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DIG Flashcards

1
Q

What is the start and end of the foregut?

A

Starts at the mouth and ends where the bile duct meets the Duodenum D2 (major duodenal papilla)

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2
Q

What is the sphincter of Oddi?

A

A muscular valve that controls the flow of digestive juices (bile and pancreas secretions) from the Ampulla of Vater into the duodenum.

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3
Q

What is the Ampulla of Vater?

A

Point at which the common bile duct meets the Pancreatic duct.

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4
Q

What is the start and the end of the midgut?

A

Starts at the point where the bile duct meets the duodenum and ends two thirds of the way across the transverse colon.

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5
Q

What is the start and the end of the hindgut?

A

Starts after two thirds of the way along the transverse colon and ends at the anus.

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6
Q

What is the parasympathetic supply to the foregut?

A

Vagus nerve (X)

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7
Q

What is the parasympathetic supply to the midgut?

A

Vagus nerve (X)

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8
Q

What is the parasympathetic supply to the hindgut?

A

S2-S4

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9
Q

How is visceral peritoneum pain felt?

A

Autonomic nerves- Dull, diffuse, aching pain, poorly localised.

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10
Q

How is parietal peritoneum pain felt

A

Somatic nerves- Sharp, stabbing, well localised pain

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11
Q

What is the function of mesentries?

A

Stops organs from moving too much and provides conduit for other body systems.

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12
Q

What does the falicform ligament do?

A

Connects the liver to the anterior body wall

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13
Q

List 6 things that cause abdominal distension?

A 
Fluid
Faeces
Flatus
Foetus
Fat
Mass
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14
Q

Where are the three common sites of abdominal hernias?

A

Inguinal, Umbilical and epigastric

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15
Q

How are the muscles of the abdominal wall innervated?

A

multi-segmental innervation by spinal nerves T7-T12

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16
Q

What can be the result of damage to the nerves of the anterolateral abdominal wall?

A

Can weaken or paralyse muscles of the abdominal wall resulting in predisposition to hernias e.g. inguinal hernia

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17
Q

What surface marking allows the appendix to be found?

A

McBurney Point, its a third of the way between the ASIS and the umbilicus.
This is the point where the base of the appendix is attached to the caecum.

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18
Q

What is an indirect inguinal hernia?

A

Herniation of the parietal peritoneum through the deep inguinal ring of the inguinal canal.
This means it will pass laterally to the inferior epigastric vessels.

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19
Q

What is a direct inguinal hernia?

A

Herniation of the parietal peritoneum directly through transversalis fascia in the inguinal triangle.
This means it will pass medially to thee inferior epigastric vessels.

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20
Q

What are the borders of the inguinal triangle?

A

Laterally- inferior epigastric vessels
Medically- Rectus abdominus
Inferiorly- Inguinal ligament

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21
Q

What is the lesser omentum?

A

Double layered peritoneal fold connection the lesser curvature of the stomach to the liver.

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22
Q

What is the greater omentum?

A

A 4 layered peritoneal fold that hang down connecting the greater curvature of the stomach to the transverse colon

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23
Q

What are the boundaries of the omental foramen?

A

Anteriorly- Hepatoduodenal ligament (free edge of lesser omentum), portal triad (hepatic artery, portal vein, bile duct)
Posteriorly- IVC and a muscular band overlaid with peritoneum.
Superiorly- Liver
Inferiorly- first part of the duodenum

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24
Q

What is ascites?

A

Excess accumulation of fluid in the peritoneal cavity (greater than 25ml) up to 35 litres are possible.

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25
Where is inflammatory exudate in the peritoneal cavity accumulate in an upright patient?
Will be carried along the paracolic gutters into the pelvis
26
Why would a patient with ascites be positioned in a sitting position?
To assist the flow of exudate into the pelvic cavity where absorption of toxins is slow
27
What artery supplies the lesser curvature of the stomach?
Left gastric artery anastomoses with right gastric artery. Left gastric is a branch off the celiac trunk. Right gastric is a branch off the hepatic artery
28
What artery supplies the greater curvature of the stomach?
Left gastro-omental artery- branch from splenic artery | Right gastro-omental artery meets it on greater curvature- branch of gastroduodenal artery
29
What is the venous drainage of the stomach?
Drains into the portal vein either directly via the left and right gastric veins (lesser curvature) or indirectly from the splenic or superior mesenteric vein (greater curvature)
30
what saliva is produced by the parotid gland?
Watery serous saliva
31
What saliva is produced by the submandibular gland?
mixed serous and mucous saliva
32
What saliva is produced by the sublingual gland?
Mixed thick mucous saliva
33
Which salivary gland produces the majority of saliva?
Submandibular (60%)
34
What is thee innervation of the parotid gland?
CN IX Glossopharangeal nerve
35
What is the innervation of the submandibular gland?
Chorda tympani branch of facial nerve
36
What is the innervation of the sublingual gland?
Chorda tympani branch of facial nerve
37
what are the muscles of mastication?
Massater, temporalis, lateral pterygoid and medical pterygoid
38
What nerve innervates the muscles of mastication?
Mandibular branch of the trigeminal nerve
39
What nerves are responsible for the gag reflex?
CN IX glossopharangeal and CN X vagus
40
What is likely to paralyse the hypoglossal nerve? what is the result of this?
Fracture of the mandible is likely to paralyse it. | tongue deviates towards affected side and eventually may atrophy on that side.
41
What is hiatal hernia? where would pain be experienced?
Protrusion of part of the stomach into the mediastinum through the oesophageal hiatus of the diaphragm. Pain would be felt as heartburn from reflux so would be a central chest pain.
42
What is barrett's oesophagus? when is this seen?
Barrett's oesophagus refers to a metaplasia (abnormal change in cells) of the lower oesophagus. This is a change from stratified squamous cells of the oesophageal epithelium to simple columnar epithelium of the stomach. It is caused by repeated reflux of stomach acid.
43
Where is the myenteric plexus located?
Between the circular and longitudinal muscle.
44
Where is the submucosal plexus located?
In the submucosa, betwen the muscular layers and the mucosal layers
45
What does the myenteric plexus do?
Increases the rate and intensity of contractions when stimulated.
46
What does the submucosal plexus do?
Increases secretions when stimulated.
47
what is the meedical name for heartburn?
pyrosis
48
What is pyloric stenosis?
Hypertrophy of the pyloric sphincter resulting in reduced gastric emptying, this causes dilation of the stomach
49
What causes oesophageal varicoces?
Portal hypertension may haemorrhage common in alcohol cirrhosis
50
What is the main cause of gastric and peptic ulcers and how do they occur?
Helicobacter Pylori, erodes protective mucus lining of the stomach, inflamming the mucosa and making it vulnerable to the effects of gastric acid.
51
What are two different types of papilla on the tongue?
Fungiform papilla-tooth shaped, contain taste buds | Filiform papilla-spiky heavily keratonised, makes tongue rough
52
histologically what are the clear flask shaped objects found in tongue papilla?
Taste buds
53
What is intrinsic factor necessary for?
Absorption of vitamen B12 later on in the digestive system.
54
What is vitamin D important for?
Uptake of calcium
55
Which cells produce CCK in the digestive system?
I-cells in the duodenum
56
What is CCK produced in responce to and what does this do?
Produced in responce to fat in duodenum. | Stimulates pancreatic enzyme release and inhibits acid production in stomach
57
Where does the jejunum start?
duodenojejunal flexure after the duodenum has crossed the aorta
58
How does Helicobacter Pylori resist the acidic environment in the stomach?
It has urease enzymes of its cell surface that convert urea and water to ammonia which is basic so neutralises the HCL around it.
59
Why does Helicobacter Pylori cause stomach ulcers?
Creates channels down through the mucus to the epithelial cells that allows HCL to reach and damage them along with H. Pylori toxins. Inflammation caused by this promotes further acid secretion that further damages cells
60
How does H. Pylori cause duodenal ulcers?
Hyper secretion from the stomach due to the bacteria means some stomach acid gets through to the duodenum and causes ulcers.
61
How do you diagnose a H. Pylori ulcer?
Urea breath test: Chemically tagged urea consumed If H. Pylori present then urea converted to CO2 and ammonia Co2 breathed out and chemical tag can be identified.
62
How can NSAIDs lead to gastric bleeding?
They block both COX 1 and 2 leading to blockage of the physiological and inflammatory pathways. As COX 1 is blocked this causes a reduction in the prostaglandins required for maintenance of mucosal barrier. Leads to gastric bleeding
63
What affect do Glucocorticoids have on the COX Pathways?
Phospholipase A2 is inhibited by the glucocorticoids This inhibits production of aracidonic acid from phospholids This Inhibits COX 2 as there is not enough aracidonic acid so affects production of prostaglandins Hence has anti inflammatory effect
64
What enzyme is involved with the first step of eicosanoid synthesis?
Phospholipase A2
65
What are the two alternative pathways in the second step of eicosanoid synthesis?
``` COX (cycloxygenase) pathway (prostaglandins and thromboxanes) Lipoxygenase pathway (leukotrienes) ```
66
What converts Pepsinogen to Pepsin?
HCL
67
What is the main enzyme that breaks down proteins into amino acids?
Trypsin from the the prohormone trypsinogen
68
How are small peptides and dipeptides absorbed in the Intestine?
Through PEPT1 channels that co-transport them with H+ ions into the cell. broken down by intracellular peptidases to amino acids They then diffuse into the blood.
69
How are amino acids absorbed in the intestine?
Through channels that couple their transport with sodium
70
How is starch absorbed into the blood stream?
Broken down by enzymes to glucose Glucose cotransported into enterocytes with sodium (2 Na+ for every glucose) Glucose then moved into blood by Glut2 transporter
71
What is the difference between the GLUT2 transporter and the GLUT4 transporter?
GLUT2 is not affected by insulin | GLUT4 is affected by insulin
72
What is a cholymicron?
Lipoprotein that is predominantly lipids | How fatty acids are packaged in cells
73
How are cholymicrons absorbed into the blood from enterocytes?
Via the lymphatic system
74
How do statins work?
Inhibit enzyme that converts acetyl CoA to cholesterol | Hence reduces cholesterol levels resulting in less atheroma
75
What does the liver do with fatty acids?
Makes lipoproteins
76
How does hepcidin regulate iron uptake?
It is produced by the liver and inhibits iron uptake | Does this by binding to ferroportin transporters causing then to be internalised and degraded
77
Give an example of a condition with excess body iron?
Heamochromatosis- genetically recessive condition leading to non functioning hepcidin resulting in high iron levels Can cause cirrhosis
78
What is an example of a condition that could present with erosive damage to the inside of the palate and teeth?
Bulimia nervosa
79
What causes excess ketone bodies in the blood?
Usually from diabetes This is because there is no insulin to inhibit lipolysis so there are lots of fatty acids present These saturate the TCA so are converted to ketone bodies
80
What causes urea blood levels to be high?
Increased protein catabolism Can happen if starving and breaking down muscle Amino acids can then be used for gluconeogenesis
81
How can ketone bodies be used in starvation?
They can be converted to acetyl CoA and used by the brain for Krebs cycle
82
What are the stages of starvation?
- Use up glucose in food - Use up glycogen (around 24 hours) - Gluconeogenesis (first 2 days, break down proteins + lose muscle mass) - Liver converts fat to ketone bodies (day 8+, lasts 3 months)
83
What are the three types of movement in the GIT?
- Propulsive movements by peristalsis - Non-propulsive movements by Segmentation - Interdigestive by the Migratory Motor Complex
84
What does the Migratory Motor Complex do?
Interdigestive movements of GIT Appears in fasting and is nutritional and cleansing Clears small intestine of residual content Prevents backflow of particulates
85
What is gastric dumping syndrome?
If the pyloric sphincter is defective then chyme can move quickly into the blood This causes water to move out of the blood into the lumen causing a fall in blood pressure and faintness It also triggers excessive insulin release causing a fall in blood glucose
86
What are the intestinal smooth muscle pacemaker cells?
The ICC (Interstitual cells of CAJAL)
87
Which part of haemoglobin produces unconjugated bilirubin?
Haem part minus the Fe2+
88
What happens when conjugated bilirubin is excreted into the intestine with bile salts?
Converted by intestinal bacteria to urobilinogen | This can then either be reabsorbed or converted to sterocobulin
89
What is pre-hepatic jaundice due to? give an example?
Increased haemolysis causing a back up of unconjugated bilirubin. An example of this is Sickle cell anaemia
90
Describe the process by which dietary lipids are digested?
Chewing, gastric churning mixes enzymes Bidirectional segmentation in the small intestine Bile salts emulsify lipid droplets linguinal and gastric lipases begin breakdown of triglycerides to fatty acids Inactivated when they reach duodenum and cck stimulates bile realease and pancreatic lipase takes over Requires colipase to function
91
Describe the process by which dietary lipids are absorbed?
Short/Medium Chain fatty acids readily diffuse into enterocytes then pass through the enterocyte into the blood Long chain fatty acids are contained in micelles When they encounter the low pH enterocyte border they are protonated and leave the micelle moving into the enterocyte Here they are re-esterified and packaged into chylomicrons that pass into the lymphatic system
92
What are eicosanoids?
Inflammatory mediators that are produced from phospholipid precursors The main eicosanoids are Leukotrienes, Thromboxanes and prostaglandins
93
What are the effects of thomboxane A2?
Vasodilation platelet aggregation bronchoconstriction
94
Which cell types produce which eicosanoids?
Endothelium- prostaglandin (PGI2) | Platelets- Thromboxanes (TXA2)
95
What are the effects of PGL2?
Vasodilation | Antiplatelet aggregation
96
What are the 4 drug modulation pathways of the COX pa
1. Non-selective NSAIDs (non-steroidal anti-inflammatory drugs) -Inhibit COX 1/2 -Includes aspirin (irreversible) and ibuprofen (competitive inhibitor, reversible) 2. Selective NSAIDs (anti-inflammatory as COX-2 is inducible) -Inhibit COX2 -Includes celecoxib 3. Glucocortidoids -Inhibit COX-2 (only affects production of prostanoids) -Induce expression of annexin I (inhibits PLA2) (affects production of all eicosanoids) 4. TX synthase inhibitor Includes ridogrel

charlies medicine (9 decks)

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