids
Stress
Changes in gastric mucin consistency (may be genetically determined).
Acid producing tumours
70
What are the symptoms of peptic ulcers?
Burning/gnawing central abdo pain
Indigestions
Black/tarry stools
Heartburn
Loss of appetite
Nausea/vomiting (w/ haemetemesis)
Bloating
Weight loss
Some people also find they burp or become bloated after eating fatty foods.
**Nearly 75 percent of people who have gastric or duodenal ulcers don’t have any symptoms**
71
What is the treatment for peptic ulcers?
Anti-biotics - treat for H. Pylori
Medication for acid suppression (Clarithromycin, Omeprazole, Ranitidine)
Avoid NSAIDs
Stop smoking/alcohol
72
How is peptic ulcer disease diagnosed?
Endoscopy and testing for H.pylori
73
What is coeliac disease?
Coeliac disease is a chronic autoimmune disorder where the ingestion of gluten triggers an immune response in the small intestine. This response damages the intestinal lining, leading to malabsorption of nutrients.
74
What is the pathophysiology of coeliac disease?
It is an auto immune condition where the immune system mistakenly attacks healthy cells in response to the presence of “gliadin” which is a protein found in gluten.
Gliadin is an amino acid, the body does not break it down as it normally would, it tries to but can’t and breaks it into chains of ‘peptides’.
As soon as the immune system sees these peptides crossing the cell membrane it tries to kill them. The antibodies are trying to kill these short chains of peptides and the villi are damaged in the process.
This constant process damages a large proportion of the intestinal villi.
75
What is the difference between coeliac disease and gluten intolerance?
When a celiac person ingests gluten, his or her immune system will attack against its own body's tissue. Whereas, if a person is gluten intolerant, the consumption of gluten will cause short-term bloating and belly pain. Unlike celiac disease, gluten intolerance doesn't usually cause long-term harm to the body.
76
What are the causes of coeliac disease?
Genetic Predisposition
Environmental Triggers such as viral infections, stress, or surgery, can activate the disease in genetically predisposed individuals.
77
What are the GI and non-GI symptoms of coeliac disease?
**GI Symptoms;**
Diarrhoea
Bloating
Constipation
Vomiting
Abdominal pain
Lactose intolerance
**Non-digestive symptoms;**
Fatigue
Weight loss
Anaemia
Aphthous ulcers
Irregular periods
Dermatitis herpetiformis (Itchy Rash)
Fertility issues
Joint pain
Oesto problems #
Peripheral neuropathy
Gluten ataxia
78
How is coeliac disease diagnosed?
Celiac Disease is diagnosed through blood tests, genetic tests, and endoscopy.
Positive results often lead to endoscopy.
79
What is the treatment for coeliac disease?
As yet the only effective treatment for Coeliac Disease is a strict gluten-free diet. - Villi can recover.
Regular healthcare follow up
Emotional and social support
80
What is appendicitis?
Infammation of the mucus lining of the appendix
81
What is the pathophysiology of appendicitis?
Obstruction of the appendiceal lumen
Fluid builds up inside the appendix and micro-organisms proliferate
Appendiceal wall becomes inflamed and purulent exudate forms
Increased congestion and pressure leads to ischaemia and necrosis of the wall which causes it to become more permeable
Increased permeability allows toxins and bacteria to escape into the surrounding area
The increasing pressure may cause rupture or perforation
Localised infection or peritonitis may result
82
What is peritonitis?
Inflammation of the peritoneal membrane
83
What causes peritonitis?
84
How does peritonitis cause symtpoms and complications?
85
What is hepatitis?
Inflammation of the liver
86
What causes hepatitis?
Infection (Hep B, C etc.)
Toxins (Toxic hepatitis)
Autoimmune disease
**Cell injury results in inflammation and necrosis of the liver**
87
Is hepatitis an acute or chronic condition?
Can be both
88
What are the symptoms of hepatitis?
Pain or bloating in the belly area.
Dark urine and pale or clay-colored stools.
Fatigue.
Low grade fever.
Itching.
Jaundice (yellowing of the skin or eyes)
Loss of appetite.
Weight loss
Nausea and vomiting.
89
What are the differences between hepatitis A, B &C?
**A:**
Acute rather than chronic
No carrier or chronic state
Vaccine availible
Oral-faecal transmission
No cure
**B:**
Acute or chronic
May be asymptomatic
May exist in a carrier state
Transmission through carrier state
Transmission through bodily fluids
Vaccine availible
Deaths can occur from the associated cirrhosis and cancer (increase chance of hepatocellular cancer)
No cure
**C:**
Acute or chronic
Blood to blood transmission
May exist in a carrier state
Treatable with medication (Cures approx. 90% of cases)
Deaths can occur from the associated cirrhosis and cancer (increase chance of hepatocellular cancer)
90
What is gastritis?
General term for acute or chronic conditions which cause inflammation of the stomach lining leading to mild transient irritation up to severe ulcerative or haemorrhagic episodes. It is usually self limiting with complete regeneration of the gastric mucosa
91
What can cause gastritis?
Causes of gastritis include:
-infection with a bacteria called helicobacter pylori (H. pylori)
-taking anti-inflammatory painkillers (such as ibuprofen) and aspirin
-drinking too much alcohol
-being very stressed and unwell, such as after surgery
Gastritis can also be caused by a problem with the immune system where it attacks the lining of the stomach.
92
What complications can arise from gastritis?
Dehydration
Electrolyte disturbances
Peptic ulcer disease
Immune thrombocytopenia (ITP)
Iron-deficiency anemia
Vitamin B12 deficiency
93
What are the symptoms of gatritis?
Gnawing or burning ache or pain (indigestion) in your upper abdomen that may become either worse or better with eating
Nausea
Vomiting
A feeling of fullness in your upper abdomen after eating
94
What is the treatment for gastritis?
Antibiotics (If caused by H. Pylori)
Proton pump inhibitors (Reduce acid production)
Histamine (H2) blockers (Reduce acid secretion)
Antacids
Lifestyle changes
95
What is gastroenteritis?
Inflammation of the stomach lining AND intestinal lining, usually caused by infection or allergies
96
What are the symptoms of gastrienteritis?
Gastritis symptoms plus diarrohea rather than just vomiting
97
What are the common pathogens that cause gastroenteritis and their sources?
98
What is the treatment for gastroenteritis?
Usually no direct treatment as it is usually self limiting but can include:
Cease any cause
Prevent dehydration
99
What controls the vomiting response?
The vomiting centre in the brainstem, triggered by muscarinic receptors
100
What and where is the CTZ, and what is its role in the vomiting response?
The Chemoreceptor Trigger Zone (CTZ) is located in the brainstem but outside the **blood brain barrier**. It has dopamine 2 and 5-HT (serotonin) receptors and is also sensitive to cytotoxic agents. It signals the vomiting centre.
101
Where does motion sickness stem from?
The labrynth of the inner ear, specifically the vestibules.
102
How does the motion sickness response happen?
Signals from the vestibule are sent to the vestibular nuclei in the brainstem via the vestibuo cochlear nerve (VIII). The vestibular nuceli contains H1 and muscarinic receptors and when stimulated sends signals to the CTZ which in turn activates the vomiting centre.
103
What stimuli can trigger the vomiting centre via the higher brain centre?
Severe pain
Repulsive smells and sights
Strong emotions
104
How is the stomach involved in the vomiting reflex?
Enterochromafin cells release serotonin in response to cytotoxic agents. This triggers the 5-HT3 receptors of the vagal nerve and then triggers the vomiting centre
105
How does the vomiting centre produce the vomiting reflex?
Lower oesophageal sphincter relaxation
Contraction of diaphragm and abdominal muscles
Tachycardia
Increased salvation
Increased peristalsis
Epiglotttis closing
106
Where is the vomiting centre found?
The medulla oblongata in the brainstem
107
How do antihistamines help relieve nausea and vomiting?
They block the H1 receptors of the vestibular nuclei
Good for motion and morning sickness, can result in drowsiness/sedation
108
What is ondansetron and how does it relieve nausea and vomiting?
It is a **5-HT (Serotonin) receptor antagonist** which blocks the **5-HT receptors on the CTZ**. They also work on the **5-HT3 receptors around the stomach** to reduce nausea and vomiting.
5-HT receptor antagonists are effective anti-emetics for **chemo/radio-therapy patients** and **post surgery patients**, also used for pregnancy induced nausea **after the first trimester**. Side effects include headaches and stomachaches
109
What are the 3 classes of Dopamine-2 receptor antagonists and their effects?
1) Antipsychotics (end in -azine) - block D-2 (mainly) and histamine and muscarine. Effective for chemo/radio-therapy patients. Side effects include sedation, hypotension and extra-pyramidal effects
2) Metaclopromide, block D-2 and stimulate GI activity. Effective for chemo/radio-therapy patients. And reflux/hepato-biliary disorder patients. Side effects include stomach upset fatigue and extra-pyramidal effects
3)Droperidol, blocks D-2 and also used to treat schitzophrenia. Effective for acute chemo-induced nausea.
The CTZ has D-2 receptors, inhibiting these will help prevent nausea and vomiting
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What is hyoscine and what is it used for in relation to GI syptoms?
A muscarinic receptor antagonist used to treat abdominal spasms and pain and nausea/vomiting.
Effective as a prophylactic and for motion sickness. Can cause normal anti-cholinergenic side effects (dry mouth, blurry vision, drowsiness etc.)
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What extra-pyramidal side effects can antipsychotic drugs used to treat emesis have?
Akasthesia
Tardive dyskinesia
Spasmodic turticollis
Occulogyric crisis
Increased prolactin release:
- Galacticurrhoea
- Menstural problems
- Lactation
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What are PPIs and what do they do?
Proton Pump Inhibitors (PPIs), ending in **-prazole**, are a class of pro-drugs activated by stomach acid used to treat conditions such as acid reflux, heart burn and oesophagitis and prevention and treatment of peptic ulcers. They reduce the amount of excess acid produced by the stomach.
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How are PPIs usually administered?
Orally, however they can be administered IV to treat bleeding from peptic ulcers
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What are some examples of common PPIs?
Omeprazole
Pantoprazole
Lansoprazole
Dexlansoprazole
Rabeprazole
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How do the parietal cells of the stomach work?
When stimulated by gastrin, histamine or acytlecholine they move hydrogen into the stomach and potassium back into the parietal cell via a proton pump. The hydrogen binds with chlorine to form hydrochloric acid
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What is the mode of action of PPIs?
They bind to the proton pumps of the parietal stomach cells, reducing the amount of hydrogen released thereby reducing the amount of acid produced in the stomach. Reducing symptoms of acid reflux and heartburn and allowing better healing of gastric ulcers and oesophagitis
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How long do PPIs take to reach peak effect, and how long does that effect last?
They take 2-3 days to reach peak effect
Each dose lasts approximately 1-2 days
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How are doses of PPIs ceased?
They must be reduced gradually to prevent the rebound effect (sudden re-increase of acid)
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What are the short term side effects of PPIs?
Headache
Diarrhea
Abdominal pain
Nausea
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What are the long term side effects of PPIs?
Increased risk of infection (Decreased acid causes decreased immune function)
- C. Diff
-Pneumonia
Increased risk of deficiencies (Decreased acid causes decreased absorption)
- Vitamin B12
- Magnesium
- Iron
- Calcium (Osteoporosis/fractures)
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What are basic symptoms of excess stomach acid?
Heartburn, stomach pain and indegestion
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How do antacids work?
They neutralise the acid via a chemical action, providing short term relief from symptoms of excess stomach acid
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What suffixes do antacids commonly have?
-carbonate or -hydroxide
124
What is GERD?
Gastroesophageal reflux disease (GERD) occurs when stomach acid repeatedly flows back into the tube connecting your mouth and stomach (esophagus). This backwash (acid reflux) can irritate the lining of your esophagus.
Many people experience acid reflux from time to time. However, when acid reflux happens repeatedly over time, it can cause GERD.
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What are the symtpoms of GERD?
Common signs and symptoms of GERD include:
-A burning sensation in your chest (heartburn), usually after eating, which might be worse at night or while lying down
-Backwash (regurgitation) of food or sour liquid
-Upper abdominal or chest pain
-Trouble swallowing (dysphagia)
-Sensation of a lump in your throat
If you have nighttime acid reflux, you might also experience:
-An ongoing cough
-Inflammation of the vocal cords (laryngitis)
-New or worsening asthma
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What are common side effects of antacids?
**Calcium and aluminium** containing antacids can cause **constipation**
**Magnesium** containing antacids can cause **general GI upset** as well as **diarrhea**
127
What are the different types of laxative?
Stool softeners
Bulk forming
Stimulant
Osmotic
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What is CVS?
Cyclic vomiting syndrome is persistent and repeated episodes of severe vomiting lasting anywhere from hours to days
129
What are the symptoms of CVS?
Fatigue
Loss of appetite
Abdominal pain
Diarrhoea
Dizziness
Headaches
Photophobia
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What causes CVS?
It is not known currently. But migraines can be risk factors
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How can CVS be managed at home?
Anti sickness medication
Pain relief medication
Identifying and avoiding triggers such as certain foods, stress, lack of sleep, caffeine or alcohol
Getting lots of rest and sleep in a quiet dark room
Taking sips of water or diluted juice during and after episodes
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What are the possible serious complications of CVS?
Severe dehydration
Oesophageal tears
Esophagitis
Tooth decay
