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Medicine A100 > GI > Flashcards

GI Flashcards

1
Q

What is a Diverticula?

A

When pressure is too high in the colon it can produce an abnormal ‘out pouching’ to form a hollow. Most likely in the sigmoid colon as blood supply causes an area of weakness

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2
Q

What is Meckels’ Diverticulum?

A

Pouch in lower part of the small intestine, a vestigial remnant of the yolk sac. It can produce ectopic gastric mucosa which then produces gastric acid causing irritation

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3
Q

What are Haemorrhoids?

A

Vascular structures in the anal canal that aid with stool control. When they become swollen + inflamed they are painful, itchy + blood may be present in stool.

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4
Q

Where do you find the Oropharynx?

A

Below Nasopharynx + above the Laryngopharynx, extends from the uvula to the hyoid bone. Contains the epiglottis

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5
Q

What is Xerostomia?

A

Insufficient saliva production. You can still eat moist foods but teeth + mucosa degrade very quickly

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6
Q

Name the three paired Salivary Glands + their secretions

A
  • Parotid Glands (Serous Saliva- 25% of volume secreted)
  • Sublingual Glands (Mucus Saliva - 5%)
  • Submaxillary Glands (Mixed Serous + Mucus - 70%)
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7
Q

Describe the Secretion of Hypotonic Saliva

A
  1. Acinar Cells secrete an isotonic fluid containing enzymes, it does this by secreting Cl ions into lumen, water + Na then follow passively.
  2. Duct cells remove Na + Cl and add HCO3
  3. Gaps between duct cells are tight so water doesn’t follow the osmotic gradient + saliva remains hypotonic
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8
Q

How does flow rate effect the tonicity + pH of saliva?

A
  • At a high flow rate there is less chance for Na to be removed so saliva is less hypotonic
  • Stimulus for secretion promotes HCO3 secretion so at high flow rates you have more alkaline saliva
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9
Q

What is the Parasympathetic Stimulation of the salivary glands?

A

Glossopharyngeal (9th cranial nerve)

Stimulates increase in production of primary secretion (acinar cells) and increased the addition of HCO3

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10
Q

Describe the process of Swallowing

A
  1. Voluntary Phase - Tongue moves bolus up + posteriorly
  2. Pharyngeal Phase - Triggered when bolus touches anterior tonsillar pillars. Soft Palate moves upwards blocking off nasopharynx from oropharynx, hyoid bone is raised to block airway with epiglottis. Tongue moves upwards + backwards to force bolus into oesophagus
  3. Oesophageal Phase - Begins when bolus passes upper oesophageal sphincter. When it passes it it initiates peristaltic wave. If primary peristalsis doesn’t clear oesophagus second peristaltic wave is triggered above site of bolus
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11
Q

What muscle lies between the Pharynx + Oesophagus?

A

Cricopharyngeus Muscle

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12
Q

What is the Arcuate Line (Line of Douglas)?

A

Line that marks the level at which the posterior part of the rectus sheet disappears

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13
Q

What is a Rectus Sheath Haematoma?

A

Bleeding into the Rectus Abdominas, as its a tight space this is can be very painful. Sometimes seen in patients of Warfarin

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14
Q

What is a Hernia?

A

A protrusion of an organ through the wall of the cavity containing it

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15
Q

What is the structure of the Inguinal Canal? What runs through it?

A

Passage that extends inferiorly + medially through the inferior part of the abdominal wall. Opening is the deep inguinal ring, exit is the superficial Inguinal ring.
In men the Spermatic cord runs through it. In women its the round ligament of the uterus

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16
Q

What is a Direct Inguinal Hernia?

A

Protrudes into the Inguinal canal through a weakened area of transversalis facia near the medial inguinal fossa within Hesselbach’s triangle.

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17
Q

What is an Indirect Inguinal Hernia? What do most of these result from?

A

Protrudes through the deep inguinal ring. Most due to failure of embryonic closure of the deep inguinal ring after testicle has passed through it.

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18
Q

Describe Femoral Hernias

A

Protrusion of abdominal viscera through the femoral ring, appears as a mass in the femoral triangle. Often painful. More common in females due to wider pelvis. Can cause strangulation due to rigid boundaries of femoral ring

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19
Q

What complications can arise from Herniation?

A
  • Strangulation - Constriction of blood vessels prevents blood flow to the herniated tissues
  • Incarnation - Can’t be removed or pushed back into place
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20
Q

What do Parietal Cells secrete?

A

HCL

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21
Q

What do Chief Cells secrete?

A

Proteolytic enzymes (Pepsin)

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22
Q

Explain the mechanism for secretion of stomach acid

A

Because most bodily fluids are slightly alkaline they need to produce large quantities of H+ to be able to secrete it. Water is split into H+ and OH- in the mitochondria of parietal cells. OH- is combined with CO2 to form HCO3- which is exported into the blood.
Parietal cells have invaginations (Canaliculi) which have proton pumps to excrete H+ into stomach.
For every mol of H+ into stomach there is 1 mol of HCO3- into the blood

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23
Q

What stimulates the production of HCL?

A
  • Gastrin (binds CCK Receptors to insert H/K pumps)
  • Vagus nerve stimulates through musclarinic Ach receptor
  • Histamine binds to H2 receptors on Parietal cells
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24
Q

What controls the secretion of Gastrin? Where are G-cells located?

A
  • Peptides + Amino acids in stomach
  • Ach Stimulation by Vagus nerve
  • Gastrin releasing peptide
  • Somatostatin released by D-cells when pH is low inhibit gastrin
    G-cells found in Antrum of stomach
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25
Q

What are the 3 phases of Digestion and what do they do to HCL production?

A
  • Cephalic (Smelling, tasting, chewing, swallowing. Causes stimulation of parietal cells + G cells via vagus nerve)
  • Gastric (Distension of stomach stimulates vagus nerve to increase stimulation of Parietal + G-cells. Presence of Amino acids stimulates G cells. Food acts as a buffer increasing pH decreasing production of somatostatin by D-cells)
  • Intestinal (Chyme stimulates Gastrin secretion. Low pH causes somatostatin production by D-cells)
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26
Q

What defences does the stomach have?

A

Mucus + HCO3 released by surface mucus cells + neck cells in gastric glands. This forms a thick alkaline layer which sticks to epithelial surface keeping it at a higher pH.
Prostaglandins help to maintain a high mucosal blood flow.

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27
Q

What can cause breaches in the stomachs defences + what does this lead to?

A
  • Alcohol - Dissolves the mucus layer
  • Helicobacter pylori - Causes Gastritis by invading the stomach lining + producing cytotoxins
  • Non Steroidal Anti Inflammatories - Inhibit prostaglandin production
    These can all lead to Gastritis, Ulceration + GORD
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28
Q

What pharmacological interventions can be used to combat Stomach ulcers + other problems of the GI tract? How do they work?

A
  • H2 Blockers (Cimetidine, Ranitidine) - Block the binding of Histamine to H2 receptors on Parietal cells
  • Proton Pump Inhibitors (Omeprazole) - These block the H/K ATPase which presents H+ from being pumped into the stomach. As its the terminal step its a preferred target.
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29
Q

What is Gastro Oesophageal Reflux Disease? What can it be caused by? What problems can it cause? Whats the treatment for it?

A
  • Its the reflux of stomach contents into the oesophagus, presents with heartburn, cough, sore throat + dysphagia.
  • Caused by; Lower oesophageal sphincter problems, Delayed gastric emptying, Hiatus hernia, Obesity
  • Treated with lifestyle changes (not lying down after food) H2 blockers, Antacids (neutralise acid), PPI’s
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30
Q

What is Chronic Gastritis? What can cause it?

A
  • Chronic inflammation of the the stomach lining
  • H. pylori - infects lining of the stomach + produces cytotoxins
  • Autoimmune - Body produces antibodies against Gastric Parietal Cells, this means no Intrinsic factor (Needed to absorb B12) is produced so patients have Pernicious Anaemia.
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31
Q

What can cause Acute Gastritis and why? How does it present?

A
  • Heavy use of NSAID’s - these inhibit prostaglandins which are responsible for maintaining mucosal blood + nutrient supply
  • Alcohol - Dissolves protective mucus layer
  • Chemotherapy - Damages rapidly dividing cells
  • Bile reflux - Bile is an irritant to the stomach lining, can happen with reverse peristalsis
    It can be asymptomatic but can also present with pain nausea, vomiting + bleeding which can be fatal
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32
Q

What are Peptic Ulcers? Where are they most common? What can it be caused by? How does it present?

A
  • Defects in the Gastric or Duodenal mucosa, it must extend through the muscularis mucosa.
  • Most common in the first part of the Duodenum although can also affect the lesser curvature of the stomach
  • Can be caused by; Stomach acid, H.pylori, NSAID’s, Smoking + Massive Phycological stress (Extreme trauma, ITU)
  • Present with burning gnawing epigastric pain, often worse after a meal or at night time (more Duodenal than Gastric). More serious causes can have bleeding + anaemia (erodes through artery), Satiety (feeling full early), weight loss + perforated bowel
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33
Q

What is Functional Dyspepsia?

A

Patient has symptoms of Ulcer disease but no physical evidence of organic disease, its diagnosed by exclusion

34
Q

What is used to diagnose Gastric Pathology? What are they used to test for?

A
  • Biopsies can be used from Endoscopes, used for Benign + Malignant tumours
  • Urease Breath test used to test for H. pylori
  • Chest X-Rays used to check for bowel perforation
  • Blood tests used to check for anaemia
35
Q

What is H. pylori? How does it cause damage? How does its colonisation point change the affect it has?

A
  • Helix shaped, Gram -ve Microaerophilic Bacteria, spread by faecal oral transmission
  • Produced Urease to convert urea into ammonia which toxic to epithelia. Lives in mucous layer and adheres to epithelia releasing cytotoxins causing direct damage. Promotes inflammatory response causing self damage
  • Antrum (Located here causes increased Gastrin secretion from G-cells increasing acid secretion by parietal cells. Causes Duodenal metaplasia which allows colonisation of Duodenum -> Duodenal ulceration), Predominant Body (Forms a Gastric Ulcer and can lead to intestinal metaplasia, dysplasia + cancer)
36
Q

What is Zollinger-Ellison Syndrome?

A

Caused by a Non-Beta islet cell Gastrin secreting tumour of the pancreas. The high levels of Gastrin cause proliferation of the Parietal cells which means there is a V. high production of acid which causes sever ulceration of the stomach + small bowel.

37
Q

What sort of cancers do you get of the Stomach? Cancer has to be quite large to present with symptoms but what are they?

A
  • Majority of cancers are Adenocarcinomas, small number or Lymphomas, Carcinoid + Stromal
  • Presents with; Dysphagia, Weight loss, Loss of appetite, Nausea/Vomiting, Malaena + Virchow’s nodes (Lymph node in left Subclavicular fossa
38
Q

What are the qualities of Chyme after it leaves the stomach?

A
  • Acidic (This is corrected by HCO3 secreted by the Pancreas, Liver + Duodenal mucosa. HCO3 is produced during the production of Gastric acid)
  • Hypertonic (Food produces lots of solutes dissolved in chyme + stomach is impermeable to water. Corrected by Osmotic movement into lumen)
  • Partly Digested
39
Q

What is the Structure of Liver lobules?

A

Central Vein surrounded by Interlobular Triads (Hepatic Portal Vein, Hepatic Artery, Biliary Duct) In between these are Hepatocytes. Bile drains out of Biliary ducts. Blood flows from Interlobular Triads to the central veins being filtered by Hepatocytes. Bile flows the other way along Canaliculi

40
Q

What is Inflammation of the Gallbladder called?

A

Cholecystitis

41
Q

Describe the Secretion and passage of Bile

A

In response to Gastric emptying he duodenum secretes Cholecystokinin (CCK) which causes contraction of the bladder + secretion of Bile acid with enzymes from pancreas through the Ampulla of Vater. Continue to the terminal Ileum where they are actively reabsorbed by the epithelium and returned to the liver where they are actively uptake by Hepatocytes + re secreted into Canaliculi

42
Q

What enzymes are produced in the Pancreas?

A
  • Active (Amylase, Lipases)

- Inactive (Trypsin, Chymotrypsin, Elastase, Carboxypeptidase)

43
Q

Describe the Production + Secretion of Pancreatic Enzymes

A

Enzymes are formed + packaged into Zymogen Granules + secreted by exocytosis to be activated in the duodenum by enzymatic cleavage to prevent digestion of Pancreas.
Secreted into the Acinus + Duct cells modify the aqueous secretions

44
Q

Describe the breakdown of Fats + their transport into the vascular circulation

A

Bile acids emulsify fats and form Micelles (Carry Cholesterol, Monoglycerides, Free Fatty Acids). Diffuse down conc. gradient into cells + re-esterified back to Triglycerides, Phospholipids + Cholesterol, these are then converted into Chylomicrons with Apoproteins + exocytosed from the basolateral membrane into Lymph capillaries, re-enter vascular circulation via the thoracic duct into the left subclavian vein

45
Q

What is Steatorrhoea? When do you get this?

A

Fat appearing in stool. Happens when bile acids or pancreatic lipases are not secreted in adequate amounts.

46
Q

Whats the name of the innate defensive cells in the Liver?

A

Kupffer Cells

47
Q

What is Xerostomia? What can it be caused by? What does it lead to?

A
  • Reduction in salivary flow
  • Can be caused by Severe Dehydration, Diabetes, HIV, some Medication
  • Leads to Microbacterial overgrowth in the mouth, this can lead to Parotitis
48
Q

What is Achlorhydria? Whats it caused by? What does it lead to?

A
  • Reduced production of of Gastric Acid
  • Caused by Pernicious Anaemia, H2 Antagonists, PPI’s
  • Patients more susceptible to Cholera, Shigella + salmonella. Hospital patients have an increased risk of C. diff
49
Q

Which organisms are resistant to Gastric Acids?

A

Mycobactum TB + Enteroviruses (Hep.A, Polio + Coxackie) are resistant to Gastric acid.
H. pylori produces urease which breaks down urea into ammonia to produce a cloud of protective ammonia

50
Q

What can cause Appendicitis?

A
  • Lymphoid hyperplasia at base of appendix causing reduced flow (stasis -> Infection)
  • Appendix may be obstructed by a faecolith (calcified faeces)
  • May be obstructed by worm
51
Q

What can cause Liver Failure? What does Liver failure cause?

A
  • Caused by (Hepatitis, Alcohol, Drugs (Paracetamol), Industrial solvents, Mushroom poisoning
  • Leads to; increased susceptibility to infections, toxins eat. Increased blood ammonia due to failure of urea cycle. Increased ammonia levels can cause Hepatic Encephalopathy
52
Q

What does Liver Cirrhosis lead to?

A

Portal venous hypertension -> Portosystemic shunting + therefore toxin shunting
This causes Oesophageal Varices due to increased BP from collateral blood flow of liver. Haemorrhoids + Caput Medusa

53
Q

What is Pre-Hepatic Jaundice caused by? What would the lab findings be for a patient suffering with Pre-Hepatic Jaundice?

A
  • Caused by excessive production of Bilirubin usually with the increased breakdown of RBC’s and liver is unable to cope with abnormally high levels
  • Lab results would show; Unconjugated Hyperbilirubinaemia, Reticulocytosis (High reticulocytes), Anaemia, high Lactate Dehydrogenase, low Hepatoglobin
54
Q

What is Hepatic Jaundice caused by? What would the lab findings be for a patient suffering with Hepatic Jaundice?

A
  • Caused by reduced capacity of liver cells to secrete conjugated bilirubin into the blood
  • Lab results would show; Mixed unconjugated + conjugated bilirubin, Increased liver enzymes ALT/AST, Abnormal clotting
55
Q

What is Post-Hepatic Jaundice caused by? What would the lab findings be for a patient suffering with Post-Hepatic Jaundice?

A
  • Caused by obstruction to drainage of bile causing a back up of Bile acids into the liver
  • Lab results would show; Conjugated Bilirubin, Bilirubin in urine (Dark in colour), Increase in canicular enzymes, ± Increase in liver enzymes
56
Q

What does Excessive Alcohol consumption do to the Liver?

A
  • Fatty liver - Alcohol metabolism produces NADH which induces production of TAG’s from Glycerol which accumulates in Liver
  • Alcoholic Hepatitis - inflammation of Hepatocytes
57
Q

What is Liver Cirrhosis?

A

Liver cell necrosis followed by nodular regeneration + fibrosis resulting in resistance to blood flow + deranged function

58
Q

How is Ascites developed in Portal Hypertension?

A

Increased Pressure in portal system means blood backs up into the abdomen causing an increase in Hydrostatic pressure. If you have liver damage reduced albumin can cause reduced oncotic pressure in the vessels as well.

59
Q

What is Acute Pancreatitis? Whats the presentation? What can cause it?

A
  • Inflammatory process caused by effects of enzymes released from pancreatic acini
  • Acute presents with; Oedema, Haemorrhage, Severe Pain, Vomiting, Dehydration, Shock. Have increased Amylase
  • Chronic presents with Pain, Malabsorption due to Fibrosis + calcification
  • Causes - GET SMASHED (Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion bite, Hyperlipidaemia, Endoscopic Retrograde Cholangiopancreatography, Drugs)
60
Q

Whats the presentation of Pancreatic Carcinoma?

A

Initially asymptomatic then lots of symptoms at once; Obstructive jaundice, Pain, Vomiting, Malabsorption, Diabetes

61
Q

Whats absorbed by the Jejunum?

A

Carbohydrates + Amino acids

62
Q

Whats absorbs in the Ileum?

A

Anything not absorbed in the Jejunum + Vit. B12 + Bile

63
Q

How are Carbohydrates ingested?

A

In the form of Amylose (straight chain with α-1,4 bonds) and Amylopectin (Branched with α-1,6 bonds at branches)

64
Q

How are Amino Acids absorbed?

A

Proteins are digested to short peptides, 10-20AA’s long by pepsin secreted by chief cells in stomach + Peptidases from pancreas in Duodenum.

65
Q

How is Iron absorbed?

A

Can only be absorbed in ferrous form (Fe2+), Gastric acid makes it ferrous + is bind by Gastroferrin which is secreted by stomach to keep it ferrous. Transferrin then transports it to epithelial cells

66
Q

How is Vitamin B12 absorbed?

A

Intrinsic factor secreted by Parietal cells binds B12 to keep it soluble and absorbed together. This can be damaged if Parietal cells are damaged or if the terminal Ileum is removed

67
Q

Describe the Motility through the Intestines

A
  • Small intestines (Segmenting - SI divided into sections which each contain a pacemaker, the frequency gets slower from Duodenum to terminal Ileum, The Intestinal Gradient. This causes net movement down tract)
  • Large Intestine (Haustral Shuffling, LI divided into Haustra which contract in the same intestinal gradient as SI. Mass Movement happens a couple of times a day which is peristaltic propulsion of faeces from transfers through descending colon into the rectum inducing urge to defecate)
68
Q

Describe Defecation

A

Once Mass movement has filled rectum pressure receptors cause an urge to defecate. Waves of contraction in rectal muscle then forces faeces towards the anus. There is an Internal Anal Sphincter under parasympathetic control + External Anal Sphincter under voluntary control. Once both sphincters are relaxed intra abdominal pressure is increase + there is an expulsion of Faeces

69
Q

What is Ulcerative Colitis?

A

Inflammatory Disorder which affects Rectum + extends proximally with no breaks in inflammation. Patients present with Rectal bleeding, Diarrhoea + Abdominal pain

70
Q

What is Crohn’s Disease?

A

Chronic inflammation potentially involving any location of GI tract. Presentation depends on the location in the tract. Upper GI (Nausea/Vomiting, Dysplasia, Small bowel obstruction, Weight loss) Terminal Ileum (Pernicious Anaemia), Lower GI (Diarrhoea, Passage of Blood)

71
Q

Whats the treatment of Ulcerative Colitis?

A

Topical Corticosteroids, for Extensive Colitis (Up to Hepatic Flexure) use Oral Corticosteroids + Infliximab (Antibody against Tumour Necrosis Factor)

72
Q

Whats the treatment of Crohn’s Disease?

A

Induction of Remission (Oral or IV Glucocorticoids), Maintenance of Remission (Immunosuppressant [Methotrexate] + Infliximab [Anti-TBF Antibodies]), Perianal Disease (Antimicrobials [Ciprofloxacin + Metronidazole]), Surgical Management (Colectomy, Ileorectal Anastomosis)

73
Q

What Vitamins are excreted by Normal Flora in the intestines?

A

Vit. K, Vit. B12, Thiamine

74
Q

What is given Prophylactically to patients who are undergoing dirty surgery?

A

Metronidazole (Kills all anaerobes), Broad Spectrum Antibiotics (Gentamicin or Cephalosporin)

75
Q

What is the Normal Flora of the Vagina and what is its function?

A

Lactobacillus (Gram +ve Bacilli) is normal Flora. It converts Glycogen into Lactic Acid which provides a slightly acidic environment to prevent other bacteria + Candida albicans (Thrush) from growing

76
Q

What causes Travellers Diarrhoea? How does it cause symptoms?

A

Enterotoxinogenic E. Coli.

Produces Heat Stable or Labile Toxins which result in severe Cholera like Diarrhoea

77
Q

What is Cholera caused by and how does it cause Diarrhoea?

A
  • Caused by Vibrio cholerae

- Causes massive movement of Salt + water into the lumen causing Diarrhoea

78
Q

What sort of cancer would an Oesophageal Carcinoma be? Whats the Prognosis?

A
  • Squamous cell carcinoma - most common type, Can occur at any level
  • Adenocarcinoma - Rare, found in the lower third often in association with Barrettes oesophagus
  • Normally presents at an advanced disease state, direct spread through oesophageal wall, only 40% are resectable. 5% 5 year survival.
79
Q

How does Gastric Cancer present? Whats the Prognosis?

A
  • Presents with vague symptoms - Epigastric pain, Vomiting + weight loss. Signet ring cells
  • Early Gastric cancer confined to the submucosa has a good prognosis. Spread is direct through the Gastric wall into Duodenum, Transfers Colon, Pancreas, Lymph Nodes, Liver + Peritoneum. When presenting with advanced cancer it has a 10% 5 year survival.
80
Q

Describe the pathway of the involvement of H. pylori with Gastric Cancer. What cancer is H. pylori Commonly associated with?

A

Normal Gastric Mucosa -> H. pylori Infection -> Acute Gastritis -> Chronic Gastritis -> Intestinal Metaplasia -> Dysplasia -> Advanced Gastric Cancer
Has a strong association with Gastric Lymphoma, eradication of H. pylori can cause regression of tumour

81
Q

What is the spread and staging of Colorectal Carcinomas?

A
  • Spread direct through bowel wall to adjacent organs (Bladder), via lymph to mesenteric Lymph nodes, via portal venous system to liver
  • Dukes staging
  • A - Confined to bowel wall
  • B - Through wall, Lymph nodes clear
  • C - Involvement of Lymph nodes
  • D - Widespread Metastases
82
Q

Where is the most common site of Pancreatic Tumours? What is the most common type of Pancreatic Tumour? Whats the spread of the tumours?

A
  • 2/3rd are in head of pancreas, normal a pale firm mass with a necrotic centre
  • 80% are ductal Adenomas, some acinar tumours contain zymogen granules
  • Spread to adjacent structures (spleen)

Medicine A100 (6 decks)

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