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GI for Finals > High Yield Exam Cram > Flashcards

High Yield Exam Cram Flashcards

1
Q

Which cells in the stomach produce mucous?

A

Mucous cells

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2
Q

Name the two nerve plexuses that give the gut independent neural control

A

Submucosal + myenteric plexuses = enteric nervous system (ENS)

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3
Q

Which cells in the stomach produce pepsinogen?

A

chief cells

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4
Q

Which cells in the stomach produce hydrochloric acid and intrinsic factor?

A

Parietal cells

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5
Q

What is intrinsic factor required for?

A

vitamin B12 absorption

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6
Q

What produces intrinsic factor?

A

Parietal cells

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7
Q

Where in the body is vitamin B12 absorbed?

A

Terminal ileum

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8
Q

Which glands produce bicarbonate?

A

Brunner’s glands

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9
Q

Explain where the secretions from the exocrine and endocrine pancreas are secreted to and what they are

A

Endocrine pancreas -> secretes insulin into blood

Exocrine pancreas -> secretes bicarb and digestive enzymes into duodenum

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10
Q

Why doesn’t the pancreas digest itself?

A

Enzymes made in the pancreas are inactivated and then become active in duodenum when they come into contact with Enterokinase (a brush border enzyme)

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11
Q

What are the constituent monomers of lactose

A

glucose + galactose

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12
Q

What brush border enzyme breaks down lactose?

A

Lactase

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13
Q

What are the constituent monomers of sucrose?

A

glucose + fructose

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14
Q

What brush border enzyme breaks down sucrose?

A

sucrase

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15
Q

What are the constituent monomers of maltose?

A

glucose + glucose

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16
Q

What brush border enzyme breaks down maltose?

A

Maltase

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17
Q

What are the fat soluble vitamins?

A

A, D, E, K

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18
Q

What is segmentation?

A

Pushes chyme back and forwards to mix and aid digestion

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19
Q

When does segmentation occur?

A

Occurs while you are still eating

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20
Q

Name the two different types of anal sphincters

A

internal anal sphincter (smooth muscle under automatic control)

external anal sphincter (skeletal muscle under voluntary control)

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21
Q

What is the most common typeof GI cancer

A

Adenocarcinoma

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22
Q

How do you differentiate an upper and lower GI bleed?

A

High urea = upper GI bleed

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23
Q

How should GI bleeds be investigated?

A

Endoscopy
Colonoscopy

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24
Q

What is the name of the scoring system used to assess the likelihood that somebody has had a GI bleed

A

Glasgow-Blachford Score

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25
Q

What is the Rockall score used for?

A

Estimating the risk of re-bleeding and mortality

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26
Q

What is a Mallory-Weiss tear?

A

tear and bleeding associated with vomiting

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27
Q

What is Boerhaave’s and what is the triad associated with it?

A

Full thickness perforation of oesophagus.

Triad of Vomiting, chest pain, surgical emphysema.

Look out for gastric contents in chest cavity.

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28
Q

What are the red flag symptoms associated with GORD?

A
  • Dysphasia
  • Weight loss
  • > 55
  • Mass on palpation
  • Low haemoglobin
  • Raised platelet count
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29
Q

What is the surgical management of GORD

A

Nissan Fundoplication

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30
Q
A
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31
Q

What is the classical finding on barium swallow in diffuse oesophageal spasm?

A

Corkscrew

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32
Q

How is diffuse oesophageal spasm managed?

A

Muscle relaxants

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33
Q

How does diffuse oesophageal spasm present?

A

Severe, episodic chest pain with or without dysphasia

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34
Q

How does achalasia look on barium swallow?

A

Bird’s beak

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35
Q

What causes achalasia?

A

loss of the myenteric plexus ganglion cells in lower oesophagus -> lack of relaxation

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36
Q

How does achalasia present?

A

Dysphasia to solids and liquids at the same time

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37
Q

How can achalasia be managed?

A

balloon dilatation +/- botulism

or

Heller cardiomyotomy

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38
Q

What kind of cancer tends to affect the upper 2/3rds of the oesophagus?

A

Squamous cell carcinoma

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39
Q

What kind of cancer tends to affect the lower 1/3 of the oesophagus?

A

Adenocarcinoma

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40
Q

What condition pre-disposes to oesophageal adenocarcinoma?

A

Barrett’s oesophagus

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41
Q

Explain the process that sees normal oesophageal cells become an adenocarcinoma

A

Stratified squamous epithelium -> METAPLASIA ->
Simple columnar epithelium -> DYSPLASIA->
Adenocarcinoma

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42
Q

How is an oesophageal cancer imaged?

A

endoscopy, contrast swallow, CT

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43
Q

What are the two options to help prevent rupture of oesophageal varices?

A
  • Propranolol
  • Band ligation
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44
Q

What are the acute management options in oesophageal varices?

A

Broad spectrum abx
Terlipressin
Bind ligation
Sengstaken-Blakemore tube
TIPSS stenting can be used in cases of re-bleeding

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45
Q

What test is used to identify H. Pylori?

A

Urease breath test

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46
Q

What drug must be stopped prior to urease breath test and for how long before must it be stopped?

A

must be off PPI for 2 weeks!

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47
Q

If symptoms have not cleared, when should patients be re-tested for H.Pylori?

A

4 weeks

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48
Q

What is the treatment for H.Pylori?

A

clarithromycin, amox, omeprazole (abx for 7 days)

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49
Q

What is Zollinger-Ellison Syndrome?

A

Duodenal or pancreatic tumour produces excess gastrin. Causes gastric ulcers.

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50
Q

When should patients treated for a gastric ulcer be re-scoped?

A

4-8 weeks after treatment

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51
Q

How can a gastric ulcer be differentiated from a duodenal ulcer?

A

Peptic = worse on eating

Duodenal = relieved on eating, sore 2-3 hrs later

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52
Q

What is an absolute contraindication to NG tube?

A

Basal skull fracture

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53
Q

What should the pH of safe NG aspirate be?

A

<5

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54
Q

What are the surgical resection options for a gastric cancer?

A
  • Subtotal Gastrectomy (preserving some of the stomach)

Total Gastrectomy and Roux en Y reconstruction (remove the stomach and attach the distal oesophagus to small bowel

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55
Q

What is ALWAYS the distal margin when resecting a gastric tumour, regardless of where it is?

A

1st part of the duodenum

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56
Q

When would bariatric surgery be considered?

A

BMI > 35 and you have made efforts at weight loss

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57
Q

Name the causes of acute liver injury

A
  • Viruses (hepatitis)
  • Alcohol
  • Drugs
  • Prolonged bile duct obstruction
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58
Q

What are the 4 most common causes of liver cirrhosis?

A

Alcoholic liver disease
Non-alcoholic fatty liver disease
Hepatitis B
Hepatitis C

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59
Q

What is the difference between compensated and decompensated liver disease?

A

Compensated = patient is well and bloods are not deranged

Decompensated = AHOY
- Ascites
- Hepatic encephalopathy
- Oesophageal varies bleeding
- Yellow (jaundice)

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60
Q

Which scans are useful for identifying liver cirrhosis?

A

liver ultrasound (increased echogenicity) or a fibro scan

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61
Q

What blood test can be used to identify cirrhosis?

A

Enhanced liver fibrosis (ELF) blood test

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62
Q

What is the gold standard for diagnosing liver cirrhosis?

A

Liver biopsy

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63
Q

What is the function of the Child-Pugh score?

A

Assesses severity of cirrhosis and prognosis

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64
Q

How should patient’s with liver cirrhosis be monitored?

A

MELD score done every 6 months to estimate 3 month mortality

Ultrasound and AFP every 6 months to screen for hepatocellular carcinoma

Endoscopy every 3 years to check for oesophageal varices

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65
Q

What are the 3 basic steps in the pathological progression of alcoholic liver disease?

A
  1. Fatty change
  2. Alcoholic hepatitis
  3. Cirrhosis
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66
Q

What is the function of the AUDIT questionnaire?

A

Screens for harmful alcohol use

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67
Q

What blood test finding is classical for alcoholic liver disease?

A

AST:ALT >2:1

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68
Q

What occurs at the following times during alcohol withdrawal:

6-12 hours
12-24 hours
24-48 hours
24-72 hours

?

A

6-12 hours = tremor, sweating, headache, craving & anxiety

12-24 hours = hallucinations

24-48 hours = seizures

24-72 hours = delirium tremens

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69
Q

What would you expect to see in a patient withdrawing from alcohol at 6-12 hours after their last drink?

A

tremor, sweating, headache, craving & anxiety

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70
Q

What would you expect to see in a patient withdrawing from alcohol at 12-24 hours after their last drink?

A

Hallucinations

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71
Q

What would you expect to see in a patient withdrawing from alcohol at 24-48 hours after their last drink?

A

seizures

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72
Q

What would you expect to see in a patient withdrawing from alcohol at 24-72 hours after their last drink?

A

delirium tremens

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73
Q

What can be used in acute withdrawal to:

A) Manage symptoms
B) protect against wernicke’s encephalopathy

A

Chlordiazepoxide (benzo)

Pabrinex (thiamine B1)

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74
Q

What scoring system is used to estimate the amount of liver scarring in non-alcoholic fatty liver disease?

A

NAFLD (Non-Alcoholic Fatty Liver Disease) Fibrosis Score

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75
Q

What characteristic blood test finding is seen in non-alcoholic fatty liver disease?

A

ALT: AST >1:5

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76
Q

Which hepatitis strain is a notifiable disease?

A

All strains!

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77
Q

Which Hepatitis strains are
A) DNA viruses
B) RNA viruses

A

Hep B is the only DNA, the rest are all RNA viruses.

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78
Q

How is acute hepatitis managed?

A

Supportive management for all

+ antivirals for Hep B & C

+ pegylated interferon alpha for 48 weeks for Hep D

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79
Q

Which strains of hepatitis are spread via the fecal-oral route?

A

A & E

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80
Q

Which strain of hepatitis can you NOT vaccinate against?

A

C

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81
Q

Which strain of hepatitis can only occur in combination with a current hepatitis B infection

A

Hepatitis d

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82
Q

What does the hepatitis surface antibody indicate?

A

current infection or recent vaccine (not +ve in chronic infection)

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83
Q

What does the hepatitis E antibody indicate?

A

the virus is currently replicating and the patient is infectious

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84
Q

What does the hepatitis c antibody indicate?

A

high IgM = acute infection

Low IgM = chronic infection

IgG +ve = previous infection

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85
Q

Who gets Type 1 autoimmune hepatitis?

A

Ladies, during or after menopause.

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86
Q

Who gets type 2 autoimmune hepatitis?

A

Children

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87
Q

How does type 1 autoimmune hepatitis present?

A

fatigue and features of liver disease

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88
Q

How does type 2 autoimmune hepatitis present?

A

Symptoms of acute hepatitis

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89
Q

Which autoantibodies are associated with

A) Type 1 autoimmune pancreatitis

B) Type 2 autoimmune pancreatitis

A

Type 1: - ANA & anti-SMA

Type 2: - Anti-LKM1 & anti-LC1

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90
Q

How is autoimmune pancreatitis managed?

A

Steroids
Azathioprine

91
Q

How is a paracetamol OD managed if the patient presents within the 1st hour?

A

1st hr = activated charcoal

92
Q

What timeframe is considered a ‘staggered overdose”?

A

taken over >1hr

93
Q

What is the treatment of a staggered overdose?

A

NAC regardless

94
Q

What could be causing acute SOB in response to NAC?

A

a non-IgE mediated mast cell release

95
Q

Explain the dosing of NAC

A
96
Q

What criteria must be met in order to qualify for a liver transplant following a paracetamol overdose?

A

pH < 7.3, 24 hours after ingestion

or all of: INR > 6.5, creatinine >300, grade III or IV encephalopathy

97
Q

What causes ascites?

A

portal hypertension resulting from cirrhosis

98
Q

How should new onset ascites be investigated?

A

diagnostic paracentesis

99
Q

What are the two different types of ascitic fluid and what do they indicate?

A

Transudative (low protein) = cirrhosis

Exudative (high protein) = infection or malignancy

100
Q

How should ascites be managed?

A

Low sodium diet

Regular, high calorie meals

Spirnolactone

Ascitic tap/drain

Abx

TIPS

101
Q

What are the 2 most common bacterial causes of spontaneous bacterial peritonitis?

A

e.coli or Klebsiella

102
Q

What is hepatorenal syndrome?

A

Liver cirrhosis and portal hypertension causes impaired blood flow to the kidneys

103
Q

How is hepatorenal syndrome managed?

A

volume expansion fluids with albumin

vasopressors which vasodilate splanchnic vessels

Stents

Liver transplantation

104
Q

What is hepatic encephalopathy?

A

Hepatic encephalopathy is confusion (graded 1-4) caused by ammonia build up resulting from liver disease

105
Q

How is hepatic encephalopathy managed?

A

Manage with lactulose and broad spectrum abx (rifaximin)

106
Q

What are the main risk factors for hepatocellular carcinoma?

A

Alcoholic liver disease

Non-alcoholic fatty liver

Hepatitis B & C

107
Q

What is the tumour marker for hepatocellular carcinoma?

A

Alpha-fetoprotein (AFP)

108
Q

How are at risk patients monitored for hepatocellular carcinoma?

A

screened every 6 months with ultrasound and AFP

109
Q

At what plasma level does jaundice become visible?

A

50 micromols/L

110
Q

List the 3 types of jaundice and their basic patholphysiology

A
  1. Pre-hepatic jaundice caused by increased release of haemoglobin from red blood cells
  2. Hepatic jaundice caused by poor bile metabolism
  3. Post-hepatic jaundice caused by Cholestasis or Intrahepatic Bile Duct Obstruction
111
Q

What is the mode of inheritance for haemochromatosis?

A

Autosomal recessive

112
Q

What is the gene mutation in haemochromotosis and what chromosome is It on?

A

282Y mutation in HFE gene on chromosome 6

113
Q

What happens in Hemochromatosis

A

Excess iron deposition in tissues

114
Q

How is Hemochromatosis managed?

A

Venesection

115
Q

What is the inheritance pattern in Wilson’s disease?

A

Autosomal recessive

116
Q

which protein is mutated in Wilson’s disease and where can it be found?

A

Chromosome 13- mutation of copper transporting protein

117
Q

What happens in Wilson’s disease?

A
  • Excessive copper deposition in body tissues
118
Q

How does Wilson’s disease cause neurological signs?

A

Copper deposits in the brain

119
Q

what is the ocular finding in Wilson’s disease?

A

Keyser-Fleischer rings

120
Q

How is Wilson’s disease diagnosed

A

serum caeruplasmin

121
Q

How is Wilson’s disease treated?

A

copper chelation (penicillamine or trientine)

122
Q

How should gall bladder polyps be managed?

A

<5mm = leave alone

5-9mm = observe

> 1cm = resect

123
Q

What is Cholelithiasis?

A

gallstones

124
Q

What is choledochal-lithiasis?

A

gallstones in the bile duct

125
Q

What is the difference between primary and secondary choledochal-lithiasis?

A

primary = a gall stone forms in the bile duct

secondary = the stone travels from the cystic duct and lodges in the bile duct

126
Q

What are gallstones most commonly formed from?

A

cholesterol

127
Q

Which demographic tends to get gallstones?

A
  • Fat
  • Female
  • Forty
  • Fair
  • Fertile
128
Q

What condition is Murphy’s sign a useful diagnostic test for?

A

Cholecystitis

129
Q

Explain cholecystitis

A

palpation of RUQ causes pain on expiration

130
Q

What are the 2 causes of Ascending Cholangitis?

A

obstruction (e.g. stones/strictures) or infection introduced during ERCP

131
Q

What is chariots triad and Reynolds pentad?

A

Charcot’s triad:
RUQ pain
Jaundice
Fever

Reynolds Pentad (Charcot’s triad + …):
Shock
Altered mental status

132
Q

What is the difference between Primary biliary cholangitis and Primary sclerosing cholangitis

A

Primary biliary cholangitis = Intrahepatic duct damage. AMA antibody & IgM

Primary sclerosing cholangitis = Intra AND extrahepatic duct damage. pANCA antibody

133
Q

What medication is given in Primary biliary cholangitis?

A

Ursodeoxycholic acid (helps the bile flow)

134
Q

What characteristic finding might you see on MRCP in Primary sclerosing cholangitis?

A

presence of a stone and “beading” strictures in the biliary tree

135
Q

Which autoimmune condition is associated with Primary sclerosing cholangitis?

A

ulcerative colitis

136
Q

How is Primary sclerosing cholangitis managed?

A

Liver transplant and biliary stents

137
Q

why must patients with primary sclerosis cholangitis be carefully observed?

A

A stricture carries a risk of cholangiocarcinoma developing

138
Q

What is the most common presenting feature of cholangiocarcinoma?

A

Painless jaundice

139
Q

What is the tumour marker for cholangiocarcinoma?

A

Ca 19-9

140
Q

What is the most important step in the management of pancreatitis?

A

IV fluids

141
Q

Describe Cullens sign. Which condition is it associated with?

A

bruising around umbilicus

Pancreatitis

142
Q

Describe Grey-Turner’s sign. Which condition is it associated with?

A

bruising around flank, pancreatitis

143
Q

What are the causes of pancreatitis?

A

Causes = I GET SMASHED

I -Idiopathic

G- Gallstones
E- Ethanol
T- Trauma

S-Steroids
M- mumps/coxsackie A- Autoimmunity & Ascaris infection
S- Scorpion venom
H- Hypertriglycerideaemia, Hyperchylomicronaemia, Hypercalcaemia, Hypothermia
E-ERCP
D- Drugs

144
Q

if you are sick <1 hour after eating, what is the likely cause?

A

Psychogenic

145
Q

What is the mechanism of action of cyclizine?

A

Antihistamine (H1 antagonist)

146
Q

What are the two big side effects of cyclizine?

A

Can precipitate cardiac failure
Sedating

147
Q

what is the mechanism of action of Prochlorperazine/ Metoclopramide/ Haloperidol?

A

Dopamine antagonists

148
Q

Which antiemetic is contraindicated in Parkinson’s?

A

Haloperidol and metoclopromide

149
Q

What significant side effects are associated with metoclopromide?

A

Prokinetic side effects
Acute dystonic oculogyric crises

150
Q

In which clinical scenarios are metoclopromide contraindicated?

A

bowel obstruction
Parkinson’s

151
Q

What is the MOA of dexamthosone?

A

Neurokinin 1 receptor antagonists

152
Q

What is the MOA of ondansetron?

A

5HT3-receptor antagonists

153
Q

Give a brief explanation of refeeding syndrome

A

Refeeding with high levels of carbohydrates causes a rapid insulin spike. This causes extracellular ions such as potassium, calcium and magnesium to be pulled into cells. This drops the plasma concentrations of these ions which can destabilise the heart

154
Q

What are hr electrolyte derangement associated with re-feeding syndrome?

A

Decreased Magnesium, potassium & phosphate

155
Q

How is referring syndrome treated

A

Replace phosphate

156
Q

What genotype is associated with coeliac disease?

A

HLA genotype (HLA-DQ2 or HLA-DQ8)

157
Q

Which antibody is tested for in coeliac?

A

Anti-TTg

158
Q

What is the gold standard for diagnosing coeliac?

A

duodenal biopsy (villous atrophy)

159
Q

What must patients with suspected coeliac disease do prior to diagnostic biopsy?

A

Eat gluten for at least 6 week

160
Q

What is the classic skin condition associated with coeliac disease?

A

Dermatitis herpetiform = caused by IgA deposits in skin

161
Q

Describe the patient demographic affected by
A) Crohnes
B) UC

A
162
Q

Where in the body is affected by
A) Crohnes
B) UC

A
163
Q

What are the genes associated with
A) Crohnes
B) UC

A
164
Q

Describe the features of
A) Crohnes
B) UC

A
165
Q

Describe the extent of fibrosis in
A) Crohnes
B) UC

A
166
Q

Describe the systemic manifestations of
A) Crohnes
B) UC

A
167
Q

Describe flare management in
A) Crohnes
B) UC

A
168
Q

Describe how to maintain remission in

A) Crohnes
B) UC

A
169
Q

How is IBS defined?

A

presence of abdominal pain (for over 3 consecutive days in the last 3 months according to the ROME criteria) alongside altered bowel habits or abdominal bloating (or both) in the absence of any other symptoms

170
Q

what is the difference between diverticulosis, diverticular disease & diverticulitis ?

A

Asymptomatic disease = diverticulosis

Symptomatic disease with no inflammation = diverticular disease

Symptomatic disease with inflammation = diverticulitis

171
Q

What is the inheritance pattern of familial adenomatous polyposis?

A

Autosomal dominant

172
Q

Which disease are you at increased risk of if you have familial adenomatous polyposis?

A

Bowel cancer

173
Q

Which gene is affected in familial adenomatous polyposis and what chromosome is it on?

A

APC gene, chromosome 5

174
Q

How does pre-cancerous familial adenomatous polyposis present?

A

Multiple adenomas throughout the colon

175
Q

How is familial adenomatous polyposis monitored?

A

Annual colonoscopy from age 10/12

176
Q

What prophylactic procedure can be offered to patients with familial adenomatous polyposis?

A

Prophylactic proctocolectomy usually by the age of 16 - 25 yrs

177
Q

What is the inheritance pattern of Lynch syndrome?

A

autosomal dominant

178
Q

Which condition does Lynch syndrome increase your risk of?

A

Bowel cancer

179
Q

What is the genetic mutation in Lynch syndrome?

A

mutation in DNA mismatch repair genes (MLH1 & MSH2)

180
Q

What genetic feature on Lynch syndrome tumours results in short, repeated DNA sequences?

A

Microsatellite instability

181
Q

What side is the colorectal cancer usually on in Lynch syndrome patients?

A

Right side

182
Q

What age do Lynch syndrome patients classically present with cancer?

A

40s

183
Q

Lynch syndrome is associated with cancer at which other sites?

A

endometrial, genitourinary, stomach and pancreatic cancers

184
Q

How is known Lynch syndrome monitored?

A

colonoscopy every two years from age 25

185
Q

What is the inheritance pattern of MUTYH-associated polyposis?

A

autosomal recessive condition

186
Q

What is the genetic mutation associated with MUTYH-associated polyposis?

A

MUTYH base excision repair gene

187
Q

Which side of the colon are tumours caused by MUTYHassociated polyposis most likely to be on?

A

R

188
Q

at what age is surveillance for MUTYH-associated polyposis commenced?

A

18 to 20 years old

189
Q
A
190
Q

What are the 3 biggest causes of bowel obstruction?

A
  • Adhesions
  • Hernias
  • Malignancy
191
Q

What x-ray sign indicates a volvulus?

A

Coffee bean sign

192
Q

Is C.Diff gram positive or gram negative?

A

Gram positive

193
Q

Is C.diff an aerobe or an anaerobe?

A

Anaerobe

194
Q

Is c. diff a cocci or a bacilli?

A

Bacilli

195
Q

How is c. diff tested for?

A

Stool antigen

196
Q

Name the antibiotics likely to cause c. diff

A
  • Clarithromycin
  • Co-amoxiclav
  • Ceftriaxone
  • Ciprofloxacin
197
Q

How is a 1st episode of c. diff treated?

A

oral vancomycin

198
Q

How is life threatening c. diff treated?

A

oral vancomycin AND IV metronidazole

199
Q

How is a recurrence of c.diff within 12 weeks treated?

A

oral fidaxomicin

200
Q

What is the distinctive clinical finding in cholera?

A

“rice-water” stools

201
Q

How is Giardia lamblia spread?

A

through contaminated water (commonly from private water supplies)

202
Q

What kind of organism is Giardia?

A

Protozoa

203
Q

What distinctive finding associated with Giardia can be found on stool microscopy?

A

cysts

204
Q

What condition does Entamoeba histolytica cause?

A

amoebic dysentery

205
Q

Name the hepatic complication of Entamoeba histolytica

A

amoebic liver cysts

206
Q

Describe Rovsing’s sign

A

RIF pain on palpation of LIF

207
Q

Where is McBurney’s point?

A

one third of the distance from the anterior superior iliac spine (ASIS) to the umbilicus

208
Q

What is the purpose of a loop stoma?

A

can be reversed – often used to divert bowel contents out of the bowel upstream of an anastomosis which is further down to allow it to heal (defunctioning)

209
Q

Describe the difference between a direct and an indirect inguinal hernia

A
210
Q

Are femoral hernias more common in males or in females?

A

Females

211
Q

What are the three main complications of a hernia?

A

Bowel obstruction
Incarceration
Strangulation

212
Q

What is the difference between incarceration and strangulation?

A

Incarceration = unable to reduce

Strangulation = sore (unable to reduce and ischaemic)

213
Q

What can be given for symptomatic relief in cases of anal fissures?

A

GTN/ diliazem ointment and lignocaine ointment

214
Q

What are the surgical management options for anal fissures?

A

Botox

Sphincterotomy

215
Q

How is rectal prolapse managed?

A

Surgical management - rectopexy

216
Q

What kind of laxative is ispaghula?

A

Bulk forming

217
Q

Name 2 stool softening laxitives

A

Docusate
glycerol suppository

218
Q

How do stool softening laxatives work?

A

Made up of detergent like molecules which incorporate more water

219
Q

Name 2 osmotic laxatives

A

lactulose, laxido

220
Q

How do osmotic laxatives work?

A

made of compounds which are not absorbed by the gut and therefore draw water into the gut.

221
Q

Name a stimulating laxative

A

Senna

222
Q

Explain how stimulating laxatives work

A

These drugs irritate the bowel which encourages peristalsis

223
Q
A

GI for Finals (1 decks)

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