Monday [abdomen muscles, intestine physiology, IBD, spinal curvatures] Flashcards

1
Q

How is the abdominal superficial fascia divided?

A

Location - above umbilicus = single sheet connective tissue - below umbilicus = two layers; fatty superficial layer [Camper’s fascia] and the membranous deep layer [Scarpa’s fascia]

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2
Q

Where do the superficial nerves/vessels run?

A

Between these two layers of fascia

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3
Q

Annotate

A
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4
Q

What are the two main muscles of the anterolateral abdominal wall?

A

Flat muscles – three flat muscles, situated laterally on either side of the abdomen. Vertical muscles – two vertical muscles, situated near the mid-line of the body

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5
Q

How are the flat muscles strengthened?

A

Fibres run in different directions and cross each other to strengthen wall and to dercease chance of herniation.

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6
Q

What are the three flat muscles? [from superficial to deep]

A

External oblique Internal oblique Transverses abdominis

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7
Q

What do the aponeurosis of the flat muscles form in the midline?

A

linea alba (a fibrous structure that extends from the xiphoid process of the sternum to the pubic symphysis)

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8
Q

The way each flat muscle is arranged and the function of each

A
  • EO = largest, runs inferomedially, contralateral rotation of the torso - IO = smaller and thinner, runs superomedially, bilateral contraction compress the abdomen, while unilateral contraction ipsilaterally rotates the torso - TA = deepest with transversely running fibres, compression of the abdominal contents
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9
Q

Annotate

A

image

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10
Q

What are the two vertical muscles anterolateral compartment abdomen? Bonus: what forms the six-pack?

A

Rectus abdominis [intersected by fibrous strips, known as tendinous intersections + linea alba = six pack]. Pyramidalis

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11
Q

Functions of the vertical muscles

A

rectus abdominis =As well as assisting the flat muscles in compressing the abdominal viscera, the rectus abdominis also stabilises the pelvis during walking, and depresses the ribs pyramidalis =This is a small triangular muscle, found superficially to the rectus abdominis. It is located inferiorly, with its base on the pubis bone, and the apex of the triangle attached to the linea alba. Tenses the linea alba.

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12
Q

What is the rectus sheath

A

The rectus sheath is formed by the aponeuroses of the three flat muscles and encloses the rectus abdominis and pyramidalis muscles. It has an anterior and posterior wall for most of its length: The anterior wall is formed by the aponeuroses of the external oblique, and of half of the internal oblique. The posterior wall is formed by the aponeuroses of half the internal oblique and of the transversus abdominis. Approximately midway between the umbilicus and the pubic symphysis, all the aponeuroses move to the anterior wall of the rectus sheath. At this point, there is no posterior wall to the sheath; the rectus abdominis is in direct contact with the transversalis fascia. The demarcation point where the posterior layer of the rectus sheath ends is the arcuate line

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13
Q

What are the horizontal/vertical planes o the surface of the abdomen?

A

Horizontal - Transpyloric plane – halfway between the jugular notch and the pubic symphysis, approximately the level of the L1 vertebrae. - Intertubercular plane – horizontal line that runs between the superior aspect of the right and left iliac crests Vertical - run from the middle of the clavicle to the mid-inguinal point (halfway between the anterior superior iliac spine of the pelvis and the pubic symphysis). These planes are the mid-clavicular lines

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14
Q

Annotate

A
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15
Q

What is the midline, paramedian, Kocher and McBurney incision? When would you use these?

A

Midline = access abdominal cavity []linea alba poorly vascularised Paramedian = laterally to midline for structures like kidney/spleen/adrenals. Ligates muscles medially to incision = atrophy. Kocher = gain access gallbladder and/or biliary tree pathology McBurney = a McBurney is a called a ‘grid iron’ incision, because it consists of two perpendicular lines, splitting the fibres of the muscles without cutting them – this allows for excellent healing. McBurney incision is performed at McBurney’s point (1/3 of the distance between the ASIS and the umbilicus) and is used in an open appendicectomy

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16
Q

Annotate

A
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17
Q

What are the five muscles in the posterior abdominal wall?

A

Iliacus, psoas major, psoas minor, quadratus lumborum, diaphragm

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18
Q

Where is the quadratus and what is it’s function?

A

The quadratus lumborum muscle is located laterally in the posterior abdominal wall. It is a thick muscular sheet which is quadrilateral in shape. The muscle is positioned superficially to the psoas major. Actions: Extension and lateral flexion of the vertebral column. It also fixes the 12th rib during inspiration, so that the contraction of diaphragm is not wasted

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19
Q

Locatio and function of psoas major

A

The psoas major is located near the midline of the posterior abdominal wall, immediately lateral to the lumbar vertebrae. Actions: Flexion of the thigh at the hip and lateral flexion of the vertebral column

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20
Q

Location and function of the psoas minor, diaphragm and iliacus

A

The psoas minor muscle is only present in 60% of the population. It is located anterior to the psoas major. Actions: Flexion of the vertebral column The iliacus muscle is a fan-shaped muscle that is situated inferiorly on the posterior abdominal wall. It combines with the psoas major to form the iliopsoas – the major flexor of the thigh. Actions: Flexion and lateral rotation of the thigh at the hip joint The posterior aspect of the diaphragm is considered to be part of the posterior abdominal wall. It is described in detail here.

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21
Q

what is psoas sign?

A

The psoas sign is a medical sign that indicates irritation to the iliopsoas group of muscles. The sign is elicited by flexion of the thigh at the hip. The test is positive if the patient reports lower abdominal pain. A right sided psoas sign is an indication of appendicitis. As the iliopsoas contracts, it comes into contact with the inflamed appendix, producing pain.

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22
Q

Annotate

A
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23
Q

Bonus: describe the fascia of the posterior abdomen

A

Fascia of the Posterior Abdominal Wall A layer of fascia (sheet of connective tissue) lies between the parietal peritoneum and the muscles of the posterior abdominal wall. This fascia is continuous with the transversalis fascia of the anterolateral abdominal wall. Whilst the fascia is one continuous sheet, it is anatomically correct to name the fascia according to the structure it overlies. Psoas Fascia The psoas fascia covers the psoas major muscle. It is attached to the lumbar vertebrae medially, continuous with the thoracolumbar fascia laterally and continuous with the iliac fascia inferiorly Thoracolumbar fascia The thoracolumbar fascia consists of the three layers; posterior, middle and anterior. Muscles are enclosed between these layers: Quadratus lumborum – between the anterior and middle layers. Deep back muscles – between the middle and posterior layers. The posterior layer extends between the 12th rib and the iliac crest posteriorly. Laterally the fascia meets the internal oblique and transversus abdominis muscles, but not the external oblique. As it forms these attachments it covers the latissimus dorsi. The anterior layer attaches to the anterior aspect of the transverse processes of the lumbar vertebrae, the 12th rib and the iliac crest. Laterally the fascia is continuous with the aponeurotic origin of the transversus abdominis muscle. Superiorly the fascia thickens to become the lateral arcuate ligament, which joins the iliolumbar ligaments inferiorly.

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24
Q

annotate fascia

A
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25
Q

In the posterior abdominal wall, which muscle is located between the anterior and middle layers of the thoracolumbar fascia?

A

hm

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26
Q

How to distinguish abdominal vertebral bodies?

A

Although the lumbar vertebrae lack some of the more distinctive features of other vertebrae, there are several characteristics that help to distinguish them. The vertebral bodies are large and kidney-shaped. They are deeper anteriorly than posteriorly, producing the lumbosacral angle (the angle between the long axis of the lumbar region and that of the sacrum). The vertebral foramen is triangular in shape. Other features of a typical lumbar vertebrae: Transverse processes are long and slender. Articular processes have nearly vertical facets. Spinous processes are short and broad. Accessory processes can be found on the posterior aspect of the base of each transverse process. They act as sites of attachment for deep back muscles. Mammillary processes can be found on the posterior surface of each superior articular process. They act as sites of attachment for deep back muscles.

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27
Q

What’s different about the 5th lumbar verebrae?

A

The fifth lumbar vertebrae, L5, has some distinctive characteristics of its own. It has a notably large vertebral body and transverse processes as it carries the weight of the entire upper body

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28
Q

Annotate

A
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29
Q

What are the two types of joints in the vertebral body?

A

There are two types of joint in the lumbar spine. Both of these articulations are not unique to the lumbar vertebrae, and are present throughout the vertebral column. Between vertebral bodies – adjacent vertebral bodies are joined by intervertebral discs, made of fibrocartilage. This is a type of cartilaginous joint, known as a symphysis. Between vertebral arches – formed by the articulation of superior and inferior articular processes from adjacent vertebrae. It is a synovial type joint

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30
Q

How can the ligaments of the spine be split?

A

Ligaments The joints of the lumbar vertebrae are supported by several ligaments. They can be divided into two groups; those present throughout the vertebral column, and those unique to the lumbar spine.

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31
Q

Which ligaments are present thoughout the vertebral column?

A

Anterior and posterior longitudinal ligaments: Long ligaments that run the length of the vertebral column, covering the vertebral bodies and intervertebral discs. Ligamentum flavum: Connects the laminae of adjacent vertebrae. Interspinous ligament: Connects the spinous processes of adjacent vertebrae. Supraspinous ligament: Connects the tips of adjacent spinous processes. (Note: In the cervical spine, the interspinous and supraspinous ligaments thicken and combine to form the nuchal ligament)

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32
Q

Which ligaments are unique to the lumbar spine?

A

The lumbosacral joint (between L5 and S1 vertebrae) is strengthened by the iliolumbar ligaments. These are fan-like ligaments radiating from the transverse processes of the L5 vertebra to the ilia of the pelvis

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33
Q

Annotate

A
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34
Q

When does the spinal cord terminate?

A

Throughout the vertebral column, the spinal cord travels through the vertebral canal (made up by the foramina of all vertebrae). At around the level of L1, the spinal cord terminates and the cauda equina begins. This is a bundle of lumbar, sacral and coccygeal nerve roots.

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35
Q

Where do the spinal nerves exit?

A

Spinal nerves exit the vertebral canal through the intervertebral foramina.

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36
Q

What is lumbar spinal stenosis and how can this treated?

A

Thought to be hereditary, lumbar spinal stenosis results in a stenotic (narrow) vertebral foramen in one or several lumbar vertebrae. This can cause compression of the spinal cord and exiting nerves. This condition can be worsened by age-related degenerative changes, such as bulging of the intervertebral discs. Lumbar spinal stenosis can sometimes be treated surgically with a decompressive laminectomy

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37
Q

What is excessive lumbar lordosis and who often develops it?

A

This is an abnormal anterior curvature of the vertebral column in the lumbar region, characterised by anterior tilting of the pelvis. Women develop temporary excessive lumbar lordosis in late pregnancy, but this resolves after childbirth. In either sex, obesity can similarly cause lordosis due to the increased weight of the abdomen. Both examples can cause back pain, and occur as a result of an altered line of gravity.

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38
Q

What are the three carbohydrate products absorbed by the small intestine?

A

Glucose, galactose, fructose

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39
Q

What is the digestion of starch initiated in the body by?

A

Digestion of starch is initiated in the mouth, facilitated by salivary amylase

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40
Q

Where does the majority of carbohydrate digestion occur, and which enzyme is active in particular?

A

The majority of carbohydrate digestion occurs in the small intestine. The main enzyme is pancreatic amylase, which yields disaccharides from starch by digesting the alpha 1-4 glycosidic bonds. The disaccharides produced (maltose, maltotriose, and α-dextrins) are all converted to glucose by brush border enzymes

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41
Q

Dissaccharides naturally occuring in food get broken down how?

A

Disaccharides occurring naturally in food do not require amylase to break them down. Brush border enzymes (lactase, sucrase, trehalase) hydrolyse these compounds into molecules of glucose, galactose and fructose

42
Q

How are carbohydrates absorbed?

A

Glucose and galactose are absorbed across the apical membrane by secondary active transport (along with Na+) through the Sodium-Glucose cotransporter (SGLT1). Both glucose and galactose exit the cell via GLUT2 receptors across the basolateral membrane into the blood. Fructose enters the cell by facilitated diffusion via GLUT5 and is transported into the blood via GLUT2 receptors.

43
Q

Which enzyme starts the digestion of protein in the body?

A

Protein digestion begins in the stomach with the action of pepsin, which breaks protein into amino acids and oligopeptides. The process of digestion is completed in the small intestine with brush border and pancreatic enzymes. They split the oligopeptides into amino acids, dipeptides and tripeptides.

44
Q

How are amino acids then absorbed into the body?

A

Amino acids are absorbed via a Sodium cotransporter, in a similar mechanism to the monosaccharides. They are then transported across the basolateral membrane via facilitated diffusion. Di and tripeptides are absorbed via separate H+ dependent cotransporters and once inside the cell are hydrolysed to amino acids

45
Q

Describe the digestion of lipids?

A

Lipids are hydrophobic, and thus are poorly soluble in the aqueous environment of the digestive tract. Their digestion is started by lingual and gastric lipases, but this only digests 10% of ingested lipids. The remainder of the lipids are digested in the small intestine. Here, bile aids digestion by emulsifying the fat goblets into smaller chunks, called micelles, which have a much larger surface area. Pancreatic lipase, phospholipase A2 and cholesterol ester hydrolase (3 major enzymes involved in lipid digestion) hydrolyse the micelles, breaking them down into fatty acids, monoglycerides, cholesterol and lysolecithin

46
Q

Describe the absorption of lipids

A

The products from digestion are released at the apical membrane and diffuse into the enterocyte. Inside the cell, the products are re-esterified to form the original lipids, triglycerides, cholesterol and phospholipids. The lipids are then packaged inside apoproteins to form a chylomicron. The chylomicrons are too large to enter circulation, so they enter lymphatic system via lacteals.

47
Q

How much water does the average adult ingest per dfay, and where does most of the absoprtion occur?

A

The average adult usually ingests 1-2 L of water each day, but the fluid load to the small intestine is 9 to 10 L, 8 to 9 L being added by secretions of the GI system. Most absorption of water and electrolytes occurs in the small intestine, with some water absorbed in the colon as well.

48
Q

Describe water absorption

A

Water absorption is dependent on the absorption of solutes such as (Na+ and Cl−). Na+ is absorbed from the intestinal lumen, most use the cotransport with glucose and amino acids and the Na+/H exchange, which allow Na+ ions to move from the lumen into the enterocyte. Na+ is rapidly removed from the enterocyte via the Na+ pumps, allow water via osmosis to follow either transcellularly or paracellularly (between the tight junctions of the enterocytes). Water as well as Na+ ions can then diffuse into the capillaries

49
Q

Describe and explain steatorrhoea

A

Steatorrhea is due to a disruption to the normal absorption of lipids, leading to fat filled faeces. There are numerous underlying causes for this such as pancreatitis, which prevents the correct secretion of pancreatic lipase and so lipids remain undigested. Another cause is gallstones which prevent bile from entering the duodenum and again prevents maximal absorption of lipids. However, the absorption in the small intestine can be compromised, such as in inflammatory bowel diseases. To distinguish between the underlying causes of Steatorrhea, the small intestine and biliary tree must be visualised. The small intestine can be visualised via endoscopy or radiography whilst the biliary tree can be visualised with endoscopic retrograde cholangiopancreatography

50
Q

How to distinguish between the causes of steatorrhoea

A

To distinguish between the underlying causes of Steatorrhea, the small intestine and biliary tree must be visualised. The small intestine can be visualised via endoscopy or radiography whilst the biliary tree can be visualised with endoscopic retrograde cholangiopancreatography

51
Q

How long is the small intestine on average? Parts of it

A

23ft long; duodenum, jejunum, ileum

52
Q

What are the four main layers of the small intestine?

A

The histological structure of the small intestine is similar to the other organs in the digestive tract. There are four main layers: Mucosa (Innermost layer) – Contains the epithelium, lamina propria and muscularis mucosae. Submucosa – Connective tissue layer, which contains blood vessels, lymphatics and the submucosal plexus. Muscularis externa – Consists of two smooth muscle layers; the outer longitudinal layer and inner circular layer. The myenteric plexus lies between them. Adventitia (Outermost layer) – Comprised of loosely arranged fibroblasts and collagen, with the vessels and nerves passing through it. The majority of the small intestine adventitia is covered by mesothelium and is commonly called the serosa

53
Q

Modifications of the small intestine for absoprtion

A

The small intestine is the major absorptive site in the gastrointestinal tract, and therefore has a number of modifications to aid its function. The mucosa and submucosa form large numbers of folds (or plicae) arranged in a circular fashion in the lumen (therefore called plicae circulares). Additionally, the plicae contain microvilli to further increase the surface area, which increases absorption

54
Q

What are in the components of the cells of the epithelioum?

A

The epithelium of the small intestine lines the luminal surface. There are a number of components to the epithelium: Enterocytes – Tall columnar cells, which have an absorptive function. They contain brush border enzymes on the surface which have an important digestive function. Goblet cells – Exocrine glands which secrete mucin. Crypts of Lieberkuhn The Crypts of Lieberkuhn are glands found in the epithelial lining. They contain numerous cells such as stem cells to produce new cells to replenish the cells lost due to abrasion, as well as enteroendocrine cells to synthesise and secrete hormones. To protect from pathogens, there are Paneth cells which secrete protective agents (such as defensins and lyzozymes) and Peyer’s patches which are only found in the ileum. Peyer’s patches contain mucosal-associated lymphatic tissue (MALT) which house white blood cells and lymphocytes. These cells can produce antibodies to further protect the small intestine from infection

55
Q

Annotate

A
56
Q

What are THE FOUR MAIN CLASSES of enteroendocrine cells? What do these secrete?

A

The enteroendocrine cells are located within the Crypts of Lieberkuhn. They secrete hormones in response to various stimuli. There are four main classes of enteroendocrine cell, each with a different secretory product. These are I cells, S cells, K cells and enterochromaffin cells. I Cells secrete Cholecystokinin (CCK) in response to the presence of fat in the small intestine. CCK stimulates the contraction of the gallbladder (which pushes bile out into the cystic duct) and the release of pancreatic enzymes. Both bile and pancreatic enzymes have a key role in lipid digestion. S Cells secrete Secretin in response to the low pH of chyme in the small intestine. Secretin induces HCO3– secretion from the pancreas and inhibits gastric emptying. K Cells secrete Gastric-Inhibitory Peptide (GIP), in response to chyme entering the small intestine. GIP has a misleading name as it actually stimulates insulin release, ready to put the newly digested carbohydrates into cells for storage. Finally, Enterochromaffin Cells are mechanically stimulated by the presence of chyme in the small intestine. They release serotonin, which acts on the enteric nervous system to activate the cystic fibrosis transmembrane regulators (CFTR). This ion channel secretes Cl– ions into the intestinal lumen, with Na+ ions and H2O following. Na+ is required in the lumen for the absorption of a number of nutrients.

57
Q

What are the three main substances that the small intestine recieves/

A

Bile, pancreatic enzymes, alkaline juice [HCO3-]

58
Q

Function of bile, pancreatic enzymes and alakaline juice

A

here are three main substances that the small intestine receives: bile, pancreatic enzymes and alkaline juice (HCO3–). Bile serves an important role in lipid digestion, and is secreted from the gallbladder into the common bile duct, in response to CCK. Pancreatic enzymes and alkaline juice are secreted from the pancreas into the pancreatic duct, in response to CCK and secretin

59
Q

What do the common bile duct and pancreatic duct form? How is this marked? What is this regulated by?

A

The common bile duct and pancreatic duct unite to form the hepatopancreatic ampulla (also known as the Ampulla of Vater). This opens out onto the internal surface of the duodenum, and is marked by the major duodenal papilla. The major duodenal papilla serves as an important anatomical landmark, as it is where the embryonic foregut becomes midgut. The secretions into the small intestine are regulated by the sphincter of Oddi

60
Q

Describe the lumen of the small intestine

A
61
Q

Describe the pancreatic enzymes

A

The pancreas plays an important role in digestion, as it produces many of the enzymes needed in digestion. These enzymes come in two forms. Some enzymes are already active, such as pancreatic lipase and pancreatic amylase, whilst some are secreted as inactive enzymes such as trypsinogen. The inactive enzymes are released as zymogens (precursors of the active form) – this prevent the enzymes digesting the pancreas itself. Trypsinogen is converted to trypsin (active form) in the small intestine by coming into contact with the brush border enzyme enterokinase. Trypsin then converts the remaining inactive proteases to their active form.

62
Q

What is coeliac disease and how common is it?

A

Coeliac disease is a condition which causes inflammation of the small intestine. It is autoimmune in aetiology, and affects roughly 1 in 100 people.

63
Q

What triggers coeliac in particular?

A

The immune-mediated damage of the small intestine occurs secondary to gluten exposure. When gluten is absorbed, it is broken down into a number of products. One product is gliadin, a protein. In coeliac disease, gliadin is presented to the T cells of the immune system as a foreign antigen. This stimulates the production of antibodies against gliadin and an inflammatory response to occur

64
Q

Which part of the duodenum does the ampulla of vater empty into?

A

2nd

65
Q

Whihc cells cholecystokinin released from?

A

I cells

66
Q

What are the histological changes seen biopsy coeliac disease?

A

Villous atrophy, flattending of the villous, intraepithelial lymphocytes and crypt hyperplasia

67
Q

How si the large intestine specialised for its function>?

A

The large intestine is lined by mucosa with crypts of Lieberkühn containing glands and mucus-producing goblet cells. These protect the intestinal wall from the plethora of anaerobic bacteria in the colon and from the pressure exerted on the walls by the concentrated chyme (soon to become faeces). The walls also contain gastrointestinal lymphoid tissue (GALT) that contributes to the body’s immune defences. The colon helps to absorb a small volume of water from the lumen (400ml/day). As the chyme is very concentrated by the time it reaches here, the colon must work against a larger osmotic pressure gradient than in the rest of the GIT. In other words, it must move water against the gradient for osmosis. The colon also helps to transport ions

68
Q

Water and ion aborption in the large intestine

A

In the large intestine, there is a net absorption of sodium ions and chloride ions are actively absorbed. Sodium – this ion may be absorbed by various methods: Sodium-hydrogen antiporter on the luminal membrane Epithelial sodium channels Enhanced by absorption of short-chain fatty acids in the colon via specialised symporters Chloride and bicarbonate – the movement of sodium into the plasma produces an electrochemical gradient to allow absorption of chloride. Chloride ions are exchanged for bicarbonate ions (causing net bicarbonate secretion). Water – the absorption of these electrolytes creates an osmotic gradient to allow further absorption of water. Potassium – absorption of water along the length of the bowel concentrates potassium in the lumen. This provides an electrochemical gradient for the movement of potassium into the plasma. In the colon potassium may be absorbed or secreted depending on the remaining concentration in the lumen and the electrochemical gradient created by the active absorption of sodium. Secretion usually occurs when the luminal concentration of potassium ions is below 25mM. Vitamins and fats – short-chain fatty acids, crucial B vitamins (such as B6 and B12) and vitamin K (required for blood clotting) are produced by the digestion of chyme by the commensal microbial flora of the colon.

69
Q

Describe how the absorption in the GI tract is regulated by endocrine mechanisms

A

Absorption in the gastrointestinal tract is regulated by neuroendocrine mechanisms. In the colon endocrine mechanisms used include: Aldosterone – increases the net absorption of water and electrolytes by stimulating the basolateral sodium-potassium ATP-ase. This increases the electrochemical gradient and driving force for sodium absorption. It also increases transcription of epithelial sodium channels. Glucocorticoids and somatostatin – act to increase water and electrolyte absorption by increasing the action of the basolateral sodium-potassium ATP-ase

70
Q

Describe how the absorption in the GI tract is regulated by neuro mechanisms

A

The intestines are innervated by the enteric nervous system whose: Parasympathetic innervation promotes net secretion from the intestines Sympathetic innervation promotes net absorption from the intestines

71
Q

What is the function fo the rectum? Where does the function for defecating come from?

A

The rectum is reponsible for temporary storage of faeces before defecation. As it becomes filled the rectal walls expand and stretch receptors stimulate the desire to defecate. The urge to defecate arises from contraction of rectal muscles, relaxation of the internal anal sphincter and an initial contraction of the external anal sphincter

72
Q

When is the urge for defecated acted upon?

A

If the urge is not acted upon further water is absorbed and the faeces is stored until the next mass movement occurs.

73
Q

Annotate

A
74
Q

Which fibres control defecation?

A

There are two main anal sphincters; an internal and external sphincter. The internal anal sphincter is controlled by parasympathetic fibres which relax involuntarily. The external anal sphincter is skeletal muscle that is controlled by somatic nerve supply from the Inferior anal branch of the Pudendal nerve (S2,3,4), which allows conscious control of defecation

75
Q

What is the rectoshpincteric reflex?

A

When the rectum is distended the rectosphincteric reflex is initiated and relaxes the internal sphincter. If defecation is not desired, voluntary contraction of the external sphincter can delay it. If defecation is appropriate, then a series of reflexes take place that lead to: Relaxation of the external sphincter Contraction of abdominal wall muscles Relaxation of pelvic wall muscle. Peristaltic waves can then faciliate movements of faeces through the anal canal.

76
Q

How cna defecagtion be assisted?

A

Defecation can also be assisted by taking a deep breath and attempting to expel the air against a closed glottis, this is known as the Valsalva maneuver. However, if a delay in defection is needed then voluntary contraction of the external sphincter is usually sufficient to override the reflexes that anal distension initiates

77
Q

When can faecal incontinence occur?

A

Defecation can either be voluntary or involuntary depending on the situation. Young children learn voluntary control of the process during toilet training and it typically remains under voluntary control throughout life. However in some situations loss of control may occur, particularly if defecation occurs too quickly, before excess water has been absorbed and diarrhoea occurs. Other causes of faecal incontinence include: Physical injury Nerve injury Surgery Intense fright Inflammatory bowel disease Childbirth Treatments can vary depending on the cause of the incontinence and how easily it can be corrected.

78
Q

What are the two main types of laxatives? How are they used?

A

Laxatives are used in the treatment of constipation. There are two main types of laxative: bulk laxatives e.g: Isphagula husk and stimulant laxatives e.g. Senna. A bulk laxative adds fibre to the contents of the intestine increasing the mass thus stimulating the walls of the intestine to cause peristalsis, thus increasing movement of the bowels, reducing constipation. Stimulant laxatives work on sensory receptors in the wall of the intestine to increase the amount of water and electrolytes being retained in the gut. This in turn causes peristalsis helping to empty the bowels

79
Q

Does contraction of the internal sphincter occur during defecation?

A

No

80
Q

What happens in the rectum?

A

GI tract water is reabsorbed and any waste material is stored asd faeces to be removed

81
Q

What is haustral shuttling?

A

The large intestine is naturally separated into segments known as haustra. Along the course of the walls are groups of cells called pacemaker cells. These send signals to the smooth muscle cells on the walls of the large intestine causing them to contract at regular intervals. The contraction causes the food to be churned in the intestine exposing the gut contents to a larger surface area of epithelium maximising absorption. Each group of cells control a certain number of haustra. The pacemaker cells closer to the ileum emit signals slightly faster than those towards the end of the length of bowel. This gradient allows a gentle progression of bowel contents towards the rectum

82
Q

What is mass movement and gastro-colic reflex?

A

Mass Movement Whilst haustral shuttling occurs continuously mass movement only occurs once or twice per day. This involves a sudden, uniform peristaltic contraction of smooth muscle of the gut which originates at the transverse colon and rapidly moves formed faeces into the rectum, which is normally empty. The result of this is feeling the urge to defecate. The contraction may be stimulated by eating. When this occurs it is called the gastro-colic reflex

83
Q

Which part of the bowel does UC affect?

A

Ulcerative colitis (UC) is a structural condition caused by the inflammation of the large bowel. It can affect any part of the large colon or rectum. It will usually stop at the caecum, although some patients may have irritation of the ileum due to backwash ileitis.

84
Q

Type of inflammation for UC? Sx of UC as well.

A

Inflammation is continuous, although up to 30% of patients may experience patchy inflammation, making endoscopic diagnosis uncertain. UC patients usually experience bloody diarrhoea, tenesmus, pain and fatigue

85
Q

Extraintestinal features of UC

A

There may also be extraintestinal features of the disease present such as; uveitis, scleritis, arthritis, erythema nodosum, pyoderma gangrenosum and mouth ulcers

86
Q

Dx and Tx of UC

A

To confirm a diagnosis of UC patients will undergo a detailed history and examination. This will then be followed by blood tests which would include an FBC for anaemia, U & E’s, LFT’S, amylase for pancreatitis and CRP/ESR for inflammation. Faecal calprotectin levels can also be assessed, as it is a sensitive marker for inflammation of the bowel and distinguishes between IBD and IBS. Endoscopy and CT scans can also be utilised to assist with diagnosis and to assess the severity of the condition. Treatment is dependent on the severity and location of disease. Severe disease requires urgent intravenous steroids and ‘rescue’ therapy with anti-TNF-alpha agents or ciclosporin – although some patients may require emergency colectomy. Mild-moderate disease is managed step-wise with a variety of inflammatory agents such as aminosalicylates, corticosteroids, anti-TNF-alpha agents and thiopurines. Surgery is sometimes performed acutely, however many patients undergo elective surgery due to drug side effects or failed medical treatment. There are broadly two types of surgeries, both of which require temporary ileostomy formation. It is important to make sure that a patient can take care of a stoma and the psychological implications of this need to be addressed, especially as patients may be quite young.

87
Q

What can blood test faecal calprotectin help differentiate between?

A

IBD and IBS

88
Q

Which of these is not a cause of faecal incontinence? Nerve injury, childbirth, perineal injury, retroverted uterus.

A

It’s a retroverted uterus

89
Q

Classic Sx of coeliac disease

A

Diarrhoea, abdominal distention, malabsorption ,loss of appetite, among children failure to grow normally.

90
Q

Tx for coeliac disease and Cx if left untreated

A

STRICT GLUTEN-FREE FIET, LEADS TO RECOVERY of intestinal mucosa, improves Sx. Can lead to cancers like lymphomam slightly increased risk of eath.

91
Q

What does lordosis, kyphosis, hyperlordosis, hyperkpyhosis?

A

Lordosis = curve in Kyphosis = curve out

92
Q

Why does lumbar regions curve in?

A

Anterior part of intervertebral discs larger than posterior part

93
Q

Example associated underlying conditions with lordosis and kyphosis

A

Osteoporosis, mislagined vertebrae, spondylisthesis, EDS, marfans, obesity and inflammation of intervertebral discs

94
Q

Types of kyphosis

A

Postural kyphosis [repeated poor posture, common young females] Scheuermann’s kyphosis [often associatee with scoilioiss] Congenital kyphosis [vertebrae get deformed durgin development -> can compress the heart and lungs]

95
Q

Underlying cause often in scoliosis

A

Often unclear; defect in composiiotn of intervertebral discs - decreased amount of glycoaminoglycans -> spine gets misshappen - see in NMD like cerebral palsy or muscular dystrophy

96
Q

Sx of spinal problems

A

Mild to severe pain difficulty moving SOB in severe casses and inability to exercise

97
Q

Dx spinal problems

A

Done by physical excamination of th eback Measure CObb angle [determine extend of deformity] Radiography

98
Q

Tx of lordosis/kyphosis

A

Physical exercises to limit disease progression and maintain ROM Pain medication fixing braces Surgery in young perople rarely

99
Q

Which part of the bowel does Crohn’s disease effect?

A

IBD type that may affect any segment of the Gi tract from the mouth to the anus

100
Q

Big RF for Crohn’s disease

A

Tobacco smokers are twice as likely to develop Crohns as nonsmokers