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Question 1

explain lateral flexures in the rectum

3:
-> 2 on the left (superior, intermediate)
-> 1 on the right (inferior)

Answer 1

• formed by transverse rectal folds
  (i.e. internal infoldings of rectum’s mucosa)
• helps to store and organise fecal contents INSIDE rectum

Question 2

5

location of sphincters

Answer 2

Upper Eosophagus Sphincter (EOS): bet pharynx and eosophagus
Lower Eosophagus Sphincter (LES): bet esophagus and stomach
pyloric sphincter: bet stomach and duodenum (start of SI)
ileocecal sphincter: bet ileum (end of SI) and cecum (start of LI)
internal and external anal sphincters: bet rectum (end of LI) and anus

main functions:
* UES and LES: prevent reflux of food into pharynx and esophagus respectively
* pyloric and ileoecal: regulates flow of contents
1. partially digested food from stomach into duodenum
2. digested material from small intestine into large intestine
* IAS and EAS: controls passage of stool during bowel movements

Question 3

a flexure and a muscle

what helps stool to remain in retum until defecation is consciously initiated

Answer 3

• anorectal flexure (80º angle)
  => makes it harder for stool to pass through anal canal until defecation is consciously initiated
• puborectalis muscle
  which is in normally contracted state
  => helps maintains anorectal angle,
  esp during peristaltic contractions
  (i.e. stronger contractions to counteract the push of feces towards anal canal)

when defecaction is to occur,
puborectalis muscle relaxes
-> anorectal angle is straightened
=> stool can pass through anal canal

Question 4

and at what vertebrae levels

what do the anterior branch of the abdominal aorta give rise to

Answer 4

• celiac: T12
• superior mesenteric: L1
• inferior mesenteric: L3

Question 5

and its origin

what artery is the gall bladder supplied by

Answer 5

cystic artery
← R hepatic artery
← common hepatic artery
<= celiac trunk

Question 6

and their origin

what arteries form the anastomosis which supplies the inferior border of stomach

Answer 6

• left gastric artery
  <= celiac
• right gastric artery
  <- common hepatic
  <= celiac

Question 7

and their origin

what arteries form the anastomosis which supplies the superior border of stomach

Answer 7

• celiac → splenic
  ⇒ left gastro-omental artery
• celiac → common hepatic
  ⇒ right gastro-omental artery

Question 8

and their origin

what arteries supply the fundus and upper part of stomach

Answer 8

short gastric arteries
← splenic artery
← celiac trunk

Question 9

and their respective function

what is the 2 types of cells found in the gland

general gland (acinus) structure

Answer 9

• acinar secretory cells: secrete digestive enzymes
• epithelial cells: form the intercalated duct
  AND modify secretions
  (e.g. changing pH by secreting bicarbonate)

Question 10

and what is below it

where does the posterior wall of the rectus sheath end

Answer 10

arcuate line
(found below umbilicus)
→ below line: rectus abdominis is in contact with transversalis fascia

Question 11

and what organs do they connect

what are the 4 ligaments found in the GIT

Answer 11

• hepatogastric ligament: liver and stomach
• hepatoduodenal ligament: liver and duodenum
• gastrophrenic ligament: stomach and diaphragm
• gastrosplenic ligament: stomach and spleen

Question 12

and where in stomach they occur

3 motor functions of stomach

pylorus = antrum (connect to body of stomach) + pyloric canal (connect to duodenum)

Answer 12

• reservoir function @ proximal
• churning function @ distal (antrum)
• gastric emptying @ even more distal (antrum-pylorus-duodenum unit)

Question 13

and where is it found

what does the anorectal junction/line indicate

Answer 13

• where rectum joins anal canal
• found at superior ends of anal columns

anal columns = series of longitudinal ridges

Question 14

and where is it found

what does the pectinate line indicate

diff from PECTINEAL line!

Answer 14

• formed by the inferior (comb-shaped) limit of anal valves
• indicates the junction of the superior and inferior parts of the anal canal

Question 15

and why

where is pepsinogen inactivated

Answer 15

inactivated irreversibly at duodenum
<- pH of duodenum is alkaline

Question 16

as manifestations in oral cavity

examples of ulcers

describe common characteristics, etiology

Answer 16

• apthous ulcers
  (i.e. canker sores):
  gray-white exudate w/ erythemayous rim, painful, shallow
  idiopathic
  (VITAMIN CDE)
• cold sores:
  vesicles containing clear fluid, most common on and around lips,
  due to HSV infection (likely type 1)
  (VITAMIN CDE)

Question 17

dermatome + name

where is visceral pain from stomach referred to

Answer 17

reaches T5-T9 spinal segments
=> referred to epigastric region

recall!
T10 = umbilicus
thus ABOVE T10 (T7-T9) = epigastrium
and BELOW T10 = inferior to umbilicus,
with L1 = specifically inguinal and pelvis

Question 18

early vs late in course of disease

what types of pain are felt when there is diseased appendix

Answer 18

• EARLY: pain in umbilicus
  due to visceral pain fibres travelling along sympathetic nerves to T10 spinal segment
  → brain interprets pain as coming from T10 dermatome
  “take it as pain is still in visceral peritoneum”
• LATE: pain in RLQ
  due to appendix swelling and touching parietal peritoneum
  → irritates somatic sensory nerve supplying parietal peritoneum in RLQ
  (which is L1 spinal nerve)
  “take it as pain travel out to parietal peritoneum”

Question 19

for parietal and visceral peritoneum respectively

what is the blood and lymphatic supply
and innervation of the peritoneum like

Answer 19

• parietal peritoneum: same as the region of the abdominopelvic WALL it lines
• visceral peritoneum: same as the organs it covers

Question 20

found in the rectus abdominis

function of the tendinous intersections

Answer 20

• divide the rectus abdominis muscle into segments
  (forms the “six-pack” 😏)
• attach the muscle to the anterior rectus sheath
  ⇒ prevents excessive movements and thus provides stability

Question 21

function

difference in sympathetic vs parasympathetic innervation of stomach

Answer 21

• sympathetic: stimulate (i.e. constrict) pyloric sphincter
  -> results in food staying longer in stomach
  => slowing digestion
• parasympathetic:
  stimulate peristalsis movement of stomach,
  stimulation secretion of gastric glands

recall!
sympathetic = “shoot”
thus need to divert energy away from digestive processes
towards more important body functions

Question 22

hint: blood vessels = arteries AND VEINS

which blood vessels do the liver receive blood from

Answer 22

• portal vein (75-80%)
• hepatic artery (20-25%)

recall! portal vein drains blood from stomach
via gastric veins, splenic vein and superior mesentric vein
⇒ blood from portal vein will be nutrient rich but poorly oxygenated

Question 23

it’s a muscle!

what abdominal structure lies within the rectus sheath

Answer 23

rectus abdominis

rectus sheath encloses this muscle

Question 24

other than kidneys

which organs are retroperitoneal

Answer 24

• duodenum
  (except first part)
• pancreas
  (except tail part)
• ascending and descending colon

Question 25

# xout of the 4 quadrants where can you find the colon

Answer 25

* ascending colon: **R**LQ * descending and sigmoid colon: **L**LQ

Question 26

# skeletal framework what makes up the superior border of the abdominal cavity

Answer 26

* costal margin * xiphoid process * floating ribs (11th and 12th ribs)

Question 27

# skeletal framework what makes up the inferior border of the abdominal cavity

Answer 27

* hip bones * illiac crest * ASIS * pubic tubercle * pubic symphysis * pectineal line

Question 28

# tip of which costal cartilage? left or right? where can the gallbladder area be palpated at

Answer 28

tip of **right** **9th** costal cartilage ## Footnote also known as the **transpyloric** plane (transpyloric bcos it cuts pylorus of stomach)

Question 29

where is the transpyloric plane located | i.e. at which level of the vertebrae

Answer 29

L1

Question 30

# what ducts, where do each drain from, final destination describe the biliary system

Answer 30

* liver: R and L hepatic ducts which unite to form comon **hepatic** duct, gallbladder: **cystic** duct, pancreas: **pancreatic** duct * flow: common hepatic duct joins with cystic duct => forms **bile duct** => which then merges with pancreatic duct and **open into duodenal wall** at **ampulla of Vater**

Question 31

# what is includes, what demarcates the division describe functional division of liver

Answer 31

* demarcated by fossae for **gallbladder** * separated such that **left** side includes **caudate and quadrate lobes** | fossae = shallow depression where gallbladder is located

Question 32

# what the stomach lies on structures that are posterior to stomach

Answer 32

* spleen * pancreas * transverse colon * left kidney and suprarenal gland

Question 33

# think abt the adjective where is the subcostal plane located | i.e. which lumbar vertebrae does it cut through

Answer 33

L3 "**sub**costal (3 letters) plane found at L**3**"

Question 34

at which costal cartilage is the subcostal plane located

Answer 34

inferior border of **10th** costal cartilage

Question 35

# think of the adjective where is the intertubercular plane located | i.e. which lumbar vertebrae does it cut through

Answer 35

L5 "**inter**tubular (5 letters) plane found at L**5**"

Question 36

# which muscles describe the walls of the inguinal canal * anterior wall: (...), laterally reinforced by internal oblique * floor: (...) * roof: (...) and medially (...) * posterior wall: (...) and medially (...)

Answer 36

* **anterior** wall: **external** oblique, laterally reinforced by internal oblique * **floor**: **inguinal ligament** (which is rolled inferior edge of **external** oblique) * **roof**: **internal** oblique and medially **conjoint tendon** (which is lowest fibres of internal oblique + transversus abdominis) * **posterior** wall: **transversalis fascia** and medially **conjoint tendon**

Question 37

# which virus what are squamous papilloma and squamous cell carcinoma associated with

Answer 37

HPV

Question 38

Appendicitis is the inflammation of the appendix, often leading to acute abdominal pain with **maximum tenderness** at **McBurney's point**. Where is McBurney's point located? A) mid-inguinal point B) two-thirds of the distance between the umbilicus and the right ASIS C) midpoint of a line between the ASIS and the umbilicus D) mid point of inguinal ligament E) midpoint of a line drawn between the xiphoid process and the umbilicus | tenderness = pain felt when area is **touched**

Answer 38

B) two-thirds of the distance between the umbilicus and the right anterior superior iliac spine (ASIS)

Question 39

arterial and venous circulation of spleen

Answer 39

* receives blood from splenic artery (← celiac trunk ← abdominal aorta) * drained by splenic vein (→ hepatic portal vein → IVC)

Question 40

arterial supply of rectum

Answer 40

* **proximal** part: **superior** rectal arteries ← inferior mesenteric artery <= abdominal aorta * **middle and inferior** parts: R and L **middle** rectal arteries ← inferior vesical (male) or uterine (female) arteries ← internal illiac artery ← common illiac artery <= abdominal aorta * **anorectal junction and anal canal**: **inferior** rectal arteries ← internal pudendal arteries ← internal illiac artery ← common illiac artery <= abdominal aorta

Question 41

at what level of the vertebrae is the cisterna chyli located ## lymphatic structure located at the origin of the thoracic duct, receiving lymph from the lower body and abdominal viscera

Answer 41

L1 and L2

Question 42

between which arteries in the large intestine is there an arterial anastomosis

Answer 42

* right colic (ascending colon) and middle colic (transverse colon) * middle colic (transverse colon) and left colic (mainly descending colon)

Question 43

branches of the inferior mesentric artery: * l... c... artery * s... arteries * s... r... artery

Answer 43

* left colic artery: transverse colon (last 1/3), descending colon * sigmoid arteries: sigmoid colon * superior rectal artery: rectum (superior part)

Question 44

branches of the celiac trunk

Answer 44

* left gastric artery * splenic artery * common hepatic artery | recall! celiac trunk branch out from abdominal aorta @ T12

Question 45

# compare with arterial circulation commen on the pressure in the portal venous system

Answer 45

**lower** than arterial circulation => **prevents backflow** and thus congestion in GI organs ## Footnote pressure too high = portal hypertension

Question 46

comment on the effectiveness of agents that reduce gastric acidity: * antacids * H2-receptor antagonists * proton pump inhibitors (PPI)

Answer 46

most to least effective: 1) PPI 2) H2-receptor antagonists 3) antacids

Question 47

# compare with arterial and venous circulation comment on the resistance in the portal venous system

Answer 47

* **lower** than arterial circulation => allows blood to flow smoothly into liver * **higher** than (systemic) venous circulation => **slows** blood flow through liver for **proper filtration**

Question 48

definition of lesser and greater omentum

Answer 48

a **double layered** peritoneal fold extending * (LESSER omentum) from the **liver** to the LESSER curvature of the **stomach** * (GREATER omentum) between the GREATER curvature of the **stomach** and the **transverse colon**

Question 49

describe the venous drainage of the stomach ## Footnote hint: portal vein, gastric veins, splenic vein, superior mesentric vein, gastro-omental veins

Answer 49

* L and R **gastric veins** directly drain into **portal vein** * L **gastro-omental vein** drains into **splenic vein**, while R **gastro-omental** vein drains into **superior mesentric vein** (SMV) => splenic vein and SMV combine to form **portal vein** | portal vein drains into **IVC** ## Footnote all veins run parallel to arteries

Question 50

diff in moa of sucralfate and bismuth compound as mucosal protective agents

Answer 50

both physically **coats** ulcer and protect it from further damage by **acid and digestive enzymes**, but * sulcralfate also stimulates **secretion of mucus and bicarbonate** → **neutralises** gastric acid * bismuth also has **antimicrobial** properties (e.g. against **H. pylori**)

Question 51

which mucoprotective agent causes harmless *blackening* of **stool** and reversible *darkening* of **tongue**

Answer 51

bismuth

Question 52

Which of the following is TRUE regarding the use of bismuth? (A) Bismuth can be used long-term without risk of toxicity. (B) Bismuth is safe for use in patients with renal insufficiency. (C) Long-term use of bismuth may lead to encephalopathy.

Answer 52

(C) **Long-term** use of bismuth may lead to **encephalopathy**. (B): Bismuth is primarily eliminated via **renal** clearance → should be **avoided** in patients with **renal insufficiency**

Question 53

MOA of misoprostol

Answer 53

synthetic PGE1 **analogue** → binds to **PGE2** receptors ⇒ low doses: promotes **HCO3- and mucus** secretion, enhances **mucosal blood flow** high doses: **inhibit gastric acid** secretion

Question 54

difference bet gastritis and gastropathy

Answer 54

* both involves **mucosal injury** (i.e. damage to mucosal layer) due to damaging forces >> protective mechanisms * gastr**itis** involves **inflammation**, while gastropathy has little or no inflammation | main inflammatroy cells present = **neutrophils**

Question 55

difference in **cause** of congenital vs acquired pyloric stenosis

Answer 55

* congenital: **hyperplasia** of pyloric **muscularis propria** * acquired: 1. **benign inflammatory** conditions (e.g. antral gastritis, peptic ulcers) 2. **malignant**: carcinomas | end result of both = obstruction of gastric outflow tract

Question 56

difference in appearance (and underlying pathology) of leukoplakia vs erythroplakia

Answer 56

* leukoplakia: well-defined, **WHITE** **patch or plaque** that cannot be scraped off ← **hyper**KERATosis * erythroplakia: **thin**, erythematous (i.e. **RED**) **mucosa** ← **absence** of KERATIN production

Question 57

difference in contents of inguinal canal in males vs females

Answer 57

both contain illoinguinal nerve * males: **spermatic cord** * females: round ligament ## Footnote in males, **testis** also **descends through inguinal canal** during fetal development

Question 58

difference in sympathetic vs parasympathetic innervation of gallbladder

Answer 58

* sympathetic: relaxation of gallbladder * parasympathetic: contraction of gallbladder, relaxation of **Sphincter** of Oddi

Question 59

Does giving a drug orally achieve a higher drug level in blood than giving it intravenously

Answer 59

**No** when given orally -> absorbed in small intestine (via capillary bed) -> delivered by hepatic portal vein to liver -> undergoes **FIRST-PASS metabolism** -> some of the drug is **broken down by liver enzymes** => lesser active drug enters systemic circulation

Question 60

explain an important implication of portal-systemic anastomoses (PSA) | PSA are where veins draining to **portal vein** and **IVC** communicate

Answer 60

liver or **portal obstuction** (e.g. due to liver cirrhosis) -> veins **dilate** => can rupture and cause **haemorrhage** ## Footnote haemorrhage is more common in * lower eosophagus * rectum (remember as the start and end)

Question 61

features of acute gastritis

Answer 61

* DIFFUSE mucosal *hyperemia* associated with **bleeding**, erosions and ulcers <- *congestion* and **haemorrhage** <- *engorgement* of and **damage** to blood vessels * clinical presentations: **haematemesis, melena, iron-deficiency anaemia**, epigastric pain, nausea and vomiting

Question 62

function of smooth muscle in normally PARTIALLY contracted state

Answer 62

muscles can **contract further** or **relax** ⇒ allows for **efficient** and coordinated digestion without issues like dumping syndrome (**too fast** emptying) or stasis (**too slow** movement)

Question 63

functions of falciform ligament

Answer 63

* **divides** liver into right and left lobes (anatomical division) * attaches liver to **anterior abdominal wall**

Question 64

how do uraemic states and urease-secreting *H. pylori* disrupt secretion of HCO3- into mucus layer

Answer 64

increase **ammonia** production → **inhibits HCO3- transporters** in gastric EPITHELIAL cells ⇒ less HCO3- secreted into mucus layer

Question 65

in which quadrant of the abdomen is the **appendix** located in

Answer 65

RLQ

Question 66

is it the arterial supply or venous drainage of rectum that has a (portocaval) anastomosis

Answer 66

Venous drainage bet **superior** rectal vein AND **middle & inferior** rectal veins * superior rectal vein: drains proximal part of rectum -> inferior mesenteric vein => **hepatic portal vein** (**PORTAL** circulation) * **middle and inferio**r rectal veins: drain middle and inferior parts of rectum -> internal illiac vein => **IVC** (**SYSTEMIC** circulation) ## Footnote function: primarily to provide **alternative** route to bypass **blocked or elevated** PORTAL circulation

Question 67

location and function of anal sinuses

Answer 67

* between anal valves * compressed by **feces** → exude **mucus** ⇒ that aids in **evacuation of feces** from anal canal

Question 68

name and explain the protective mechanisms of gastric mucosa: * m... secretion * b... secretion * epithelial b... * mucosal b... f... * p...

Answer 68

* mucus secretion: act as **physical barrier** which prevents acid- & pepsin-containing fluid from contacting surface epithelial cells * bicarbonate secretion: secreted into **mucus layer**, resulting in a **pH-neutral microenvironment** adjacent to surface of epithelial cells * epithelial barrier: **intercellular tight junctions** LIMIT back-diffusion of H+ and pepsin * mucosal blood flow: provides bicarbonate and removes H+, plus provides oxygen and nutrients to support rapid epithelial cell turnover * prostaglandins

Question 69

name the divisions of the GIT * foregut = (...) of eosophagus to 2nd part of (...) * midgut = 2nd part of (...) to (...) along transverse colon * hindgut = (...) of transverse colon to rectum

Answer 69

* foregut = distal **3rd** of eosophagus to **2nd** part of **duodenum** * midgut = 2nd part of duodenum to **two-thirds** along **transverse colon** * hindgut = distal **3rd** of transverse colon to rectum

Question 70

Name the vitamin and explain 1 impact

Answer 70

impaired **production of VITAMIN K** by gut bacteria → impaired activation of coagulation factors (II, VII, IX, X) ⇒ impaired coaguation ## Footnote recall: PT (and thus INR) will increase ← factor VII (extrinsic pathway) has the shortest half-life and is the first to be affected

Question 71

parts of the large intestine: 1. c... 2. a... 3. t... 4. d... 5. s... 6. r... 7. a...

Answer 71

1. caecum 2. ascending colon 3. transverse colon 4. descending colon 5. sigmoid colon 6. rectum 7. anal canal

Question 72

relation of anal sphincters to puborectalis muscle

Answer 72

**external** anal sphincter **blends superiorly** with puborectalis muscle

Question 73

visualise how the superior epigastric artery comes about

Answer 73

aorta (→ branchiocephalic trunk) → subclavian artery → internal thoracic artery ⇒ superior epigastric artery

Question 74

visualise how the inferior epigastric artery comes about

Answer 74

aorta → thoracic aorta → abdominal aorta → common iliac artery → external iliac artery ⇒ inferior epigastric artery

Question 75

what are found at the inferior ends of the anal columns

Answer 75

anal valves

Question 76

what are the 2 "feeding centres" and what signals do they release | function is control of food intake

Answer 76

* ventromedial nucleus (**V**MN): **satiety** signals (anorexigenic signals) * lateral nucleus (**L**N): **hunger** signals (orexigenic signals) "feeling **full** is a **V**ictory, feeling **hungry** is a **L**"

Question 77

what are the 3 important structures found in the lesser omentum

Answer 77

* hepatic artery * portal vein * bile duct ## Footnote found near to the **free edge** of the lesser omentum (i.e. R side where hepatoduodenal ligament is)

Question 78

what are the 3 key features of neural regulatory systems in GIT

Answer 78

* sensors * neural network * effector systems

Question 79

what are the arteries that supply the rectus abdominis

Answer 79

* superior epigastric artery * inferior epigastric artery ## Footnote rectus abdominis is drained by veins that bear the same names

Question 80

what are the common manifestations seen in oral cavity

Answer 80

* mucosal changes * ulcer * lumps and bumps ## Footnote ulcer: local defect due to **sloughing of necrotic tissue**, leading to BREACH in covering epithelium lumps and bumps: RAISED **lesions** on or beneath tissue surface

Question 81

what are the common pathology of the oral cavity and oesophagus

Answer 81

lined by stratified **squamous** epithelium => **squamous** papilloma (benign) => **squamous** cell carcinoma (malignant)

Question 82

what are the common pathology of the stomach, small bowel, colon and rectum

Answer 82

lined by simple columnar epithelium (which is **glandular**) => **adeno**ma (benign) => **adeno**carcinoma (malignant)

Question 83

what are the protective effects of prostaglandins on gastric mucosa

Answer 83

promote * **mucus** secretion * **bicarbonate** secretion * **blood flow**

Question 84

what are the rectus abdominis attached to (superiorly and inferiorly)

Answer 84

superior: costal margin and xiphoid proess inferior: pubic crest and pubic symmphysis

Question 85

what are the secretory substances released by **parietal** cells | secretory = released into LUMEN of stomach

Answer 85

* acid (mainly HCl): **lower pH** for pepsinogen -> pepesin, kill ingested bacteria * intrinsic factor: helps with **absorption of vit B12** (via forming a **complex** with B12 in intestines which is then **absorbed**)

Question 86

what are the secretory substances released by **chief** cells | secretory = released into LUMEN of stomach

Answer 86

pepsinogen: converted into pepsin -> digests **protein** ## Footnote note: as pepsin is a **proteolytic** enzyme, it also helps with conversion of pepsinogen to pepsin (i.e. **autocatalytic**)

Question 87

what attaches the liver to the diaphragm

Answer 87

coronary ligaments, which are found at the **bare area** of the liver (which is not covered by peritoneum, directly in contact with diaphragm)

Question 88

what cells in the gastric glands are gastrin secreted by

Answer 88

G cells "**G** for **G**astrin" ## Footnote mostly by gastric glands in **antrum**, in contrast to ghrelin which is secreted mostly by gastric glands in **fundus**

Question 89

what direction does the external oblique muscles run

Answer 89

downwards and forwards "imagine the direction of your hands when you put them in your pockets" ## Footnote **internal** oblique muscles run in the **opposite** direction ⇒ downards and **backwards**

Question 90

what direction does the transverse abdominis muscle run

Answer 90

horizontally

Question 91

what disruptive process impacts both epithelial barrier function and epithelial regeneratieve capacity

Answer 91

chemotherapy * direct **cellular damage** * inhibition of epithelial regenerative capacity

Question 92

what does the neurovascular bundle run between

Answer 92

internal oblique and transversus abdominis

Question 93

what features can use to differentiate large intestine from small intestine

Answer 93

* omental appendices: **fatty** projections attached to **external surface** * taenia coli: 3 bands of **smooth muscle** running along **entire length** of large intestine * haustra: **pouch-like segments** of large intestine

Question 94

what hormones are secreted in stomach | hormones = released into BLOOD

Answer 94

* ghrelin: MORE secreted during **empty stomach** → travels to hypothalamus and **stimulates appetite** * gastrin: MORE secreted during **full stomach** → travels to hypothalamus and **decreases appetite**

Question 95

what is between the visceral peritoneum and parietal peritoneum

Answer 95

peritoneal cavity holding a small amount of fluid (peritoneal fluid)

Question 96

what is one function that the greater omentum has that the lesser omentum does not

Answer 96

moves towards and **wraps around inflamed** organ → acting as a physical barrier to **localise the infection** ⇒ **protect other organs** from inflammation

Question 97

what is the arterial supply of the transverse colon

Answer 97

* middle colic artery (from **SMA**) * left colic artery (from **IMA**) ## Footnote recall! * midgut: last part of duodenum to **2/3** of transverse colon hindgut: **last 1/3** of transverse colon to anus * midgut: supplied by **superior mesentric artery** hindgut: supplied by **inferior mesentric atery**

Question 98

what is the conjoint tendon formed by

Answer 98

fusion of lowest fibers of **internal oblique** and **transversus abdominis**

Question 99

what is the dilated **terminal** portion of the rectum which acts as a **storage area** for feces before defecation called?

Answer 99

ampulla

Question 100

what is the epithelium that covers the majority of GIT

Answer 100

simple columnar epithelium ## Footnote except in **oral cavity, oesophagus** and **anus** (i.e. START and END of GIT) whichhas **stratified squamous** epithelium to protect them from **mechanical damage**

Question 101

what is the head of the pancreas attached to

Answer 101

2nd part (i.e. descending part) of duodenum

Question 102

what is the neck of the pancreas anterior to

Answer 102

superior mesenteric vessels

Question 103

what is the body of the pancreas posterior to

Answer 103

stomach, omental bursa and lesser sac

Question 104

what is the tail of the pancreas attached to

Answer 104

spleen

Question 105

what is the implication of the superior and inferior epigastric arteries forming an **anastomosis** | anastomosis = connection or junction bet 2 tubular structures

Answer 105

if blood supply from one artery is **reduced**, the other artery can **compensate** ## Footnote the superior artery originates from the internal thoracic artery and the inferior artery from the external iliac artery, and they anastomose (connect) near the umbilicus

Question 106

what is the inguinal ligament formed by

Answer 106

lower edge of the **external oblique** aponeurosis **rolling inwards** → form a thick band

Question 107

what does the anterior wall of the inguinal canal consists of

Answer 107

* **external** oblique aponeurosis * *reinforced* by *internal* oblique at *lateral* 1/3 (i.e. the 1/3 closer to the ASIS)

Question 108

what does the roof of the inguinal canal consist of

Answer 108

* **internal** oblique aponeurosis * conjoint tendon *medially*

Question 109

what does the floor of the inguinal canal consist of

Answer 109

inguinal ligament

Question 110

what does the posterior wall of the inguinal canal consist of

Answer 110

* **transversus abdominus** * conjoint tendon *medially*

Question 111

what nerve controls the external anal sphincter

Answer 111

under **voluntary** control → contraction is stimulated by **somatic** fibers = **inferior rectal nerve** (branch of pudendal nerves which come from **S2-S4**) ## Footnote external anal sphincter is located **below the pectinate line**

Question 112

what nerves control the internal anal sphincter

Answer 112

under **autonomic** control * **contraction** (tonus) is **stimulated and maintained** by the **sympathetic** fibers (tonic contraction = normally contracted state), * **inhibited** (loses its tonic contraction and is allowed to expand passively) by the **parasympathetic** fibers ## Footnote internal anal sphincter is located **above the pectinate line**

Question 113

what is the pelvic pain line and what implications does it have for the visceral innervation of the rectum

Answer 113

inferior limit of visceral peritoneum * **ABOVE** the pelvic pain line (= covered by visceral peritoneum): visceral afferent fibers follow sympathetic fibers to **L1-L2** spinal segments * **BELOW** the pelvic pain line (= not covered by visceral peritoneum): visceral afferent fibers follow parasympathetic fibers to **S2-S4** spinal segments

Question 114

descibe the autonomic innervation of the rectum and anal canal

Answer 114

* sympathetic: from *lumbar* **splanchnic** nerves (*L1-L2*) * parasympathetic: from *pelvic* **splanchic** nerves (*S2-S4*) ## Footnote NO autonomic innervation **below the pectinate line**

Question 115

what physiologic response will be acting against a person when they lose weight

Answer 115

weight loss → less **adipose tissue** → lower levels of **leptin** → less anorexigenic signals ⇒ increased appetite

Question 116

what structures enhance absorption of nutrients in GI tract

Answer 116

* villi in small intestine * crypts in colon | via increasing **surface area**

Question 117

what type of epithelium is the peritoneum made of

Answer 117

simple squamous epithelium (known as mesothelium)

Question 118

what's the difference in the order of the aponeuroses above and below the umbilicus

Answer 118

* ABOVE umbilicus: aponeurosis of **external** oblique is **anterior** to rectus abdominis, aponeurosis of **internal** oblique **split and encloses** muscle, aponeurosis of **transversus abdominis** is **posterior** to rectus abdominis * BELOW umbilicus: aponeuroses of **all 3** are **anterior to** muscle

Question 119

where are the 3 abdominal muscles (external oblique, internal oblique and transversus abdominis) found

Answer 119

* **lateral** region: generate **movement** * **anterior** region: transition into **aponeurotic sheets** → form the **rectus sheath**

Question 120

where are the "feeding centres" found | function is control of food intake

Answer 120

hypothalamus

Question 121

where are the lunar semilunaris located

Answer 121

they pass along the **lateral border** of the **rectus abdominis** "form the 11 abs ;)" ## Footnote mark the **transition** between the abdominal **muscles** and their **aponeurotic portions**

Question 122

where are the openings of the deep inguinal ring (DIR) and superficial inguinal ring (SIR) found respectively

Answer 122

* DIR: transversalis fascia (above **midpoint** of inguinal ligament) * SIR: external oblique aponeurosis (above and slightly lateral to **pubic tubercle**)

Question 123

where do nutrients go after being absorbed in GIT | in general (i.e. **water-soluble** nutrients)

Answer 123

absorbed in **small intestine** through **capillaries** in villi -> carried via **hepatic portal vein** to liver -> processed by liver -> eventually carried into **systemic circulation** ## Footnote flows from hepatic portal veins to **capillaries** in liver -> processed by liver -> then carried into **hepatic veins** -> **IVC** -> heart (R side) -> lungs (via pulmonary artery) -> heart (L side) => **systemic circulation** (via aorta)

Question 124

where do the lymph nodes of the bowel drain into

Answer 124

cisterna chyli

Question 125

where is visceral pain from gall bladder referred to

Answer 125

* reaches **T7-T9** spinal segments ⇒ referred to **right hypochondriac** region * right **phrenic** nerve passes in vacinity of gallbladder ⇒ referred pain in **right shoulder and neck**

Question 126

Where would the incision most likely be made to separate the left and right rectus sheaths? A) Mid clavicular line B) Transpyloric plane C) Linea alba D) Subcostal plane E) Linea semilunaris

Answer 126

C) Linea alba * Rectus sheaths formed by the aponeurotic sheets of the 3 abdominal muscles * Linea alba formed by the **interweaving** of the **aponeuroses** at the **midline** ## Footnote **rectus abdominis** lies **lateral to the linea alba** on both sides

Question 127

Which abdominal muscle does the **L1** nerve provide **MOTOR innervation** to

Answer 127

internal oblique * external oblique: T7-T11 * internal oblique: T7-T12, L1 * rectus abdominis: T7-T12

Question 128

which artery supplies the midgut

Answer 128

superior mesenteric artery ## Footnote foregut = celiac trunk hindgut = inferior mesenteric artery

Question 129

which molecules stimulate appetite centrally (i.e. send orexigenic signals)

Answer 129

* ghrelin (secreted usually before meals, when **stomach is empty**) * cortisol (secreted in response to **stress**)

Question 130

which molecules suppress appetite centrally (i.e. send anorexigenic signals)

Answer 130

* insulin (secreted in response to **glucose**) * cholecystokinin (CCK) (secreted in response to **fat and protein**) * leptin

Question 131

Which of the following clinical presentations does NOT help to differentiate pyloric stenosis from other conditions which also present with regurgitation and vomiting (e.g. eosophagal atresia, physiological regurgitation)? A) projectile non-bilious vomiting after feeds B) presents in 3rd-6th week of life C) frequent demands for re-feeding

Answer 131

A) projectile non-bilious vomiting after feeds * B: presentation in **3rd-6th week of life** differentiates it from eosophagal atresia, which presents **right after birth** * C: **frequent demands for re-feeding** is due to **malnourishment** of infants, differentiating it from physiological regurgitation, which does not have this presentation ## Footnote note: vomiting is **non-bilious** due to the obstruction before **duodenum, where bile enters**

Question 132

which of the following dermatomes supply the umbilical region

Answer 132

T10

Question 133

Which of the following histological findings is characteristic of acute gastritis? A) Lymphocytic infiltration and intestinal metaplasia B) Superficial mucosal defect with fibrinous exudate and neutrophilic infiltration C) Abundnat subepithelial plasma cells within superficial lamina propria D) Glandular atrophy with eosinophilic infiltration

Answer 133

B) Superficial mucosal defect with fibrinous exudate and neutrophilic infiltration * **superficial mucosal defect** looks like **mucosal layer is missing** * **fibrinous exudate** is due to capillary damage -> leakage of plasma proteins like fibrinogen which forms fibrin => looks like a **pink layer on surface of mucosa** * **neutrophilic** infiltrates

Question 134

Which of the following is NOT a branch of the superior mesenteric artery (SMA)? A) Ileocolic artery B) Right colic artery C) Ileal arteries D) Left colic artery E) Jejunal arteries F) Middle colic artery G) Inferior pancreaticoduodenal artery

Answer 134

D) Left colic artery * Inferior pancreaticoduodenal artery: Pancreas, Dudodenum * Jejunal and ileal arteries: Jejunum, Ileum * **Ileocolic** artery: Ileum, Cecum, Appendix, **Ascending colon** * **Right colic** artery: **Ascending colon** * **Middle colic** artery: 2/3 of **Transverse colon** ## Footnote arteries supplying ascending colon collectively known as **right branches** of SMA

Question 135

Which of the following is NOT a function of the liver? A) Secretion of bile to aid in fat digestion B) Storage of glycogen for energy C) Production of digestive enzymes for carbohydrate breakdown in the duodenum D) Detoxification of blood by filtering bacteria and foreign particles

Answer 135

C) Production of digestive enzymes for carbohydrate breakdown in the duodenum * Liver is involved in carbohydrate, fat and protein **metabolism** * however, it does NOT directly digest carbohydrates but rather contributes by **storing and releasing glucose** | carbohydrate = sugar

Question 136

Which of the following nerves provides **SENSORY innervation** to the skin around the **umbilicus** (T10 dermatome)? A) T7-9 intercostal nerve B) T10 intercostal nerve C) T11-12 intercostal nerve D) L1

Answer 136

B) T10 intercostal nerve * T7-9: epigastrum * T11-12: inferior to umbilicus * L1: inguinal and pubis

Question 137

Which of the following statements about the diaphragmatic surface of the liver is TRUE? A) It is directly attached to the inferior surface of the diaphragm with no separation. B) The hepatorenal recess is located between the liver and the left kidney. C) The subphrenic recess separates the liver from the diaphragm. D) The hepatorenal recess is found on the left side of the liver.

Answer 137

C) The **subphrenic** recess separates the liver from the diaphragm. * Only certain parts of the liver is separated from the diaphragm, there is one part of the liver which is **NOT covered by peritoneum** and is directly **in contact with diaphragm** * Diaphragmatic surface also has **hepatorenal** recess, but it is on the **right** side bet the liver and the **right** kidney with adrenal gland

Question 138

which parts of the large intestine are retroperitoneal vs intraperitoneal

Answer 138

* cecum: intraperitoneal * appendix: intraperitoneal * ascending colon: retroperitoneal * transverse colon: intraperitoneal * descending colon: retroperitoneal * sigmoid colon: intraperitoneal * rectum: retroperitoneal "rmb as structures are **alternately** intra and retroperitoneal" ## Footnote * all the intraperitoneal parts (except cecum) are suspended by a **mesentry** ⇒ **mobile** * while all the retroperitoneal parts are **fixed** to posterior abdominal wall

Question 139

Which specialized cells in the gastrointestinal tract generate slow waves to regulate the rhythmic contraction of smooth muscle? A) Parietal cells B) Chief cells C) Interstitial Cells of Cajal D) Enterochromaffin-like (ECL) cells

Answer 139

C) Interstitial Cells of Cajal which connect longitudinal and circular smooth muscles → generate cycles of contraction and relaxation

Question 140

which vein does blood from liver drain into

Answer 140

hepatic vein

Question 141

why are smooth muscles in GIT able to exist in these 2 states, normally **contracted** and normally PARTIALLY **contracted**? ## Footnote depending on location and function, SM can exist in 4 functional states 1. normally contracted 2. normally partially contracted 3. normally relaxed 4. phasic contraction

Answer 141

sustained tonic contraction (i.e. can sustain contractions w/o continuous ATP contractions)

Question 142

why do people tend to empty their bowels after a meal

Answer 142

* main contributor is **gastrocolic (and gastroduodenal) reflex**: triggered by **distension of stomach (and duodenum)** as they fill with food, stimulates colon to **increase motility** * another contributor is secretion of **gastrin** secreted in response to food in GIT, stimulates colon to **increase motility** ## Footnote * gastrocolic reflex = **long reflex**: involves CNS, mediated mainly by vagus nerve * tends to happen more after **breakfast** as it is the first meal after a **long period of fasting** -> gastrocolic reflex stimulated more strongly

Question 143

why is it important to do biopsy for patients with leukoplakia and erythroplakia

Answer 143

may see findings of **dysplasia** and **malignancy** (usually squamous cell carcinoma) | dysplasia = PREcancerous changes

Question 144

what are the lines which divide the abdomen into **4 quadrants**

Answer 144

* median plane: at **midline** * transumbilical plane: at **umbilicus**

Question 145

order the layers of the abdominal fascia (from superficial to deep): * extraperitoneal fat * muscle * parietal peritoneum * skin * subcutaneous tissue * deep fascia

Answer 145

* skin * subcutaneous tissue * muscle * deep fascia * extraperitoneal fat * parietal peritoneum

Question 146

# and what happens during each phase what are the 3 swallowing phases

Answer 146

* oral phase: a. **chewing** b. formation of **food bolus** c. *tongue* pushes bolus backwards towards *pharynx* * pharyngeal phase: **swallowing reflex** triggered by bolus reaching oropharynx a. nasopharynx closes b. pharynx wall contracts, pushing food bolus *down pharynx* c. larynx moves upwards, while epiglottis is pushed down by food bolus -> epiglottis meets larynx => trachea closes d. **inhibition of respiration** e. UES opens * oesophagal phase a. **primary peristalsis**, which pushes food blolus *down oesophagus* b. **secondary peristalsis**, which occurs if food is **stuck in eosophagus** ## Footnote * voluntary: oral phase <- actions of chewing and of tongue are voluntary * involuntary: pharyngeal phase <- reflex mah oesophagal phase <- peristalsis is by smooth muscles

Question 147

what temporarily relaxes LES

Answer 147

* belching (i.e. burping): releases **swallowed air** * gastric distension: accomodate pressure changes when **stomach is overly full** ## Footnote tone of LES is impt as **relaxation** (= decreased tone) results in **acid reflux** (i.e. GERD)

Question 148

which hormones control the tone of LES

Answer 148

* gastrin: released at **start** of meal, triggered by food **entering stomach**, **increases tone** (i.e. contraction) to prevent reflux * CCK: released at **later phase** of meal, triggered by FATTY food **entering duodenum**, **decreases tone** (i.e. relaxation) to aid movement of food from stomach into small intestine

Question 149

how does nicotine, coffee and tea affect tone of LES

Answer 149

**decrease** tone of LES (i.e. relaxation)

Question 150

# what stimulates each, mediators for which what are the 3 types of gastric relaxation

Answer 150

* **receptive** relaxation: triggered when **food is swallowed** and stimulate the stretch receptors in eosophagus, signals then sent through **vagus nerve** to relax stomach * **adaptive** relaxation: trigger when **food enters stomach** and stimulate stretch receptors in it, triggering **vago-vagal pathway** to relax stomach further * **feedback** relaxation: triggered when **food enters small intestines**, release **hormones** like CCK and secretin to relax stomach and thus slow gastric emptying ## Footnote vagus nerve activation: * any stimulation of vagus nerve * **one-way (e.g. brain → stomach)** vago-vagal reflex: * reflex loop involving both afferent (sensory) and efferent (motor) vagus fibers * **two-way (stomach → brain → stomach)**

Question 151

Which of the following antacids is most potent? A) Aluminium hydroxide — Al(OH)3 B) Sodium bicarbonate — NaHCO3 C) Magnesium hydroxide — Mg(OH)2 D) Calcium carbonate — CaCO3

Answer 151

B) Sodium bicarbonate — NaHCO3 From most effective → least effective: NaHCO3, CaCO3, Mg(OH)2, Al(OH)3 "**carbonates** are more effective than hydroxides" "**2 together** is always the best, thus sodium **bi**carbonate and Mg(OH)**2** are more effective"

Question 152

He took an over-the-counter antacid that caused belching and bloating. The drug was MOST LIKELY which of the following? A) Magnesium hydroxide B) Famotidine C) Aluminium hydroxide D) Sodium bicarbonate

Answer 152

D) Sodium bicarbonate all compounds containing H**CO3-** and **CO3-** will result in **CO2 gas formation** => thus resulting in gastric distention, belching and flatulence

Question 153

Which drug can be added to the formulation to reduce belching and flatulence

Answer 153

simethicone acts as an anti-foaming agent via **easing release of gas** within GIT via burping or flatulence

Question 154

what are the DDI of antacids

Answer 154

can affect **absorption** of other medications => do NOT take within **2 hours** of other meds

Question 155

in what group of patients should you avoid long-term use of antacids

Answer 155

patients with **renal insufficiency** the elements in antacids which can cause **adverse effects** (e.g. Na+ and Ca2+ → metabolic alkalosis, Mg2+ → osmotic diarrhoea, Al3+ → constipation) are **filtered, regulated and/or excreted by kidneys**

Question 156

what is milk-alkali syndrome

Answer 156

**excessive calcium intake** → **hypercalcemia** → kidney dysfunction → **metabolic alkalosis** (could be worsened if there is excessive bicarbonate intake as well) → worsens hypercalcemia ⇒ **cycle repeats**

Question 157

MOA of H2-receptor antagonists

Answer 157

**competitive** inhibitors of H2 receptors on **parietal** cells ⇒ suppresses **acid secretion** by parietal cells

Question 158

Which of the following is the most potent H2-receptor antagonist? A) Famotidine B) Cimetidine C) Ranitidine D) Omeprazole

Answer 158

A) Famotidine ## Footnote H2-receptor antagonists all end with "**tidine**"

Question 159

H2-receptor antagonists are most effective at reducing gastric acidity when taken at **what time**

Answer 159

At **night** * effective at inhibiting **nocturnal** acid secretion, which is due to **histamine** * not that effective at inhibiting *meal-induced* acid secretion, as they are triggered by *other mediators (e.g. ACh, gastrin)*

Question 160

how effective are H2 receptor antagonists at inhibiting **meal-induced** acid secretion

Answer 160

**modest** only * H2 blockers ONLY block **histamine-mediated** stimulation of **parietal cells** * meal-induced acid secretion also involves stimulation of parietal cells via **gastrin** and acetylcholine **(ACh)** (**independent** of histamine) | recall: **parietal** cells secrete **acid**!

Question 161

Which of the following statements about omeprazole is/are correct? A) Omeprazole is a prodrug B) Omeprazole works directly from within the stomach to block acid release C) Omeprazole contains esomeprazole D) Omeprazole irreversibly blocks proton pumps in the parietal cells

Answer 161

A) Omeprazole is a prodrug route: taken orally → absorbed in small intestine → enters bloodstream ⇒ activated in **acidic environment** of parietal cells D) Omeprazole **irreversibly** blocks proton pumps in the parietal cells via forming **covalent** disulphide bonds with **H+-K+-ATPase** ## Footnote (C) is wrong as *esome*prazole is **isomer** of omeprazole, ("*isomer*-prazole") but they are NOT the same drug

Question 162

why should patients not crush omeprazole capsule

Answer 162

destroys the **enteric coating** which protects drug against **activation by stomach acidity** before absorption

Question 163

When is the BEST time for her to be administered the omeprazole? A) When she experiences acid reflux B) Immediately after her largest meal of the day C) 1 hour before bedtime D) 1 hour before breakfast

Answer 163

D) 1 hour before breakfast * bioavailability of omeprazole is **reduced by food** ⇒ best given on an **empty stomach** * omeprazole inhibits **active pumps**, not resting pumps ⇒ should be given **1 hour** before meal

Question 164

# and what is stimulated to be released what hormones stimulate pancreatic secretion

Answer 164

* CCK: stimulates release of **digestive enzymes** (e.g. proteases, lipases) by **acinar secretory cells** * secretin: stimulates release of pancreatic juice which are **bicarbonate-rich** and contain water and electrolytes by **ductal cells** ## Footnote CCK = stimulated by **fat-** and protein-containing chyme in small intestine secretin = stimulated by **acidic** chyme **entering** small intestine from stomach

Question 165

how is CCK-stimulated release of digestive enzymes regulated by food content in duodenum

Answer 165

if food is present → **trypsin** is busy breaking down proteins → less **CCK-RP and monitor peptides** broken down → increased stimulation of **I cells** by them to **release CCK** ⇒ CCK stimulates further release of pancreatic enzymes

Question 166

describe secretion of Cl- in small intestines

Answer 166

**Na+-K+-ATPase** pump actively transports 3 Na+ out of cell and 2 K+ in → **higher extracellular [Na+]** and higher intracellular [K+] → Na+ gradient allows **Na+-coupled transporters** on *basolateral* side of cell to bring in **Cl-** from blood ⇒ **Cl- exits** through **CFTR channels** on *apical* side of cell into intestinal lumen

Question 167

describe secretion of HCO3- in small intestines

Answer 167

**Na+-K+-ATPase** pump actively transports 3 Na+ out of cell and 2 K+ in → **higher extracellular [Na+]** and higher intracellular [K+] → Na+ gradient allows **Na+-coupled transporters** on *basolateral* side of cell to bring in **HCO3-** from blood ⇒ **HCO3- exits** through **Cl-/HCO3- exchanger** on *apical* side of cell into intestinal lumen (Cl- which entered will exit through **CFTR channels** on *apical* side of cell into intestinal lumen)

Question 168

process of gastric churning

Answer 168

* pylorus **closes** * **contactions** of antrum **crush food** against closed pyloric sphincter -> further breaking it down * chyme is then **pushed backward** into stomach for further mixing (retropulsion)

Question 169

what mechanisms protect pancreas from autodigestion by its own enzymes

Answer 169

* most are synthesised as **inactive proenzymes (zymogens)** (which are packaged within secretory granules) * which are then **activated by trypsin**, which itself is activated by enzymes in the **small intestines** * acinar and ductal cells secrete **trypsin inhibitors** (including SPINK1)

Question 170

what is pancreatitis due to

Answer 170

**derangement or overwhelming** of protective mechanisms, resulting in **autodigestion** of pancreas by its own enzymes

Question 171

# reversibility, parts of pancreas affected differences bet exocrine and endocrine pancreatitis

Answer 171

* acute: reversible chronic: irreversible * acute: mainly exocrine parenchyma (acinar cells) chronic: destruction of exocrine parenchyma first, then destruction of endocrine parenchyma in late stages

Question 172

Which of the following statements is TRUE regarding the epidemiology and causes of pancreatitis? A) Autoimmune pancreatitis is the most common cause of chronic pancreatitis. B) Alcohol and gallstones together account for the majority of acute pancreatitis cases in Western countries. C) Chronic pancreatitis is primarily caused by gallstones. D) Hereditary pancreatitis accounts for over 50% of chronic pancreatitis cases.

Answer 172

B) Alcohol and gallstones together account for the majority of acute pancreatitis cases in Western countries. * **Biliary tract disease** and **alcohol** account for ~80% of **acute pancreatitis** cases in Western countries * (A) and (C) is wrong as most common cause of **chronic pancreatitis** is long-term **alcohol abuse** * (D) is wrong as while **hereditary** pancreatitis is one other cause of chronic pancreatitis (alongside **long-standing obstruction of pancreatic duct** and **autoimmune injury**), it only takes up to 25% of cases

Question 173

how does gallstones lead to acute pancreatitis

Answer 173

**obstructs** bile duct → increase in intrapancreatic ductal **pressure** → **enzyme-rich** fluid **leaks** into pancreatic interstitium (i.e. connective tissue surrounding pancreas) ⇒ *destruction* of pancreatic tissue which thus elicits an acute *inflammatory* response

Question 174

Which of the following correctly describes how chronic alcohol consumption contributes to pancreatitis? A) It causes a transient increase in contraction of the sphincter of Oddi, which can **obstruct** pancreatic outflow. B) It leads to secretion of protein-rich pancreatic fluid, resulting in the formation of protein plugs that **obstruct** small pancreatic ducts. C) It has direct toxic effects on acinar cells, leading to **oxidative stress** and cellular injury. D) All of the above. ## Footnote recall: sphincter of Oddi is the muscular valve surrounding the exit of the **bile duct** and **pancreatic duct** into the **duodenum**.

Answer 174

D) All of the above.

Question 175

Which of the following is NOT a typical histological feature of acute pancreatitis? A) Microvascular leak and interstitial edema B) Fat necrosis with calcium deposition (saponification) C) Chronic lymphocytic infiltration and fibrosis D) Hemorrhage and pancreatic parenchymal destruction

Answer 175

C) Chronic lymphocytic infiltration and fibrosis (A): *inflammatory mediators* increase **vascular permeability** -> fluid accumulation and thus swelling (D): *elastase* **damages blood vessels** => haemorrhage (B): *lipase* **breaks down** peripancreatic **fat** or fat within pancreas and forms **calcium deposits**

Question 176

A 45-year-old male with a history of chronic **alcohol use** presents with severe **epigastric pain radiating to the back, nausea, and vomiting**. He is hypotensive, tachypneic, and has decreased urine output. Laboratory tests show **elevated amylase and lipase**. Over the next 48 hours, he develops progressive **hypoxemia**, requiring mechanical ventilation. Which of the following complications is MOST likely responsible for his respiratory distress? A) Pancreatic abscress B) Disseminated intravascular coagulation C) Acute respiratory distress syndrome (ARDS) D) Pancreatic pseudocyst

Answer 176

C) Acute respiratory distress syndrome (ARDS) * Symptoms indicate that patient has acute pancreatitis * All of the options are thus possible complications (systemic organ failure, DIC, sterile or infected pancreatic abscess, pancreatic pseudocyst) * ARDS is most likely and is due to *inflammatory cytokines* increasing pulmonary **vascular permability** ⇒ pulmonary **oedema**

Question 177

Which of the following features is characteristic of autoimmune pancreatitis (AIP) and helps differentiate it from pancreatic carcinoma? A) Presence of IgG4+ plasma cells B) Poor response to corticosteroids C) Metastatic spread to distant organs D) Vascular invasion on imaging

Answer 177

A) Presence of **IgG4+** plasma cells * (B) is wrong as autoimmune pancreatitis **mimics pancreatic cancer** (e.g. present with pancreatic mass), but its key distinguishing feature is its **good response to steroid therapy** * (C) and (D) are just features of pancreatic cancer

Question 178

Arrange the key pathological mechanisms seen in chronic pancreatitis: A) repeated bouts of acute pancreatitis -> acinar cell injury and inflammation B) atrophy and dropout of acini C) fibrosis D) dilatation of pancreatic ducts with protein plugs / calcified concretions

Answer 178

(A), (C), (D), (B) (D) doesn't occur in all causes repeated bouts of acute pancreatitis (A) -> acinar cell injury and inflammation -> activation of **FIBRINOGENIC FACTORS** (which are actually inflammatory mediators) -> fibrosis (C) (+ if if cause is alcohol, there is also secretion of **protein-rich pancreatic juice** (D) -> formation of **protein plugs** -> **calcification** of protein plugs to form concretions -> **block** pancreatic ducts and cause **ductal dilation**) => atrophy of acinar cells (B) ## Footnote note: **predominance of fibrinogenic factors** in chronic pancreatitis **distinguishes it from acute** pancreatitis

Question 179

Which of the following correctly describes the order of genetic mutations in pancreatic carcinoma? A) TP53 mutation → KRAS mutation → SMAD4 mutation → Invasive carcinoma B) KRAS mutation → CDKN2A inactivation → TP53 & SMAD4 mutations → Invasive carcinoma C) SMAD4 mutation → TP53 mutation → CDKN2A inactivation → PanIN formation → Invasive carcinoma D) CDKN2A inactivation → KRAS mutation → TP53 mutation → Invasive carcinoma

Answer 179

B) KRAS mutation → CDKN2A inactivation → TP53 & SMAD4 mutations → Invasive carcinoma * **KRAS** mutation: **earliest event** in pancreatic carcinogenesis → formation of **PanIN** (Pancreatic Intraepithelial Neoplasia) * **CDKN2A (p16)** inactivation: causes dysplastic PanINs → allowing uncontrolled cell proliferation * **TP53** & **SMAD4** mutations: **final step** in progression to **invasive carcinoma**

Question 180

Which of the following statements about pancreatic carcinoma is correct? A) The tumor is soft and well-circumscribed, without an infiltrative border. B) The presence of desmoplasia makes the tumor hard and fibrotic. C) PDAC originates from acinar cells rather than ductal epithelium. D) Perineural invasion is uncommon and does not contribute to pain in pancreatic cancer.

Answer 180

B) The presence of desmoplasia makes the tumor hard and fibrotic. * (B): presence of **desmoplasia**, which is a **fibrotic** reaction, allowing it to be *firm* and also aiding in tumour *invasion* ⇒ large, pale, *firm* mass with *infiltrative border* * (D): **perineural** invasion is common → tumor cells spread along **nerve fibers** ⇒ severe *pain*

Question 181

Which of the following statements about insulinomas is correct? A) Most insulinomas are malignant and have a high metastatic potential. B) Insulinomas are the most common type of PanNET and are usually benign. C) Gastrinomas are more benign than insulinomas. D) Non-functioning PanNETs are less aggressive than functioning ones.

Answer 181

B) Insulinomas are the **most common** type of PanNET and are usually **benign**. compared to other functioning and non-functioning PanNET which are malignant (e.g. gastrinoma (which causes ZES))

Question 182

A **solid, pale** pancreatic mass with areas of **cystic change** is surgically removed. Histological examination reveals **nests and trabeculae of small round cells** with **SALT-AND-PEPPER CHROMATIN**. The tumor is **highly vascular**. What is the most likely diagnosis? A) Pancreatic ductal adenocarcinoma B) Pancreatic neuroendocrine tumor (PanNET) C) Acinar cell carcinoma D) Solid pseudopapillary neoplasm

Answer 182

B) Pancreatic neuroendocrine tumor (PanNET) * cystic change: **fluid-filled** spaces due to necrosis or degeneration * highly vascular: indicates **abundant blood supply**

Question 183

Pancreatic ductal adenocarcinoma (most common form of pancreatic carcinoma) has no precursor lesions. True or False?

Answer 183

False Precursor lesions include * pre-malignant masses (e.g. IPMN, MCN) * pancreatic intraepithelial neoplasia (PanIN) ## Footnote orde for **cystic** neoplasms: **serous** cystadenoma — benign → **mucinous** cystic neoplasm (MCN) — pre-malignant → **intraductal** papillary mucinous neoplasm (IPMN) — pre-malignant ⇒ **solid-pseudo**papillary neoplasm (SPN) — malignant

Question 184

# think of a tube, what are 3 ways it can become obstructed what are the 3 main causes of large bile duct obstruction

Answer 184

* intraluminal (i.e. sth **within lumen**): e.g. gallstones * mural (i.e. sth wrong with **wall of bile duct**): e.g. inflammatory bile duct strictures, malignancies of biliary tree * extramural (i.e. **compression** from outside bile duct): e.g. porta hepatis lymphadenopathy, malignancies of head of pancreas

Question 185

Which of the following statements about large bile duct obstruction is TRUE? A) Chronic obstruction can lead to biliary cirrhosis. B) Ascending cholangitis is caused by viral infections. C) Acute obstruction always leads to irreversible liver damage. D) Intermittent obstruction has no risk of infection.

Answer 185

A) Chronic obstruction can lead to biliary cirrhosis. * (C) and (D) are wrong as 1. **acute** obstrucion: **reversible** (C) 2. **subtotal / intermittent** obstruction: **stasis** of bile -> envt for **bacterial OVERgrowth** -> **infection** of bile duct, followed by liver and then systemically (D) => ascending cholangitis, intrahepatic cholangitic abscesses and sepsis 3. **chronic** obstruction: permanent bile stasis => progressive biliary **fibrosis and cirrhosis** * (B) is wrong as infections are caused by **gut-associated BACTERIA** (e.g. E.coli)

Question 186

where are plicae circulares (folds), villi, microvilli and crypts found in

Answer 186

* plicae circulares: **circular folds** of mucosa and submucosa, most prominent in **jejunum** but sparse in ileum * villi: **finger-like projections** extending from folds, found throughout **small intestine** * microvilli:**microscopic projections** on individual enterocytes, found throughout **small intestine** * crypts: **invaginations** bet VILLI. found throughout **small AND large intestine** ## Footnote so small intestine has everything, while colon only has crypts

Question 187

what is the function of small intestinal secretion

Answer 187

* **ALKALINISE** contents -> provide optimal envt for enzyme activity BY secreting **HCO3-** * maintain **FLUIDITY** of chyme BY secreting **Cl-** and thus secreting **water** (snd Na+) via **paracellular** pathway

Question 188

what is secreted in the colon and why

Answer 188

* K+ in response to aldosterone which works to increase **sodium (and thus water) absorption** * HCO3- to **buffer** against **H+** produced by **bacterial fermentation**

Question 189

what is the molecule that drives absorption in small intestines

Answer 189

Sodium (Na+) * helps with absorption of other nutrients either via 1. **co-transporters**, where nutrients (e.g. glucose, amino acids) are actively transported into the cell along with Na+ 2. creating as **osmotic gradient**, with draws water (and **dissolved solutes** like Cl- and K+) into cell via osmosis through **paracellular** route (also known as **solvent drag**) * gradient is maintained by Na+ being **pumped out** of enterocyte via **Na+/K+ ATPase**

Question 190

how does osmolarity and processes change as we move along small intestine

Answer 190

* start: **hyper**osmolarity due to digestion of chyme * as we move along, hyperosmolar chyme **pulls water into lumen** AND **secretion** of mucus, Na+, Cl- and HCO3- into lumen for better digestion and absorption * eventually, luminal contents become **iso**-osmolarity * thus **absorption** then occurs

Question 191

# hormone and protein involved how is availability of iron regulated | use iron deficiency as example situation

Answer 191

deficiency: lesser **hepcidin** (produced by liver) → increase in **ferroportin** activity (as less inhibition) → **less iron is transported out** from intestinal cells into bloodstream ⇒ more iron excreted in feces once intestinal cells **slough off** and are **excreted** OR more iron **stored as ferritin**

Question 192

what is another name for vitamin B12

Answer 192

cobalamin (CBL)

Question 193

Which protein is responsible for transporting B12 in the blood after absorption? A) Haptocorrin B) Intrinsic Factor C) Transcobalamin II D) Pepsin

Answer 193

C) Transcobalamin II INSIDE enterocytes → B12 **dissociates** from IF and **binds** to TCII → B12-TCII **complex** is then **transported in the bloodstream** to be delivered to tissues.

Question 194

transport of vit B12 in GIT: * stomach: 1. B12 is released from **dietary proteins** by (...), and (...) then binds to it to **protect it from stomach acid** 2. (...) cells secrete (...) * duodenum: (...) degrade (...) to release free B12, which then binds to (...) to form (...) complex * ileum: (...) complex binds to **specific receptors** on enterocytes and are absorbed via (...)

Answer 194

* stomach: 1. B12 is released from **dietary proteins** by *stomach acid and pepsin*, and *haptocorrin* then binds to it to **protect it from stomach acid** 2. *parietal* cells secrete *intrinsic factor (IF)* * duodenum: *pancreatic proteases* degrade *haptocorrin* to release free B12, which then binds to *IF* to form *B12-IF* complex * ileum: *B12-IF* complex binds to **specific receptors** on enterocytes and are absorbed via *receptor-mediated endocytosis*

Question 195

# think of water slowing in a river causes of diarrhoea

Answer 195

* increased intestinal **secretions** (*secretory*) ("more **water put into** river, resulting in increased vol of water in river") * decreased **absorptive capacity** (*malabsorptive*) ("less **water removed** from river, resulting in increased vol of water in river") * **osmotic** ("also less **water removed** from river, resulting in increased vol of water in river") * shortened **intestinal transit** (*motility-related*) ("water in river **flows** faster, so less time to remove water, thus resulting in increased vol of water in river")

Question 196

main location where each type of diarrhoea occurs: secretory, malabsorptive, osmotic, motility-related)

Answer 196

* small intestine and colon: motility-related * small intestine only: secretory * jejunum and ileum (of small intestine) only: malabsorptive and osmotic

Question 197

what substances are mainly absorbed in the ileum

Answer 197

* bile salts * vitamin B12 (particularly at **terminal** ileum)

Question 198

where are mineral ions (e.g. calcium, iron) mainly absorbed

Answer 198

stomach as its **acidic** pH enhances **solubilisation** (i.e. acid converts minerals into *ionic form* which is *more soluble* and thus can be *absorbed more efficiently*)

Question 199

why does osmotic diarrhoea tend to involve jejunum and ileum

Answer 199

* majority of absorption occurs in jejunum and ileum <- same folds, villi and microvilli as duodenum, but has a **longer length** * fewer **active transporters** to counter **osmotic absorption** 1. duodenum has co-transporters which *actively transport solutes* into blood 2. colon has transport proteins which *actively reabsorb water* ## Footnote note that site where **MAJORITY** of absorption occurs (**jejunum and ileum**) is different from site where absorption of **MOST (number of) SOLUTES** occur (**duodenum**)

Question 200

how can the impaired absorption of bile salts lead to elevated ALP levels

Answer 200

bile salt malabsorption → impaired **absorption** of fat-soluble vitamins, including **vit D** → decreased levels of **calcium** in blood (as vit D is crucial for Ca2+ homeostasis) → stimulation of **parathyroid gland** to release **parathyroid hormone (PTH)** → which increases Ca2+ levels via **bone resorption** (i.e. activation of **osteoclasts** to break down bone and release Ca2+) ⇒ at the same time **releasing ALP**

Question 201

describe the digestion of carbohydrates in the small intestine

Answer 201

1. pancreatic amylase: carbohydrates → disaccharides 2. brush border enzymes: disaccharides → monosaccharides ## Footnote carbohydrates are already partially digested by **salivary amylase** in mouth

Question 202

how is the absorption of fructose in small intestines different from the other monosaccharides (glucose, galactose, xylose)

Answer 202

* glucose, galactose & xylose: **Na+**-dependent **secondary active transport** system ← move against their conc gradient with help of Na+ gradient (maintained by Na+/K+-ATPase) * fructose: **facilitated** diffusion ← moves down its conc gradient (maintained by fructose being **rapidly converted** into glucose and lactic acid **upon entering** epithelial cell)

Question 203

describe the digestion and absorption of proteins in the small intestine

Answer 203

1. *pancreatic* **proteases** break down proteins into smaller peptides and free AAs 2. *brush border* **peptidases** further break down the smaller peptides into tripeptides, dipeptides and free AAs 3. free AAs are absorbed via **Na+-dependent** transport systems (2º active transport), while tripeptides and dipeptides are absorbed via **carrier** transport 4. tripeptides and dipeptides are then broken down into free AAs by *intracellular* **peptidases** ## Footnote * proteins are already partially digested by **gastric pepsin** in stomach * rate of absorption of peptides > free AAs ⇒ peptides are more efficient at getting AA into cell

Question 204

in which parts of the small intestine are carbohydrates and proteins mainly absorbed

Answer 204

duodenum and jejunum

Question 205

is it normal for there to be a small amount of protein in person's stool

Answer 205

yes → protein in stool comes from * bacteria debris (i.e. bacteria die and release their proteins into stool) * cellular debris (i.e. sloughed-off intestinal cells from constant renewal of intestinal epithelium)

Question 206

which salivary gland are neoplasms most commonly found in? A) minor salivary glands B) parotid gland C) sublingual gland D) submandibular gland

Answer 206

B) parotid gland

Question 207

Which of the following statements correctly describes the common characteristics of salivary gland neoplasms? A) **Pleomorphic adenom**a is most commonly associated with male smokers, while *Warthin tumour* has no known associations. B) *Warthin tumour* is the most common salivary gland neoplasm, and it is frequently associated with male smokers. C) **Pleomorphic adenoma** is the most common salivary gland neoplasm, followed by *Warthin tumour*, with *Warthin tumour* being associated with male smokers. D) Both **pleomorphic adenoma** and *Warthin tumor* are strongly associated with male smokers.

Answer 207

C) **Pleomorphic adenoma** is the most common salivary gland neoplasm, followed by *Warthin tumour*, with *Warthin tumour* being associated with male smokers.

Question 208

Which of the following is a key diagnostic feature differentiating Boerhaave syndrome from Mallory-Weiss tears? a) Haematemesis b) Pneumomediastinum or subcutaneous emphysema c) Presence of dysphagia d) Occurrence after minor vomiting

Answer 208

b) Pneumomediastinum or subcutaneous emphysema * Mallory-Weiss tears are **superficial** ⇒ **haematemesis** * Boerhaave syndrome are **transmural** (deep) → air and other GI contents leaking into mediastinum ⇒ severe **chest pain** and tachypnea

Question 209

which risk factors can be used to differentiate adenocarcinoma and SCC? A) diet B) gender C) smoking D) past medical history

Answer 209

A) diet and D) past medical history * most important risk factors are **GERD** for adenocarcinoma and **low fibre diet** for SCC * **male** gender is risk factor for both (B) * **tobacco** is also a risk factor for both (C)

Question 210

One option is true while the other is false. Choose. A) Adenocarcinoma affects the upper 2/3 of the eosophagus, while SCC affects the lower 1/3 of the eosophagus. B) Squamous cell carcinoma (SCC) is the most common form of eosophagal cancer.

Answer 210

B) is true and A) is false It is the other way round, with SCC affecting the proximal and mid eosophagus (upper 2/3)

Question 211

what is the difference in histology between Squamous Cell carcinoma (SCC) and adenocarcinoma

Answer 211

* SCC: keratin pearls * adenocarcinoma: mucin production

Question 212

# think of the 4 Bs what are the clinical features and complications of eosophagal cancer

Answer 212

clinical features: * **B**lock: progressive dysphagia, odynophagia * **B**leed: invasion of tumour into mucosal and submucosal layers → breach of blood vessels ⇒ haemorrhage complications: * Burrow: 1. aspiration pneumonia, (due to **fistula** → **infection** from inhaled food/liquid) 2. aortic **invasion** → **haemorrhage** 3. mediastinitis (due to mediastinal **invasion** → **infection** from food/liquid) 4. **metastasis** ## Footnote recall: blood vessels are usually found in submucosal layer!

Question 213

definition of oesophagal varices

Answer 213

**dilated** submucosal veins in **lower 1/3** of oesophagus and **proximal stomach**

Question 214

pathogenesis of oesophagal varices

Answer 214

liver **cirrhosis** → portal **hypertension** → portosystemic **shunting** bet **L gastric** veins and **eosophagal** veins ## Footnote L gastric veins: * drains **lower 1/3** of oesophagus * drains INTO **portal vein** Eosophagal veins: * drains **middle 1/3** of oesophagus * drains INTO (hemiazygos vein →) **azygos** vein → **SVC**

Question 215

pathogenesis of GERD

Answer 215

transient **LES** relaxation → **reflux of gastric contents** into lower eosophagus → squamous epithelial cells release secretory **inflammatory cytokines** in response to bile acids and salts ⇒ **DAMAGE** to eosophagus

Question 216

# complication of GERD what is Barrett's eosophagus

Answer 216

mucosal damage -> stratified squamous epithelium being **replaced** by **NONciliated COLUMNAR epithelium** and **GOBLET cells** (i.e. intestinal **metaplasia**)

Question 217

why is Barrett's eosophagus concerning

Answer 217

precancerous, increased risk of **dysplasia** and **cancer**

Question 218

causes of acute gastritis

Answer 218

* chemical (e.g. NSAIDs, alcohol, chemotherapy) * stress ulcers: 1) **curling** ulcer: usually due to severe *burns* -> systemic hypovolemia => decreased mucosal blood flow (too LITTLE protection) "*burn*ed by the **curling** iron" 2) **cushing** ulcer: due to *increased intracranial pressure* from e.g. brain injury -> vagal stimulation => increased gastric acid secretion (too MUCH acid) "**cushion** the *brain*" | acute gastritis = too much acid and/or too little protection

Question 219

causes of chronic gastritis

Answer 219

* H pylori (majority) * autoimmune

Question 220

pathogenesis of H pylori gastritis

Answer 220

mucosal **damage** and inflammation due to: * H pylori produces **urease** which **neutralises HCl** -> **G cells** detect the rise in pH -> and thus increase **gastrin secretion** => which then stimulates increased **ACID secretion** from **parietal cells** * H pylori producing **endotoxins and exotoxins**

Question 221

Which of the following best describes the typical distribution of lesions in Ulcerative Colitis? A. Involves only the terminal ileum and spares the rectum B. Involves the colon and rectum with skip lesions C. Continuous involvement of colon with rectal involvement D. Affects any portion of the GI tract, including esophagus

Answer 221

C. Continuous involvement of colon with rectal involvement * Ulcerative colitis **ALWAYS involves the rectum** and progresses *continuously proximally*. * while Crohn's **spares the rectum**, and presents as *skip lesions*

Question 222

Which of the following is a distinguishing gross feature of Crohn disease? A. Friable mucosa with superficial and deep ulcers B. Lead pipe appearance due to loss of haustra C. Cobblestone mucosa with creeping fat D. Thin bowel wall

Answer 222

C. Cobblestone mucosa with creeping fat * Crohn's shows **transmural** inflammation, leading to thickened walls (D), creeping fat and *cobblestone* mucosa * while UC shows inflammation only in **mucosa and submucosa**, and has lead pipe appearance (due to loss of haustra) and *friable* mucosa with superficial and deep ulcers

Question 223

Granulomas are seen in Crohn disease. True or False?

Answer 223

True specifically **non-caseating** ones

Question 224

Which of the following is true regarding diarrhea in Ulcerative Colitis? A. It is typically watery and non-bloody B. May or may not be bloody C. Almost always bloody D. Always associated with malabsorption

Answer 224

C. Almost always **bloody** while Crohn's may present with **non-bloody** diarrhoea

Question 225

What is the direction of blood and bile flow in the liver, and why are they opposite?

Answer 225

* Blood in **portal vein & hepatic artery** flows toward the central vein (**inwards**) <- blood is brining nutrients and oxygen **TO hepatocytes** (e.g. nutrients and oxygens, substances to detoxify) * Bile flows toward the **bile duct** in the portal triad (**outwards**). This happens because blood <- bile is synthesized **BY hepatocytes** and must exit the liver via bile duct

Question 226

# recall that it is under chronic gastritis! pathogenesis of autoimmune gastritis

Answer 226

**autoantibodies** to **parietal** cells -> parietal cell death -> **G cells** detect **rise in pH** -> increase **gastrin** secretion -> stimulate increased **acid secretion** from remaining parietal cells => mucosal damage and inflammation

Question 227

# think of the pathogenesis clinical features of autoimmune gastritis

Answer 227

* hypochlorhydria <- parietal cell death * hypergastrinemia <- increased gastrin secretion by G cells * **pernicious anemia** which is **megaloblastic anemia** due to loss of IF <- parietal cell death ## Footnote recall: **IF** helps with absorption of **B12** which is needed for proper **DNA synthesis** in **RBCs**

Question 228

in peptic ulcer disease, where is the solitary mucosal ulcer usually seen

Answer 228

* proximal duodenum or antrum of stomach (MAJORITY) * distal stomach

Question 229

what is the characteristics of pain in peptic ulcer disease

Answer 229

* **burning**/aching * @ **epigastric** * relieved by food/alkali ← (esp milk) **buffers** stomach acid due to their **calcium** and **protein** content AND **delays gastric emptying**, thus prolonging buffering effect and temporarily protecting ulcerated area (usually duodenum) * occurs again **1-3 hours after food** * worse at **night** ← increased acid secretion

Question 230

causes of peptic ulcer disease

Answer 230

"think of chemicals which burn through stomach" * NSAIDs * H pylori (which produces urease)

Question 231

# think of amt of gastric contents lost + content of gastric contents what electrolyte imbalances will be seen in patients with prolonged vomiting (and inability to retain food)

Answer 231

* metabolic alkalosis due to prolonged vomiting → loss of **HCl** → loss of H+ ⇒ blood becomes more **alkaline** * **hypochloremia** (low Cl-) due to prolonged vomiting → loss of **HCl** ⇒ loss of Cl- * hypokalemia (low K+) due to prolonged vomiting resulting in: a) loss of **K+** b) **renal compensation** for alkalosis where need to **lose cation** to balance out loss in Cl- and thus maintain **electroneutrality** → choice of cation is K+ and not **Na+** as will **worsen volume-depleted state**

Question 232

3 possible types of polyps in stomach

Answer 232

* hyperplastic * adenoma * oxyntic/fundus gland

Question 233

pathophysiology of hyperplastic polyps

Answer 233

**chronic gastritis** (e.g. from H pylori) → reactive **hyperplasia** of mucosa ⇒ may lead to **dysplasia**

Question 234

which of the stomach polyps have risk of malignancy

Answer 234

* hyperplastic polyps * adenoma polyps

Question 235

what are the 2 types of stomach cancer (Lauren classification)

Answer 235

* intestinal type * diffuse type

Question 236

what is a unique histological feature of diffuse type stomach cancer

Answer 236

signet ring cells!

Question 237

what does diffuse type stomach cancer look like

Answer 237

plastic bottle = linitis plastica

Question 238

which type of stomach cancer has a ***poorer* prognosis**

Answer 238

diffuse type bcos *poorly* **differentiated**

Question 239

where is intestinal type stomach cancer most commonly found

Answer 239

**lesser** curvature of **antrum**

Question 240

in which cancers in GIT do the T in TNM staging system refer to **depth of invasion** instead of size | depth = no of **layers** invaded

Answer 240

* gastric * colorectal ## Footnote in contrast, look at size in liver, pancreatic and gallbladder cancer

Question 241

definition of early gastric carcinoma

Answer 241

gastric cancer that invades **no more deeply** than **submucosa** (irrespective of lymph node metastasis) | i.e. does not go BEYOND submucosa

Question 242

clinical significance of early gastric carcinoma

Answer 242

**good prognosis** with complete excision | much better prognosis than gastric carcinomas in general

Question 243

what is the mos likely cause of appendicitis in children? A) Faecalith obstruction (i.e. hardened stools) B) Foreign matter C) Lymphoid hyperplasia D) Tumor of the appendix E) Parasitic infection

Answer 243

C) Lymphoid hyperplasia * **faecolith** is more common cause in **adults** * foreign matter is a possible cause in both children and adults, but less common

Question 244

what can cause **painless** obstructive *jaundice*

Answer 244

pancreatic cancer (esp **HOP**) bcos HOP is **anterior** to **common bile duct**

Question 245

what is the treatment for H pylori eradication

Answer 245

**triple** therapy (*CAO*) * *C*larithromycin (antibiotic) * *A*moxicillin (antibiotic) (or **metronidazole** in case of **penicillin allergy**) * *O*meprazole (PPI)

Question 246

why is PPI included in treatment for H pylori eradication | as part of triple therapy

Answer 246

* raises intragastric **pH** -> lowers **MIC** and thus making antibiotics **more effective** AND also **reduces symptoms** * **antimicrobial** properties

Question 247

why is double antibiotic therapy required in treatment of H pylori eradication | as part of triple therapy

Answer 247

* H pylori is **inherently very resistant** (to vancomycin, trimethoprim, etc) * H pylori **becomes resistant** to clarithromycin and metronidazole if **given alone**

Question 248

* triple therapy is carried out for (...) to (...) days * after completion of triple therapy, PPI is continued for: (...) to (...) weeks in duodenal ulcers (...) to (...) weeks in gastric ulcers

Answer 248

* **triple therapy** is carried out for **7 to 14 days** * after completion of triple therapy, *PPI* is *continued* for: *4 to 8* weeks in *duodenal* ulcers *8 to 12* weeks in *gastric* ulcers

Question 249

what does quadruple therapy for H pylori eradication involve

Answer 249

**TOMB** * **T**etracycline (antibiotic) * **O**meprazole (PPI) * **M**etronidazole (antibiotic) * **B**ismuth (mucoprotective agent)

Question 250

difference bet antiemetics vs antimimetics

Answer 250

* antiemetics: drugs to prevent or treat **nausea and vomiting** * antimimetics: **subset** of antiemetics, drugs that specifically prevent or treat **motion sickness**

Question 251

where are *serotonin* 5-**HT3** receptors found

Answer 251

*serotonin* 5-**HT3** receptors found on vagal efferent fibers in **GIT** <- athlete throwing *smiley* hammer from **stomach**-shaped area (sign says "1, 2, **3**, **H**ammer **T**hrow!")

Question 252

example of 5-*HT*3 *antagonists*

Answer 252

on**danse**tron <- ribbon **dancer** *blocking* *H*ammer *T*hrow in stomach-shaped area ## Footnote other examples: granisetron, palonosetron

Question 253

clinical indications of 5-HT3 antagonists

Answer 253

* prevention of ACUTE **chemotherapy**-induced vomiting * prevention of nausea and vomiting caused by other forms of **noxious GIT stimulation** (e.g. distension, inflammation)

Question 254

what can 5-HT3 antagonists be prescribed with to enhance its efficacy as it is **not effective alone** ## Footnote allows for * **increased** control over ACUTE n/v * **extend** control over DELAYED n/v <- 5-HT3 antagonists are not effective when used alone

Answer 254

corticosteroids and NK1-receptor antagonists

Question 255

what is 1 major adverse effect of 5-HT3 antagonists

Answer 255

cardiac arrhythmia (QT **prolong**ation) <- ribbon dancer has an **elongated** ribbon

Question 256

where are dopamine D2 receptors found

Answer 256

*D2* receptors are found at the chemoreceptor trigger zone located **adjacent to NTS** <- guy in gymnastics competition holding onto *2 D-shaped rings* **adjacent to Track with a Solitary runner** ## Footnote nucleus *Tractus Solitaire* (NTS) = vomiting center

Question 257

# give example of the drug also MOA of dopamine receptor antagonists

Answer 257

me**toclo**pramide antagonises D2 receptors, and also has *prokinetic* effect which *stimulates GIT motility* <- gymnast from opposing team **tickling** the gymnast which was holding the 2 D-shaped rings, causing him to *fall onto a STOMACH-shaped cushion and make it move*

Question 258

what are some adverse effects of dopamine receptor antagonists

Answer 258

* **extra***pyrimidal* symptoms (esp in ELDERLY) <- OLD judge of the gymnastics competition getting bored and wearing an "**EXTRA**" *pyrimidal* newspaper hat * another judge of the gymnastics competition laughing so hard that **milk** shoots *upwards* out of his nose <- *elevate* **prolactin** levels ## Footnote since prolactin is responsible for lactation, elevated prolactin levels = gynecomastia, impotence, galactorrhoea

Question 259

where are neuokinin (NK1) receptors found

Answer 259

*NK*1 receptors are found at the chemoreceptor trigger zone located **adjacent to NTS** <- guy in gymnastics competition holding a pla*NK* on gymnastics beam **adjacent to Track with a Solitary runner**

Question 260

example of NK1 receptor antagonists

Answer 260

a**prepitant** <- **participants** lining up to get their pee checked before they their turn to performa plaNK at the beam

Question 261

what are some severe adverse effects associated with NK1 receptor antagonists

Answer 261

* peripheral neuropathy * blood dyscrasias (i.e. abnormalities in composition or function of blood)

Question 262

MOA of antipsychotics | e.g. **promethazine**, prochlorperazine, droperidol, olanzapine

Answer 262

* **M**uscarinic antagonism * **A**ntihistamine * **D**opamine receptor antagonism "stop them from going **MAD**"

Question 263

adverse effect of **D**roperidol (antipsychotic)

Answer 263

exhibits **D**2 receptor antagonism (MA**D**) => QT *prolongation* ("*elongated* ribbon across judging table of gymnastics competition")

Question 264

what is olanzapine good for

Answer 264

controlling CINV **delayed** nausea with **less EPS**

Question 265

function of the epiploic foramen

Answer 265

allows **communication** between **greater and lesser** sac

Question 266

# hint: blood vessels! what structures are anterior and posterior to the epiploic foramen respectively

Answer 266

* anterior: hepatic artery, bile duct, portal vein * posterior: IVC

Question 267

what is superior to the epiploic foramen

Answer 267

caudate lobe of **liver** ## Footnote i think what they trying to say is that the *middle* of the liver is above it

Question 268

what is inferior to the epiploic foramen

Answer 268

*1st part* of the **duodenum**

Question 269

how does the lesser sac relate to the lesser and greater omentum | lesser sac

Answer 269

think abt function of lesser sac = allow stomach to move freely => posterior to stomach * **lesser omentum** forms **anterior wall** of lesser sac * greater omentum forms inferior extension of lesser sac (i.e. **inferior** recess of lesser sac **extends into greater omentum**)

Question 270

what organs are anterior and posterior to the lesser sac respectively

Answer 270

* anterior: stomach * posterior: pancreas

Question 271

what are the classes of physical drugs used to treat constipation | i.e. does not directly affect bowel motility or physiological processes

Answer 271

* stool surfactant agents * bulk-forming laxatives * osmotic laxatives

Question 272

MOA of stool surfactant agents

Answer 272

lowers surface tension of stool -> allow **water and lipids** to **penetrate stool** => stool becomes softer and **easier to pass**

Question 273

how is MOA of mineral oil different from other stool surfactant agents

Answer 273

also makes stool **easier to pass**, but via * **lubrication** * preventing **water reabsorption** from stool => keep stools **soft**

Question 274

A/E of long-term use of stool surfactant agents

Answer 274

impaired absorption of **fat-soluble vitamins** (ADEK) <- lipids needed have penetrated and gone into stool

Question 275

what are some A/Es of mineral oil

Answer 275

* unpleasant taste (cos oil doesn't taste good) => should **mix with fruit juice** * **aspiration** -> lipid **pneumonitis** due to the oil being non-absorbable and thus possibly regurgitated and then accidentally aspirated

Question 276

example of stool surfactant agents

Answer 276

glycerin + sodium chloride (= docusate)

Question 277

MOA of bulk-forming laxatives

Answer 277

contain **indigestible, hydrophilic colloids (fibers)** -> **absorb water** in intestines -> form a bulky, gel-like **mass** that increases stool mass and **distends colon** => thus **stimulating peristalsis**

Question 278

what is the 1st-line drug for constipation in healthy patients

Answer 278

psyllium (bulk-forming laxative) ## Footnote other examples of bulk-forming laxatives: * methyl**cellulose** (**natural** fiber) * *polycarbo*phil (*synthetic* fiber)

Question 279

instructions for administration of bulk-forming laxatives * administer with (...) * do not take within (...) hours of other oral drugs * A/Es include (...) * avoid if suspected (...)

Answer 279

* administer with **lots of water** * do not take within **2** hours of other oral drugs * A/Es include **bloating, flatulence and abdominal pain** * avoid if suspected **obstruction**

Question 280

MOA of osmotic laxatives

Answer 280

**osmotically**-mediated water movement **into bowel** -> increases stool **liquidity** AND **volume** => stimulates **peristalsis**

Question 281

Which of these statements regarding osmotic laxatives is false? A) Lactulose osmotically mediates water movement into bowel and increases stool liquidity and volume B) High doses of osmotic laxatives can produce purgation within 3 hours C) Osmotic laxatives can cause severe flatus and abdominal cramps D) Patients with hepatic insufficiency should not be put on osmotic laxatives E) Balanced macrogol is a good alternative as it does not cause significant electrolyte shifts

Answer 281

A) Lactulose osmotically mediates water movement into bowel and increases stool liquidity and volume * literally the MOA B) **High doses** of osmotic laxatives can produce purgation within 3 hours * in fact within **1-3 hours** C) Osmotic laxatives can cause severe flatus and abdominal cramps * abdominal cramps due to **increased motility** (indirectly) * bloating and flatulence due to **fermentation** of the drug (e.g. lactulose) **by colonic bacteria** D) Patients with hepatic insufficiency should not be put on osmotic laxatives * should be patients with **renal** insufficiency or **cardiac** diseases who should not be put on osmotic laxatives <- can cause cardiac **arrhythmias** and **renal failure** <- likely due to it causing changes in **Na+ and K+** balance E) **Balanced macrogol** is a good alternative as it does NOT cause **significant electrolyte shifts**

Question 282

what are the classes of physiological drugs used to treat constipation

Answer 282

* opioid receptor antagonists * serotonin 5-HT4 receptor agonists * stimulant laxatives * Cl- channel activators

Question 283

MOA of opioid receptor antagonists

Answer 283

blocks **μ**-opioid receptors in **GI tract** => reverses opioid-induced **inhibition of gut motility and secretion**

Question 284

If μ-opioid receptors are antagonised, will pain relief by opioids still be effective?

Answer 284

Yes! bcos the antagonist does NOT **cross the BBB** => does NOT block **CNS analgesic effects**

Question 285

clinical indication of opioid receptor antagonists

Answer 285

opioid-induced constipation in patients under palliative care

Question 286

MOA of serotonin 5-HT4 receptor agonists

Answer 286

Stimulation of **serotonin 5-HT4** receptors -> Increases **neurotransmitter** release -> increase **smooth muscle** motor activity (e.g. peristalsis) => **prokinetic** effect on GIT motility

Question 287

for *serotonin 5-HT4 receptor agonists*, why is prucalo*pride* better than cisa*pride*?

Answer 287

* higher affinity * NO cvs effects

Question 288

MOA of stimulant laxatives

Answer 288

stimulate **enteric nerves** in intestinal wall -> increase migrating colonic **contractions** AND increase colonic electrolyte and fluid **secretions**

Question 289

clinical indication for stimulant laxatives

Answer 289

used **long-term** in **neurologically impaired / bed bound** patients

Question 290

what should patients not take **within 1 hour** of taking **milk** products

Answer 290

oral bisacodyl (stimulant laxative) as milk products will cause **enteric coating** of oral bisacodyl to **break down** -> risk of **gastric irritation / dyspepsia**

Question 291

what is the last resort drug given to patients who are unresponsive to other laxatives

Answer 291

Cl- channel activators

Question 292

MOA of Cl- channel activators

Answer 292

stimulation of ***type 2* Cl- channels** -> increased **secretion** of **chloride-rich fluid** into intestinal lumen => stimulate motility and shorten intestinal transit time

Question 293

What are the drug classes used in treatment of diarrhoea

Answer 293

"**I** **L**ike **OCS** **B**oys" * **I**ntestinal adsorbents * **L**yophilizate of killed Lactobacillus * **O**pioid agonists * **C**olloidal bismuth compounds * **S**omatostatin-like peptides * **B**ile salt binding resins

Question 294

which drugs are used in **acute** diarrhoea

Answer 294

"**I** **L**ike **OC**S Boys" * **I**ntestinal adsorbents * **L**yophilizate of killed Lactobacillus * **O**pioid agonists * **C**olloid bismuth compounds

Question 295

MOA of intestinal adsorbents

Answer 295

absorbs **bacteria**, bacterial **toxins** and **fluid** => decrease stool **liquidity and number**

Question 296

A/E of intestinal adsorbents

Answer 296

low risk of significant A/Es as NOT absorbed into **systemic circulation**

Question 297

which anti-diarrhoeal drugs should not be taken within 2 hours of taking other meds

Answer 297

* Intestinal *adsorbents* cos can impair *absorption* of other drugs * bile acid *binding* resins cos can *bind* to other drugs

Question 298

MOA of lyophilizate of killed Lactobacillus ## Footnote think abt how it affects * harmful microbes * normal intestinal flora

Answer 298

**adheres** onto surface of **intestinal cells**, and thus * interfering with **intestinal adherence of microbes** => **prevent overcolonisation** of those *microbes* * occupying **space** and competing for **nutrients** (**competitive exclusion**) => **normalises** *intestinal flora*

Question 299

what are the clinical indications of lyophilizate of killed Lactobacillus

Answer 299

* **bacterial** diarrhoea * **traveller's** diarrhoea

Question 300

who is lyophilizate of killed Lactobacillus contraindicated in

Answer 300

patients with **lactose** intolerance

Question 301

examples of opioid agonists used in treatment of diarrhoea

Answer 301

* loperamide * diphenoxylate

Question 302

Which of the following statements regarding opioid agonists are FALSE? A) Use of opioid agonists may potentially lead to addiction B) Loperamide does not cross the blood-brain barrier C) Consuming high doses of loperamide can cause cardiac abnormalities D) Diphenoxylate may be prescribed with another drug that could lead to cholinergic effects- prescribed with atropine which causes ANTIcholinergic effects E) Loperamide is typically used for acute rapid relief of diarrhoea

Answer 302

A) Use of opioid agonists may potentially lead to **addiction** * esp diphenoxylate B) Loperamide does NOT **cross the blood-brain barrier** * thus does not have potential to cause addiction C) Consuming **high doses** of **loperamide** can cause **cardiac** abnormalities D) *Diphenoxylate may be prescribed with another drug that could lead to cholinergic effects* * **diphenoxylate** prescribed alongside **atropine** as it will lead to **anticholinergic** ADVERSE effects, thus **discourage overdose** AND atropine also has **antidiarrhoeal** actions E) Loperamide is typically used for **acute** rapid relief of diarrhoea * acute relief: **I** **L**ike **OCS** **B**oys

Question 303

Which is the **first line** drug for **rapid** symptomatic relief of diarrhoea?

Answer 303

opioid agonists "I Like **O**CS Boys"

Question 304

MOA of Colloidal bismuth compounds | I Like O**C**S Boys

Answer 304

rapid **dissociation** in stomach allowing **absorption of salicylate** -> salicylate then **inhibits prostaglandin** production and **chloride** secretion => reduce stool **frequency and liquidity**

Question 305

what kind of diarrhoea is Bile acid binding resins used to treat ## Footnote recall that it's not used in acute as drugs used in acute are **I** **L**ike **OC**S Boys

Answer 305

diarrhoea caused by EXCESS faecal **bile salts** * usually watery and persistent * buzz words: **ileum diseases** or **surgical resections** that lead to bile salts malabsorption

Question 306

MOA of somatostatin-like peptide used in treatment of diarrhoea

Answer 306

INHIBITS release of **hormones/transmitters** => reduces intestinal and pancreatic **secretions** AND slows **GIT motility**

Question 307

what type of diarrhoea is somatostain-like peptides used to treat ## Footnote recall that it's not used in acute as drugs used in acute are **I** **L**ike **OC**S Boys

Answer 307

secretory diarrhoea caused by **GIT/neuroendocrine tumours** (e.g. VIPoma/ carcinoid tumour <- *STOP* **VIP** **Customers** only! = *somatostatin-like peptide* treats **VIPoma** and **Carcinoid tumour**)

Question 308

what structures pass through the transpyloric plane | located @ **L1** level

Answer 308

* hilum of (left) **kidney** * 1st PART of **duodenum** * neck of **pancreas** * origin of **SMA** ## Footnote recall! * celiac trunk originate from abdominal aorta @ **T12** * SMA originate from abdominal aorta @ **L1** * IMA originate from abdominal aorta @ **L3**

Question 309

orders of layers of abdomen wall: 1. skin 2. superficial FASCIA, consisting of (...), the fatty layer, and (...), the membranous layer 3. (...) FASCIA, surrounding the abdominal muscles — external oblique, internal oblique, transversus abdominis 4. also the (...), which is found bet the internal oblique and transversus abdominis muscles 5. (...) FASCIA 6. (...) fat 7. (...) peritoneum

Answer 309

1. skin 2. *superficial* FASCIA, consisting of **Camper's**, the fatty layer, and **Scarpa's** the membranous layer 3. ***deep* investing** FASCIA, surrounding the abdominal muscles — external oblique, internal oblique, transversus abdominis 4. also the **neurovascular bundle**, which is found bet the internal oblique and transversus abdominis muscles 5. ***transversalis*** FASCIA 6. **extraperitoneal** fat 7. **peritoneal** peritoneum

Question 310

what can be palpated at the **mid-inguinal point** | recall! mid-inguinal pt = halfway bet ASIS and **pubic symphysis**

Answer 310

femoral artery

Question 311

# medial, lateral, inferior what structures bound the **Hesselbach** triangle

Answer 311

* medial: rectus abdominis * lateral: inferior epigastric vessels * inferior: inguinal ligament

Question 312

how does the Hesselbach triangle relate to (direct and indirect) inguinal hernias

Answer 312

**weaker** region => it is where **direct** inguinal hernias occur

Question 313

which type of inguinal hernia may enter the scrotum

Answer 313

**indirect** inguinal hernia bcos it enters the DIR, travels through inguinal canal, then **exits via SIR**, sometimes reaching the scrotum

Question 314

how does coughing affect direct vs indirect inguinal hernias

Answer 314

* direct: **tightening of abdominal muscles** -> **push hernia back** or at least stop it from coming out too far * indirect: **increased intra-abdominal pressure** -> push hernia **outwards** => tend to **bulge** out more ## Footnote use this analogy to understand better! * Direct hernia: You're pressing on a hole in a **soft balloon** — when you squeeze elsewhere, the hole might close. * Indirect hernia: You're squeezing toothpaste through a narrow **tube** — once it starts coming out, pressure just pushes more out.

Question 315

which type of organ is fixed, intraperitoneal or retroperitoneal

Answer 315

retroperitoneal * **fixed** to abdominal wall * compared to **intraperitoneal** organs which are attached to abdominal wall via **mesentery**

Question 316

# left/right, anterior/posterior what is the order of the vessels in the portal triad

Answer 316

* bile duct (right), hepatic artery (left) * portal vein (posterior)

Question 317

what kind of epithelium lines the inner surface of the lungs

Answer 317

still stratified squamous epithelium but * non-keratinised * covered by **mucous membrane**

Question 318

which of the papillae found on the tongue is the **most numerous** A) filiform B) circumvallate C) fungiform

Answer 318

A) filiform

Question 319

do each of the papillae found on the tongue have **taste buds** A) filiform B) circumvallate C) fungiform

Answer 319

* filiform: **no** taste buds * circumvillate: **a lot** of taste buds * fungiform: has taste buds

Question 320

what do each salivary gland produce, mucus or serous fluid A) parotid B) sublingual c) submandibular

Answer 320

* parotid: **serous** only * submandibular: **mix** of serous and mucus * sublingual: majority **mucus**

Question 321

layers of wall in GIT: 1. MUCOSA, containing epithelium, (...) and muscularis (...) 2. SUBMUCOSA, containing (...) submucosal plexus and the bigger (...) 3. MUSCULARIS (...), containing outer (...) muscle and inner (...) muscle, (...) myenteric plexus and (...some type of cell...) 4. SEROSA/ADVENTITIA, whereby (...) is in contact with visceral peritoneum and (...) is for retroperitoneal organs

Answer 321

1. MUCOSA, containing epithelium, lamina **propria** and muscularis **mucosa** 2. SUBMUCOSA, containing **Meissner's** submucosal plexus and the bigger **blood vessels** 3. MUSCULARIS **EXTERNA/PROPRIA** containing **outer longitudinal** muscle and **inner circular** muscle, **Auerbach's** myenteric plexus and **Interstitial cells of Cajal (ICC)** 4. SEROSA/ADVENTITIA, whereby **serosa** is in contact with visceral peritoneum and **adventitia** is for **retroperitoneal** organs

Question 322

# function difference between muscularis mucosa (in mucosa) vs muscularis externa (in muscularis externa)

Answer 322

* muscularis mucosa: responsible for **local** movements of **mucosal layer** (e.g. adjusting surface area to form villi) * muscularis externa: responsible for **peristalsis and segmentation**

Question 323

difference between Meissner's plexus (in submucosa) and Auerbach's plexus (in muscularis externa/propria)

Answer 323

* Meissner's plexus: local **secretion** (e.g. of digestive enzymes), local **absorption** (e.g. of nutrients) local movements of mucosa (by **muscularis mucosa**) * Auerbach's plexus: peristalsis and segmentation (by **muscularis externa/propria**) ## Footnote Auerbach's plexus is also located **bet circular and longitudinal muscles** (like ICC), but the diff is * **ICC** (like a "*clock*") sets a **basic rhythm** (e.g. 3 contractions per minute in the stomach) * The **Auerbach’s plexus** (like a "*traffic control center*") listens to that rhythm but **decides if, when, and how strong the actual contractions should be** — depending on food content, stretch, and signals from the brain

Question 324

what type of muscles are seen in the muscularis externa in the eosophagus

Answer 324

* upper third: **striated** muscle <- **voluntary** phase of swallowing * middle third: **mixed** <- **transition** zone * lower third: **smooth** muscle <- **involuntary** phases of swallowing

Question 325

explain roles of ligamentum teres and ligamentum venosum in embryological development

Answer 325

* ligamentum teres: fibrous remnant of fetal **umbilical vein** which carried **oxygenated blood** from placenta to fetus * ligamentum.venosum: fibrous remnant of **ductus venosus**, which **shunted** oxygenate blood from **umbilical vein -> directly to IVC** so that it can bypass liver and reach heart directly

Question 326

what is found posteriorly in the liver

Answer 326

**fissure** for ligamentum venosum and ligamentum teres

Question 327

what are macrophages found in the liver called

Answer 327

**Kupffer** cells

Question 328

what is the function of hepatic **stellate** cells in healthy liver

Answer 328

store vit **A** in lipid droplets ## Footnote recall! during liver injury, they become **myofibroblast**-like cells and produce **collagen** for **fibrosis**

Question 329

inferior relations of gallbladder

Answer 329

* 1st part of duodenum * transverse colon

Question 330

list the following parts of the liver

Answer 330

Question 331

a fracture in which ribs will pose a risk of gallbladder rupture

Answer 331

ribs **9-11**

Question 332

inferior relations of the spleen

Answer 332

left colic flexure

Question 333

what can cause **painless** obstructive jaundice

Answer 333

HOP tumour

Question 334

# relate function to where it is found what is the function of Brunner's glands | which are found in **submucosa**

Answer 334

**alkaline** secretion to **neutralise** stomach **acid** => found in **duodenum** (esp at **1st part**)

Question 335

# relate function to where it is found what is the function of Peyer's patches | which are found in **submucosa**

Answer 335

large **lymphoid** patches in **immune defense** => found in **ileum** so as to prevent **bacteria in colon** from invading

Question 336

which part of the small intestine has the most pronounced villi and plicae circularis

Answer 336

jejunum bcos it is where the **most absorption** occurs

Question 337

differences bet jejunum and ileum in: A) thickness B) prominence of arterial arcades C) length of vasa recta

Answer 337

A) thickness * jejunum: thicker * ileum: thinner B) prominence of arterial arcades and C) length of vasa recta * jejunum: less prominent arterial arcades and longer vasa recta => fast and rich blood supply for rapid **nutrient absoprtion** * ileum: more prominent arterial arcades and shorter vasa recta => more distributed and low-pressure blood supply ## Footnote * arterial arcades: **"network of roads"** in the mesentery that interconnect. -> create **redundancy** — so if one branch is blocked, another can still supply * vasa recta: **“exit ramps**” from the arterial arcades that actually **deliver blood to the intestinal wall**

Question 338

what does the gastrosplenic ligament contain | gastrosplenic ligament = greater curvature of stomach to spleen

Answer 338

* gastro-omental vessels * short gastric vessels ## Footnote recall! * L gastro-omental artery <- splenic artery <= celiac trunk * R gastro-omental artery <- common hepatic artery <= celiac trunk * short gastric arteries <- splenic artery <= celiac trunk

Question 339

what does the splenorenal ligament contain

Answer 339

splenic vessels ## Footnote recall! splenic artery <= celiac trunk

Question 340

what pathology is related to the ileocecal sphincter ## Footnote recall! ileocecal sphincter is a **functional/physiological** sphincter i.e. a **thickening** of the muscularis layer at junction bet ileum and cecum

Answer 340

surgical **resection** of terminal **ileum** where **loss** of ileocecal sphincter -> **faster transit** of intestinal contents => **decrease absorption time**

Question 341

does the majority of water absorbed by GIT come from food/water intake or its own secretions

Answer 341

own secretions!

Question 342

what factors is the speed of gastric emptying dependent on

Answer 342

* state of food: liquid > solid * pH: low pH (**acidic**) inhibits * tonicity: **hyper**tonicity inhibits * food type: **fatty** acids inhibit ## Footnote Why? bcos * duodenum isn't built to handle extreme acidity. -> time is needed for pancreatic bicarbonate to neutralize the acid * load would cause water loss from blood into gut (can result in e.g. diarrhoea) -> time is needed for gradual adjustment of osmolality * fats take longer to digest (need bile + pancreatic lipase) -> time is needed to ensure proper emulsification and absorption

Question 343

what hormone stimulates gastric function and motility

Answer 343

gastrin <- secreted by G cells in antrum

Question 344

which hormones inhibit gastric function and motility

Answer 344

* CCK <- secreted by I cells in *duodenum* * secretin <- secreted by S cells in *duodenum* * gastric inhibitory peptide (GIP) <- secreted by cells in *duodenum* ## Footnote to allow *duodenum* time to process incoming chyme, especially if it's acidic, fatty or hyperosmolar

Question 345

which veins in stomach drain directly into portal vein vs drain into 1 of the branches (splenic vein OR SMV)

Answer 345

* drain **directly**: L and R **gastric** veins * drain into *splenic* vein: L *gastro-omental vein*, *short gastric* veins drain into *SMV*: R *gastro-omental* vein

Question 346

what is the *s*ympathethic innervation of the * foregut * midgut * hindgut

Answer 346

* foregut: **greater** *s*planchnic nerve (T5-T9), via **celiac** ganglion * midgut: **lesser** *s*planchnic nerve (T10-T12), via **superior** mesenteric ganglion * hindgut: **lumbar** *s*planchnic nerve (L1-L2), via **inferior** mesenteric ganglion ## Footnote remember that bcos it's **S**ympathetic innervation, will always have **S**planchnic but won't have *P*elvic *S*planchnic = *P*ara*S*ympathetic innervation

Question 347

what is the *p*ara*s*ympathetic innervation of the * foregut * midgut * hindgut

Answer 347

* foregut: **vagus** nerve * midgut: **vagus** nerve * hingut: ***p*elvic *s*planchnic** nerve ## Footnote remember that bcos it's **P**ara**S**ympathetic innervation, will be **P**elvic **S**planchnic but won't have *S*planchnic alone = *S*ympathetic innervation

Question 348

# movements, what it is stimulated by difference between peristalsis and segmentaton

Answer 348

* peristalsis: moves bolus **forward**, stimulated by **stretching of walls** by food bolus * segmentation: coordinated contraction moves bolus **back and forth** -> **dividing** it into smaller pieces, **local reflex** stimulated by **presence** of bolus

Question 349

when is migrating motor complexes (MMC) present

Answer 349

during **interdigestive** periods (i.e. only when **food is absent**) <- stimulated by *motilin* (hormone which regulates gut *motility*, esp during **fasting**)

Question 350

what does migrating motor complexes (MMC) do

Answer 350

* **sweeps remaining** food debris INTO colon * PREVENTS **migration of colonic bacteria** into distal ileum

Question 351

what stimulates the relaxation of the internal anal sphincter

Answer 351

**distension** of rectum ## Footnote integrating it all: rectum is full -> **stretch receptors** in rectal wall activated -> signal goes to spinal cord, triggering the **rectosphincteric reflex** -> **parasympathetic nerves** are activated -> inhibit **sympathetic tone** => relaxation of internal anal sphincter => creates **sensation to VOID**

Question 352

what happens to stool that reaches EAS if defecation is desired

Answer 352

* **relaxation** of external sphincter AND ALSO * relaxation of **pelvic** muscles * contraction of **abdominal** muscles

Question 353

# 2 different mechanisms/pathways involved! what happens to stool that reaches EAS if defecation is not desired

Answer 353

**voluntary** decision to contract -> brain sends signal to spinal cord -> **involuntary reflex** by **sacral** nerves coordinates contraction of EAS ## Footnote i.e. You choose whether to contract (**voluntary**) But how it's contracted is **reflexively** controlled by somatic motor pathways

Question 354

reason behind *post-prandial* **alkaline tide** (i.e. blood leaving stomach *after a meal* is **alkaline**)

Answer 354

**Cl-** is taken up from blood in **exchange** for **HCO3-** => release of HCO3- thus raises pH ## Footnote * Why? CO2 (main substrate) combines with H2O to form H2CO3 (catalysed by carbonic anhydrase) -> H2CO3 dissociate to form H+ and HCO3- * note that H+ leaves from **H+/K+ ATPase pump** while HCO3- leave via a separate channel

Question 355

# 2 processes how does Na+/K+ ATPase help with gastric acid production

Answer 355

* results in **higher intracellular [K+]** (and extracellualar [Na+]) -> intracellular K+ can be exchanged for extracellular H+ via **H+/K+ ATPase** * results in **lower intracellular [Na+]** -> **secondary** active transport where **Cl-/HCO3- exchanger** is linked to **Na+/Cl- co-transporter**