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MPharm 2 - PH2113 > PH2113 - GI 2 > Flashcards

PH2113 - GI 2 Flashcards

1
Q

What is the function of the liver?

A
  1. Central to maintenance of homeostasis.
  2. Storage, Clearance, Filtration, Secretion, Excretion, Synthesis, Metabolism, Homeostasis.
  3. detoxification of:
    - endogenous and exogenous substances
    - cellular debris and invading bacteria (Immune system),
    - Removal of bilirubin (break down of RBC)
    - Hormone deactivation
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2
Q

What are the classifications of liver disease?

A

Acute:
-less than 6 months
-Often resolves spontaneously, self limiting ( ultimately resolving itself without treatment.)
-Rapid decline in liver function
-May be asymptomatic
100% association with encephalopathy (means disorder or disease of the brain) and coagulopathy
Can result in acute liver failure (ALF)

Chronic:
-Over six months duration
-Often symptomatic
-Secondary to long-standing cell damage
-Permanent structural change
-Loss of normal liver architecture
-Cirrhosis (Fibrous scars
Divides the liver into nodules)
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3
Q

Causes of liver disease:

A
  1. Viral infection:
    - Hep A-/E- transmission through fecal infection/ contamination of food and water.
    - Hep B/C- Blood to blood needle contamination
    - Hep D- have to have Hep B to get it.
  2. Alcohol:
    - most common cause in western world.
    - will lead to cirrhosis (fibrous tissue in the liver), which increases resistance to blood flow from the Hepatic portal vein resulting in portal hypertension (PHT)
    - Liver cells die = liver failure
    - Rate of progression (and regression) linked to further alcohol consumption
  3. obesity, diabetes and metabolic syndrome causes:
    - Non-alcoholic steatohepatitis- alcoholic liver disease symptoms, but occurs in people who drink little or no alcohol
    - Non-alcoholic fatty liver disease- build-up of fat in the liver. It’s usually seen in people who are overweight or obese.
  4. Cholestasis (reduction or stoppage of bile flow.) :
    Intra-hepatic
    Extra-hepatic
  5. Immune disorders
  6. Vascular abnormalities
  7. Metabolic disorders
  8. Genetic disorders
9. Drugs: 2 types:
Type A:
-Related to the dose of the drug
-Withdrawal of precipitating drug results in reversal
e.g. paracetamol (NAPQI)
Type B:
- related to the property of the drug.
- To do with hypersensitivty or how its metabolised
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4
Q

What are some signs of drug induced liver disease?

A

Signs and symptoms similar to other causes of liver disease
History of exposure is best marker
Onset can be acute
Fever, chills, rash, pruritis, abdominal pain, n+v
Overt symptoms may develop over time

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5
Q

What are the risks of drug induced liver disease?

A 
Race
Age
Gender
Alcohol consumption
Pre-existing liver disease
Genetics
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6
Q

How is drug induced liver disease managed?

A 
Withdraw causative agent
Inform patient
Avoid future exposure
Acute patients
Avoid physical exertion, alcohol, paracetamol and hepatotoxic agents
Supportive management
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7
Q

What is paracetamol overdose?

A
  • Rapid deterioration in liver function in a previously healthy individual
  • Complicated to manage because:
    CNS, CV and renal systems affected
    Infection and bleeding can be life threatening
    -20-30 tablets consumed within 24hours can result in severe hepatocellular necrosis
    Saturation of glutathione dependent pathway
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8
Q

What are the stages in paracetamol toxcity?

A

> 1 hour- activated charcoal is used to treat since it absorbs the paracetamol- no harmfull effects.

2-24hrs - asymptomatic or non-specific signs.
8 Hours- N acetylcysteine- effective

24-48hrs - RUQ pain, jaundice, deranged bloods.
>72hrs - jaundice, somnolence, liver failure
Results in
Cerebral oedema
Shock
Sepsis
Renal failure

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9
Q

What are the non specific symptoms of liver disease?

A
  • Weakness, fatigue, general malaise
  • Chronic - weight loss, anorexia
  • Advanced - loss of muscle bulk
  • Abdominal discomfort/pain
  • Jaundice- yellowing of the skin
  • Increase in the size of the liver
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10
Q

What are some cutaneous signs of liver disease?

A

Hyperpigmentation
Scratch marks
Spider naevi

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11
Q

What are some abdominal signs of liver disease?

A
  1. Distension- enlargement/ballooning effect of the liver
  2. Hepatomegaly (abnormal enlargement of the liver.)
  3. Splenomegaly (abnormal enlargement of the spleen.)
  4. Umbilical and paraumbilical veins- increase in venous pressure, because volume of blood moving through the veins changes.
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12
Q

What are signs of liver disease?

A
  • Jaundice- yellowing of skin
  • Pruritus: itchy skin because of the deposition of bile salts.
  • Portal hypertension: Increase in BP in veins.
  • Ascites- Swelling of the abdominal cavity die to fluid.
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13
Q

What is jaundice and how can it be treated?

A
  • Sign of liver disease but non specific to liver disease.
  • Yellowing of sclerae, skin
  • Hepatocellular
  • Cholestatic (bile cannot flow from the liver to the duodenum)
  • Prehepatic (Increased blood breakdown)
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14
Q

What is pruritus and how can it be treated?

A
  • Itchy skin because of deposition of bile salts in the skin.
  • Most debilitating in cholestatic conditions- Obstruction relieved by endoscopy, radiology, surgery

Treatment (several treatments):

  1. Anion exchange resins e.g. cholestyramine, colestipol
    - Bind bile acids and prevent reabsorption
    - helps body remove bile acids which can lower cholesterol levels in the blood.
    - Side effects : GI (constipation, diarrhoea, flatulence), fat and vitamin malabsorption
    - Poor adherence due to palatability

Counselling patients on taking drug
Take interacting drugs 1hr before or 4hrs after cholestyramine
Benefits may take up to one week to become apparent

  1. Antihistamines
    - Sedating properties useful if pruritus affects sleep
  2. Ursodeoxycholic acid
  3. Topical therapies: Calamine lotion, menthol 2% in aqueous cream
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15
Q

What is portal hypertension?

A
  • increase in the blood pressure of veins leading to:
  • collateral vein formation (re-routing of blood circulation around a blocked vein).
  • shunting of blood to systemic circulation

Contributes to:

  • Formation of ascites (accumulation of fluid in the peritoneal cavity, causing abdominal swelling).
  • Development of encephalopathy (disorder of the brain).
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16
Q

What is Ascites?

A 
Accumulation of fluid within the abdominal cavity
Caused by:
Central hypovolaemia
Reduced serum albumin
PHT and splanchic artery vasodilation
17
Q

How can ascites be treated?

A

Simple measures include:
1. Reduce sodium intake
2. Fluid restriction
Moderate to severe ascites requires diuresis or paracentisis

  • Diuretics: Spironolactone:
    1. Blocks sodium reabsorption in kidney tubules
    2. Dose range 50-400mg daily
    3. Titrate slowly
    4. Side effects : gynaecomastia, hyperkalaemia
  • Paracentsis:
    1. procedure to take out fluid that has collected in the belly.
    2. Combined with albumin administration
    3. Does not affect mechanisms responsible for fluid accumulation
    4. Repeated every 2-4 weeks in outpatient setting
18
Q

What is encephalopy

A
  • Can be caused by PHT
  • It is a reversible disorder of the brain
  • Lack of awareness, altered mental state, disorientation, coma
  • Ammonia levels heavily implicated
19
Q

How can encephalopy be treated?

A

Lactulose:

  • Acidifies colonic contents, leading to ionisation of nitrogenous products and therefore reduction in absorption.
  • 30-40ml/day titrated to achieve 2-3 soft stools per day
  • Side effects : bloating, diarrhoea

Antibiotics:
-Metronidazole reduces ammonia production by GI bacteria

20
Q

how is clotting abnormality treated?

A

Phytomenadione IV/ Vitamin K
10mg daily for 3 days
Oral not as effective as IV, therefore not used

Not effective in patients with significant disease

Also avoid NSAIDs, aspirin and anticoagulants, since the contribute to bleeding

21
Q

What is varices?

A
  • Portal hypertension (an increase in the pressure within the portal vein) is a consequence of bleeding varices
  • Dilated blood vessels
  • Bleeding may be a gentle ooze in which case anaemia is the most common symptom.
  • Active angiogenesis (the development of new blood vessels.)
22
Q

How can varices be treated?

A

Initial treatment
1. Stop immediate bleeding:
Terlipressin (vasopressin analogue)
Systemic vasoconstrictor, infused for 2-5 days

  1. Treat hypovolaemic shock
  2. Aim to prevent recurrent bleeding:
    Band ligation
    Long term non-selective β-blockers e.g. propranolol
    PHT by splanchic vasoconstriction and portal blood flow
23
Q

What are some common symptoms of dyspepsia?

A

heartburn
acid regurgitation
excessive burping/belching, abdominal bloating
nausea
feeling of abnormal or slow digestion or early satiety

24
Q

What are the 8 factors that constitute a risk for GI complications

A
  1. 65 years or over.
  2. history of peptic ulcers, gastrointestinal bleeding.
  3. serious comorbidity
  4. heavy smoking or alcohol use
  5. The particular NSAID used (see exercise)
  6. use of NSAID at maximum daily dose
  7. prolonged NSAID use
  8. concurrent use of drugs that increase the likelihood of upper GI adverse effects (e.g. anticoagulants, aspirin [including low-dose], clopidogrel, corticosteroids, SSRIs, venlafaxine, duloxetine).
25
Q

What are the 2 differences in the 2 types of COX enzymes (Cyclo-oxygenase)?

A
  • cox1: constantly present, responsible for prostaglandin production. E.g Ibuprofen and naproxen
  • Aspirin had the most antithrombotic effect (reduces the formation of blood clots) of all NSAIDs, as it irreversibly inhibits COX-1 in platelets.
  • COX-2 induces inflammatory stimuli, tissue damage or malignancy. E.G Rofecoxib
  • COX-2 selective NSAIDs are associated with a lower incidence of serious upper GI events
  • Thought that COX-2 would non selective NSAIDS (ibuprofen)- but research showed link to cardiovascular safety.

NSAIDS vary in how selective they are for the COX1 and COX2 pathways, so there selectivity can be used to classify them in to non selective (works for cox1 and 2) partially selective and cox-2 selective

26
Q

How are COX1 and COX2 enzymes stimulated/produced?

A
  • Arachidonic acid is precursor for COX1/2.
  • Psychological stimuli= cox1
  • inflammatory stimuli= cox2
27
Q

What are some strategies elderly people can try to prevent GI injury

A

As an alternative to treatment with an NSAID, in older patients it may be useful to first try:
weight reduction
warmth
exercise
use of a walking stick
switching to a simple analgesic, e.g. paracetamol

28
Q

What are nice guidelines for diagnosed peptic ulcers?

A
  • Do not use NSAIDS,
  • Not always possible e.g for patients with rheumatic disease, since dependent on NSAIDS doe pain relief so PPI should also be given for 2 months.

-Patients who are receiving long-term therapy with aspirin and have a history of PUD should also be tested for H.pylori infection and treated if positive

29
Q

What are the 3 types of stimuli by which gastric acid would be secreted by the parietal cells?

A
  1. histamine is the most significant contribution and stimulates H2 histamine receptors.
  2. Acetylcholine from parasympathetic activity via the vagus nerve and enteric nervous system stimulates M3 receptors.
  3. gastrin, released from G cells in the gastric epithelium via vagal stimulation, primarily induces acid secretion indirectly by increasing histamine synthesis in enterochromaffin-like (ECL) cells. ECL cells are located in the gastric glands, close to parietal cells, and release of histamine from them stimulates H2 receptors of the parietal cells.
    - Gastric acid release is inhibited by somatostatin released from the D cells
30
Q

What is misoprostol?

A
  • Synthetic prostaglandin E1 analogue licensed for the prevention of NSAID-associated ulceration.
  • acts on the parietal cells to reduce gastric acid output by decreasing levels of intracellular cyclic AMP, which in turn reduces the activity of the proton pump at the apical surface of the proton pump.
  • only clinically effective at high doses to reduce gastric acid secretion.
31
Q

What is Gastro-oesophageal reflux disease?

A
  • Digestive disorder that affects the lower esophageal sphincter.
  • reflux of stomach contents causes troublesome symptoms

Subdivided into:
1. Reflux oesophagitis - patients usually have typical reflux symptoms that respond well to acid suppression and show healing of mucosal erosions.

Endoscopy-negative reflux disease (ENRD) shows no evidence of injury to the mucosa. This should not necessarily be viewed as a mild disease such patients often have severe and atypical symptoms, and an incomplete response to acid-suppressing drugs

32
Q

Gastro-oesophageal reflux disease symptoms:

A

Typical: Heartburn (burning feeling rising from the stomach or lower chest towards the neck.) acid regurgitation

Atypical: Dysphagia (feeling of obstructed swallowing), odynophagia (Pain in the oesophagus on swallowing), water brash (a sudden flow of saliva associated with indigestion), globus sensation, non-cardiac chest pain, dyspepsia or abdominal pain

Extra-oesophageal symptoms- Hoarseness or sore throat, or both; sinusitis; otitis media; chronic cough; laryngitis or polyps on the vocal cords, or both; dental erosions; non-atopic asthma; recurrent aspiration or pulmonary fibrosis, or both

-Malignancy: Oesophageal adenocarcinoma, head and neck cancer.

33
Q

risk factors of GORD

A

Genetic factors possibly contribute 18-31% to the cause of GORD, with evidence that reflux symptoms cluster within families.

-Lifestyle: Inappropriate relaxation of the lower oesophageal sphincter. Obesity can disrupt this sphincter. other lifestyle factors: over-eating, poor posture, tight-fitting clothing and pregnancy.

Environmental:

  • lower incidence of GORD in patients who are H. pylori-positive
  • H. pylori might protect against the disease.
34
Q

what is the pathophysiology (physiological processes) of GORD?

A

Clearing mechanisms:
-Sphincter relaxes in response to oesophageal peristalsis to allow the passage of food, liquid, or saliva into the stomach.

Tissue resistance:
-The stratified squamous cells of the oesophageal mucosa = resistance to swallowed irritants and to an acidic environment due to their ability to produce mucus and bicarbonate. Reflux normally will cause a greatly increased cell production rate (hyperplasia) to counteract the erosion.

Gastric and duodenal contents:
pesin (enzyme breakdowns of protein) action increased at low PH, forms corrzive mix with gastic acid in deudoenal. reflux of duodenal contents goes into the stomach, which can lead to a reflux into the oesophagus. results in bile and other enzymes being forced into contact with the oesophageal mucosa and this will cause damage.

35
Q

What are some questions to ask the patient if there symptoms are similar to GORD?

A
  • Where is the pain?
  • When is the pain most frequent?
  • Does it change when you lie down or bend over?- BENDING WILL MAKE IT WORSE
  • How do you feel after meals?- if more discomfort after meals- gord
  • Do you ever wake up with the symptoms?
  • Do you have any chest pain, cough or hoarseness?
  • Have you noticed a change in your voice pitch?
  • Do you ever have a bitter taste in your mouth?- due to acid reflux
  • Do you ever have food flowing back into your mouth?
  • How do citrus fruit juices, alcohol, coffee, chocolate, fatty foods or very spicy foods affect your heartburn?
  • What medicines are you taking?
36
Q

OTC treatment for dyspesia: Antacids

A 
Active Ingredients
Aluminium salts,
Magnesium salts,
Bismuth Salts,
Calcium salts,
OTC brands
- gaviscon advance
Rennie,
Tums,
Pepto-Bismol

-Mechanism of Action
Direct neutralising action on stomach acid.

Counselling points
QDS after meals and at bed. Leave 2 hour gap between other meds.

MPharm 2 - PH2113 (50 decks)

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