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GI Flashcards

1
Q

Describe the main components of saliva

A

-Hypotonic solution containing water, mucous and electrolytes, antibodies, amylase and lysozyme, lymphocytes and neutrophils

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2
Q

Give 3 consequences of failure of continuous saliva secretion (xerostomia)

A
  • halitosis
  • poor dentition
  • Bacterial over growth
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3
Q

What physical mechanisms trigger the release of saliva from the major salivary glands?

A

-Senses ie sight, smell, taste and thought of food

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4
Q

Describe the location of the 3 major paired salivary glands and state whether their secretions are mainly serous, mucus or mixed

A
  • Parotid = in front of ears (preauricular) -> serous
  • Sublingual =under tongue -> mucous
  • Submandibular = floor of mouth -> mixed
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5
Q

What are the main purposes of saliva?

A
  • Lubrication of food for swallowing
  • Maintenance of teeth integrity by neutralising acid
  • Iodide is a bacteriostatic
  • Initiate digestion of foods by amylase/lipase
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6
Q

Name the ducts of parotid and submandibular glands

A
  • Parotid = stensons (second molar tooth of maxilla)

- Submandibular = whartons (either side of lingual frenulum)

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7
Q

Describe the general secretory units of a salivary gland and what each component does to produce saliva

A
  • Acinus -> secretion of fluid isotonic with plasma
  • Striated ducts -> ductal modifiction of isotonic solution by removing Na and Cl and adding K+, I-and HCO3-. ducts are impermeable so water cannot follow
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8
Q

Describe the difference between unstimulated and stimulated saliva

A
  • Unstimulated -> low flow rate provides lots of time to remove Na/Cl and basal hco3 added.
  • Stimulated -> high flow rate means limited time to remove Na and lots of HCO3- added
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9
Q

What does the gag reflex test?

A
  • Sensation of soft palate

- Motor innervation of soft palate

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10
Q

Name the two arches anterior and posterior to the palatine tonsils

A
  • Anterior = palatoglossus

- Posterior = palatopharyngeal

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11
Q

Describe the three phases of swallowing

A
  • Oral -> food chewed to form bolus, pushed to back of mouth causing reflex activation of pharyngeal phase
  • Pharyngeal -> involuntary control - pharyngeal receptors communicate with swallowing centres in brain causing soft palate to raise and close off nasopharynx, hyoid bone and larynx raise closing epiglottis, food passes into oesophagus
  • Oesophageal -> passage through upper oesophageal sphinter causing constriction of sphincter and peristaltic wave causing relaxation of lower oesophageal sphincter
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12
Q

What is achalasia?

A

-Failed relaxation of lower oesophageal sphincter causing dysphagia

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13
Q

Give 3 common causes of dysphagia

A
  • Stroke causing paralysis of muscles on one side
  • Benign stricture
  • Achalasia
  • Oesophgitis
  • Malignancy
  • Ulcer
  • Candida
  • Spasm
  • Pharyngeal pouch
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14
Q

What is a pharyngeal pouch?

A
  • also known as zenkers diverticulum

- diverticulum of oesophagus through killians dehiscence between cricopharyngeus and inferior pharyngeal constrictor

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15
Q

How does the autonomic nervous system affect salivary glands?

A
  • Parasympathetic -> stimulates acinus and ductal cells to add HCO3-
  • Sympathetic -> reduction in bloodflow to glands limits salivary flow
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16
Q

describe the differences in voluntary and unvoluntary control of the oesophagus

A
  • Upper 1/3 voluntary striated muscle

- Lower 2/3 unvoluntary smooth muscle

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17
Q

Describe the results on the GI system of lateral and craniocaudal folding

A
  • Lateral = ventral body wall and pinching from yolk sac

- Craniocaudal = blind ended primitive gut tube from stomatoduem to proctoduem with opening at umbilicus

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18
Q

Of what tissue origin are epithelial linings and musculature of gut wall?

A
  • Epithelia = endoderm

- Musculature = splanchnic mesoderm

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19
Q

What are the adult derivatives of the foregut, midgut and hindgut?

A
  • Foregut -> Oesophagus, stomach, 1st part duodenum, liver, gallbladder, pancreas
  • Midgut -> distal 3/4 of duoedenum to 2/3 transverse colon
  • Hindgut-> distal 1/3 transverse colon to upper anal canal. also internal lining of bladder and urethra
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20
Q

Describe the branches of the coeliac trunk and which art og the gut it supplies

A
  • Splenic artery (left gastroepiloic, fundus)
  • Common hepatic -> proper hepatic (R/L hepatic, cystic), gastroduodenal (superior pancreaticoduodenal, right gastroepiploic) right gastric
  • Left gastric (oesopagus)
  • Foregut
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21
Q

Describe the main branches of superior mesenteric artery and which part of the gut it supplies

A
  • Inferior pancreaticoduodenal
  • Ileocolic
  • Right Colic
  • Middle colic
  • Midgut
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22
Q

Describe the main branches of inferior mesenteric artery and which part of the gut it supplies

A
  • Left colic
  • Sigmoidal
  • Continues as superior rectal
  • Hindgut
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23
Q

Which structures in the gut have a dual blood supply by CT and SMA?

A
  • Duodenum (gastroduodenal and sup. pancreatico duodenal from CT and inf. pancreaticoduodenal from SMA)
  • Pancreas (sup. pancreatico duodenal from CT and inf. pancreaticoduodenal from SMA)
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24
Q

What is a mesentery and why is it important? What is the embryonic origin of mesentery? Describe the locations of the dorsal and ventral mesentery

A
  • Double layer of peritoneum which attaches the gut to the abdominal wall
  • Allows blood and nerve supply to organs
  • Splanchnic mesoderm
  • Dorsal along length of gut tube, ventral only to foregut
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25
Q

What are omenta and describe their formation?

A
  • Double folds of mesentery formed during rotation of the stomach
  • As the stomach rotates clockwise in longitudinal axis it drags the dorsal and ventral mesentery with it producing double folds forming greater and lesser omenta.
  • As it rotates on an obligue (AP) axis it puts the omenta into their anatomical positions -> greater hangs from greater curvature of stomach, lesser from lesser curvature of stomach
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26
Q

What lays in the free edge of the lesser omentum?

A

-Portal triad

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27
Q

Where does the liver develop? How does the liver help anatomical positioning?

A
  • Within the ventral mesentery

- Grows so fast and so large within cavity that pushes stomach to left

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28
Q

What is retropetitoneal/secondary retroperitoneal and what organs?

A
  • Retroperitoneal -> organs never within the peritoneum/enveloped in mesentery - abdominal aorta and kidneys
  • Secondary retroperitoneal > once within the peritoneum and covered in mesentery but got pushed dorsally and became fused with posterior abdominal wall to loose its mesentery -> distal 3/4 duodenum, ascending/descending colon
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29
Q

Explain the association between the foregut and the respiratory tract

A
  • Resp tract started as a blind diverticular ventral outpuching from the foregut.
  • Tracheoesophageal septum gows and separates resp diverticulum from foregut. puts trachea ventrally and oesophagus dorsally
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30
Q

Describe the development of the duodenum and problems which can arise during development

A
  • Grows rapidly and pulled into a c-shape as stomach rotates
  • Growth is so rapid that lumen is obliterated and recanalised
  • Failed recanalisation causes duodenal atresia (usually upper, problem with vasculature commonly causes lower duodenal atresia)
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31
Q

List the abdominal muscles from superior to deep and describe their main features (ie fibre direction/fascia etc)

A
  • External oblique -> fibres run inferiomedially
  • Internal oblique -> fibres run superior medially
  • Transverse abdominus - transversalis fascia between inner side of muscle and parietal peritoneum
  • Rectus abdominus -> tendinous intersections, linea alba and linea semilunaris laterally, covered in rectus sheath (made from aponeurosis of surrounding muscles)
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32
Q

What is linea alba? What is a pathological lesion associated with linea alba?

A
  • Connective tissue in midline of abdomen where many abdominal muscles join
  • Divarication of recti -> separation of two sides of rectus abdominus due to stretching of linea alba -> common in pregnancy and only shows from sitting to laying
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33
Q

What is the arcuate line and its clinical significance?

A
  • Horizontal line 1/3 between umbilicus and pubic synthesis which denotes the lower limit of the posterior layer of rectus sheath
  • C-sections performed here
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34
Q

What is a rectus sheath haematoma?

A
  • Bleeding into rectus sheath from damage to superior/inferiot epigastric vessels or tear in muscle
  • Very painful and slow bruising
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35
Q

Where is mcburneys point and what is it used for?

A
  • 2/3 between umbilicus and ASIS

- Appendectomy

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36
Q

What is meckel’s diverticulum? What are the rules of 2s?

A
  • Congenital diverticulum in the small intestine due to failed closure of the vitelline duct.
  • 2 inches long
  • Within 2 feet of ileocecal valve
  • 2 tissue types present (gastric/pancreatic)
  • 2x common in males
  • 2% population
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37
Q

Decribe the difference between small, large and renal (ureteric) colic

A
  • Small -> around umbilicus every 35-40s
  • Large -> suprapubic around every 2-3 minutes
  • Renal -> loin to groin pain which is extremely painful
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38
Q

Why does diaphragmic irritation cause left shoulder tip pain and give 3 causes

A
  • Referred pain from phrenic nerve as dermatome c3,4,5
  • Ruptured spleen
  • Perforated ulcer
  • Ectopic pregnancy
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39
Q

What is the inguinal canal and inguinal ligament? What does it contain?

A
  • Oblique passageway between the deep and superficial inguinal rings formed by the fascia of the external and internal obliques. Its inferior border is the inguinal ligament which is a thickened area of the inferior border of aponeurosis of external oblique.
  • Inguinal ligament runs from ASIS to pubic tubercle.
  • Contains spermatic cord in men and round ligament of uterus in women
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40
Q

What is a hernia? Describe the differences between direct and indirect iguinal hernias

A
  • Protrusion of part of abdominal organ through the abdominal wall
  • Direct -> through hesselbachs triangle medial to inferior epigastric vessels though superficial inguinal ring
  • Indirect -> through deep inguinal ring -> inguinal canal -> superfcial inguinal rig
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41
Q

Describe a femoral hernia

A

-Bowel protrudes under the inguinal ligament and through the weak femoral ring of femoral canal

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42
Q

Which hernia is more common on males/females?

A
  • Indirect inguinal -> males

- Femoral -> females

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43
Q

Describe the margins of hesselbachs triangle

A
  • Medial -> lateral margin of rectus sheath
  • Superiolateral -> inferior epigastric vessels
  • Inferior -> inguinal ligament
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44
Q

What are umbilica hernias? What are the most common causes in children and adults?

A
  • Hernia which occurs anywhere from xiphersternum to umberlicus -> includes epigastric and paraumbilical
  • Children = weakness at umbilical scar
  • Adults = protrusion through linea alba
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45
Q

What is a diaphragmatic hernia?

A

-Developmental defect where diaphragm allows intestine to herniate into chest

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46
Q

What is a hiatus hernia and describe its subtypes

A
  • Special diaphragmatic hernia
  • Sliding -> gastrooesophageal junction slides through diaphragm into chest
  • Rolling -> Fundus of stomach passes into chest alongside oesophagus
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47
Q

What is the most common cause of an incisional hernia?

A

-Obesity

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48
Q

What is the function of the rugae of the stomach?

A

-Allow distention for storage of food

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49
Q

How is the stomach specialised for disrupting food?

A
  • Acid
  • Thick walls in the antrum for foordinated peristalsis from proximal to distal
  • Funnel shape to cause acceleration of contents towards pylorus allowing large lumps to be left behind and liquid chyme to be ejected
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50
Q

What 3 chemical mediators stimulate the parietal cells to secrete acid and where are they secreted from? What stimulates their secretion?

A
  • Gastrin -> G cells and Histamine -> ECL Cells caused by presence of peptides in stomach and distension of stomach (produces 60% of HCL)
  • Ach -> Parasympathetic neurones and senses of food (30% HCL)
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51
Q

What is receptive relaxation?

A

-Vagally mediated relaxation of the upper stomach to allow food to enter without causing increased intragastric pressure and causing reflux

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52
Q

Name the cells present in the stomach and their function

A
  • Parietal = acid
  • ECL = histamine
  • G cell = gastrin
  • Chief cell = pepsinogen
  • D cell = somatostatin
  • Mucous cell = mucus
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53
Q

How is acid production inhibited?

A

-Inhibition of G cells due to decreased pH, Somatostatin (low pH) and reduced vagal activity (reduced distension)

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54
Q

What is the function of acid in the stomach? How is it produced? What is the alkaline tide?

A
  • Disinfect
  • Helps unravel proteins
  • Activates pepsinogen
  • H2O is split into H and OH in the parietal cell-> H+ pumped into stomach lumen by H+ATPase-> OH combines with CO2 to make HCO3 -> HCO3 exchanged for Cl- in blood. Cl- diffuses down its conc gradient into stomach lumen. H+ and CL- combine to form HCl
  • Alkaline tide is the concomitant production of HCO3 which enters the blood stream
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55
Q

Name the protective mechanisms of the stomach

A
  • Mucus realeased by neck and surface mucous cells forms a thick alkaline viscous layer which adheres to epithelium and raises pH relative to the stomach lumen
  • high turn over of cells -> keeps epithelia intact
  • Prostaglandins -> vasodilates bvs to keep epithelia supplied with nutrients
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56
Q

Name 3 insults to the stomach and their outcomes

A
  • Alcohol
  • H.pylori
  • NSAIDs
  • Gastritis, ulceration, reflux
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57
Q

Very briefly describe the formation of the mid and hindgut

A
  • Elongation of the gut tube with insufficient space causes physiological herniation of the gut tube into the proximal umbilical cord
  • It rotates 3x90 degrees anticlockwise turns (one during herniation, one whilst herniated and one on return) which achieves the normal anatomical position
  • Descent of the ceacal bud greates ascending colon
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58
Q

What are the consequenes of malrotation of the gut tube?

A
  • Left sided colon if only makes 1 rotation

- Reversed rotation

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59
Q

Why can volvulus of the mid and hind gut occur?

A

-Mesentery allows structures to be mobile

60
Q

How is the anal canal anatomically divided? What is the difference between these two sections? How is this achieved?

A
  • Divided by the pectinate line
  • Above pectinate line supplied by IMA, S2,3,4 parasymp, columnar epithelia
  • Below pectinate line -> Pudendal A, S2,3,4 pudendal, stratified squamous
  • Achieved during development when cloaca (mesoderm) makes contact with cloacal membrane (ectoderm) -> Anal pit is induced and forms the lower 1/3 of the anal canal. The upper 2/3 is made by cloaca itself therefore they have different innervation and supply
61
Q

What is gastroschisis? What is Omphalocoele? How do they differ from hernias?

A
  • Gastroschisis is failed closing of abdo wall during folding leaving the gut tube outside the cavity
  • Omphalocoele is failed completion of physiological hernation leaving the gut tube outside the body but covered in peritoneum and amnion
  • Hernia is covered in skin and subcut because herniation completed and then occured again
62
Q

What is the bare area regarding the liver?

A

-An area on the diaphragmatic surface of the liver which is not covered in peritoneum

63
Q

Name the ligaments of the liver and their function

A
  • Falciform ligament -> Attaches liver to anterior abdominal wall (contains ligamentum teres)
  • Coronary ligaments -> superior liver to diaphragm
  • Triangular ligaments -> outside of coronary ligaments
  • Ligamentum venosum -> posterior
64
Q

What makes up the portal triad?

A
  • Portal Vein
  • Hepatic artery
  • Common bile duct
65
Q

Name the hepatic recesses

A
  • Subphrenic
  • Subhepatic
  • Morrison’s pouch
66
Q

Name the lobes and their positions of the liver

A
  • R and L lobe

- R Lobe gives rise to caudate lobe and quadrate lobe

67
Q

What 2 veins make up the hepatic portal vein?

A

-SMV and Splenic vein

68
Q

Describe the biliary tree

A

-Cystic duct from gb joins common hepatic duct to form common bile duct -> pancreatic duct joins and is called ampulla of varter -> When it enters 2nd part duodenum through sphincter of oddi

69
Q

What are gall stones?

A

-Components of bile eg pigments, cholesterol which precipitate out and form stones

70
Q

Describe the common presentation of gall stones

A
  • Right upper quadrant or epigastric pain which is cramping and intermittent in nature
  • Can have associated fever, vomiting, local peritonism
71
Q

Give 3 differentials of Acute cholecystitis

A
  • Biliary colic
  • Ascending cholangitis
  • Liver abscess
72
Q

What is the difference between acute cholecystitis and biliary colic?

A
  • AC -> gallstones are in neck of gall bladder and there is local peritonitis, and the pain may be refered to the right shoulder, fever is present
  • Biliary colic is physical contraction of cystic duct
73
Q

What is charcots triad?

A
  • Suggestive of ascending cholangitis

- Jaundice, RUQ pain, fever

74
Q

Describe some risk factors for gallstones

A

-Female, fat, 40, fertile

75
Q

What is GORD? Give some causes and complications. Describe the Rx,

A
  • Gastoesophageal Reflux disease -> reflux of stomach contents into oesophagus causing cough, heartburn, dysphagis and sore throat
  • LOS problems, Delayed gastric emptying, Hiatus hernia, Obesity
  • Oesophagitis, Barrets Oesophagus, benign stricture, Carcinoma
  • Lifestyle modifications, antacids and PPIs
76
Q

Describe the urease breath test. What is it used for?

A
  • Test for H.pylori
  • Pt swallows tablet with urea containing radiolabelled C13 -> 30 mins later if H.pylori present will have digested urea and isotope will be detected on breath
77
Q

What is Acute gastritis? Give some causes

A
  • Acute inflammation of the lining of the stomach causing indigestion, N+V, burning pain in stomach or asymptomatic
  • Chronic NSAID use, alcohol, Chemotherapy
78
Q

What is chronic gastritis, give some causes

A
  • Inflammation of the lining of the stomach for a prolonged period of time which often leads to atrophy and decreased protective mechanisms
  • Pernicious anaemia, H.pylori, chronic alcohol
79
Q

What is peptic ulcer disease? What are the symptoms of gastric/peptic? Which artery runs along the lesser curvature of the stomach and is prone to erosion by an ulcer?

A
  • Erosion of the mucosa of the stomach or suodenum which extends through muscularis mucosa and sloughs off into lumen
  • Epigastric burning pain in both. duodenal is relieved by eating and worse at night. Gastric is made worse by eating
  • Gastroduodenal
80
Q

What is the eradication Tx for H.pylori?

A
  • Clarythromicin
  • Amoxicillin
  • PPI
81
Q

What is zollinger ellison syndrome?

A

-Non-beta islet cell gastrin secreting tumour of the pancreas which causes proliferation of the parietal cells resulting in severe ulceration (can be part of MEN1)

82
Q

How is H.pylori spread? What type of organism is it and how is it adapted for survival in the stomach?

A
  • Feacal-oral
  • Helical gram -ve aerobe which produces urease to help survival by converting urea to ammonium to increase local pH and producing an alkali could for it to stay in. Has flagellum for motility to stay in alkaline areas following chemotaxis. Releases cytotoxin which directly injures epithelia
83
Q

How does H.pylori spread to the duodenal cap?

A

-Colonisation in the antrum leads to increased acid production -> causes duodenal metaplasia due to acid chyme

84
Q

Describe some risk factors for gallstones

A

-Female, fat, 40, fertile

85
Q

What are tenia coli?

A

-3 large strips of muscle on the large bowel which contract the wall of the bowel into haustra

86
Q

Why is the splenic flexure more prone to ischaemia?

A

-Does not have direct blood supply like rest of colon

87
Q

What is the pouch of douglas? What is the equivalent in men?

A
  • Rectouterine pouch in women between posterior uterus and colon
  • Retrovesicle pouch
88
Q

How does the hypertonic chyme which leaves the stomach become isotonic?

A

-The duodenum is permeable to water so as hypertonic chyme enters duodenum H2O is drawn in from ECF and chyme is isotonic by time it passes the pancreas

89
Q

Describe the basic structure od the pancreas and what each bit does

A
  • Exocrine pancreas made from acinus, which secretes an aqueous fluid filled with pancreatic amylase, lipase and proteases, and ducts which modify the solution by adding HCO3- and modifying electrolyte concentrations
  • Endocrine pancreas from islets of langerhans -> a secrete glucagon and b secrete insulin
90
Q

What stimulates the exocrine pancreas?

A
  • Acinus -> Vagus nerve and cholecystokinin from duodenum which is released in response to hypertonic chyme
  • Ducts -> secretin released from duodenum in response to hypertonic chyme
91
Q

Describe the microscopic structure of the liver

A
  • Lobule is a structural unit which is surrounded by CT which has invaginated from the capsule (glissens capsule) with a portal triad in each corner of lobule and a central vein (linked by hepatic sinusoids)
  • Acinus is a functional unit of the liver created by a diamond shape between two central veins and two portal triads.
92
Q

How is an acinus of the liver modified for its function?

A

-Zone 1 receives the most oxygenated blood but it also receives the most toxins

93
Q

Describe the production of bile and its components. What stimulates bile production?

A
  • Bile acid dependant component contains bile acid (cholic and chenodeoxycholic acid) and pigments and is secreted by hepatocytes into the bile canaliculi
  • Bile acid independent is an alkaline solution which helps to neutralise chyme is secreted by the ductal cells of the canaliculi
  • Secretin released from duodenum in response to hypertonic chyme
94
Q

What are bile salts?

A

-Bile acids which have been conjugated with glycine to make them soluble so they are active

95
Q

How are lipids in the gut digested? What happens to the bile salts?

A
  • Emulsified using bile salts which then make micelles with products of lipid breakdown (FAs, cholesterol, TGs) and transport them to the brush border so they can diffuse into enterocytes
  • The bile salts are recycled in the enterohepatic circulation after being absorbed in the terminal ileum
96
Q

What are chylomicrons? What is different about them to other lipid carriers?

A
  • Carriers of diertary lipids from the intestine to the liver
  • Too big to enter bvs so enter lymphatics
97
Q

What stimulates contraction of the gallbladder?

A

-CCK from the duodenum in response to hypertonic chyme and fats

98
Q

Describe some innate defences of the GI tract

A
  • Saliva -> lysoszyme, Iodine
  • Gastric Acid
  • Colonic mucus
  • Macrophages and neutrophils
99
Q

What is achlorhydria? Give some causes

A
  • Decrease in production in gastric acid leading to increased risk of infections such as salmonella and shigella
  • PPIs
  • Pernicious anaemia
100
Q

What are kuppfer cells?

A

-Specialised macrophages which line the sinusoids of liver cells

101
Q

Give some causes of liver failure

A
  • Alcohol
  • Hepatitis
  • Drugs
102
Q

What is liver cirrhosis?

A

-Hepatocellular damage producing areas of nodular regeneration separated by fibrous septae

103
Q

List some clinical signs of Alcoholic liver disease

A
  • Hands -> Clubbing, leuconychia (low albumin), dupytens contracture, palmar erythema,
  • Face -> pallor (ACD)
  • Trunk -> Spider naevi, gynaecomastia (decreased liver metabolism)
  • Abdo -> hepatosplenomegaly, caput medusa, ascites
  • General -> jaundice, bruising (coagulopathy), anorexia
104
Q

What is portal hypertension? Describe the main features. Give some causes

A
  • Raised portal blood pressure >20mmHg
  • SAVE (splenomegaly, ascites, varices (oesophageal, caput medusa, worsening piles) and encephalopathy
  • Alcohol, hepatitis, Primary biliary cirrhosis
105
Q

Describe portosystemic shunting in portal hypertension. Give the vessels involved in all 3 varices

A
  • Raised portal pressure causes a backflow and increased pressure of blood as blood cannot enter portal system. portal vessels become engorged and dilated causing shifting of blood from the portal system into the systemic system.
  • Oesophageal -> Left gastric vein to inferior oesophageal veins
  • Caput medusa -> peri-umbilical to superficial abdo
  • Haemorrhoids -> superficial rectal to inferior/middle rectal
106
Q

Why does portal hypertension cause encephalopathy?

A
  • Decreased blood flow through liver decreases detoxification of blood.
  • Build up of toxins in systemic system including ammonia ->cross bbb -> astrocytes clear causing glutamate to glutamine -> osmotic imbalance -> cerebral oedema
107
Q

Describe the pathophysiology of ascites in liver disease

A

-Back pressure due to accumulation of blood causes increased hydrostatic pressure leading to fluid exudation. This causes a decrease in circulating volume and RAAS activation which enters a cycle of increased exudation and further RAAS activation. Also decreased albumin and impaired aldosterone metabolism

108
Q

What is mesenteric adenitis?

A

-Inflammation of the mesenteric lymph nodes caused by adenovirus. Causes RIF pain which can be mistaken for appendicitis

109
Q

Give 3 causes of appendicitis

A
  • Faecolith
  • Infection which has caused proliferation of lymphoid tissue
  • Worms
110
Q

Give 3 causes of gut ischaemia

A
  • Volvulus
  • Systemic hypotension/sepsis
  • Arterial disease
111
Q

Describe the major functions of the liver

A
  • Detoxification
  • Synthetic function eg albumin , clotting factors
  • Metabolism
  • Excretion eg bilirubin
  • Glycogen storage
112
Q

Give some LFTs

A
  • AST:ALT
  • g-GGT
  • ALP
  • bilirubin
  • Albumin and PT
113
Q

What is jaundice?Give causes of pre-hepatic, hepatic and post-hepatic jaundice and what type of bilirubin is seen

A
  • Yellow discolouration of the skin and eyes due to excess bilirubin
  • Haemolytic anaemia -> Unconjugated
  • Hepatitis -> Mixed
  • Gall stone in CBD -> Conjugated
114
Q

Describe the bilirubin cycle and what happens in jaundice

A
  • Haemoglobin -> Biliverdin to bilirubin in spleen -> carried to liver -> Conjugated with glucaronic acid -> Bile -> Broken down by gut bacteria -> Stercobilin -> Stercobilinogen in faeces -> Urobilinogen in urine or reabsorbed as stercobilin
  • In jaundice excess bilirubin in blood gets filtered through kidney producing dark urine. Stools will be pale due to no stercobilinogen
115
Q

Give some causes of hepatitis

A

-Viral, autoimmune, drugs, alcohol

116
Q

What is fulminant hepatic failure? Give some causes

A
  • Acute and severe decompensation of hepatic function with hepatic encephalopathy
  • Pregnancy, Hepatitis, Alcohol, Wilsons disease
117
Q

Give 3 complications of acute cholecystitis

A

-Obstructive jaundice, acite pancreatitis, gallstone ileus

118
Q

Give the causes for pancreatitis

A

-Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmine, Scorpion bite, Hyperlipidaemia, ERCP, Drugs

119
Q

How is the small intestine specialised for its function?

A
  • Villi and microvilli increase SA
  • Plicae Circulares are permanent folds in the jejunum which slow down contents to allow absorption
  • Brush border enzymes
120
Q

Describe the intestinal motility in the small intestine

A
  • Intestinal gradient -> occurs between meals as intestinal pacemakers have a higher frequency proximally driving slow caudal progression
  • Segmentation-> following meals contents are mixed back and forth by rhythmic contractions
  • Peristalsis
121
Q

What is anoikis?

A

-Programmes cell death of enterocytes after they have detached at the top of a crypt

122
Q

What enzymes are contained within the brush border to digest starch?

A

-Amylase and amylopectin

123
Q

How is glucose taken up into enterocytes and passed to blood stream?

A
  • Secondary active transport using SGLT-1 and the Na gradient set up by NaKATPase
  • GLUT2 on basolateral membrane to blood stream
124
Q

Describe the principle of oral rehydration

A
  • Uptake of Na generates an osmotic gradient so water follows
  • Glucose stimulates Na uptake so mixture of glucose and salt stimulates maximal water uptake
125
Q

How is the large intestine specialised for uptaking water?

A

-Has Na chennels stimulated by aldosterone

126
Q

hat enzymes work on proteins in the gut to allow absorption?

A

-Pepsin, Typsin, chemotrypsin

127
Q

Describe how Calcium is taken up from the gut

A

1) Paracellular passage is passive later in the gut when things have digested more
2) Facilitated diffusion using Vitamin D to activate the carrier molecule

128
Q

Describe the motility in the large intestine

A
  • Haustral shuttling (segmentation)-> Mixes food back and forth
  • Mass movement -> Coordinated contraction 1-3xday which moves contrnts rapidly from transverse colon to rectum. Often triggered by eating -> gastrocolic reflex
129
Q

Describe defaecation

A
  • Rectum normally empty and when fills up to 25% there is the urge to defaecate.
  • Internal sphincter is under parasymp control (smooth muscle) and external relaxes under voluntary control
  • Intraabdominal pressure rises = expulsion
130
Q

Which vitamins rely on colonic bacteria?

A

-B12, Thiamine, Vit K

131
Q

Name some normal flora of the mouth

A

-Strep viridans, Staph, Enterococcus

132
Q

What is oral thrush? In who is it seen? How is it treated?

A
  • White patches in the mouth and throat caused by candida albicans
  • Immunocomprimised individuals, Neonates, diabetics
  • Nystatin suspension
133
Q

What is the usual causative agent of tonsillitis? What is a quincy?

A
  • Adenovirus

- Abscess of the tonil often caused by strep pneumoniae

134
Q

Name some colonic normal flora

A

-Bacteroides, E.coli, Enterococcus

135
Q

When is strep viridans more likely to cause Endocarditis?

A

-In those with prosthetic heart valves

136
Q

What is the main bacteria in the vagina?

A

-Lactobacilli

137
Q

How is the small intestine recognisable on xray? Large bowel?

A
  • Valvulae conniventes and central

- Hautra which do not go all the way across and will be peripheral

138
Q

Which pathology causes a coffee bean sign on xray?

A

-Volvulus

139
Q

What is a sign of UC on xray?

A

-Lead pipe colon

140
Q

Give clinical features of an oesophageal carcinoma. What is the most common type? What type is associated with barretts oesophagus?

A
  • Dysphagia -> progressively worsening
  • Weight loss
  • Squamous cell
  • Adenocarcinoma
141
Q

What are the clinical features of gastric cancer? What investigations?

A
  • vague symptoms
  • Weightloss
  • Epigastric pain
  • Vomiting.Haematemasis
  • Endoscopt and biopsy
142
Q

What has high associaton with gastric lymphoma?

A

-H.pylori

143
Q

NAme a genetic condition which predisposes to Tumours in the large intestine

A

-Familial adenomatous polyposis

144
Q

What system is used to describe colorectal cancer? Describe it

A
  • Dukes staging
  • A confined to bowel wall
  • B through the wall
  • C Lymph node involvement
  • D distant mets
145
Q

Where most commonly is a pacreatic carcinoma?

A

-In the head of the pancreas affecting ductal cells

PPE (15 decks)

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