GI Flashcards

Question

AAD

Answer 1

- Severe disease usually C. difficile, others C. perfringens, S aureus - Normally microflora prevents establishment - Can be severe - Pseudomem-branous colitis, dehydration, kidney failure, death - Risk factors - exposure to antimicrobials, age, hospitalisation - Prevention - very important, gloves, hand washing, probiotics?

Answer 2

- Many studies on use of probiotics to treat/prevent diarrhoea including ADD - Some evidence for efficacy - Also evidence for adverse effects in risk patients

Answer 3

- Single stranded (+) RNA, non-enveloped virus, high diversity - Sapovirus - also a human pathogen, fewer outbreaks than norovirus but similar settings. Can get co-infection with norovirus

Answer 4

- transmission - direct, contaminated food/water - Highly contagious - Outbreaks in hospitals, cruise ships, elderly care facilities common - Also sporadic cases - Acute self-limiting gastroenteritis, or can be asymptomatic

Answer 5

- 48 hour incubation period - Pathogenesis not well described - Cross intestinal epithelial barrier to then infect dendritic cells, macrophages and B cells - Sudden D&V, stomach pain +/- fever, malaise

Answer 6

- Prevention & outbreak policies (eg ward closures, isolation of cases on ships etc) and staff training - Hand hygiene - Disinfection - chlorine products recommended for surfaces

Answer 7

Obstacles - Cant grow it, highly diverse, dont understand pathogenesis or immunology

Answer 8

- Single most important cause of severe infant gastroenteritis - DS non-enveloped RNA Virus - Worldwide distribution - Incidence similar, more deaths in developing countries

Answer 9

Transmission - Faecal-oral route - virus highly contagious, stable in environment - Hospital infections a problem in developed countries - Water bourne, food bourne outbreaks are rare Clinical features - acute rotavirus gastroenteritis - vomiting 1-2 days - Watery diarrhoea lasting ~5 days - Fever, malaise, dehydration - Little inflammation

Answer 10

- - - - - -

Answer 11

Have a look on L3, pg 12

Answer 12

- Infection resolves within 1-2 weeks without treatment - Infants dehydrate very quickly so supportive care is vital - iv or oral rehydration - reintroduce age appropriate diet as soon as baby/infant wants to eat - Hyperimmune bovine colostrum

Answer 13

Rotashield vaccine introduced into the US in 1998, live oral vaccine given at 2,4,6 months of age, vaccine withdrawn 9 months later after severaal cases of intussusception (bowel obstruction) - Several large safety studies then done - Live, oral vaccine - Monovalent but has cross protection - Live virus will be shed after first vaccine

Answer 14

- Avoid contact with cases (48hr exclusion for day care) - Strict hygiene - hand washing - Surface disinfection - Breast feeding - protective maternal Ig

Answer 15

- family Picornoviridae, small, non-enveloped, + strand RNA - Spread via faecal-oral route or respiratory - Infect GI (or respiratory tracts) then spread systemically

Answer 16

- Epidemiology changed with advent of improved public hygiene - infections no longer in infants, no later - more likely to cause paralysis

Answer 17

1. GI replication (few/no GI symptoms, virus excreted for 2-8 weeks) 2. Spread to lymphoid tissue, replication 3. Invasion into blood - viremia 4. Penetration of BBB - targets motor neurons

Answer 18

- Live attenuated oral vaccine and an inactivated polio vaccine - IPV initially used, switched to OPV

Answer 19

- NZ switched from OPV to IPV in 2002 - 3 doses gives 99-100% seroconversion - Safe in pregnancy & breast feeding - Antibody does decline with time, no evidence of increased disease

Answer 20

- C.parvum, C. hominis - Protozoa - thick oocyst resistant to many disinfectants - Carried by animals & humans - Faecal-oral transmission, commonly water, also person-person & zoonotic - Acute infections in adults but diarrhoea can be prolonged (14 days) - -

Answer 21

- 1-12 day incubation - Invades gut epithelium, replicates, forming oocysts - excreted in feces - Immune response develops - CD4 cells vital (severe disease in HIV/AIDS) Symptoms - diarrhoea (1-2 weeks), stomach pain, nausea, weight loss - Can persist and spread in immune suppressed people

Answer 22

- Therapy not needed if immune-competent - No good treatments - Nitazoxanide is approved by the FDA & is on the NZ hospital medicines list

Answer 23

- Flagellated protozoa - Cysts carried by animals & humans - Faecal-oral transmission of cysts, commonly water (swimming pools, river, lakes, tank water) person-person & sexual, zoonotic - Acute infection in adults but diarrhoea can be prolonged or chronic - Non-invasive - Stool sample for diagnosis

Answer 24

- 1-2 week incubation - Infection of gut epithelium, villi shortening, malabsorption & diarrhoea, increased permeability can cause complications - Immune response develops - Symptoms - diarrhoea, abdominal pain, bloating, weight loss, temporary lactase deficiency

Answer 25

- First line treatment is metronidazole, but resistance is increasing - Prevention - cysts resistant to chlorine disinfectants - Is a high level of surface antigen variation - Animal vaccines being developed

Answer 26

- Sight, smell, taste or thought of food. These stimuli, processed by the brain, activate enteric neurons via parasympathetic preganglionic neurons travelling in the vagus nerve

Answer 27

Food stretches the walls of the stomach; - this is sensed by mechanoreceptors, activating a neural reflex to stimulate acid secretion (purple) - Peptides and amino acids in food stimulate G cells to release gastrin (blue) - Food also acts as a buffer, the pH and thus stimulus for somatostatin secretion (light blue-green)

Answer 28

- Once chyme enters the duodenum, intestinal phase stimuli activate negative feedback mechanisms to reduce acid secretion and prevent the chyme from becoming too acidic - SOmatostatin (SST) released from antral D cells when gastric ph <3 inhibits gastric release in -ve feedback loop

Answer 29

1. Primary oesophageal defence is lower oesophageal sphincter - prevents reflux of gastric acid contents 2. Key stomach defence - secretion of mucous layer - slows ion diffusion, prevents damage by pepsin 3. Prostaglandins PGE2 and PGI2 stimulate mucous production and inhibit H+ secretion by parietal cells 4. Secretion of bicarbonate by superficial gastric epithelial (or goblet) cells -> increases pH and prevents acid-related damage

Answer 30

L4, pg 10 & 11

Answer 31

- Chronic acid-related disorder - Reflux of gastric acid into the oesophagus - Left unresolved can develop erosive oesophagitis (strictures) and adenocarcinomas (bartletts metaplasia)

Answer 32

- Caustic effects of acid , pepsin and bile overwhelm the defense factors of gastrointestinal mucosa - Burning stomach pain, nausea, full/bloated/belching - Red flags (severe signs): vomiting, black or tarry stools, unexpected weight loss - Main causative factor is presence of helicobacter pylori - Other risk factors include - Smoking - Excess alcohol - Genetic factors

Answer 33

- Are rare, usually in 20-50. year olds - Symptoms - abdominal pain, diarrhoea, burning/aching/gnawing in upper abdomen, heartburn, nausea & vomiting, bleeding in digestive tract, unintended weight loss - Pancreatic or duodenal gastrinomas (produce gastrin) that stimulate production of very large amounts of acid

Answer 34

- Ulcers of stomach or duodenum in context of profound illness or trauma requiring intensive care - Risk of gastric haemorrhage - Etiology involves acid and mucosal ischemia - treatment IV H2-blocker or IV PPI - Danger of aspiration pnemonia due to gastric colonization by bacteria in alkaline milieu - Sucralfate offers protection without risk of pnemonia

Answer 35

1. Enhance Mucosal Defence - Prostaglandin analogs: Misoprostol - Antacids 2. Acid Suppression - Proton pump inhibitors (PPI) - H2-receptor antagonists (H2RA)

Answer 36

- Prostaglandin E2 (PGE2) and prostacyclin (PGI2) are the major PG's synthesised in the gastric mucosa - PGE2 & PGI2 bind to the parietal EP3 receptor - Linked to Gi subunit, therefore inhibits AC and decreases cAMP and gastric acid secretion - PGE2 can also stimulate mucin & bicarbonate ssecretion

Answer 37

- L4, pg 22

Answer 38

- Ranitidine (Zantac, peptisoothe, ranitidine relief, OTC/Rx) - More potent H2RA vs cimetidine - Also inhibits CYP450, but not clinically relevant at OTC doses (liquid and tablet) - Rx is subsidised - Famotidine (Pepzan, Rx) - Greatest affinity of all H2RAs - Does not inhibit CYP450

Answer 39

L4, pg 24 - said dont need to know something (cant remember)

Answer 40

L4, Pg 25 & 26 & (27- dont need to know)

Answer 41

L4, pg 29 & 30

Answer 42

- Impulses from the CTZ pass to areas of the brainstem referred to as the vomiting centre - Vomiting centre controls and integrates the visceral and somatic response involved in vomiting

Answer 43

- Emetic stimuli include: - Pathway and mediators include: - Enkephalins implicated in the mediation of vomiting

Answer 44

- Vomiting is regulated centrally by the vomiting centre and the chemoreceptor trigger zone (CTZ) - The CTZ is sensitive to chemical stimuli and is the main site of action of many emetic and antiemetic drugs - The blood-brain-barrier (BBB) around the CTZ is relatively permeable, therefore circulating mediators act directly on CTZ - The CTZ also regulates motion sickness

Answer 45

1. Drug therapy induced emesis 2. Others - odours - Tastes 3. Motion Sickness

Answer 46

- dehydration - malnutrition - patient discomfort

Answer 47

- 5-HT3 receptor antagonists - Centrally acting dopamine receptor antagonists - Histamine H1 receptor antagonists - Muscarinic receptor antagonists - Neurokinin receptor antagonists

Answer 48

- L5, pg 13

Answer 49

- Examples include promethazine, cyclizine, meclozine (not subsidised) - Effective treatment for nausea and vomiting arising from many causes - motion sickness - irritants in the stomach - NOT effective against substances acting on the CTZ - Most also have antagonistic activity at mACh receptors (likely to be important part of their mechanism of action) - Adverse Effects: Drowsiness and ssedation most common unwanted effect (H1 receptor involved in CNS arousal)

Answer 50

- Infrequent defecation (usually <3 times /week) with stools that are hard, uncomfortable and difficult to pass (need to strain or feeling of incomplete evacuation) - Rationale for treatment is to: - relieve symptoms and restore 'normal' defecation pattern - Avoid straining, eg postoperative, ischaemic heart disease, haemorrhoids - Laxatives, cathartics, purgatives, aperients, and evacuants

Answer 51

- Purgatives hasten food transit through the intestine - Used to relieve constipation or to clear bowel before surgery or examination 1. Bulk laxatives - Examples are methylcellulose, bran, psyllium - Polysaccharide polymers which do not get broken down - Attract water and form hydrated mass, promoting peristalsis - Generally take several days to work

Answer 52

2. Osmotic laxatives 3. Faecal Softeners 4. Stimulant laxatives

Answer 53

> 3 loose or liquid bowel movements a day - Osmotic - Secretory - Exudative

Answer 54

1. Absorbents

Answer 55

2. Morphine (& codeine)

Answer 56

3. Lopeeramide | 4. Diphenoxylate (diastop)

Answer 57

Mutation: - Any change in DNA base sequence - May change protein function or expression Polymorphism: - A change in DNA base sequence that is common in the population - > 1% frequency = polymorphism

Answer 58

genotype - DNA imprint (a set of genes) - Forever Phenotype - Observed characteristics - May change

Answer 59

- Adherence to therapy - Differences in organ function and maturation (eg kidneys and liver) - Differences in body size and composition - Drug interaction - Genetic differences in drug handling - Old age - Sex - Co-morbidities

Answer 60

many indications: - Inflammatory bowel disease - Severe inflammatory dermatoses - Rheumatic diseases - Prevention of solid organ transplant rejection Know these adverse effects: - Bone marrow depression (myelosuppression, eg leucopenia) - Hepatic toxicity

Answer 61

- elevated conc. of 6MMP are asscoiated with hepatotoxic - 6TGN - The primary active metabolite - Elevated conc. associated with an increased risk of bone marrow toxicity

Answer 62

- L16, pg 31

Answer 63

- L16, pg 32 & 33 & 34

Answer 64

- L16, pg 35

Answer 65

- Treatment of peptic ulcers and GORD

Answer 66

- Omeprazole is a PPI - Interested in the parietal cell - we want to reduce the acid secretion - Proton pump controls the stuff - Omeprazole prevents the hydrogen ions from pumping into the lumen - Omeprazole is absorbed (systemically) in the small intestine - Binds irreversibly to proton pump - Omeprazole is a prodrug (inactive) in blood - Acidic conditions of the secretory canaliculi is the trigger for the activation of omeprazole

Answer 67

- To improve bioavailability Enteric coating: - Intact at low pH and release at higher pH - Small intestine is the primary site for drug absorption - Hydroxyproplycellulose

Answer 68

- Eudragit | - Solubility stays low at low pH, when pH gets to the higher pH then solubility inc.

Answer 69

- Maintain stability of omeprazole - Ensure correct dose - Volume of dispersant

Answer 70

- L6, pg 17

Answer 71

- Many and diverse bacteria - Anaerobic - Fermentation - SCFA production - Bacterial enzymes - Caution with the concomitant use of antibiotics - Disrupts colonic microflora

Answer 72

- two different enzymes | - Inc of enzymatic activity towards end (terminal) of GI tract

Answer 73

- Sulphasalazine - the original IBD drug - inactive that requires enzymatic transformation in vivo to release the active moiety - Not absorbed from the small intestine - Once reached the colon, the nitrogen group is cleaved by colonic bacteria (azoreductase)

Answer 74

- Contain 5-aminosalicyclic acid (5-ASA) 0 Anti-inflammatory action 1. PENTASA (5-ASA) - Ulcerative colitis and crohns disease - Time-dependent release - Prolonged release microgranules - Release continuously throughout the GIT - Release at all pH conditions

Answer 75

- SR microgranules in a shachet | - SR microgranules in a tablet (500mg)

Answer 76

- Liquid enemas - Suspension in purified water - Shake well before use - Distal colon - Suppositories - Sustained release base

Answer 77

2. Asacol Oral formulation - Delayed release formulation - Enteric coated tablets (gastro-resistant) - Film coating dissolves at ph >7 Rectal formulation - Suppository

Answer 78

1. The population method (same dose given to everyone) - Some patients would be under - or over-dosed - The clinical significance of this variability is negligible 2. Covariate-based dosing (same dose for similar group) - A dose is adjusted based on covariate (eg weight or creatinine CL) - Assumes people of the same value of a covariate handle drug similarly 3. Dose-individualisation (response-based dosing) - When even a small variability in response is detrimental to the patient - Therapeutic drug monitoring 'TDM'

Answer 79

defrgtyhuj

Answer 80

- We usually measure a drug conc. (usually in plasma) | - But response is usually variable

Answer 81

- Between-subject - Within-subject - Random

Answer 82

- An 'average' dose may be appropriate for one patient, toxic for a second patient, and sub-therapeutic for a third patient

Answer 83

- Refers to the plasma conc. that should lead to effectiveness without toxicity in most patients - Defined as the drug concentration range above the minimum effective conc. (MEC) and below the minimum toxic conc. (MTC)

Answer 84

a) Disintegration and dissolution of the drug b) Absorption across the membranes in the gut wall c) Pre-systemic metabolism (or 'first-pass') and elimination

Answer 85

1. Disintegration and dissolution of the drug 2. Physiology of gastrointestinal tract 3. Food or drug interactions in the gut lumen 4. Passage through the gut wall

Answer 86

- Only dissolved drug can readily traverse the gut wall Will depend on: - The release characteristics of dosage form - Physiochemical properties of the drug

Answer 87

- Gastric emptying - highly variable b/w people - Small intestine transit time - much less variability - Gastric emptying time may impact absorption rate for drugs that readily dissolve in the stomach (paracetamol) or enteric coated drugs - Insoluble drugs may have enhanced absorption if transit time is slow

Answer 88

- Altered pH | - Complexation

Answer 89

- Passive diffusion - Carrier-mediated transport - Active transport

Answer 90

- The primary absorption process for most drugs - Drug diffuses from high conc. to low conc. - After oral drug administration, when drug is reaching the gut lumen, the conc. in the gut will be much higher than in the plasma

Answer 91

- May be against a conc. gradient - Energy is required - Transporters are saturable and can be competitively inhibited (drug interactions) - Include efflux transporters (eg P-glycoprotein) that limit drug absorption from the gut

Answer 92

- Cross sectional - Case-control studies - Cohort studies

Answer 93

- Data obtained from groups who have already been exposed, or not exposed, to the factor of interest. No allocation of exposure is made by the researcher. Best risk factors on an outcome

Answer 94

Advantages: - Ethically safe - Participants can be matched - Can establish timing and directionality of events - Eligibility criteria and outcome assessments can be standardised Disadvantages - Controls may be difficult to identify - Exposure may be linked to a hidden confounder - Blinding is difficult - For rare disease, large sample sizes or follow-up necessary

Answer 95

- Patient with a certain outcome or disease and an appropriate group of controls, without the outcome or disease, are selected (usually with some matching) then information is obtained on whether the subjects have been exposed to the factor under investigation

Answer 96

Advantages - Quick and cheap as fewer people needed than cross-sectional studies - Only feasible method for very rare disorders or those with long lag b/w exposure and outcome Disadvantages: - Reliance on recall or records to determine exposure status - Confounders - Selection of control groups is difficult - Potential bias: recall, selection

Answer 97

Advantages: - Cheap and simple - Ethically safe Disadvantages: - Establishes association at most, not causality - Recall bias, social desirability bias - Researchers (Neyman) bias - Group sizes may be unequal - Confounders may be unequally distributed

Answer 98

- Random error = random variation, or 'noise in the system', chance - Systematic error = is consistent, repeatable error associated with faulty equipment or a flawed experiment design - Random error can be reduced by large study sizes: bigger studies give more precise estimates Systematic error can't

Answer 99

1. Control selection bias 2. Loss to follow-up bias 3. Self-selection bias 4. "Healthy worker" effect

Answer 100

Information bias - L8, pg 26, 27 Confirmation Bias - L8, pg 28

Answer 101

measure of association | -L8, pg 31, 32, 33, 34, 35

Answer 102

1. Bulk-forming laxatives 2. Stool softeners 3. Stimulant laxatives 4. Osmotic laxatives

Answer 103

- Exert effect by mimicking increased fibre consumption and increasing feacal mass - Patients should inc. fluid intake at the same time - Effect seen 12-36 hours but can take as long as 72 hours - Side effects: flatulence and abdominal distension - Safe in pregnancy - Tip: briskly stir in powder and drink immediately

Answer 104

- Effective for mild constipation (especially prevention of haemorroids) - Examples docusate sodium - Docusate works as a stool softener as well as a stimulant - Poloxamer is a non-ionic surfactant with similar properties to docusate - X liquid paraffin

Answer 105

- Increase GI motility & irritate lining of colon to produce contractions - Examples: bisacodyl, senna - Quicker onset than other laxatives (6-12 hours) hence take at night - Most commonly abused laxative - Nu-lax (natural alternative) contains senna leaves

Answer 106

- Act by retaining fluid in the bowel by osmosis - Example: Lactulose, macrogols - Common side effects: Flatulence, abdominal pain and colic - Can take 48 to 72 hours before an effect is seen

Answer 107

- Haemorrhoids or "piles" are common and affect around 50% of adults at some point in their lives - They occur when vascular-rich connective tissue cushions become engorged and swollen - They can be categorised into two types based anatomically: internal or external

Answer 108

- Anatomical (degeneration of elastic of connective tissue due to ageing) - Physiological (increased anal canal pressure from heavy lifting, obesity, chronic diarrhoe, childbirth, standing for long periods of time) - Mechanical (straining at stool from constipation and prolonged sitting on toilet interfering with blood flow to and from rectal area)

Answer 109

Symptoms - bleeding from rectal areas, especially after bowel motion - Perianal itching and pain Red flags - Symptoms longer than 3 weeks - Large volume of blood - Sharp or stabbing pain at time of defecation - Over 50 years of age Treatment: - Inc. fibre in diet - Avoid becoming constipated - Pharmacological - anaesthetics - Astringents - Anti-inflammatories

Answer 110

L9, pg 21 - more about them in Lt

Answer 111

Characterised by abdominal pain and discomfort; usually associated with at least 2 of the following symptoms - Pain and discomfort relieved by defecation or passing wind - Bowel motions more or less often usual - Change in bowel habit - diarrhoe and/or constipation - Symptoms occuring at least 3 time a month Other symptoms include - Feeling of incomplete defacation - Passing mucus - Bloating Treatment: - Diet and lifestyle changes are first line treatment - Smaller, more frequent meals - A low FODMAP diet - Avoid triggers eg alcohol, caffeine - Manage stress - Ensure adequate hydration - Increasing physical activity - Pharmacological options (L9, pg 27) Red flags - Children under 16 years of age - Over 45 years of age with recent change to bowel habit - Change in nature and severity of pain - Pain that is not normal in the left lower quadrant - Blood in stool

Answer 112

- Also known as pinworm - Most common in children but can also affect adults - Most children between 5-14 will be infected at some stage - Small, thin, white worms between 2mm an 13mm long - look like cotton threads

Answer 113

Transmission via - Self-infection - ingestion of eggs - Person to person via contaminated cloths and bed linen

Answer 114

Clinical maifestations: - Itchy anal region - Secondary infection from scratching - Teeth grinding and isomnia due to disturbed sleep - Loss of appetite - Abdominal pain Red flags: - Pregnant women - Children under 1 year old - Secondary skin infection from scratching - Recent travel (exotic worms) Hygiene measures and advice: - Shower in the morning to remove infected eggs - Frequently change cloths, bedding etc - Avoid scratching - Treat the whole family Treatment options: - Mebendazole - Pyrantel

Answer 115

- One side is good for protecting the gi tract from pathogens and the other is for absorbing nutrients

Answer 116

in the leaky barrier the antigens are getting in and the T cells respond - Inflammation causes more damage - Leaky barrier is due to genetics & environment which cause inflammation

Answer 117

Inflammatory disease of the small intestine triggered by gluten in susceptible individuals, characterised by damage to villi and nutrient malabsorption - GI symptoms (D&V, weight loss) and/or malnutrition related problems eg fatigue, anemia, bone/joint pain depression

Answer 118

- Female bias (2-3:1) - Genetic influence - Environmental - Exposure to gluten peptides - gliadins & glutenins (high proline & glutamine content) - These are not easily digested in the GI tract - Breast feeding - increased duration, reduced risk

Answer 119

Diagnosis: - History, biopsy, Ig to TG2 or deamidated gluten peptides (blood test) Treatments: - Gluten free diet - Decrease/remove immunogenic epitopes from gluten - Sequester gluten - Prevent gluten uptake - TG2 inhibition

Answer 120

- Crohns disease | - Ulcerative colitis

Answer 121

Risk factor: - Genetics, environment (smoking) Location: - Inflammation frequently affects distal ileum and colon Pathology: - Discontinuous, patchy gut inflammation with skip lesion Histology: - Transmural inflammation (all layers of the bowel wall)

Answer 122

Risk factors: - Genotype and environment Location: - Inflammation affects the colon only (distal colitis or proctitis, left-sidedd colitis and pancolitis Pathology: - Continuous inflammation from the rectum to proximal parts of the colon

Answer 123

- its protective for UC | - Nicotine may be a therapeutic for UC

Answer 124

- No definitive diagnostic test | - History, presentation, endoscopy, blood tests for inflammation & infection

Answer 125

Genetic Factors: Environment: - Diet? - Stress? - Drugs? - Smoking? - Microflora/infection?

Answer 126

- Presence of these bacteria stimulates the immune system to keep them in check - Protects against colonisation by pathogens

Answer 127

- Environment induces changes in bacterial composition - dec. diversity - Inc. pathogen adherence - Combined with genetic predisposition = IBD

Answer 128

- Alterations in epithelial barrier function - Translocation of luminal antigens - Aberrant and excessive cytokine responses - Failure to resolve acute intestinal inflammation leads to chronic intestinal inflammation & pathology

Answer 129

- Numerous biologics available - Lack of head to head studies to address differences in efficacy - many target TNF - Side effects - increased risk of malignancy or serious infection - Data on long term efficacy still coming in - As always the issue of cost

Answer 130

- Use fresh or frozen faeces preps - Various delivery - top or bottom - UC - 33% remission - CD - 52% remission - Safe - some transient bloating, flatulence, cramping

Answer 131

- Inflammatory reaction restricted to the colon | - From the rectum, inflammation is uniform and continuous

Answer 132

- If GI epithelium damaged, bacterial antigens gain access to antigen presenting cells (APC) who present antigens to CD4+ cells - APC either secrete IL-12 and IL-18 to induce differentiation of Th1 cells (CD or IL-4 to induce differentiation of Th2 (T helper cells) (UC) - Pro-inflammatory and anti-inflammatory balance governed by Th17 (inc. inflam) and Treg cell (dec inflam) - Transforming growth factor (TGFb) and IL-6 drive expansion of Th17 and Treg cells

Answer 133

1. Induce and maintain remission 2. Ameliorate symptoms 3. Improve pts quality of life 4. Adequate nutrition 5, Prevent complication of both the disease and medications

Answer 134

1. Anti-inflammatory drugs - Aminosalicylates (mesalazine) - Glucocorticosteriods (prednisolone) 2. Antibiotics - Metronidazole - Ciprofloxacin 3. Immunosuppressants - Azathioprine - Methotrexate - Ciclosporin - Mercaptopurine 1. Biological response modifiers - Infliximab - Adalimumab

Answer 135

- 5-aminosalicylate (mesalazine), sulfasalazine | - Administered by oral or rectal formulations

Answer 136

- Anti-inflammatory and immunosuppressant drugs - Prednisone is the major steroid for UC and CD - Routes of administration - Oral prednisone, budesonide - IV methylprednisolone, hydrocortisone (HC) - enema (HC) and rectal foams (HC)

Answer 137

Adrenal axis suppression: - Risk of death with abrupt cessation of dosing - Requirement for dose-tapering Effects on carbohydrate, protein and fat metabolism: - Promotes gluconeogenesis - Can precipitate hyperglycemia (diabetics need to monitor) - Skeletal muscle wasting - hypertension - Redistribution of body fat ('moon face', 'buffalo humps') - Elevation of mood - Skin thinning

Answer 138

Uses: - Cytotoxic and immunosuppressive actions, potent anti-rheumatoid action MoA: - Folic acid antagonist - competitively inhibits dihydrofolate reductase important for de novo synthesis of thymidine (nucleotide) SE: - Blood dyscrasias (sometime fatal, folic acid) and liver cirrhosis

Answer 139

- L11, pg 25

Answer 140

- Target the virus = DAA (direct acting antivirals)

Answer 141

1. Receptor/co-receptor binding 2. Fusion to release subvirion 3. Release viral genome 4. Translation for viral proteins 5. Genome multiplication 6. Assembly, packaging, and release

Answer 142

- Acute, self limiting infection - +ve strand -non-enveloped, acid stable, heat resistant - Transmission via contaminated food and water person-person transmission, blood transmission

Answer 143

- +ve strand RNA virus - direct translation of enzymes and structural proteins - Transcription of RNA by viral polymerase occurs in a cytoplasmic vesicle - Virus does not enter nucleus - Virus is released by lysis

Answer 144

- 2-7 week incubation - Symptoms - malaise, nausea, dark urine, jaundice, hepatomegaly Treatment: - No specific therapy - Alcohol avoidance - Monitor medications Prevention - Passive immunisation - Active immunisation

Answer 145

- Acute and chronic hepatic infection - Enveloped virus - Partially ds circular DNA virus, -ve strand, incomplete (+) strand

Answer 146

Transmission: - Via blood, blood products, sexual contact, perinatal transmission, insects - In areas with high HBV prevalence, childhood infections are common - In areas of low HBV prevalence, most infections occur in adult

Answer 147

1. Immune-tolerant phase - elevated HBV DNA, normal ALT 2. HBeAg-positive - immune-active phase - elevated ALT & HBV DNA levels, liver injury from immune response 3. Inactive/chronic phase - HBV DNA and ALT down/normal, anti-HBe is present, liver recovery, ~ 0.5%/year will get disease resolution (clearance of HBsAg with acquisition of antibody to HBsAg) 4. HBeAg-negative immune reactivation phase - elevated ALT & HBV DNA levels, liver injury

Answer 148

- serology for antigen & antibody | - Provides information on phase of infection

Answer 149

- Aim to suppress viral replication & stop progression

Answer 150

- Public Health measures & education. - Blood product screening, no needle sharing (IDU, tattoos, piercings), safe sex - Passive immunisation - Active immunisation

Answer 151

- Acute and chronic hepatic infection - +ve strand, RNA virus - Huge sequence diversity (high replication rate and poor proof reading) - Replication - similar to HAV - Transmission - blood, both HCV & HBV more infectious than HIV, high risk of co-infection

Answer 152

- History of drug use - Sexual contact - Tattoo

Answer 153

- received a blood transfusion or organ transplant prior to 1992 - Use of injectable drugs - spent time in prison - Have a tatoo

Answer 154

- move away from drugs that only work on afew genotypes to drugs that work on many genotypes - eg Maviret

Answer 155

- Blood product screening, no needle sharing, safe sex | - No vaccine is present

Answer 156

HAV - self limiting HBV - control with vaccination (on schedule) and treat HCV - no vaccine, screen, treat & now cure

Answer 157

- Intracellular enzymes involved in the production of amino acids - Ubiquitous throughout the body but conc. vary greatly in different tissues - Increased plasma conc. caused by leakage (injury) from enzyme-rich tissue

Answer 158

- Very high conc. in the liver compared to other organs | - Elevations suggest liver injury

Answer 159

- High conc. in several organs - cardiac muscle>skeletal muscle>Kidneys>Lungs>RBC - Elevations may suggest - cardiac muscle injury - Skeletal muscle injury - Haemolysis - Hepatocyte injury - Not specific for liver injury

Answer 160

Mild/moderate elevations (2 - 20x normal) - Non-specific (eg a night out at the pub) - most chronic viral hepatitis - Alcohol hepatitis - Various drugs - Marked elevations (20 - 1000x normal) - Suggest severe liver injury - Ischemic liver injury - Acute viral hepatitis - Fulminant necrosis - Some acute drug toxicities

Answer 161

AST/ALT ratio > 2 - Alcohol hepatitis - Alcoholics are often malnourished and lacking in vitamin B6 - required for the formation of ALT Fluctuating AST and ALT - Hepatitis C (LFTs may be normal)

Answer 162

- Enzymes that cleaves phosphate from proteins (and other molecules) - Found on canalicular surface of hepatocytes, bone, kidney, placenta - Elevated in plasma when there is damage to biliary tract (but not a specific marker) - The clinical value of this test is detection of cholestatic disease

Answer 163

Mild elevation: - Hepatic disease - Pregnancy - Bone growth in children Marked elevation - Cholestatic disease - Bone disease (osteomyelitis, bony metastasis) - Cancer

Answer 164

- Found on canalicular surface of hepatocytes, kidney, pancreas and gut - Not a specific marker of liver disease Clinical value: 1. inc. GGT and inc. ALP is suggestive of cholestasis 2. Isolated inc. GGT can occur in alcohol abuse

Answer 165

- A metabolic product of heme (RBCs) - Hyperbilirubinaemia may be due to: 1. over production (eg haemolysis) 2. Impaired metabolism (rare genetic disorders) 3. Under-excretion - Hyperbilirubinaemia involves blockage of the biliary tree due to; - Obstruction (eg cholelithiasis) - Inflammation (cholangitis) - In excess, bilirubin is deposited in skin, sclera, mucus membranes (jaundice)

Answer 166

- "direct bilirubin" = conjugated = glucuronidated in the liver - "Indirect bilirubin" = unconjugated = not glucuronidated

Answer 167

- Elevated conjugated bilirubin suggest an obstructive cause

Answer 168

L15, pg 24 & 25

GI Flashcards

(212 cards)