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JMP Semester 2 > Week 16 > Flashcards

Week 16 Flashcards

1
Q

What are the main motor patterns in the GIT?

A

Constant movement by smooth muscle cells contracting in either:
Tonic - maintained for several minutes up to several hours
Phasic fashion - alternating periods of relaxation and contraction.

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2
Q

What are the main layers in the GIT From outer to inner?

A
  1. Mesentary (fold of peritoneum)
  2. Serosa
  3. Longitudinal muscle
  4. Myenteric plexus
  5. Submucosa
  6. Submucosal plexus
  7. Muscularis mucosae
  8. Mucosa
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3
Q

What is the MMC migrating motor complex?

A

It is a distinct electromechanical activity in the gastro intestinal smooth muscle. (cyclic every 1.5-2 hours IN BETWEEN MEALS. )

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4
Q

What is the phases in the MMC?

A
  1. Smooth muscles are inactive- low number of AP and contractions (40-60 mins in length)
  2. Peristaltic contractions (begin and increase in frequency). Contractions originate in stomach–> small intestine (30 mins in length)
  3. Rapid peristaltic contractions (pyloric sphincter remains open) allowing indigestible material to pass into the intestine (lasts 15 minutes)
  4. Transition period - system resets for the first phase.
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5
Q

What is thought to be the reason that MMC continuously occurs even without food?

A
  1. Housekeeping function
  2. Sweeping of undigested material/foreign bodies
  3. moving bacteria from the small intestine to the large intestine
  4. inhibiting retrograde bacterial movement
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6
Q

What two movements/contractions occur after meals?

A

PERISTALSIS AND SEGMENTATION

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7
Q

What do peristalsis and segmentation do to the MMC?

A

They override it.

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8
Q

What is Peristalsis?

A

Contraction of circular muscles behind bolus

Relaxation of circular muscles in front of the bolus

Contraction of longitudinal muscles in front of the bolus (makes it move down the tube)

Drives the MOVEMENT of the bolus down the GIT

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9
Q

What is Segmentation?

A

Contraction of segments of circular muscle

Bolus is moved backwards and forwards

Contents are broken down mechanically

Drives MIXING

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10
Q

How many muscle layers are present in the wall of the GIT?

A

There is two layers in the wall of the GIT Circular and longitudinal

The Stomach however has 3

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11
Q

Which areas of the GIT is more likely to show peristalsis?

A

Small intestine

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12
Q

Which area of the GIT is more likely to show segmentation?

A

Small and large and stomach

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13
Q

What are the neuron connections to smooth muscle known as?

A

Varicosities (boutons)

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14
Q

What are the factors that influence contraction in the GIT?

A

Neural, Mechanical and hormonal.

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15
Q

Neural facts/factors that relate to contraction in the GIT.

A

Neural:

Single neuron have many connections to a smooth muscle unit

AP in the neuron causes neurotransmitter release from the varicosities. These neurotransmitters can be both excitatory (acetylcholine) and inhibitory (noradrenaline)

Smooth muscle cells may respond to stimulation from different nerve fibres

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16
Q

What are the mechanical factors that influence contraction in the GIT.

A

Mechanical:

Stretch can cause smooth muscle contraction. (through mechanosensitive ion channels that induce depolarisation.

Physical deformation of the enteroendocrine cells along the GIT can cause both hormone release and contractions.

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17
Q

What are the hormones that influence contraction in the GIT.

A

Hormonal

Cholecystokinin - increases contraction of gall bladder and pancreas and increases intestinal motility.

Gastrin - Increases secretion of gastric acid and increases gastric and intestinal motility.

Vasoactive intestinal polypeptide (VIP)- reduces GIT smooth muscle activity.

Somatostatin- Decreases pancreatic and gastric secretions

Serotonin- Can increase or decrease gastric and intestinal motility depending on receptor it binds (5HT4 - increase) (5HT3- decrease)

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18
Q

What is the enteric nervous system?

A

The nervous system of the gut.

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19
Q

What is the benefits of the enteric nervous system?

A

Allows the GIT to act independently from the brain while still allowing for some brain control.

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20
Q

What is the two separations of the ENS?

A

Myenteric plexus (Auerbach’s plexus)

Submucosal plexus (Meissner’s plexus)

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21
Q

Where is the Myenteric plexus located in the GIT wall and what is its main purpose?

A

It is located between the longitudinal and circular smooth muscle layers in the MUSCULARIS layer.

Involved in GIT Motility.

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22
Q

Where is the Submucosal plexus located in the GIT wall and what is its main purpose?

A

Located in the submucosa

Involved in “sensing the luminal environment, regulating blood flow and controlling epithelial cell function.

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23
Q

What are the three neuron types of the ENS?

A

Sensory neurons- gathers info from GIT (mechanical, thermal, osmotic and chemical) N.B chemical sensors (acid, glucose etc.) allow tasting of contents)

Motor neurons- controls motility and secretion in the GIT (act on large number of effector cells.

Interneurons- integrate and relay info to the enteric motor neurons

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24
Q

What is the Interstitial cells of Cajal (ICC)?

A

The cells of Cajal form branched networks through the muscle layers in the GIT. These cells spontaneously generate slow, rhythmic electrical waves which spread to the smooth muscle cells and cause contraction. (pacemakers of the GIT).

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25
Q

What is the use of the waves generated by the ICC?

A

The waves help organise the gut contractions into phasic contractions (peristalsis and segmentation)

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26
Q

How does the GIT firing frequency differ down the length of the GIT?

A

5 per min in stomach

10 per min in the duodenum (connection of stomach to small intestine)

3 per minute in the colon.

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27
Q

What are the three types of Interstitial cells of Cajal (ICC)?

A

ICCMY - present between the longitudinal and circular muscles (most active)

ICCIM - present within the circular muscle layer

ICCSM - Found at the interface of the submucosa and the circular muscle layer (least active)

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28
Q

What is the general effects of sympathetic and parasympathetic inputs on the body?

A

Sympathetic = excitatory “fight or flight”

Parasympathetic = inhibitory “rest and digest”

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29
Q

What do sympathetic and parasympathetic nerves do in the gut?

A

Sympathetic = inhibitory –> inhibits enteric plexus activity, and decreases motility and secretion.

Parasympathetic = excitatory –> increases enteric plexus activity and increases motility and secretion.

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30
Q

Where do the sympathetic fibres in the GIT originate from and where do they terminate?

A

Originate–> T5 to L2

Terminate–> directly on the enteric plexus and a few on the mucosal layer.

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31
Q

What are the two types of parasympathetic fibres in the GIT?

A

Proximal and Distal

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32
Q

Where do the Proximal and Distal GIT fibres originate?

A

Proximal - from the vagus nerve (cranial nerve)

Distal - from the sacral parasympathetic nerves.

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33
Q

What is distension in the GIT?

A

It is characterized by an increase in abdominal pressure together with a visible increase in overall abdominal diameter.

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34
Q

What is the normal functions of distension in the GIT?

A

The pressure acts on stretch receptors which signal the flow of material through the GIT

Activated stretch receptors by normal food distension in one part of the GIT triggers increased peristalsis in the next part of the GIT.

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35
Q

What are the main reflex types in the GIT?

A

Intrinsic

Extrinsic (short and long)

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36
Q

What are INTRINSIC reflexes in the GIT?

A

They are reflexes that act via the ENS:

Irritation or distension of the mucosa trigger sensory fibre stimulation to the local intrinsic ganglia (in the enteric plexus)

Efferent signals travel to relevant local cells.

Results in increased secretion or motility.

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37
Q

What is the flow of Extrinsic reflexes in the GIT (particularly in distension)?

A

Sensory afferent fibres are activated and send signals to: (prevertebral sympathetic ganglia, spinal cord or the brain)

Trigger many reflexes some being short and others being long.

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38
Q

What are some examples of SHORT Extrinsic reflexes in the GIT

A

Enterogastric reflex (Stretch in duodenum shuts down gastric emptying)

Ileogastric reflex (Stretch in ileum shuts down gastric emptying)

Gastrocolic reflex (stretch in stomach and duodenum increases peristalsis in the ileum and the opening of the ileocaecal valve. Material flows into colon and triggers colonic peristalsis)

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39
Q

What are some examples of LONG Extrinsic reflexes in the GIT?

A

Vomitting reflex

Pain reflex

Vagovagal reflex - stretch in oesophagus trigger relaxation of gastric smooth muscle in preparation for the food bolus.

Defecation reflex

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40
Q

What are some other less obvious effects of distension in the GIT?

A

Stretching GIT muscles can affect the activity of the interstitial cells of Cajal (pacemakers), which may lead to uncoordinated GIT contractions

Release of hormones from the enteroendocrine cells, which can effect motility and secretion.

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41
Q

What is the most common cause of GIT distension?

A

Accumulation of gas from ingestion during eating, GIT disease or some infections

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42
Q

Why does abnormal distension in the GIT trigger pain?

A

Abnormal distension leads to dysmotility of the GIT, which in itself may cause pain, vomiting diarrhoea or constipation.

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43
Q

What is Nociception?-

A

detection of the tissue injury by the nervous system to stimuli (not pain) (only a relative factor in pain)

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44
Q

What is Pain?-

A

conscious experience involving: evaluation of nociception, context of other sensory input alongside coordination with other information such as learning and memory. (pain requires brain input) (unconscious people do not feel pain)/

For example 2 equal injuries will affect 2 people different, and even the same person differently.

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45
Q

What type of neuron is a Nociceptive neurons-

A

Are high threshold - requires a greater than normal stimulus to activate (associated with substantial cell injury/death.

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46
Q

What are Peripheral nociceptive neurons activated by?-

A

activated by chemical, mechanical and thermal stimulus. (all of these are classified as noxious stimuli)

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47
Q

What categories of compounds are Nociceptive neurons activated by one or a combination of-

A

injury-related compounds- (eg capsaicin, heat,ATP, H+)

Inflammation associated compounds- (eg bradykinin, prostaglandins, nerve growth factor (NGF))

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48
Q

Nociception activation lead to action potentials to travel where-

A

they are conducted to the spinal cord (dorsal horn).

Dorsal horn fibres continue signal onto ascending spinothalamic fibres.

Signal goes to the thalamus

Thalamus delivers signal to all parts of the cortex.

All information from them is then processed and “pain response level” is determined.

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49
Q

What do presynaptic cells release specifically when activated?-

A

glutamate (Glu)

Substance P

other substances such as calcitonin gene-related peptide (CGRP) to ensure signal is sent.

50
Q

What is the different between Glutamate and substance P neurotransmitters compared to the other compounds eg (CGRP)?

A
  • the first 2 have a fast mechanism of action in the spinal cord synapse (depolarisation) whereas the CGRP has a slow modulatory response (eventually causes depolarisation)
51
Q

What are the main ways of blocking nociception?

A

By targeting both the:

Presynaptic inhibition- reduced activity of voltage gated calcium channels (reduces neurotransmitter release (reduces spinal cord depolarisation)

Postsynaptic inhibition- increasing Cl- influx and/or K+ efflux to drive hyperpolarisation. (reduces post synaptic neuron activation chance)

52
Q

What happens with nociception in diabetics and the elderly?

A

Diabetics and the elderly can have issues with nociception so don’t know that they have been hurt (as they do not get the signals to then interpret them as pain)

53
Q

Why does the body adapt to opioids and other pain killers?

A

They body priorities nociception for survival so will develop some form of it eventually and essentially negating the pain relief.

54
Q

What is the general difference between paracetamol and ibuprofen?

A

Paracetamol is an analgesic not an anti-inflammatory.

Ibuprofen is both. (so can prevent injury healing through suppressed inflammatory response.)

55
Q

Why is nociception blocking harder than other “classical neurons”?

A

They have many more neurotransmitters that they release.

56
Q

What is different in nociceptive neurons compared to other neurons in regards to neurotransmitter release and other effects?

A

They can release neurotransmitters from both ends (unlike normal neurons that only release from one end (the other end has a dendritic tree).

Substance P and CGRP cause a neuroinflammatory response to facilitate inflammation and healing in the activated area. (this is self regulated as when activation signal disappears so does the inflammation by substance P etc.

57
Q

What ion allows for neuron vesicle mobilisation?

A

Calcium

58
Q

What receptor targets are there at the nociception neuron synapse?

A

U opiod receptors

GABAB receptors

Alpha2 adrenergic receptors.

59
Q

What are the 4 main types of opioids? -

A

endogenous opioid peptides (ignoring pain when needed (fight or flight etc.))

naturally occurring opioids

synthetic opioid dugs

semisynthetic opioid drugs.

60
Q

What is the main mechanism of action for opioids?

A

They inhibit synaptic transmission.

61
Q

Where are opioid receptors located?

A

Incoming nociceptive fibre (C-fibre)

Ascending fibre (dorsal horn neuron)

62
Q

What is the use of opioid receptors being located on both the incoming nociceptive fibre and the ascending fibre?

A

Allows control of neurotransmitter release and responsiveness of the ascending fibre.

63
Q

How do opioids inhibit synaptic transmission?

A

They are Agonists

Stimulate opioid receptors (Which are G-protein coupled receptors)

Mainly stimulate the u receptor associated with analgesia.

Prevents AP generation.

64
Q

What is the presynaptic mechanism for u opioid receptor binding (agonist)

A

Inhibits AdCy to reduce cAMP

Inhibits Voltage gated Ca++ channels

Reduces synaptic vesicle mobilisation

Reduces neurotransmitter release

65
Q

What is the postsynaptic mechanism for u opioid receptor binding (agonist)

A

Activates G proteins to activate K+ channels

K+ net efflux causes hyperpolarisation of the cell.

66
Q

What is the difference in nociceptive neurons and normal neurons when it comes to increased/rapid firing?

A

Nociceptive neurons - sensitises the receptors

Normal neurons- desensitises receptors

67
Q

What are the main effects of opioids in the GIT?

A

Reduce Ach release –>

Disrupts Intersegment coordination (reduced motility)

Decreased GIT secretion.

From these effects can cause:

Delay gastric emptying

Nausea/vomiting (through increased fluid absorbtion)

Increase GIT transit time

Constipation

Abdominal discomfort/pain.

68
Q

What are the three main areas for Opioid effects on the CNS?

A

Brain, Brainstem, Spinal Cord

69
Q

What are the effects of opioids on the brain? -

A

mood alteration

Sedation- (reducing brain activity)

Reduced emotional reaction to pain (can get euphoria or dysphoria).

70
Q

What are the effects of opioids on the brainstem?

A

Increased neuron activity that provide descending inhibition in the spinal cord. (reduces nociception (reduces pain)).

71
Q

What are the effects of opioids on the spinal cord? -

A

Inhibit synaptic vesicle release from primary afferents and causes hyperpolarisation in postsynaptic neurons (reduces nociception)

Hence pre and post synaptic effect to prevent AP generation.

72
Q

What are the clinical adverse effects of opioids?

A

Respiratory depression- due to decreased activity of the brainstem and hence reduction in activity of respiratory centers.

Nausea and vomiting- from activation of the chemoreceptor trigger zone.

Sedation- may be seen as a sign of overdose (but can be beneficial in sleep deprived patients)

Tolerance, dependence and “addiction”

73
Q

Definition of acute abdomen-

A

sudden severe abdominal pain of unclear aetiology that is less than 24 hours in duration.

74
Q

Mechanisms/reasons for inflammation in the abdomen?

A

Peritonitis (secondary to other infection of pelvic infection, appendicitis)

Inflammatory conditions (diverticulitis, pancreatitis, cholecystitis)

Contamination by gastrointestinal contents (perforated duodenal or gastric ulcer)

75
Q

Mechanisms/reasons for obstruction in the abdomen?

A

Intestinal obstruction from:

Intestinal adh esions (fibrous scar tissues)

Cancer

Hernias

Impacted feces

Twisting of the colon (volvulus)

IBS

76
Q

Mechanisms/reasons for vascular issues in the abdomen?

A

Vascular processes (aortic dissection, ruptured aortic aneurysm)

Hemorrhage (ectopic pregnancy, ruptured aortic aneurism)

77
Q

Mechanisms/reasons for trauma in the abdomen?

A

Penetrating or blunt trauma (rupture of intestinal organs and or contamination of content)

78
Q

What abdominal structures are pain sensitive and what can induces pain within them?

A

Liver, Spleen and Biliary tract

Urinary tract

Gynecologic disorders

Vascular disorders

Peritoneal disorders

79
Q

What are the different causes for visceral pain -

A

deep, dull aching or cramping (poorly localised)

Stimulated by stretching, distension or contraction.

Traction on the bowel mesentery

Inflammation or ischemia

Midline focused accompanied by tenderness

80
Q

What are the different causes for abdominal somatic pain.

A

Sharper and better localised and easily described.

Aggravated by stimulation or irritation of the parietal peritoneum with movement coughing or walking.

Clinical signs (pain, guarding, rebound and absent bowel sounds)

81
Q

Describe referred pain in the abdomen.

A

Pain felt over a site other than the true location of stimulus

Occurs in an area supplied by the same neurosegment as the involved organ

The most common form of visceral pain

Most often secondary to in inflammatory lesion

Eg subdiaphragm - shoulder pain

 Biliary tract - right shoulder 

 Small bowel- back pain 

 Appendicitis - umbilical region
82
Q

Definition of peritonitis-

A

Inflammation of the peritoneum develops if bacteria are introduced to the cavity or if chemical irritants (bile, stomach acid or pancreatic juice) find their way into the cavity

83
Q

Common mechanisms leading to peritonitis-

A

Bacterial infection of the peritoneum may be spontaneous in patients with cirrhosis of the liver or ascites (intestinal bacteria move through the intestinal wall or through lymphatic vessels into the enlarged peritoneal cavity)

84
Q

What is Peritonism

A
  • Any condition having the symptoms of peritonitis but without the inflammation of the peritoneum
85
Q

What are the potential consequences of infection and/or manipulation of the peritoneum?

A

A bloodstream infection (bacteraemia).

An infection throughout your body (sepsis). Sepsis is a rapidly progressing, life-threatening condition that can cause shock and organ failure.

Adhesions to neighbouring structures/organs

86
Q

What is an abdominal abscess?

A

Purulent collection of fluid, necrotic debris, bacteria, inflammatory cells that is encapsulated by adjacent healthy cells in an attempt to keep the pus from infecting other neighbouring structures.

87
Q

Describe the formation of an abdominal abscess.

A

A barrier may include the omentum, inflammatory adhesions or contiguous viscera.

These abscesses usually contain a mixture of aerobic and anaerobic bacteria from the GIT

Bacteria in the peritoneal cavity stimulate an influx of inflammatory cells.

The omentum and viscera tend to localise the site of infections producing a phlegmon. (inflammation of soft tissue)

The resulting hypoxia in the area facilitates the growth of anaerobes and impairs the bactericidal activity of the granulocytes.

The phagocytic activity of these cells degrades cellular and bacterial debris, creating a hypotonic milieu that expands and enlarges the abscess cavity in response to osmotic forces.

If untreated, the process continues until bacteraemia develops and can progress to generalized septic shock.

88
Q

What are the imaging types available for the abdomen?

A

Xray

Ultrasound

CT scan

MRI

PET

89
Q

What are the steps for viewing an abdominal x-ray?

A 
Confirm details 
name 
DOB 
Imaging time (when was it taken) 
Presence of other imaging for comparison.

Image quality
Anterior-posterior (either supine or erect)
Expose issues (ensure entire abdomen from the diaphragm to pelvis is visible)
If bowel perforation is suspected need an erect chest x-ray to see risen free gas.

Bowel/other organs
Small bowel usually more central
Sizes normally - SB 3cm, colon 6cm, 9cm caecum.

Bones Calcification/artefact
White areas.

90
Q

Small bowel obstruction signs on plain abdominal films:

A

Dilation of the small bowel (larger than 3cm)

Small bowel folds (white) more visible (looks like a coiled spring)

Most obstructions are caused by previous adhesions

91
Q

Large bowel obstruction signs on plain abdominal films:

A

Most large bowel obstructions are from colorectal carcinoma.

Volvulus (twisting of the bowel)

Dilation of the large bowel over 6cm

92
Q

What is acute abdomen?

A

A condition of severe abdominal pain, usually requiring emergency surgery, caused by acute disease of or injury to the internal organs.

93
Q

What are the signs of acute abdomen?

A

Severe pain

Signs of shock (tachycardia, hypotension, diaphoresis(sweating), confusion)

Signs of peritonitis

Abdominal distension

94
Q

Why is there radiating pain within the abdomen?

A

Organs typically invoke initial visceral level pain which is diffuse and may not correspond to the actual location of the organ. As the condition develops the pain may then focus on the area of the organ more sharply as somatic pain innervation begins most commonly causes by peritonitis

95
Q

What are is an example of pain radiation in the abdomen?

A

Appendicitis- dull pain near navel, becomes more sharp towards the lower right abdomen.

96
Q

What are some common causes of acute abdominal pain?

A

Gas

Overeating

Menstrual cramping

Pulled muscle

97
Q

What are some serious causes of acute abdominal pain?

A

Ectopic pregnancy

Appendicitis

Bowel perforation

Hemorrhage

Obstruction

Trauma

98
Q

What are the patient history features that can help determine causes of abdominal pain?

A

surgical history (appendectomy, adhesions

Patient age (cancer risk, preg, hernia)

Gender (pregnancy risk, menstruation, hernias, ovarian cyst

Medications (opioids constipate)

Recent bowel movement/flatulence (rules out obstruction)

Diet/intolerances.

99
Q

What are the common causes of bowel obstruction in different age groups? (children vs elderly)

A

Children- hernias, adhesions from surgery, volvulus (twisted),

Elderly- cancer, adhesions, impacted feces, gallstones,

100
Q

What are the clinical signs of bowel obstruction?

A

Abdominal cramps

Loss of appetite/vomiting

Constipation

Inability to have bowel movement/pass gas

Abdominal distension

101
Q

What is ileus?

A

The term for a lack of movement in the intestines, a temporary arrest in intestinal peristalsis. (can cause a backlog and subsequent obstruction)

102
Q

What causes an ileus?

A

Drugs that slow down GIT (opioids)

Cancer

Crohns disease (thicker intestinal wall from inflammation)

Electrolyte imbalance (especially potassium and calcium (impairs contraction when absent)

103
Q

What are some risks of surgery in abdomen?

A

Infection

Adhesions

Bleeding

Shock

Paralytic ileus.

104
Q

What would be the nutritional considerations in certain abdominal surgeries?

A

Liver Bile interruption - fat metabolism and fat soluble vitamin deficiency.

Pancreatic enzymes - protein, fat and cholesterol metabolism

Methods to help.- small meals, low fat, low sugar.

105
Q

What is rovsings sign?

A

If palpation of the left lower quadrant of a person’s abdomen increases the pain felt in the right lower quadrant, the patient is said to have a positive Rovsing’s sign and may have appendicitis.

106
Q

What is rovsings sign?

A

If palpation of the left lower quadrant of a person’s abdomen increases the pain felt in the right lower quadrant, the patient is said to have a positive Rovsing’s sign and may have appendicitis.

107
Q

What is Guarding?

A

the tensing of the abdominal wall muscles to guard inflamed organs within the abdomen from the pain of pressure upon them. The tensing is detected when the abdominal wall is pressed.

108
Q

What is the difference between voluntary and involuntary Guarding?

A

Voluntary - patient chooses to protect themselves from the pressure

Involuntary- even when distracted the patients body will tense abdominally when pressed.

109
Q

What is an NG tube?

A

A nasogastric (NG) tube is a flexible tube of rubber or plastic that is passed through the nose, down through the oesophagus, and into the stomach. It can be used to either remove substances from or add them to the stomach.

110
Q

What is intraperitoneal scar tissue called?

A

Adhesions, typically caused by surgery.

111
Q

How do adhesions cause obstruction?

A

Adhesions cause tissues and organs to stick together. This results in an abnormal bond between two parts of the body.

112
Q

What is a Hernia?

A

A hernia occurs when an organ pushes through an opening in the muscle or tissue that holds it in place. For example, the intestines may break through a weakened area in the abdominal wall. Hernias are most common in the abdomen, but they can also appear in the upper thigh, belly button, and groin areas.

113
Q

What is a volvulus?

A

A volvulus is when a loop of intestine twists around itself and the mesentery that supports it, resulting in a bowel obstruction.

114
Q

What is riglers’ (double wall) sign?

A

When there is air on both the luminal and peritoneal side of the bowel wall, the two sides of the wall are clearly visualised (white (wall) with dark patches (gas) on both sides.)

115
Q

Where is the Abdominal aorta?-

A

begins at the diaphragm and splits into the paired common iliac arteries in the lower abdomen (4th lumbar vertebrae.

116
Q

Where is the Common iliac?

A
  • they are the two arteries that branch of the abdominal aorta
117
Q

Where is the external iliac?

A

They are the arteries that branch off the common iliac and ultimately supply the leg (becomes femoral) travels more laterally.

118
Q

Where is the inferior epigastric arteries?-

A

they are a branch off the external iliac.

119
Q

Where is the Internal iliac?

A

They are the arteries that branch off the common iliac and ultimately supply the pelvic organs travels more medially.

120
Q

Visceral peritoneum

A

(the side of the peritoneum wrapping the organs)

121
Q

Greater omentum-

A

is a fold of visceral peritoneum that hangs down from the stomach in front of the small intestines and doubles back to ascend to the transverse colon then reaches to the posterior abdominal wall.

122
Q

Lesser omentum-

A

is the double layer of peritoneum that extends from the liver to the lesser curvature of the stomach (hepato-gastric ligament) and the first part of the duodenum

JMP Semester 2 (8 decks)

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