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Flashcards in GI Deck (82)
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1
Q

What are the three variants of saliva that can be produced by the body?

A
  1. Serous - watery with low mucus content. Produce by the parotid gland.
  2. Mucus - Thick mucus saliva, produced by the sublingual gland.
  3. Mixed
2
Q

What is the drainage of the parotid gland into the oral cavity?

A

Stensons duct adjacent to the upper second molar

3
Q

What is the drainage of the submandibular gland into the oral cavity?

A

Wharton duct on either side of the lingual frenulum

4
Q

Name the three portions of a salivary secretory unit

A
  1. Acinus
  2. Intercalated duct
  3. Striated duct
5
Q

Describe the production of saliva in its two stages, secretory and modification

A
  1. Occurs in the acinus, fluid (which is isotonic with the blood plasma) is secreted into the lumen.
  2. Duct cells remove Na and Cl adding HCO3. Gaps between cells are tight so water doesn’t follow producing a hypotonic solution.
6
Q

What difference does the flow rate make to the tonicity and pH of saliva?

A

At low flow rates most of the Na and Cl is removed so saliva is very hypotonic. The stimulation of of the ducts promotes the secretion of HCO3 so at high flow rates the saliva is more alkaline.

7
Q

How are serous secreting cells in the acinus seen on stained slides?

A

Stain pink and form a serous demilune

8
Q

Name and describe the two phases of the oral phase of swallowing

A
  1. Preparatory phase - food is chewed + mixed with saliva to form a bolus. It is positioned on the tongue.
  2. Transit phase - Tongue pushes the bolus upwards and posteriorly. The bolus activates sensory receptors on the anterior tonsillar pilar and pharyngeal part of the tongue initiating the pharyngeal phase of swallowing.
9
Q

Describe the pharyngeal phase of swallowing

A

Triggered when food touches the anterior tonsillar pillars. Soft palate is raised to close of the nasopharynx. Hyoid bone + larynx are raised leading to the epiglottis sealing off the airway. Movement of the tongue up and back forces food backwards into the oesophagus.

10
Q

Describe the oesophageal phase of swallowing

A

When the bolus passes through the upper oesophageal sphincter it constricts initiating a peristaltic wave. If the first wave doesn’t clear the oesophagus a second is initiated above the site of the bolus.

11
Q

What muscle attends the upper oesophageal sphincter?

A

Cricopharyngeus

12
Q

What is the arcuate line (line of Douglas)?

A

The point where the posterior rectus sheath disappears. Used as the point of incision for Caesarian sections.

13
Q

What is Divarication of Recti?

A

Linear alba can become weak after pregnancy causing it to be pushed out a little.

14
Q

What is a Rectus Haematoma?

A

Bleeding into the recuts abdominis. Can happen in patients on warfarin

15
Q

What is a patent vitellointestinal duct?

A

Connection between the small intestine and the umbilicus

16
Q

What is exomphalos?

A

Gut is outside of the abdomen covered in peritoneum

17
Q

What is Gastroschisis?

A

Gut outside of the abdomen. Not covered in peritoneum

18
Q

Where does pain in the forgut refer to?

A

Epigastric region

19
Q

Where does pain in the midgut refer to?

A

Periumbilical region

20
Q

Where does pain from the hind gut refer?

A

Suprapubic region

21
Q

What is the area of weakened fascia through which a direct inguinal hernia is most likely to occur? What are its boundaries?

A
  • Hesselbach’s triangle
    Inferior: Inguinal ligament
    Medial: Rectus abdominus
    Latteral: Inferior epigastric artery
22
Q

What are the two complications of hernias?

A
  1. Strangulation

2. Incarceration

23
Q

What are the four main parts of the stomach from top to bottom?

A
  1. Fundus
  2. Body
  3. Antrum
  4. Pylorus
24
Q

What are the 5 main cell types in the stomach and what do they produce?

A
  1. Parietal cells - HCL + Intrinsic factor
  2. G cells - Gastrin
  3. Enterochromafin cells - Histamine
  4. Chief cells - Pepsinogen
  5. D cells - Somatostatin
25
Q

In what there ways are parietal cells stimulated?

A
  1. Vagus nerve stimulates production through Ach receptor.
  2. Gastrin binds to CCK receptors.
  3. Histamine binds to H2 receptors.
26
Q

What cells produce HCL and intrinsic factor in the stomach?

A

Parietal cells

27
Q

Which cells produce Gastrin?

A

G cells

28
Q

Which cells produce histamine in the stomach?

A

Enterochromafin cells

29
Q

Which cells produce pepsinogen in the stomach?

A

Chief cells

30
Q

Which cells produce somatostatin in the stomach?

A

D cells

31
Q

Where are G cells located in the stomach? What are three things that stimulate them?

A
  • Antrum
    1. Vagus nerve
    2. Peptides + amino acids in stomach
    3. Gastrin releasing peptide
32
Q

How is the production of HCL inhibited?

A
  • When food leaves the stomach the pH drops activating D-cells to produce somatostatin which inhibits the secretion of Gastrin.
  • As the stomach shrinks there is reduced stimulation from the vagus nerve.
33
Q

How is HCL produced and pumped into the stomach?

A
  1. Water splits into H+ and OH-.
  2. Co2 enters cell and combines with OH- by carbonic anhydrase to produce HCO3-.
  3. HCO3 leaves cell and Cl enters through anion antiporter. Cl moves into stomach through Cl channel.
  4. H+ is pumped into the stomach by the K/H ATPase.
  5. K+ leaks back into the stomach. H+ combines with Cl to produce HCL
34
Q

Name the three phases of digestion

A
  1. Cephalic - smelling, tasting, swallowing of food.
  2. Gastric
  3. Intestinal
35
Q

What function do prostaglandins have in the stomach?

A

Maintain the mucosal blood supply to provide the epithelium with nutrients.

36
Q

Name three things which can breach the stomachs defences and how it causes damage.

A
  1. Alcohol - Breaks down mucus layer
  2. H. pylori - Invades stomach lining + produces cytokines causing gastritis.
  3. NSAID’s - Inhibit prostaglandins reducing blood supply to epithelium.
37
Q

Name the two forms of pharmacological interventions used to reduce gastric acid and how they work

A
  1. H2 blockers - Prevent the binding of histamine to H2 receptors on Parietal cells.
  2. Proton Pump Inhibitors - Block the H/K ATPase preventing H+ from being pumped into the stomach.
38
Q

Name the 5 ligaments of the liver

A
  1. Falciform - Attaches the liver to the anterior body wall. Divides liver into right and left lobes.
  2. Round ligament of Liver - Remnant of umbilical vein. Divides left part of liver into medial and lateral parts.
  3. Left triangular - Continuous with falciform. Attaches to the diaphragm.
  4. Right triangular - Attaches to the diaphragm.
  5. Coronary - Holds liver to the inferior surface of the diaphragm.
39
Q

Describe the Biliary tree

A
  1. Bile is continuously secreted into canaliculi.
  2. These drain into interlobar biliary ducts which merge to form the left and right hepatic bile ducts.
  3. After leaving the ports hepatis they fuse to form the common hepatic bile duct.
  4. The cystic duct from the gall bladder joins the common hepatic bile duct to form the common bile duct.
  5. The pancreatic duct joins the common bile duct shortly before the Ampulla of Vater where it drains into the duodenum.
40
Q

Where are four common places that gall stones can be found/become lodged? What do they cause?

A
  1. Within gall bladder - Asymptomatic.
  2. Cystic duct - Acute cholecystitis.
  3. Common bile duct - Biliary obstruction (abdominal pain, dark urine).
  4. Terminal Duct - Pancreatitis
41
Q

What is the arterial supply for the gallbladder and cystic duct?

A

Cystic artery

42
Q

What is the arterial supply of the pancreas?

A

Pancreatic branches of the splenic artery. The head is supplied by superior and inferior pancreaticoduodenal arteries which are branches of the gastroduodenal and the superior mesenteric arteries.

43
Q

Which arteries supply the greater curve of the stomach?

A

Left and right gastro-omental arteries

44
Q

What is intrinsic factor needed for? What can a deficiency cause?

A
  • Absorption of vitamin B12

- Pernicious anaemia due to B12 being needed for the formation of stable erythrocytes.

45
Q

What is autoimmune chronic gastritis? How does it present?

A
  • Body produces antibodies against parietal cells
  • Present with symptoms of anaemia, glossitis (large inflamed tongue), anorexia and neurological symptoms (numbness + balance due to B12 deficiency)
46
Q

Name four causes of acute gastritis

A
  1. NSAID’s
  2. Alcohol
  3. Chemotherapy
  4. Bile reflux
47
Q

What are the interlobular portal triads in the liver made up of? Which direction do products move?

A
  1. Hepatic portal vein
  2. Hepatic artery
  3. Biliary duct
    - Blood flows from the interlobular portal triads to the central vein. Bile flows the opposite way along canaliculi into the biliary ducts.
48
Q

Describe the release and re-uptake of bile

A
  1. Gastric emptying causes the release of Cholecystokinin from the duodenum.
  2. CCK causes contraction of the gall bladder and the secretion of bile.
  3. Bile is actively reabsorbed in the terminal ileum.
  4. Venous return from the gut enters the hepatic portal blood where hepatocytes actively uptake bile salts and re-secrete them into canaliculi.
49
Q

Give two examples of active enzymes and four examples of inactive enzymes produced in the pancreas

A
  1. Amylase
  2. Lipases
    Proteases
  3. Tripsin
  4. Chymotrypsin
  5. Elastase
  6. Carboxypeptidase
50
Q

What stimulates secretions from the pancreas? Three things for Acinus, one for the duct cells

A
  1. Vagus nerve
  2. Cholecystokinin
  3. Fats in the duodenum
  4. HCO3 secretion stimulated by secretin produced when a low pH in the jejunum
51
Q

What three things are carried within Micelles? What happens to the contents after the are inside epithelial cells?

A
  1. Cholesterol
  2. Monoglycerides
  3. Free fatty acids
    - Re-esterified back to triglycerides, phospholipids and cholesterol. These are formed into chylomicrons with apoproteins.
52
Q

Whats it called when there is fat in the faeces?

A

Steatorrhoea

53
Q

Where does the foregut end? Which artery is it supplied by?

A
  • Distal to the major duodenal papilla

- Celiac trunk

54
Q

Where does the Midgut begin and end? Which artery is it supplied by?

A
  • Begins distal to the major duodenal papilla and ends before the left colic flexure.
  • Supplied by the superior mesenteric artery.
55
Q

Where does the Hindgut begin? Which artery is it supplied by?

A
  • Begins before the left colic flexure

- Inferior mesenteric artery

56
Q

What is the name of the muscles that run longitudinally along the large bowel? What is the name of the pouches they cause?

A
  • Tenia Coli

- Haustra

57
Q

Which artery forms anastomoses between the superior and inferior mesenteric arteries?

A

Marginal artery of the colon

58
Q

What in children can commonly be mistaken as being appendicitis?

A

Mesenteric adeninis (inflammation of mesenteric lymph nodes)

59
Q

What is it called when you have a reduced production of saliva?

A

Xerostomia

60
Q

What is it called when there is a reduced production of gastric acid?

A

Achlorhydria

61
Q

Where are Payer’s patches found? What can cause inflammation of these patches?

A
  • Ilium

- Typhoid fever

62
Q

Name three causes of Appendicitis

A
  1. Lymphoid hyperplasia
  2. Obstruction by faecolith
  3. Obstruction by worm
63
Q

What is the name of the confusion caused by build up of waste in the blood due to liver failure?

A

Hepatic Encephalopathy

64
Q

What can be caused by portal venous hypertension?

A
  • Oesophageal varicies
  • Haemorrhoids
  • Caput medusa
65
Q

Name 5 causes of hepatic jaundice

A
  1. Congenital (Gilberts, Crigler-Nanjjar syndromes)
  2. Hepatic inflammation (Viral, alcohol, haemochromatosis, Wilson’s disease)
  3. Drugs
  4. Cirrhosis
  5. Hepatic tumours
66
Q

Explain how excessive alcohol consumption causes a fatty liver

A
  1. Alcohol metabolism produces NADH from NAD+.
  2. Reduced NAD+ means there is reduced fatty acid oxidation.
  3. Glycerol is converted to TAG’s which accumulate causing fatty liver
67
Q

Name the causes of pancreatitis

A
  • Gall stones
  • Ethanol (alcohol)
  • Trauma
  • Steroids
  • Mumps + Malignancy
  • Autoimmune
  • Scorpion bite
  • Hyperlipidaemia
  • Endoscopic Retrograde Cholangiopancreatography
  • Drugs
68
Q

What binds iron in the gut to keep it in the ferrous form?

A

Gastroferrin

69
Q

Describe the motility in the small intestine

A

Intestines are divided into segments, each with their own pacemaker. From duodenum to terminal ilium there is a reduction in frequency called the intestinal gradient which causes the net movement down the intestine.

70
Q

What are the two types of motility in the large intestine?

A
  1. Haustral shuffling

2. Mass movement

71
Q

What are the macro and microscopic changes seen in ulcerative colitis?

A
Macroscopic 
- Mucosa is reddened, inflamed and bleeds easily. 
- In severe ulceration normal mucosa looks like polyps 
Microscopic 
- Superficial inflammation 
- Chronic inflammatory infiltrate. 
- Goblet cell depletion 
- Crypt abscesses
72
Q

What is the treatment for Ulcerative colitis?

A

Corticosteroids

73
Q

What are the macro and microscopic changes seen in Chron’s disease?

A
Macroscopic 
- Bowel thickened and narrowed
- Deep ulcers + fissures 
- Mucosa has a cobblestone appearance 
Microscopic 
- Transmural inflammation 
- Lymphoid hyperplasia 
- Granulomas
74
Q

What is the treatment for Chron’s disease?

A

Glucocorticoids

Immunosuppressants

75
Q

What is the causative organism for gingivitis?

A

Streptococcus mutans

76
Q

What is the most common causative organism for tonsillitis?

A

Strep. pyogenes

77
Q

What is the most common cause of bacterial endocarditis?

A

Strep. viridians

78
Q

What is the causative organism for gas/wet gangrene?

A

Clostridium perfringes

79
Q

What is the causative organism for cholera?

A

Vibrio cholerae

80
Q

What is the causative organism of Travellers diarrhoea?

A

Enterotoxinogenic E. coli

81
Q

What are the two types of oesophageal carcinomas?

A
  1. Squamous cell carcinoma - most common, can occur at any hight.
  2. Adenocarcinoma - lower third, normally associated with barretts oesophagus.
82
Q

What is the staging used for colorectal adenocarcinomas? What are the stages?

A
- Dukes staging 
A. Confined to the bowel wall. 
B. Through wall, lymph nodes clear. 
C. Involvement of lymph nodes. 
D. Widespread mets.