1
Q
explain lateral flexures in the rectum
3:
-> 2 on the left (superior, intermediate)
-> 1 on the right (inferior)
A
- formed by transverse rectal folds
(i.e. internal infoldings of rectum’s mucosa) - helps to store and organise fecal contents INSIDE rectum
2
Q
5
location of sphincters
A
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
3
Q
a flexure and a muscle
what helps stool to remain in retum until defecation is consciously initiated
A
- 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
4
Q
and at what vertebrae levels
what do the anterior branch of the abdominal aorta give rise to
A
- celiac: T12
- superior mesenteric: L1
- inferior mesenteric: L3
5
Q
and its origin
what artery is the gall bladder supplied by
A
cystic artery
← R hepatic artery
← common hepatic artery
<= celiac trunk
6
Q
and their origin
what arteries form the anastomosis which supplies the inferior border of stomach
A
- left gastric artery
<= celiac - right gastric artery
<- common hepatic
<= celiac
7
Q
and their origin
what arteries form the anastomosis which supplies the superior border of stomach
A
- celiac → splenic
⇒ left gastro-omental artery - celiac → common hepatic
⇒ right gastro-omental artery
8
Q
and their origin
what arteries supply the fundus and upper part of stomach
A
short gastric arteries
← splenic artery
← celiac trunk
9
Q
and their respective function
what is the 2 types of cells found in the gland
general gland (acinus) structure
A
- acinar secretory cells: secrete digestive enzymes
- epithelial cells: form the intercalated duct
AND modify secretions
(e.g. changing pH by secreting bicarbonate)
10
Q
and what is below it
where does the posterior wall of the rectus sheath end
A
arcuate line
(found below umbilicus)
→ below line: rectus abdominis is in contact with transversalis fascia
11
Q
and what organs do they connect
what are the 4 ligaments found in the GIT
A
- hepatogastric ligament: liver and stomach
- hepatoduodenal ligament: liver and duodenum
- gastrophrenic ligament: stomach and diaphragm
- gastrosplenic ligament: stomach and spleen
12
Q
and where in stomach they occur
3 motor functions of stomach
A
- reservoir function @ proximal
- churning function @ distal (antrum)
- gastric emptying @ even more distal (antrum-pylorus-duodenum unit)
13
Q
and where is it found
what does the anorectal junction/line indicate
A
- where rectum joins anal canal
- found at superior ends of anal columns
anal columns = series of longitudinal ridges
14
Q
and where is it found
what does the pectinate line indicate
A
- formed by the inferior (comb-shaped) limit of anal valves
- indicates the junction of the superior and inferior parts of the anal canal
15
Q
and why
where is pepsinogen inactivated
A
inactivated irreversibly at duodenum
<- pH of duodenum is alkaline
16
Q
as manifestations in oral cavity
examples of ulcers
describe common characteristics, etiology
A
- 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)
17
Q
dermatome + name
where is visceral pain from stomach referred to
A
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
18
Q
early vs late in course of disease
what types of pain are felt when there is diseased appendix
A
- 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”
19
Q
for parietal and visceral peritoneum respectively
what is the blood and lymphatic supply
and innervation of the peritoneum like
A
- parietal peritoneum: same as the region of the abdominopelvic WALL it lines
- visceral peritoneum: same as the organs it covers
20
Q
found in the rectus abdominis
function of the tendinous intersections
A
- 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
21
Q
function
difference in sympathetic vs parasympathetic innervation of stomach
A
- 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
22
Q
hint: blood vessels = arteries AND VEINS
which blood vessels do the liver receive blood from
A
- 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
23
Q
it’s a muscle!
what abdominal structure lies within the rectus sheath
A
rectus abdominis
rectus sheath encloses this muscle
24
Q
other than kidneys
which organs are retroperitoneal
A
- duodenum
(except first part) - pancreas
(except tail part) - ascending and descending colon
25
# xout of the 4 quadrants
where can you find the colon
* ascending colon: **R**LQ
* descending and sigmoid colon: **L**LQ
26
# skeletal framework
what makes up the superior border of the abdominal cavity
* costal margin
* xiphoid process
* floating ribs (11th and 12th ribs)
27
# skeletal framework
what makes up the inferior border of the abdominal cavity
* hip bones
* illiac crest
* ASIS
* pubic tubercle
* pubic symphysis
* pectineal line
28
# tip of which costal cartilage? left or right?
where can the gallbladder area be palpated at
tip of **right**
**9th** costal cartilage
## Footnote
also known as the **transpyloric** plane
(transpyloric bcos it cuts pylorus of stomach)
29
where is the transpyloric plane located
| i.e. at which level of the vertebrae
L1
30
# 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**
31
# 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
32
# what the stomach lies on
structures that are posterior to stomach
* spleen
* pancreas
* transverse colon
* left kidney and suprarenal gland
33
# think abt the adjective
where is the subcostal plane located
| i.e. which lumbar vertebrae does it cut through
L3
"**sub**costal (3 letters) plane found at L**3**"
34
at which costal cartilage is the subcostal plane located
inferior border of **10th** costal cartilage
35
# think of the adjective
where is the intertubercular plane located
| i.e. which lumbar vertebrae does it cut through
L5
"**inter**tubular (5 letters) plane found at L**5**"
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 (...)
* **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**
37
# which virus
what are squamous papilloma and squamous cell carcinoma associated with
HPV
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**
B) two-thirds of the distance between the umbilicus and the right anterior superior iliac spine (ASIS)
39
arterial and venous circulation of spleen
* receives blood from splenic artery
(← celiac trunk ← abdominal aorta)
* drained by splenic vein
(→ hepatic portal vein → IVC)
40
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
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
L1 and L2
42
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)
43
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)
44
branches of the celiac trunk
* left gastric artery
* splenic artery
* common hepatic artery
| recall! celiac trunk branch out from abdominal aorta @ T12
45
# 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
## Footnote
pressure too high = portal hypertension
46
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
47
# 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**
48
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**
49
describe the venous drainage of the stomach
## Footnote
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**
## Footnote
all veins run parallel to arteries
50
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**)
51
which mucoprotective agent causes
harmless *blackening* of **stool**
and reversible *darkening* of **tongue**
bismuth
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.
(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**
53
MOA of misoprostol
synthetic PGE1 **analogue**
→ binds to **PGE2** receptors
⇒ low doses: promotes **HCO3- and mucus** secretion, enhances **mucosal blood flow**
high doses: **inhibit gastric acid** secretion
54
difference bet gastritis and gastropathy
* 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**
55
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
56
difference in appearance (and underlying pathology) of
leukoplakia vs erythroplakia
* 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
57
difference in contents of inguinal canal in males vs females
both contain illoinguinal nerve
* males: **spermatic cord**
* females: round ligament
## Footnote
in males, **testis** also **descends through inguinal canal** during fetal development
58
difference in sympathetic vs parasympathetic innervation of gallbladder
* sympathetic: relaxation of gallbladder
* parasympathetic: contraction of gallbladder,
relaxation of **Sphincter** of Oddi
59
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
60
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**
## Footnote
haemorrhage is more common in
* lower eosophagus
* rectum
(remember as the start and end)
61
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
62
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)
63
functions of falciform ligament
* **divides** liver into right and left lobes
(anatomical division)
* attaches liver to **anterior abdominal wall**
64
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
65
in which quadrant of the abdomen is the **appendix** located in
RLQ
66
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 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
67
location and function of anal sinuses
* between anal valves
* compressed by **feces**
→ exude **mucus**
⇒ that aids in **evacuation of feces** from anal canal
68
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
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
* 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
70
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
## Footnote
recall: PT (and thus INR) will increase
← factor VII (extrinsic pathway) has the shortest half-life and is the first to be affected
71
parts of the large intestine:
1. c...
2. a...
3. t...
4. d...
5. s...
6. r...
7. a...
1. caecum
2. ascending colon
3. transverse colon
4. descending colon
5. sigmoid colon
6. rectum
7. anal canal
72
relation of anal sphincters to puborectalis muscle
**external** anal sphincter **blends superiorly** with puborectalis muscle
73
visualise how the superior epigastric artery comes about
aorta
(→ branchiocephalic trunk)
→ subclavian artery
→ internal thoracic artery
⇒ superior epigastric artery
74
visualise how the inferior epigastric artery comes about
aorta
→ thoracic aorta
→ abdominal aorta
→ common iliac artery
→ external iliac artery
⇒ inferior epigastric artery
75
what are found at the inferior ends of the anal columns
anal valves
76
what are the 2 "feeding centres"
and what signals do they release
| function is control of food intake
* 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**"
77
what are the 3 important structures found in the lesser omentum
* 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)
78
what are the 3 key features of neural regulatory systems in GIT
* sensors
* neural network
* effector systems
79
what are the arteries that supply the rectus abdominis
* superior epigastric artery
* inferior epigastric artery
## Footnote
rectus abdominis is drained by veins that bear the same names
80
what are the common manifestations seen in oral cavity
* 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
81
what are the common pathology of the oral cavity and oesophagus
lined by stratified **squamous** epithelium
=> **squamous** papilloma (benign)
=> **squamous** cell carcinoma (malignant)
82
what are the common pathology of the stomach, small bowel, colon and rectum
lined by simple columnar epithelium
(which is **glandular**)
=> **adeno**ma (benign)
=> **adeno**carcinoma (malignant)
83
what are the protective effects of prostaglandins on gastric mucosa
promote
* **mucus** secretion
* **bicarbonate** secretion
* **blood flow**
84
what are the rectus abdominis attached to
(superiorly and inferiorly)
superior: costal margin and xiphoid proess
inferior: pubic crest and pubic symmphysis
85
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**)
86
what are the secretory substances released by **chief** cells
| secretory = released into LUMEN of stomach
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**)
87
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)
88
what cells in the gastric glands are gastrin secreted by
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**
89
what direction does the external oblique muscles run
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**
90
what direction does the transverse abdominis muscle run
horizontally
91
what disruptive process impacts both
epithelial barrier function and epithelial regeneratieve capacity
chemotherapy
* direct **cellular damage**
* inhibition of epithelial regenerative capacity
92
what does the neurovascular bundle run between
internal oblique and transversus abdominis
93
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
94
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**
95
what is between the visceral peritoneum and parietal peritoneum
peritoneal cavity
holding a small amount of fluid
(peritoneal fluid)
96
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
97
what is the arterial supply of the transverse colon
* 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**
98
what is the conjoint tendon formed by
fusion of lowest fibers of **internal oblique** and **transversus abdominis**
99
what is the dilated **terminal** portion of the rectum
which acts as a **storage area** for feces before defecation called?
ampulla
100
what is the epithelium that covers the majority of GIT
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**
101
what is the head of the pancreas attached to
2nd part (i.e. descending part)
of duodenum
102
what is the neck of the pancreas anterior to
superior mesenteric vessels
103
what is the body of the pancreas posterior to
stomach, omental bursa and lesser sac
104
what is the tail of the pancreas attached to
spleen
105
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**
## 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
106
what is the inguinal ligament formed by
lower edge of the **external oblique** aponeurosis **rolling inwards**
→ form a thick band
107
what does the anterior wall of the inguinal canal consists of
* **external** oblique aponeurosis
* *reinforced* by *internal* oblique at *lateral* 1/3
(i.e. the 1/3 closer to the ASIS)
108
what does the roof of the inguinal canal consist of
* **internal** oblique aponeurosis
* conjoint tendon *medially*
109
what does the floor of the inguinal canal consist of
inguinal ligament
110
what does the posterior wall of the inguinal canal consist of
* **transversus abdominus**
* conjoint tendon *medially*
111
what nerve controls the external anal sphincter
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**
112
what nerves control the internal anal sphincter
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**
113
what is the pelvic pain line
and what implications does it have for the visceral innervation of the rectum
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
114
descibe the autonomic innervation of the rectum and anal canal
* sympathetic: from *lumbar* **splanchnic** nerves (*L1-L2*)
* parasympathetic: from *pelvic* **splanchic** nerves (*S2-S4*)
## Footnote
NO autonomic innervation **below the pectinate line**
115
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
116
what structures enhance absorption of nutrients in GI tract
* villi in small intestine
* crypts in colon
| via increasing **surface area**
117
what type of epithelium is the peritoneum made of
simple squamous epithelium
(known as mesothelium)
118
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
119
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**
120
where are the "feeding centres" found
| function is control of food intake
hypothalamus
121
where are the lunar semilunaris located
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**
122
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**)
123
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**
## 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)
124
where do the lymph nodes of the bowel drain into
cisterna chyli
125
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**
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
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
127
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
128
which artery supplies the midgut
superior mesenteric artery
## Footnote
foregut = celiac trunk
hindgut = inferior mesenteric artery
129
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**)
130
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
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
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**
132
which of the following dermatomes supply the umbilical region
T10
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
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
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
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
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
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
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
B) T10 intercostal nerve
* T7-9: epigastrum
* T11-12: inferior to umbilicus
* L1: inguinal and pubis
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.
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
138
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"
## Footnote
* all the intraperitoneal parts (except cecum) are suspended by a **mesentry**
⇒ **mobile**
* while all the retroperitoneal parts are **fixed** to posterior abdominal wall
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
C) Interstitial Cells of Cajal
which connect longitudinal and circular smooth muscles
→ generate cycles of contraction and relaxation
140
which vein does blood from liver drain into
hepatic vein
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
sustained tonic contraction
(i.e. can sustain contractions w/o continuous ATP contractions)
142
why do people tend to empty their bowels after a meal
* 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
143
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
144
what are the lines which divide the abdomen into **4 quadrants**
* median plane:
at **midline**
* transumbilical plane:
at **umbilicus**
145
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
146
# 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**
## Footnote
* voluntary: oral phase
<- actions of chewing and of tongue are voluntary
* involuntary:
pharyngeal phase
<- reflex mah
oesophagal phase
<- peristalsis is by smooth muscles
147
what temporarily relaxes LES
* 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)
148
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
149
how does nicotine, coffee and tea affect tone of LES
**decrease** tone of LES
(i.e. relaxation)
150
# 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
## 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)**
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
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"
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
D) Sodium bicarbonate
all compounds containing H**CO3-** and **CO3-**
will result in **CO2 gas formation**
=> thus resulting in gastric distention, belching and flatulence
153
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
154
what are the DDI of antacids
can affect **absorption** of other medications
=> do NOT take within **2 hours** of other meds
155
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**
156
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**
157
MOA of H2-receptor antagonists
**competitive** inhibitors of H2 receptors on **parietal** cells
⇒ suppresses **acid secretion** by parietal cells
158
Which of the following is the most potent H2-receptor antagonist?
A) Famotidine
B) Cimetidine
C) Ranitidine
D) Omeprazole
A) Famotidine
## Footnote
H2-receptor antagonists all end with "**tidine**"
159
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)*
160
how effective are H2 receptor antagonists at inhibiting **meal-induced** acid secretion
**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**!
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
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
162
why should patients not crush omeprazole capsule
destroys the **enteric coating**
which protects drug against **activation by stomach acidity** before absorption
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
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
164
# 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**
## Footnote
CCK = stimulated by **fat-** and protein-containing chyme in small intestine
secretin = stimulated by **acidic** chyme **entering** small intestine from stomach
165
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
166
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
167
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)
168
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)
169
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)
170
what is pancreatitis due to
**derangement or overwhelming** of protective mechanisms,
resulting in **autodigestion** of pancreas by its own enzymes
171
# 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
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.
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
173
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
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**.
D) All of the above.
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
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**
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
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**
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
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
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
(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
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
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**
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.
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*
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.
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))
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
B) Pancreatic neuroendocrine tumor (PanNET)
* cystic change: **fluid-filled** spaces due to necrosis or degeneration
* highly vascular: indicates **abundant blood supply**
183
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)
## 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
184
# 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
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.
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)
186
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**
## Footnote
so small intestine has everything, while colon only has crypts
187
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
188
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**
189
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**
190
how does osmolarity and processes change as we move along small intestine
* 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
191
# 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**
192
what is another name for vitamin B12
cobalamin (CBL)
193
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.
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 (...)
* 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*
195
# 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")
196
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
197
what substances are mainly absorbed in the ileum
* bile salts
* vitamin B12
(particularly at **terminal** ileum)
198
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*)
199
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*
## 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**)
200
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**
201
describe the digestion of carbohydrates in the small intestine
1. pancreatic amylase:
carbohydrates → disaccharides
2. brush border enzymes:
disaccharides → monosaccharides
## Footnote
carbohydrates are already partially digested by **salivary amylase** in mouth
202
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)
203
describe the digestion and absorption of proteins in the small intestine
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
204
in which parts of the small intestine are carbohydrates and proteins mainly absorbed
duodenum and jejunum
205
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)
206
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
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.
C) **Pleomorphic adenoma** is the most common salivary gland neoplasm, followed by *Warthin tumour*, with *Warthin tumour* being associated with male smokers.
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
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
209
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)
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.
B) is true and A) is false
It is the other way round,
with SCC affecting the proximal and mid eosophagus (upper 2/3)
211
what is the difference in histology between Squamous Cell carcinoma (SCC) and adenocarcinoma
* SCC: keratin pearls
* adenocarcinoma: mucin production
212
# think of the 4 Bs
what are the clinical features and complications of eosophagal cancer
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!
213
definition of oesophagal varices
**dilated** submucosal veins
in **lower 1/3** of oesophagus
and **proximal stomach**
214
pathogenesis of oesophagal varices
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**
215
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
216
# 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**)
217
why is Barrett's eosophagus concerning
precancerous,
increased risk of **dysplasia** and **cancer**
218
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)
"*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
219
causes of chronic gastritis
* H pylori (majority)
* autoimmune
220
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**
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
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*
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
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
223
Granulomas are seen in Crohn disease.
True or False?
True
specifically **non-caseating** ones
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
C. Almost always **bloody**
while Crohn's may present with **non-bloody** diarrhoea
225
What is the direction of blood and bile flow in the liver,
and why are they opposite?
* 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
226
# recall that it is under chronic gastritis!
pathogenesis of autoimmune gastritis
**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
227
# think of the pathogenesis
clinical features of autoimmune gastritis
* 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**
228
in peptic ulcer disease,
where is the solitary mucosal ulcer usually seen
* proximal duodenum
or antrum of stomach
(MAJORITY)
* distal stomach
229
what is the characteristics of pain in peptic ulcer disease
* **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
230
causes of peptic ulcer disease
"think of chemicals which burn through stomach"
* NSAIDs
* H pylori
(which produces urease)
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)
* 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**
232
3 possible types of polyps in stomach
* hyperplastic
* adenoma
* oxyntic/fundus gland
233
pathophysiology of hyperplastic polyps
**chronic gastritis**
(e.g. from H pylori)
→ reactive **hyperplasia** of mucosa
⇒ may lead to **dysplasia**
234
which of the stomach polyps have risk of malignancy
* hyperplastic polyps
* adenoma polyps
235
what are the 2 types of stomach cancer
(Lauren classification)
* intestinal type
* diffuse type
236
what is a unique histological feature of diffuse type stomach cancer
signet ring cells!
237
what does diffuse type stomach cancer look like
plastic bottle
= linitis plastica
238
which type of stomach cancer has a ***poorer* prognosis**
diffuse type
bcos *poorly* **differentiated**
239
where is intestinal type stomach cancer most commonly found
**lesser** curvature
of **antrum**
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
* gastric
* colorectal
## Footnote
in contrast, look at size in liver, pancreatic and gallbladder cancer
241
definition of early gastric carcinoma
gastric cancer that invades **no more deeply** than **submucosa**
(irrespective of lymph node metastasis)
| i.e. does not go BEYOND submucosa
242
clinical significance of early gastric carcinoma
**good prognosis** with complete excision
| much better prognosis than gastric carcinomas in general
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
C) Lymphoid hyperplasia
* **faecolith** is more common cause in **adults**
* foreign matter is a possible cause in both children and adults,
but less common
244
what can cause **painless** obstructive *jaundice*
pancreatic cancer (esp **HOP**)
bcos HOP is **anterior** to **common bile duct**
245
what is the treatment for H pylori eradication
**triple** therapy (*CAO*)
* *C*larithromycin (antibiotic)
* *A*moxicillin (antibiotic)
(or **metronidazole** in case of **penicillin allergy**)
* *O*meprazole (PPI)
246
why is PPI included in treatment for H pylori eradication
| as part of triple therapy
* raises intragastric **pH**
-> lowers **MIC** and thus making antibiotics **more effective**
AND also **reduces symptoms**
* **antimicrobial** properties
247
why is double antibiotic therapy required in treatment of H pylori eradication
| as part of triple therapy
* H pylori is **inherently very resistant**
(to vancomycin, trimethoprim, etc)
* H pylori **becomes resistant** to clarithromycin and metronidazole if **given alone**
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
* **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
249
what does quadruple therapy for H pylori eradication involve
**TOMB**
* **T**etracycline (antibiotic)
* **O**meprazole (PPI)
* **M**etronidazole (antibiotic)
* **B**ismuth (mucoprotective agent)
250
difference bet
antiemetics vs antimimetics
* antiemetics: drugs to prevent or treat **nausea and vomiting**
* antimimetics: **subset** of antiemetics,
drugs that specifically prevent or treat **motion sickness**
251
where are *serotonin* 5-**HT3** receptors found
*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!")
252
example of 5-*HT*3 *antagonists*
on**danse**tron
<- ribbon **dancer** *blocking* *H*ammer *T*hrow in stomach-shaped area
## Footnote
other examples: granisetron, palonosetron
253
clinical indications of 5-HT3 antagonists
* prevention of ACUTE **chemotherapy**-induced vomiting
* prevention of nausea and vomiting caused by other forms of **noxious GIT stimulation**
(e.g. distension, inflammation)
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
corticosteroids
and NK1-receptor antagonists
255
what is 1 major adverse effect of 5-HT3 antagonists
cardiac arrhythmia (QT **prolong**ation)
<- ribbon dancer has an **elongated** ribbon
256
where are dopamine D2 receptors found
*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
257
# give example of the drug also
MOA of dopamine receptor antagonists
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*
258
what are some adverse effects of dopamine receptor antagonists
* **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
259
where are neuokinin (NK1) receptors found
*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**
260
example of NK1 receptor antagonists
a**prepitant**
<- **participants** lining up to get their pee checked before they their turn to performa plaNK at the beam
261
what are some severe adverse effects associated with NK1 receptor antagonists
* peripheral neuropathy
* blood dyscrasias
(i.e. abnormalities in composition or function of blood)
262
MOA of antipsychotics
| e.g. **promethazine**, prochlorperazine, droperidol, olanzapine
* **M**uscarinic antagonism
* **A**ntihistamine
* **D**opamine receptor antagonism
"stop them from going **MAD**"
263
adverse effect of
**D**roperidol (antipsychotic)
exhibits **D**2 receptor antagonism (MA**D**)
=> QT *prolongation*
("*elongated* ribbon across judging table of gymnastics competition")
264
what is olanzapine good for
controlling CINV **delayed** nausea
with **less EPS**
265
function of the epiploic foramen
allows **communication** between **greater and lesser** sac
266
# hint: blood vessels!
what structures are anterior and posterior to the epiploic foramen respectively
* anterior: hepatic artery, bile duct,
portal vein
* posterior: IVC
267
what is superior to the epiploic foramen
caudate lobe of **liver**
## Footnote
i think what they trying to say is that the *middle* of the liver is above it
268
what is inferior to the epiploic foramen
*1st part* of the **duodenum**
269
how does the lesser sac relate to the lesser and greater omentum
| lesser sac
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**)
270
what organs are anterior and posterior to the lesser sac respectively
* anterior: stomach
* posterior: pancreas
271
what are the classes of physical drugs used to treat constipation
| i.e. does not directly affect bowel motility or physiological processes
* stool surfactant agents
* bulk-forming laxatives
* osmotic laxatives
272
MOA of stool surfactant agents
lowers surface tension of stool
-> allow **water and lipids** to **penetrate stool**
=> stool becomes softer and **easier to pass**
273
how is MOA of mineral oil different from other stool surfactant agents
also makes stool **easier to pass**, but via
* **lubrication**
* preventing **water reabsorption** from stool
=> keep stools **soft**
274
A/E of long-term use of stool surfactant agents
impaired absorption of **fat-soluble vitamins** (ADEK)
<- lipids needed have penetrated and gone into stool
275
what are some A/Es of mineral oil
* 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
276
example of stool surfactant agents
glycerin + sodium chloride
(= docusate)
277
MOA of bulk-forming laxatives
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**
278
what is the 1st-line drug for constipation in healthy patients
psyllium (bulk-forming laxative)
## Footnote
other examples of bulk-forming laxatives:
* methyl**cellulose** (**natural** fiber)
* *polycarbo*phil (*synthetic* fiber)
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 (...)
* 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**
280
MOA of osmotic laxatives
**osmotically**-mediated water movement **into bowel**
-> increases stool **liquidity** AND **volume**
=> stimulates **peristalsis**
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
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**
282
what are the classes of physiological drugs used to treat constipation
* opioid receptor antagonists
* serotonin 5-HT4 receptor agonists
* stimulant laxatives
* Cl- channel activators
283
MOA of opioid receptor antagonists
blocks **μ**-opioid receptors in **GI tract**
=> reverses opioid-induced **inhibition of gut motility and secretion**
284
If μ-opioid receptors are antagonised,
will pain relief by opioids still be effective?
Yes!
bcos the antagonist does NOT **cross the BBB**
=> does NOT block **CNS analgesic effects**
285
clinical indication of opioid receptor antagonists
opioid-induced constipation in patients under palliative care
286
MOA of serotonin 5-HT4 receptor agonists
Stimulation of **serotonin 5-HT4** receptors
-> Increases **neurotransmitter** release
-> increase **smooth muscle** motor activity (e.g. peristalsis)
=> **prokinetic** effect on GIT motility
287
for *serotonin 5-HT4 receptor agonists*,
why is prucalo*pride* better than cisa*pride*?
* higher affinity
* NO cvs effects
288
MOA of stimulant laxatives
stimulate **enteric nerves** in intestinal wall
-> increase migrating colonic **contractions**
AND increase colonic electrolyte and fluid **secretions**
289
clinical indication for stimulant laxatives
used **long-term**
in **neurologically impaired / bed bound** patients
290
what should patients not take **within 1 hour** of taking **milk** products
oral bisacodyl
(stimulant laxative)
as milk products will cause **enteric coating** of oral bisacodyl to **break down**
-> risk of **gastric irritation / dyspepsia**
291
what is the last resort
drug given to patients who are unresponsive to other laxatives
Cl- channel activators
292
MOA of Cl- channel activators
stimulation of ***type 2* Cl- channels**
-> increased **secretion** of **chloride-rich fluid** into intestinal lumen
=> stimulate motility and shorten intestinal transit time
293
What are the drug classes used in treatment of diarrhoea
"**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
294
which drugs are used in **acute** diarrhoea
"**I** **L**ike **OC**S Boys"
* **I**ntestinal adsorbents
* **L**yophilizate of killed Lactobacillus
* **O**pioid agonists
* **C**olloid bismuth compounds
295
MOA of intestinal adsorbents
absorbs **bacteria**, bacterial **toxins** and **fluid**
=> decrease stool **liquidity and number**
296
A/E of intestinal adsorbents
low risk of significant A/Es
as NOT absorbed into **systemic circulation**
297
which anti-diarrhoeal drugs should not be taken within 2 hours of taking other meds
* Intestinal *adsorbents*
cos can impair *absorption* of other drugs
* bile acid *binding* resins
cos can *bind* to other drugs
298
MOA of lyophilizate of killed Lactobacillus
## Footnote
think abt how it affects
* harmful microbes
* normal intestinal flora
**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*
299
what are the clinical indications of lyophilizate of killed Lactobacillus
* **bacterial** diarrhoea
* **traveller's** diarrhoea
300
who is lyophilizate of killed Lactobacillus contraindicated in
patients with **lactose** intolerance
301
examples of opioid agonists used in treatment of diarrhoea
* loperamide
* diphenoxylate
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
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
303
Which is the **first line** drug
for **rapid** symptomatic relief of diarrhoea?
opioid agonists
"I Like **O**CS Boys"
304
MOA of Colloidal bismuth compounds
| I Like O**C**S Boys
rapid **dissociation** in stomach allowing **absorption of salicylate**
-> salicylate then **inhibits prostaglandin** production and **chloride** secretion
=> reduce stool **frequency and liquidity**
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
diarrhoea caused by EXCESS faecal **bile salts**
* usually watery and persistent
* buzz words: **ileum diseases** or **surgical resections** that lead to bile salts malabsorption
306
MOA of somatostatin-like peptide
used in treatment of diarrhoea
INHIBITS release of **hormones/transmitters**
=> reduces intestinal and pancreatic **secretions**
AND slows **GIT motility**
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
secretory diarrhoea caused by **GIT/neuroendocrine tumours**
(e.g. VIPoma/ carcinoid tumour
<- *STOP* **VIP** **Customers** only! = *somatostatin-like peptide* treats **VIPoma** and **Carcinoid tumour**)
308
what structures pass through the transpyloric plane
| located @ **L1** level
* 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**
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
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
310
what can be palpated at the **mid-inguinal point**
| recall! mid-inguinal pt = halfway bet ASIS and **pubic symphysis**
femoral artery
311
# medial, lateral, inferior
what structures bound the **Hesselbach** triangle
* medial: rectus abdominis
* lateral: inferior epigastric vessels
* inferior: inguinal ligament
312
how does the Hesselbach triangle relate to
(direct and indirect) inguinal hernias
**weaker** region
=> it is where **direct** inguinal hernias occur
313
which type of inguinal hernia may enter the scrotum
**indirect** inguinal hernia
bcos it enters the DIR,
travels through inguinal canal,
then **exits via SIR**,
sometimes reaching the scrotum
314
how does coughing affect
direct vs indirect inguinal hernias
* 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.
315
which type of organ is fixed,
intraperitoneal or retroperitoneal
retroperitoneal
* **fixed** to abdominal wall
* compared to **intraperitoneal** organs which are attached to abdominal wall via **mesentery**
316
# left/right, anterior/posterior
what is the order of the vessels in the portal triad
* bile duct (right), hepatic artery (left)
* portal vein (posterior)
317
what kind of epithelium lines the inner surface of the lungs
still stratified squamous epithelium but
* non-keratinised
* covered by **mucous membrane**
318
which of the papillae found on the tongue is the **most numerous**
A) filiform
B) circumvallate
C) fungiform
A) filiform
319
do each of the papillae found on the tongue have **taste buds**
A) filiform
B) circumvallate
C) fungiform
* filiform: **no** taste buds
* circumvillate: **a lot** of taste buds
* fungiform: has taste buds
320
what do each salivary gland produce, mucus or serous fluid
A) parotid
B) sublingual
c) submandibular
* parotid: **serous** only
* submandibular: **mix** of serous and mucus
* sublingual: majority **mucus**
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
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
322
# function
difference between
muscularis mucosa (in mucosa)
vs muscularis externa (in muscularis externa)
* muscularis mucosa: responsible for **local** movements of **mucosal layer**
(e.g. adjusting surface area to form villi)
* muscularis externa: responsible for **peristalsis and segmentation**
323
difference between
Meissner's plexus (in submucosa)
and Auerbach's plexus (in muscularis externa/propria)
* 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
324
what type of muscles are seen in the muscularis externa in the eosophagus
* upper third: **striated** muscle
<- **voluntary** phase of swallowing
* middle third: **mixed**
<- **transition** zone
* lower third: **smooth** muscle
<- **involuntary** phases of swallowing
325
explain roles of
ligamentum teres and ligamentum venosum
in embryological development
* 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
326
what is found posteriorly in the liver
**fissure** for ligamentum venosum and ligamentum teres
327
what are macrophages found in the liver called
**Kupffer** cells
328
what is the function of hepatic **stellate** cells in healthy liver
store vit **A** in lipid droplets
## Footnote
recall! during liver injury, they become **myofibroblast**-like cells
and produce **collagen** for **fibrosis**
329
inferior relations of gallbladder
* 1st part of duodenum
* transverse colon
330
list the following parts of the liver
331
a fracture in which ribs
will pose a risk of gallbladder rupture
ribs **9-11**
332
inferior relations of the spleen
left colic flexure
333
what can cause **painless** obstructive jaundice
HOP tumour
334
# relate function to where it is found
what is the function of Brunner's glands
| which are found in **submucosa**
**alkaline** secretion
to **neutralise** stomach **acid**
=> found in **duodenum**
(esp at **1st part**)
335
# relate function to where it is found
what is the function of Peyer's patches
| which are found in **submucosa**
large **lymphoid** patches in **immune defense**
=> found in **ileum**
so as to prevent **bacteria in colon** from invading
336
which part of the small intestine has the most pronounced villi and plicae circularis
jejunum
bcos it is where the **most absorption** occurs
337
differences bet jejunum and ileum in:
A) thickness
B) prominence of arterial arcades
C) length of vasa recta
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**
338
what does the gastrosplenic ligament contain
| gastrosplenic ligament = greater curvature of stomach to spleen
* 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
339
what does the splenorenal ligament contain
splenic vessels
## Footnote
recall! splenic artery <= celiac trunk
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
surgical **resection** of terminal **ileum**
where **loss** of ileocecal sphincter
-> **faster transit** of intestinal contents
=> **decrease absorption time**
341
does the majority of water absorbed by GIT
come from food/water intake
or its own secretions
own secretions!
342
what factors is the speed of gastric emptying dependent on
* 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
343
what hormone stimulates gastric function and motility
gastrin
<- secreted by G cells in antrum
344
which hormones inhibit gastric function and motility
* 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
345
which veins in stomach
drain directly into portal vein
vs drain into 1 of the branches
(splenic vein OR SMV)
* 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
346
what is the *s*ympathethic innervation of the
* foregut
* midgut
* hindgut
* 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
347
what is the *p*ara*s*ympathetic innervation of the
* foregut
* midgut
* hindgut
* 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
348
# movements, what it is stimulated by
difference between peristalsis and segmentaton
* 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
349
when is migrating motor complexes (MMC) present
during **interdigestive** periods
(i.e. only when **food is absent**)
<- stimulated by *motilin*
(hormone which regulates gut *motility*, esp during **fasting**)
350
what does migrating motor complexes (MMC) do
* **sweeps remaining** food debris INTO colon
* PREVENTS **migration of colonic bacteria** into distal ileum
351
what stimulates the relaxation of the internal anal sphincter
**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**
352
what happens to stool that reaches EAS
if defecation is desired
* **relaxation** of external sphincter
AND ALSO
* relaxation of **pelvic** muscles
* contraction of **abdominal** muscles
353
# 2 different mechanisms/pathways involved!
what happens to stool that reaches EAS
if defecation is not desired
**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
354
reason behind *post-prandial* **alkaline tide**
(i.e. blood leaving stomach *after a meal* is **alkaline**)
**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
355
# 2 processes
how does Na+/K+ ATPase help with gastric acid production
* 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**
med
flashcards
Decks in class (23)
# Cards
-
embryology30
-
biochem1
-
immunology16
-
cvs pharm (DONT USE)9
-
blood86
-
cvs233
-
respi153
-
renal123
-
thorax anatomy181
-
lungs anatomy38
-
git355
-
foundation I10
-
biochem168
-
foundation II133
-
endocrine121
-
repro194
-
mskderm160
-
mskderm 2387
-
multisystem19
-
paediatrics24
-
PE42
-
approach to passing5
-
procedural skills4
