git Flashcards
explain lateral flexures in the rectum
3:
-> 2 on the left (superior, intermediate)
-> 1 on the right (inferior)
- formed by transverse rectal folds
(i.e. internal infoldings of rectum’s mucosa) - helps to store and organise fecal contents INSIDE rectum
5
location of sphincters
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 anusmain functions:
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
a flexure and a muscle
what helps stool to remain in retum until defecation is consciously initiated
- 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
and at what vertebrae levels
what do the anterior branch of the abdominal aorta give rise to
- celiac: T12
- superior mesenteric: L1
- inferior mesenteric: L3
and its origin
what artery is the gall bladder supplied by
cystic artery
← R hepatic artery
← common hepatic artery
<= celiac trunk
and their origin
what arteries form the anastomosis which supplies the inferior border of stomach
-
left gastric artery
<= celiac -
right gastric artery
<- common hepatic
<= celiac
and their origin
what arteries form the anastomosis which supplies the superior border of stomach
- celiac → splenic
⇒ left gastro-omental artery - celiac → common hepatic
⇒ right gastro-omental artery
and their origin
what arteries supply the fundus and upper part of stomach
short gastric arteries
← splenic artery
← celiac trunk
and their respective function
what is the 2 types of cells found in the gland
general gland (acinus) structure
- acinar secretory cells: secrete digestive enzymes
- epithelial cells: form the intercalated duct
AND modify secretions
(e.g. changing pH by secreting bicarbonate)
and what is below it
where does the posterior wall of the rectus sheath end
arcuate line
(found below umbilicus)
→ below line: rectus abdominis is in contact with transversalis fascia
and what organs do they connect
what are the 4 ligaments found in the GIT
- hepatogastric ligament: liver and stomach
- hepatoduodenal ligament: liver and duodenum
- gastrophrenic ligament: stomach and diaphragm
- gastrosplenic ligament: stomach and spleen
and where in stomach they occur
3 motor functions of stomach
- reservoir function @ proximal
- churning function @ distal (antrum)
- gastric emptying @ even more distal (antrum-pylorus-duodenum unit)
and where is it found
what does the anorectal junction/line indicate
- where rectum joins anal canal
- found at superior ends of anal columns
anal columns = series of longitudinal ridges
and where is it found
what does the pectinate line indicate
- formed by the inferior (comb-shaped) limit of anal valves
- indicates the junction of the superior and inferior parts of the anal canal
and why
where is pepsinogen inactivated
inactivated irreversibly at duodenum
<- pH of duodenum is alkaline
as manifestations in oral cavity
examples of ulcers
describe common characteristics, etiology
- 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)
dermatome + name
where is visceral pain from stomach referred to
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
early vs late in course of disease
what types of pain are felt when there is diseased appendix
- 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”
for parietal and visceral peritoneum respectively
what is the blood and lymphatic supply
and innervation of the peritoneum like
- parietal peritoneum: same as the region of the abdominopelvic WALL it lines
- visceral peritoneum: same as the organs it covers
found in the rectus abdominis
function of the tendinous intersections
-
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
function
difference in sympathetic vs parasympathetic innervation of stomach
- 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
hint: blood vessels = arteries AND VEINS
which blood vessels do the liver receive blood from
- 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
it’s a muscle!
what abdominal structure lies within the rectus sheath
rectus abdominis
rectus sheath encloses this muscle
other than kidneys
which organs are retroperitoneal
- duodenum
(except first part) - pancreas
(except tail part) - ascending and descending colon
xout of the 4 quadrants
where can you find the colon
- ascending colon: RLQ
- descending and sigmoid colon: LLQ
skeletal framework
what makes up the superior border of the abdominal cavity
- costal margin
- xiphoid process
- floating ribs (11th and 12th ribs)
skeletal framework
what makes up the inferior border of the abdominal cavity
- hip bones
- illiac crest
- ASIS
- pubic tubercle
- pubic symphysis
- pectineal line
tip of which costal cartilage? left or right?
where can the gallbladder area be palpated at
tip of right
9th costal cartilage
also known as the transpyloric plane
(transpyloric bcos it cuts pylorus of stomach)
where is the transpyloric plane located
i.e. at which level of the vertebrae
L1
what ducts, where do each drain from, final destination
describe the biliary system
- 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
what is includes, what demarcates the division
describe functional division of liver
- demarcated by fossae for gallbladder
- separated such that left side includes caudate and quadrate lobes
fossae = shallow depression where gallbladder is located
what the stomach lies on
structures that are posterior to stomach
- spleen
- pancreas
- transverse colon
- left kidney and suprarenal gland
think abt the adjective
where is the subcostal plane located
i.e. which lumbar vertebrae does it cut through
L3
“subcostal (3 letters) plane found at L3”
at which costal cartilage is the subcostal plane located
inferior border of 10th costal cartilage
think of the adjective
where is the intertubercular plane located
i.e. which lumbar vertebrae does it cut through
L5
“intertubular (5 letters) plane found at L5”
which muscles
describe the walls of the inguinal canal
* anterior wall: (…),
laterally reinforced by internal oblique
* floor: (…)
* roof: (…)
and medially (…)
* posterior wall: (…)
and medially (…)
-
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
which virus
what are squamous papilloma and squamous cell carcinoma associated with
HPV
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
B) two-thirds of the distance between the umbilicus and the right anterior superior iliac spine (ASIS)
arterial and venous circulation of spleen
- receives blood from splenic artery
(← celiac trunk ← abdominal aorta) - drained by splenic vein
(← hepatic portal vein ← IVC)
arterial supply of rectum
-
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
at what level of the vertebrae is the cisterna chyli located
L1 and L2
between which arteries in the large intestine is there an arterial anastomosis
- right colic (ascending colon)
and middle colic (transverse colon) - middle colic (transverse colon)
and left colic (mainly descending colon)
branches of the inferior mesentric artery:
* l… c… artery
* s… arteries
* s… r… artery
- left colic artery:
transverse colon (last 1/3), descending colon - sigmoid arteries:
sigmoid colon - superior rectal artery:
rectum (superior part)
branches of the celiac trunk
- left gastric artery
- splenic artery
- common hepatic artery
recall! celiac trunk branch out from abdominal aorta @ T12
compare with arterial circulation
commen on the pressure in the portal venous system
lower than arterial circulation
=> prevents backflow and thus congestion in GI organs
pressure too high = portal hypertension
comment on the effectiveness of agents that reduce gastric acidity:
* antacids
* H2-receptor antagonists
* proton pump inhibitors (PPI)
most to least effective:
1) PPI
2) H2-receptor antagonists
3) antacids
compare with arterial and venous circulation
comment on the resistance in the portal venous system
-
lower than arterial circulation
=> allows blood to flow smoothly into liver -
higher than (systemic) venous circulation
=> slows blood flow through liver for proper filtration
definition of lesser and greater omentum
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
describe the venous drainage of the stomach
hint: portal vein, gastric veins, splenic vein, superior mesentric vein, gastro-omental veins
- 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
all veins run parallel to arteries
diff in moa of sucralfate and bismuth compound as mucosal protective agents
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)
difference bet gastritis and gastropathy
- both involves mucosal injury (i.e. damage to mucosal layer)
due to damaging forces»_space; protective mechanisms - gastritis involves inflammation,
while gastropathy has little or no inflammation
main inflammatroy cells present = neutrophils
difference in cause of
congenital vs acquired pyloric stenosis
- 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
difference in appearance (and underlying pathology) of
leukoplakia vs erythroplakia
- leukoplakia: well-defined, WHITE patch or plaque that cannot be scraped off
← hyperKERATosis - erythroplakia: thin, erythematous (i.e. RED) mucosa
← absence of KERATIN production
difference in contents of inguinal canal in males vs females
both contain illoinguinal nerve
* males: spermatic cord
* females: round ligament
in males, testis also descends through inguinal canal during fetal development
difference in sympathetic vs parasympathetic innervation of gallbladder
- sympathetic: relaxation of gallbladder
- parasympathetic: contraction of gallbladder,
relaxation of Sphincter of Oddi
Does giving a drug orally achieve a higher drug level in blood than giving it intravenously
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
explain an important implication of portal-systemic anastomoses (PSA)
PSA are where veins draining to portal vein and IVC communicate
liver or portal obstuction
(e.g. due to liver cirrhosis)
-> veins dilate
=> can rupture and cause haemorrhage
haemorrhage is more common in
* lower eosophagus
* rectum
(remember as the start and end)
features of acute gastritis
- 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
function of smooth muscle in
normally PARTIALLY contracted state
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)
functions of falciform ligament
-
divides liver into right and left lobes
(anatomical division) - attaches liver to anterior abdominal wall
how do uraemic states and urease-secreting H. pylori disrupt secretion of HCO3- into mucus layer
increase ammonia production
→ inhibits HCO3- transporters in gastric EPITHELIAL cells
⇒ less HCO3- secreted into mucus layer
in which quadrant of the abdomen is the appendix located in
RLQ
is it the arterial supply or venous drainage of rectum that has a (portocaval) anastomosis
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 inferior rectal veins: drain middle and inferior parts of rectum
-> internal illiac vein
=> IVC
(SYSTEMIC circulation)
function: primarily to provide alternative route to bypass blocked or elevated PORTAL circulation
location and function of anal sinuses
- between anal valves
- compressed by feces
→ exude mucus
⇒ that aids in evacuation of feces from anal canal
name and explain the protective mechanisms of gastric mucosa:
* m… secretion
* b… secretion
* epithelial b…
* mucosal b… f…
* p…
- 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
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
- 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
Name the vitamin
and explain 1 impact
impaired production of VITAMIN K by gut bacteria
→ impaired activation of coagulation factors (II, VII, IX, X)
⇒ impaired coaguation
recall: PT (and thus INR) will increase
← factor VII (extrinsic pathway) has the shortest half-life and is the first to be affected
parts of the large intestine:
1. c…
2. a…
3. t…
4. d…
5. s…
6. r…
7. a…
- caecum
- ascending colon
- transverse colon
- descending colon
- sigmoid colon
- rectum
- anal canal
relation of anal sphincters to puborectalis muscle
external anal sphincter blends superiorly with puborectalis muscle
visualise how the superior epigastric artery comes about
aorta
(→ branchiocephalic trunk)
→ subclavian artery
→ internal thoracic artery
⇒ superior epigastric artery
visualise how the inferior epigastric artery comes about
aorta
→ thoracic aorta
→ abdominal aorta
→ common iliac artery
→ external iliac artery
⇒ inferior epigastric artery
what are found at the inferior ends of the anal columns
anal valves
what are the 2 “feeding centres”
and what signals do they release
function is control of food intake
- ventromedial nucleus (VMN): satiety signals
(anorexigenic signals) - lateral nucleus (LN): hunger signals
(orexigenic signals)
“feeling full is a Victory, feeling hungry is a L”
what are the 3 important structures found in the lesser omentum
- hepatic artery
- portal vein
- bile duct
found near to the free edge of the lesser omentum
(i.e. R side where hepatoduodenal ligament is)
what are the 3 key features of neural regulatory systems in GIT
- sensors
- neural network
- effector systems
what are the arteries that supply the rectus abdominis
- superior epigastric artery
- inferior epigastric artery
rectus abdominis is drained by veins that bear the same names
what are the common manifestations seen in oral cavity
- mucosal changes
- ulcer
- lumps and bumps
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
what are the common pathology of the oral cavity and oesophagus
lined by stratified squamous epithelium
=> squamous papilloma (benign)
=> squamous cell carcinoma (malignant)
what are the common pathology of the stomach, small bowel, colon and rectum
lined by simple columnar epithelium
(which is glandular)
=> adenoma (benign)
=> adenocarcinoma (malignant)
what are the protective effects of prostaglandins on gastric mucosa
promote
* mucus secretion
* bicarbonate secretion
* blood flow
what are the rectus abdominis attached to
(superiorly and inferiorly)
superior: costal margin and xiphoid proess
inferior: pubic crest and pubic symmphysis
what are the secretory substances released by parietal cells
secretory = released into LUMEN of stomach
- 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)
what are the secretory substances released by chief cells
secretory = released into LUMEN of stomach
pepsinogen:
converted into pepsin
-> digests protein
note: as pepsin is a proteolytic enzyme,
it also helps with conversion of pepsinogen to pepsin (i.e. autocatalytic)
what attaches the liver to the diaphragm
coronary ligaments,
which are found at the bare area of the liver
(which is not covered by peritoneum, directly in contact with diaphragm)
what cells in the gastric glands are gastrin secreted by
G cells
“G for Gastrin”
mostly by gastric glands in antrum,
in contrast to ghrelin which is secreted mostly by gastric glands in fundus
what direction does the external oblique muscles run
downwards and forwards
“imagine the direction of your hands when you put them in your pockets”
internal oblique muscles run in the opposite direction
⇒ downards and backwards
what direction does the transverse abdominis muscle run
horizontally
what disruptive process impacts both
epithelial barrier function and epithelial regeneratieve capacity
chemotherapy
* direct cellular damage
* inhibition of epithelial regenerative capacity
what does the neurovascular bundle run between
internal oblique and transversus abdominis
what features can use to differentiate large intestine from small intestine
- 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
what hormones are secreted in stomach
hormones = released into BLOOD
- ghrelin:
MORE secreted during empty stomach
→ travels to hypothalamus and stimulates appetite - gastrin:
MORE secreted during full stomach
→ travels to hypothalamus and decreases appetite
what is between the visceral peritoneum and parietal peritoneum
peritoneal cavity
holding a small amount of fluid
(peritoneal fluid)
what is one function that the greater omentum has
that the lesser omentum does not
moves towards and wraps around inflamed organ
→ acting as a physical barrier to localise the infection
⇒ protect other organs from inflammation
what is the arterial supply of the transverse colon
- middle colic artery (from SMA)
- left colic artery (from IMA)
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
what is the conjoint tendon formed by
fusion of lowest fibers of internal oblique and transversus abdominis
what is the dilated terminal portion of the rectum
which acts as a storage area for feces before defecation called?
ampulla
what is the epithelium that covers the majority of GIT
simple columnar epithelium
except in oral cavity, oesophagus and anus (i.e. START and END of GIT)
whichhas stratified squamous epithelium
to protect them from mechanical damage
what is the head of the pancreas attached to
2nd part (i.e. descending part)
of duodenum
what is the neck of the pancreas anterior to
superior mesenteric vessels
what is the body of the pancreas posterior to
stomach, omental bursa and lesser sac
what is the tail of the pancreas attached to
spleen
what is the implication of the superior and inferior epigastric arteries forming an anastomosis
anastomosis = connection or junction bet 2 tubular structures
if blood supply from one artery is reduced,
the other artery can compensate
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
what is the inguinal ligament formed by
lower edge of the external oblique aponeurosis rolling inwards
→ form a thick band
what is the lateral wall of the inguinal canal reinforced by
internal oblique aponeurosis
what is the lateral wall of the inguinal canal reinforced by
(internal border of) external oblique aponeurosis
what is the floor of the inguinal canal reinforced by
- internal oblique aponeurosis
- medially: conjoined tendon
what is the posterior wall of the inguinal canal reinforced by
- transversus abdominus
- medially: conjoined tendon
what nerve controls the external anal sphincter
S4
through the inferior rectal nerve
“S4 bcos anal (4 letters)”
what physiologic response will be acting against a person when they lose weight
weight loss
→ less adipose tissue
→ lower levels of leptin
→ less anorexigenic signals
⇒ increased appetite
what structures enhance absorption of nutrients in GI tract
- villi in small intestine
- crypts in colon
via increasing surface area
what type of epithelium is the peritoneum made of
simple squamous epithelium
(known as mesothelium)
what’s the difference in the order of the aponeuroses
above and below the umbilicus
- 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
where are the 3 abdominal muscles
(external oblique, internal oblique and transversus abdominis)
found
-
lateral region:
generate movement -
anterior region:
transition into aponeurotic sheets
→ form the rectus sheath
where are the “feeding centres” found
function is control of food intake
hypothalamus
where are the lunar semilunaris located
they pass along the lateral border of the rectus abdominis
“form the 11 abs ;)”
mark the transition between the abdominal muscles and their aponeurotic portions
where are the openings of the
deep inguinal ring (DIR) and superficial inguinal ring (SIR)
found respectively
- DIR: transversalis fascia
(above midpoint of inguinal ligament) - SIR: external oblique aponeurosis
(above and slightly lateral to pubic tubercle)
where do nutrients go after being absorbed in GIT
in general (i.e. water-soluble nutrients)
absorbed in small intestine
through capillaries in villi
-> carried via hepatic portal vein to liver
-> processed by liver
-> eventually carried into systemic circulation
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)
where do the lymph nodes of the bowel drain into
cisterna chyli
where is visceral pain from gall bladder referred to
- 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
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
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
rectus abdominis lies lateral to the linea alba on both sides
Which abdominal muscle does the L1 nerve provide MOTOR innervation to
internal oblique
- external oblique: T7-T11
- internal oblique: T7-T12, L1
- rectus abdominis: T7-T12
which artery supplies the midgut
superior mesenteric artery
foregut = celiac trunk
hindgut = inferior mesenteric artery
which molecules stimulate appetite centrally
(i.e. send orexigenic signals)
- ghrelin
(secreted usually before meals, when stomach is empty) - cortisol
(secreted in response to stress)
which molecules suppress appetite centrally
(i.e. send anorexigenic signals)
- insulin
(secreted in response to glucose) - cholecystokinin (CCK)
(secreted in response to fat and protein) - leptin
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
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
note: vomiting is non-bilious due to the obstruction before duodenum, where bile enters
which of the following dermatomes supply the umbilical region
T10
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
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
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
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
arteries supplying ascending colon collectively known as
right branches of SMA
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
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
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
B) T10 intercostal nerve
- T7-9: epigastrum
- T11-12: inferior to umbilicus
- L1: inguinal and pubis
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.
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
which parts of the large intestine are retroperitoneal vs intraperitoneal
- 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”
- all the intraperitoneal parts (except cecum) are suspended by a mesentry
⇒ mobile - while all the retroperitoneal parts are fixed to posterior abdominal wall
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
C) Interstitial Cells of Cajal
which connect longitudinal and circular smooth muscles
→ generate cycles of contraction and relaxation
which vein does blood from liver drain into
hepatic vein
why are smooth muscles in GIT able to exist in these 2 states,
normally contracted and normally PARTIALLY contracted?
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
sustained tonic contraction
(i.e. can sustain contractions w/o continuous ATP contractions)
why do people tend to empty their bowels after a meal
- main contributor is gastrocolic reflex:
triggered by stretching of stomach as it fills 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
- 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
why is it important to do biopsy for patients with leukoplakia and erythroplakia
may see findings of dysplasia and malignancy
(usually squamous cell carcinoma)
dysplasia = PREcancerous changes
what are the lines which divide the abdomen into 4 quadrants
- median plane:
at midline - transumbilical plane:
at umbilicus
order the layers of the abdominal fascia
(from superficial to deep):
* extraperitoneal fat
* muscle
* parietal peritoneum
* skin
* subcutaneous tissue
* deep fascia
- skin
- subcutaneous tissue
- muscle
- deep fascia
- extraperitoneal fat
- parietal peritoneum
and what happens during each phase
what are the 3 swallowing phases
- 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
- voluntary: oral phase
<- actions of chewing and of tongue are voluntary - involuntary:
pharyngeal phase
<- reflex mah
oesophagal phase
<- peristalsis is by smooth muscles
what temporarily relaxes LES
- belching (i.e. burping):
releases swallowed air - gastric distension:
accomodate pressure changes when stomach is overly full
tone of LES is impt
as relaxation (= decreased tone) results in acid reflux (i.e. GERD)
which hormones control the tone of LES
- 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
how does nicotine, coffee and tea affect tone of LES
decrease tone of LES
(i.e. relaxation)
what stimulates each, mediators for which
what are the 3 types of gastric relaxation
-
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
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)
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
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 bicarbonate and Mg(OH)2 are more effective”
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
D) Sodium bicarbonate
all compounds containing HCO3- and CO3-
will result in CO2 gas formation
=> thus resulting in gastric distention, belching and flatulence
Which drug can be added to the formulation to reduce belching and flatulence
simethicone
acts as an anti-foaming agent
via easing release of gas within GIT
via burping or flatulence
what are the DDI of antacids
can affect absorption of other medications
=> do NOT take within 2 hours of other meds
in what group of patients should you avoid
long-term use of antacids
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
what is milk-alkali syndrome
excessive calcium intake
→ hypercalcemia
→ kidney dysfunction
→ metabolic alkalosis
(could be worsened if there is excessive bicarbonate intake as well)
→ worsens hypercalcemia
⇒ cycle repeats
MOA of H2-receptor antagonists
competitive inhibitors of H2 receptors on parietal cells
⇒ suppresses acid secretion by parietal cells
Which of the following is the most potent H2-receptor antagonist?
A) Famotidine
B) Cimetidine
C) Ranitidine
D) Omeprazole
A) Famotidine
H2-receptor antagonists all end with “tidine”
H2-receptor antagonists are most effective at reducing gastric acidity when taken at what time
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)
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
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
(C) is wrong as esomeprazole is isomer of omeprazole,
(“isomer-prazole”)
but they are NOT the same drug
why should patients not crush omeprazole capsule
destroys the enteric coating
which protects drug against activation by stomach acidity before absorption
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
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
and what is stimulated to be released
what hormones stimulate pancreatic secretion
- 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
CCK = stimulated by fat- and protein-containing chyme in small intestine
secretin = stimulated by acidic chyme entering small intestine from stomach
how is CCK-stimulated release of digestive enzymes
regulated by food content in duodenum
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
describe secretion of Cl- in small intestines
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
describe secretion of HCO3- in small intestines
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)
process of gastric churning
- 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)
what mechanisms protect pancreas from
autodigestion by its own enzymes
- 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)
what is pancreatitis due to
derangement or overwhelming of protective mechanisms,
resulting in autodigestion of pancreas by its own enzymes
reversibility, parts of pancreas affected
differences bet exocrine and endocrine pancreatitis
- acute: reversible
chronic: irreversible - acute: mainly exocrine parenchyma (acinar cells)
chronic: destruction of exocrine parenchyma first, then destruction of endocrine parenchyma in late stages
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.
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
how does gallstones lead to acute pancreatitis
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
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.
recall: sphincter of Oddi is the muscular valve surrounding the exit of the bile duct and pancreatic duct into the duodenum.
D) All of the above.
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
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
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
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
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
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
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
(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)
note: predominance of fibrinogenic factors in chronic pancreatitis distinguishes it from acute pancreatitis
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
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
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.
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
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.
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))
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
B) Pancreatic neuroendocrine tumor (PanNET)
- cystic change: fluid-filled spaces due to necrosis or degeneration
- highly vascular: indicates abundant blood supply
Pancreatic ductal adenocarcinoma
(most common form of pancreatic carcinoma)
has no precursor lesions.
True or False?
False
Precursor lesions include
* pre-malignant masses (e.g. IPMN, MCN)
* pancreatic intraepithelial neoplasia (PanIN)
orde for cystic neoplasms:
serous cystadenoma — benign
→ mucinous cystic neoplasm (MCN) — pre-malignant
→ intraductal papillary mucinous neoplasm (IPMN) — pre-malignant
⇒ solid-pseudopapillary neoplasm (SPN) — malignant
think of a tube, what are 3 ways it can become obstructed
what are the 3 main causes of large bile duct obstruction
- 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
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.
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)
where are plicae circulares (folds), villi, microvilli and crypts found in
- 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
so small intestine has everything, while colon only has crypts
what is the function of small intestinal secretion
-
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
what is secreted in the colon and why
- K+
in response to aldosterone
which works to increase sodium (and thus water) absorption - HCO3-
to buffer against H+ produced by bacterial fermentation
what is the molecule that drives absorption in small intestines
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
how does osmolarity and processes change as we move along small intestine
- start: hyperosmolarity
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
hormone and protein involved
how is availability of iron regulated
use iron deficiency as example situation
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
what is another name for vitamin B12
cobalamin (CBL)
Which protein is responsible for transporting B12 in the blood after absorption?
A) Haptocorrin
B) Intrinsic Factor
C) Transcobalamin II
D) Pepsin
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.
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 (…)
- 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
think of water slowing in a river
causes of diarrhoea
- 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”)
main location where each type of diarrhoea occurs:
secretory, malabsorptive, osmotic, motility-related)
- small intestine and colon: motility-related
- small intestine only: secretory
- jejunum and ileum (of small intestine) only:
malabsorptive and osmotic
what substances are mainly absorbed in the ileum
- bile salts
- vitamin B12
(particularly at terminal ileum)
where are mineral ions (e.g. calcium, iron) mainly absorbed
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)
why does osmotic diarrhoea tend to involve jejunum and ileum
- 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
note that site where MAJORITY of absorption occurs (jejunum and ileum)
is different from site where absorption of MOST (number of) SOLUTES occur (duodenum)
how can the impaired absorption of bile salts lead to elevated ALP levels
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
describe the digestion of carbohydrates in the small intestine
- pancreatic amylase:
carbohydrates → disaccharides - brush border enzymes:
disaccharides → monosaccharides
carbohydrates are already partially digested by salivary amylase in mouth
how is the absorption of fructose in small intestines
different from the other monosaccharides (glucose, galactose, xylose)
- 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)
describe the digestion and absorption of proteins in the small intestine
-
pancreatic proteases break down proteins into
smaller peptides and free AAs - brush border peptidases further break down the smaller peptides into tripeptides, dipeptides and free AAs
- free AAs are absorbed via Na+-dependent transport systems (2º active transport),
while tripeptides and dipeptides are absorbed via carrier transport - tripeptides and dipeptides are then broken down into free AAs by intracellular peptidases
- 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
in which parts of the small intestine are carbohydrates and proteins mainly absorbed
duodenum and jejunum
is it normal for there to be a small amount of protein in person’s stool
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)
which salivary gland are neoplasms most commonly found in?
A) minor salivary glands
B) parotid gland
C) sublingual gland
D) submandibular gland
B) parotid gland
Which of the following statements correctly describes the common characteristics of salivary gland neoplasms?
A) Pleomorphic adenoma 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.
C) Pleomorphic adenoma is the most common salivary gland neoplasm, followed by Warthin tumour, with Warthin tumour being associated with male smokers.
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
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
which risk factors can be used to differentiate adenocarcinoma and SCC?
A) diet
B) gender
C) smoking
D) past medical history
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)
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.
B) is true and A) is false
It is the other way round,
with SCC affecting the proximal and mid eosophagus (upper 2/3)
what is the difference in histology between Squamous Cell carcinoma (SCC) and adenocarcinoma
- SCC: keratin pearls
- adenocarcinoma: mucin production
think of the 4 Bs
what are the clinical features and complications of eosophagal cancer
clinical features:
* Block: progressive dysphagia,
odynophagia
* Bleed: 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
recall: blood vessels are usually found in submucosal layer!
definition of oesophagal varices
dilated submucosal veins
in lower 1/3 of oesophagus
and proximal stomach
pathogenesis of oesophagal varices
liver cirrhosis
→ portal hypertension
→ portosystemic shunting
bet L gastric veins and eosophagal veins
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
pathogenesis of GERD
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
complication of GERD
what is Barrett’s eosophagus
mucosal damage
-> stratified squamous epithelium being replaced by NONciliated COLUMNAR epithelium and GOBLET cells
(i.e. intestinal metaplasia)
why is Barrett’s eosophagus concerning
precancerous,
increased risk of dysplasia and cancer
causes of acute gastritis
- 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)
“burned 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
causes of chronic gastritis
- H pylori (majority)
- autoimmune
pathogenesis of H pylori gastritis
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
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
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
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
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
Granulomas are seen in Crohn disease.
True or False?
True
specifically non-caseating ones
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
C. Almost always bloody
while Crohn’s may present with non-bloody diarrhoea
