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PATH 300 > Gastrointestinal 3 > Flashcards

Gastrointestinal 3 Flashcards

1
Q

What is referred pain? Why does this happen?

A

Referred pain is a phenomenon where stimulation of visceral nociceptors usually produces pain referred to the surface, often in a different area. This happens because visceral and somatic afferents synapse on the same second order neurons in the spinal cord, and the brain interprets the subsequent input as somatic.

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2
Q

What is intestinal obstruction and what are the five different disorders that can cause it?

A
  • Intestinal obstruction is a condition where the transport of material through the lumen may be blocked.
  • Mechanical obstruction of the lumen
  • Volvulus or hernia,
  • Intussusception,
  • Paralytic ileus,
  • Destruction or congenital absence of neurons in the intestinal plexuses.
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3
Q

what causes Mechanical obstruction of the lumen?

A

due to tumor, severe inflammation

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4
Q

what is Volvulus (also called a hernia)?

A

which is the twisting of the bowel forming a closed loop

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5
Q

where do volvulus form?

A

in the small intestine, sigmoid colon or cecum; areas where the mesentery is longer.

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6
Q

what are the consequences and treatment for Volvulus?

A

Consequences are infarction of the intestine and gangrene, requiring immediate surgery.

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7
Q

what is intussusception?

A

the prolapse of part of the intestine into the adjacent segment. This can be intermittent, causing periodic pain, or complete, requiring surgical correction.

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8
Q

what is Paralytic ileus? what causes it? what are the consequences?

A

the temporary absence of peristalsis due to impaired neural control following abdominal surgery or peritonitis. Symptomatic treatment (nasogastric tube, IV fluids) usually results in total recovery. Otherwise, the intestine would become severely distended with fluid and electrolytes, accompanied by shock.

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9
Q

what causes Destruction or congenital absence of neurons? what is the treatment?

A

occasionally occurs in advanced inflammatory bowel disease, and some children are born with neural defects in the intestine. Removal of the aperistaltic area is often curative

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10
Q

What is the treatment for Diverticular Disease?

A

The treatment is supportive (analgesics, antibiotics, anti-inflammatory) if mild, surgical if severe (obstruction, fistula, perforation) or recurrent.

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11
Q

What is Diverticular Disease?

A

It’s a condition with pouches forming in the colon, often in the sigmoid region, due to herniation of the mucosa and submucosa through the muscular layers of the bowel.

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12
Q

where does Diverticular Disease usually occur?

A
  • often in the sigmoid region
  • occurring at the natural gaps in smooth muscle where blood vessels penetrate the colonic wall
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13
Q

how is Diverticular Disease diagnosed?

A

by radiologic examination following barium enema.

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14
Q

how big are Diverticula?

A

range in size from 1 mm - 5 cm or more

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15
Q

What is the prevalence of Diverticular Disease?

A
  • This disorder is very common in North America, the frequency increases with age, and it occurs in almost half of persons over the age of 60.
  • The incidence in North America has been rising throughout this century, whereas diverticulosis is still very rare in Africa and Asia
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16
Q

what causes Diverticular disease?

A

he environmental cause is considered to be inadequate fiber in the diet. This prolongs intestinal transit time and narrows lumen diameter, thereby increasing the force of segmental contractions, producing mini-compartments of high intraluminal pressure.

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17
Q

What are the consequences/symptoms of Diverticular Disease?

A

The majority of people with Diverticular Disease are asymptomatic, some have intermittent lower abdominal pain, distention, discomfort, which may decrease on a high fiber diet

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18
Q

What are the complications of Diverticular Disease?

A
  1. Diverticulitis - inflammation of a diverticulum, often due to blockage with fecal material. Causes increased pain, leukocytosis. Localized infection can produce fever, abscess, which may lead to perforation, adhesions, and fistulas, or general peritonitis, or septicemia. Severe inflammation can also cause physical obstruction or paralytic ileus.
  2. Bleeding - vessel rupture. This is less common.
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19
Q

How is Celiac Disease treated?

A

The treatment for Celiac Disease is a gluten-free diet.

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20
Q

What happens when gluten is ingested in Celiac Disease?

A
  1. Ingested gluten is broken into gliaden peptides which are transported to the lamina propria
  2. where modification by an enzyme, TG2, facilitates binding to antigen presenting cells, and activation of helper T cells, initiating B-cell production of antibodies against TG2 and the modified gliaden.
  3. Epithelial cells also release inflammatory cytokines, and CD8 T cells are activated.
  4. This results in tissue destruction and villous atrophy.
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21
Q

What are the consequences/symptoms of Celiac Disease?

A

Symptoms can begin at any age and include GI pain, diarrhea, malabsorption, weight loss, and chronic malnutrition

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22
Q

How is Celiac Disease diagnosed?

A

Celiac Disease is diagnosed via intestinal biopsy and antibodies (IgA anti-TG2). The biopsy reveals Villous atrophy, crypt hypertrophy, and intraepithelial lymphocytes.

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23
Q

What is the cause of Celiac Disease?

A

It’s an autoimmune T-cell mediated enteropathy, triggered by gluten proteins in wheat, rye, and barley. There’s a genetic susceptibility involving MHC class II genes, plus some environmental trigger, possibly infection, or alterations in the microbiome.

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24
Q

are women or more more susceptible to having celiac disease?

A

women

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25
Q

what is the prevalence of celiac disease in Canada?

A

1%

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26
Q

what are the two major types of inflammatory bowel disease?

A
  1. Ulcerative Colitis: the problem is mostly in the MUCOSA.
  2. Crohn’s Disease: abnormalities go right through the ENTIRE WALL of the bowel.
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27
Q

Four major distinctions between crohn’s disease and ulcerative colitis:

A
  1. In Crohn’s disease, any region of the GI tract can be affected, but most often it occurs in the small
    intestine, and sometimes it extends into the colon. In contrast, ulcerative colitis affects the colon and
    rectum only (colitis - limited to the colon). It begins in the rectum/ sigmoid colon, and extends proximally.
  2. The inflammation in Crohn’s Disease is transmural, it goes through the wall whereas in ulcerative colitis
    the inflammation is restricted to the mucosa/submucosa.
  3. In Crohn’s Disease, lesions occur in patches, with an area that is inflamed, a normal area, an inflamed
    area, a normal area and so on (“skip” lesions). In Ulcerative Colitis, the lesion is continuous.
  4. ULCERATIVE COLITIS CAN BE CURED BY SURGERY. You can live without your colon. There is NO CURE FOR CROHN’S DISEASE. You cannot live without the small intestine, and since Crohn’s Disease always involves the small intestine to some extent, you can’t cure it surgically. Also, in Crohn’s Disease the lesions occur in multiple locations, and if you remove one area, new lesions usually appear
    elsewhere. Treatment is symptomatic, mainly with a combination of drugs.
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28
Q

Features common to both Crohn’s disease and ulcerative colitis:

A
  1. They are BOTH CHRONIC, DEBILITATING DISEASES. Long-term inflammatory diseases of any type
    are difficult and stressful, particularly when incurable such as Crohn’s Disease. However, new
    medications can greatly reduce symptoms.
  2. The CAUSE IS MULTIFACTORIAL, and involves genetic predisposition, environmental triggers, and
    immune dysregulation. Changes in the microbiome are important, with bacterial, and possibly viral
    involvement. Many cell types are involved in the inflammatory process.
  3. The AGE DISTRIBUTION IS SIMILAR for both types of IBD. Often begins in adolescents and young
    adults, mainly between the ages of 10-30. There is a second smaller peak between 50-60.
  4. The techniques for DIAGNOSIS are similar: ENDOSCOPY, BIOPSY, BARIUM X-rays and the
    SYMPTOMS.
  5. BOTH MAY BE ASSOCIATED WITH NON-INTESTINAL SYMPTOMS, affecting the joints, the liver, and
    particularly the skin. Intestinal disorders are often accompanied by a variety of skin lesions.
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29
Q

symptoms of Crohn’s disease (and what do they depend on)

A

The symptoms mainly depend on: 1) the region of the intestine involved and 2) the severity of the
inflammation. About 1/3 of people have problems in the small intestine only. About 1/3 in the colon only.
The rest have mixed lesions in both locations.
Consequences of inflammation in the small intestin

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30
Q

characteristics of Crohn’s disease (where it occurs, pathology that occurs, …)

A
  • the inflammation extends throughout the entire wall of the intestine.
  • Granulomas and
    fistulas are common
  • Villous atrophy occurs in the small intestine, even in areas that are not obviously
    inflamed, leading to malabsorption
  • The ileum has a “cobblestone appearance” because of the ulcerations.
  • Skip lesions are common, with an ulcerated region, then a normal area and then lesions again
  • The
    ulcerations can cause regional enteritis, for example in the terminal ileum
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31
Q

Consequences of inflammation in the small intestine (in Crohn’s disease)

A

1) Intermittent abdominal pain. The pain may be due to partial obstruction of the intestine.
2) Inflammation and fever.
3) Fibrosis with thickening and rigidity of the wall and narrowing of the lumen, predisposing to obstruction.
4) Anemia - because of the mucosal erosion and the bleeding.
5) Weight loss - because of the malabsorption and also the loss of protein from the inflamed mucosa with
increased cell turnover.
6) Diarrhea - because of osmotically active ingredients in the intestine. The osmotic diarrhea causes
additional loss of nutrients due to rapid transit through the intestine.

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32
Q

Consequences of inflammation in the large intestine (Crohn’s)

A
  1. Abdominal pain and Diarrhea. -Major function of the large intestine is water absorption, impairment
    produces diarrhea.
  2. Bleeding, often with obvious blood in the stool.
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33
Q

course of Crohn’s disease

A

The course of Crohn’s disease is variable, and unpredictable. Patients may have bouts of severe difficulty
followed by years of feeling well, then intermittent, often severe symptoms

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34
Q

POSSIBLE COMPLICATIONS OF CROHN’S DISEASE:

A
  1. Hemorrhage
  2. Abscess
  3. Obstruction
  4. Fistula formation. Fistulas are abnormal communications between different areas, e.g. from the rectum to the skin or from a loop of small intestine to the large intestine.
  5. Perforation, causing peritonitis.
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35
Q

therapy for Crohn’s disease

A
  • The therapy depends on the circumstances.
  • Dietary supplements to try and counteract the malnutrition,
    anti-inflammatory drugs, and surgery for complications, such as a fistula, or obstruction.
  • A fistula to the
    bladder, for example, will cause infection which can spread to the kidney.
  • Many people with Crohn’s Disease require surgery to relieve the complications, but it will not cure the basic problem.
  • Newer drugs that target inflammatory cytokines are often very beneficial.
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36
Q

symptoms of ulcerative colitis

A

1) Abdominal pain
2) Diarrhea
3) Bleeding
4) Tenesmus (difficult or painful defecation)
5) Systemic symptoms: Severe cases are accompanied by fatigue, weight loss, and fever due to the
inflammatory process. There may also be involvement of other organs

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37
Q

what determines the severity of tenesmus in ulcerative colitis?

A

The severity is related to the extent of the lesions. The larger the area of colon involved, the more
severe will be the symptoms. In extensive ulcerative colitis, the entire mucosa may be missing in the colon
and only the deeper layers of the intestinal wall remain intact. This will produce a lot of bleeding, loss of
protein, and diarrhea, from loss of the absorptive capacity of the colon.

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38
Q

course of ulcerative colitis

A

Variable, only a small proportion of patients have involvement of the entire colon

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39
Q

Where is the inflammation confined in ulcerative colitis?

A

The inflammation is confined to the mucosa of the colon and the rectum, with ulceration in the mucosa.

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40
Q

What happens during acute inflammation in ulcerative colitis?

A

Acute inflammation may be accompanied by infection and abscesses. There are attempts at healing and granulation tissue is formed at the base of the ulcer.

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41
Q

What is the pattern of acute attacks in ulcerative colitis?

A

Acute attacks are usually interspersed with periods of relative relief (remission).

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42
Q

How do the lesions heal in ulcerative colitis?

A

The ulcerated lesions heal but not completely, and there is some scarring and loss of the mucosal folds and loss of some of the normal mucous secreting glands in the affected area.

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43
Q

Where do the lesions begin and how do they progress in ulcerative colitis?

A

The lesions begin in the rectum and sigmoid colon and tend to be continuous, in contrast to the skip lesions of Crohn’s disease.

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44
Q

What does an endoscopy reveal during acute attacks of ulcerative colitis?

A

Endoscopy during acute attacks will reveal a very inflamed area of intestine.

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45
Q

In what percentage of ulcerative colitis patients does the inflammation not progress beyond the sigmoid?

A

In about 60% of patients, the inflammation does not progress beyond the sigmoid, and symptoms may be fairly mild.

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46
Q

possible complications of ulcerative colitis

A

1) Hemorrhage
2) Perforation
3) Carcinoma. After about 10 years of Ulcerative Colitis, the risk of colorectal carcinoma starts to rise, in
proportion to the extent of the disease. However, the overall risk in now quite low, even after 30 years
with the disease.
4) Toxic dilatation of the colon with block of peristalsis resulting from damage to the neuromuscular control
mechanism. This is a serious complication and requires surgery

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47
Q

what is the treatment for ulcerative colitis?

A
  • Mild disease can often be successfully controlled with anti-inflammatory and anticytokine medication.
  • Severe disease involving most of the colon may require surgical removal. A surgical technique that is
    frequently used creates a direct ileo-anal junction forming a pouch of the small intestine at the anastomosis,
    so the person retains sphincter control and can have fairly normal bowel function
  • Previous techniques
    involve emptying the ileum through an opening in the abdominal wall (ileostomy). The small intestine
    compensates to some extent for the loss of the large intestine by increasing its ability to absorb fluids.
  • Removing the colon stops the pain, the bleeding, the weight loss, and the misery of the inflammatory
    disease, in addition to preventing cancer. So, there is a therapy that is effective and basically curative.
48
Q

what is the pathogenesis leading to ulcerative colitis?

A
  1. In a genetically susceptible individual, environmental factors (GI infections, smoking, dysbiosis…) impair the
    intestinal barrier
  2. Commensal bacteria and bacterial products enter the bowel wall and activate innate and
    adaptive responses in the mucosal immune system
  3. Cytokines released from a variety of cells further increase
    permeability and perpetuate a chronic cycle of inflammation with tissue injury and fibrosis
  4. Tumor Necrosis
    Factor (TNF) is responsible for many of the pathological changes and therapy with anti-TNF antibodies is very
    successful in many patients. Drugs targeting other inflammatory cytokines are currently being tested.
49
Q

what are symptoms of acute appendicitis?

A

abdominal pain and rigid abdomen

50
Q

What is Acute Appendicitis and where is it most common?

A

cute Appendicitis is a common surgical emergency associated with a low fiber diet. It’s very common in North America and rare in some other regions.

51
Q

What is the risk of Acute Appendicitis in young children and very old people?

A

In young children, appendicitis may not be correctly diagnosed because they cannot accurately describe the pain if they are not old enough to talk. Very old people, if debilitated by some other disease, may not survive the surgery.

52
Q

What is one cause of Acute Appendicitis?

A

One cause of appendicitis is fecal impaction with obstruction, leading to infection, inflammation, and ischemic necrosis. This can cause perforation followed by peritonitis.

53
Q

What happens when the appendix ruptures?

A

The appendix has ruptured in 3/4 of small children before surgery. Recovery from peritonitis takes longer and involves extensive use of antibiotics.

54
Q

What happens when there is no obvious physical obstruction in the appendix but the person has appendicitis?

A

In many cases, there is no obvious physical obstruction in the appendix, just generalized inflammation and infection and the cause is basically unknown.

55
Q

When is the normal appendix often removed?

A

When there is some other reason for abdominal surgery, the normal appendix is often removed prophylactically.

56
Q

what causes the rigid abdomen in appendicitis?

A

Sensory input from the intestine, when intense, triggers a reflex in the spinal cord that
stimulates abdominal muscle to contract. Appendicitis or any other type of acute abdominal inflammation often
produces strong contraction of the abdominal wall.

57
Q

What is the initial symptom in most people experiencing abdominal pain?

A

The initial symptom is a diffuse ache in the lower midline, around the umbilicus (visceral pain). This eventually becomes stronger and sharper and moves to another location (parietal pain).

58
Q

What are the sites of visceral, midline pain corresponding to the major abdominal organs?

A

the sites are as follows:
1. Upper abdomen: liver, stomach, duodenum
2. Umbilicus: jejunum; ileum, lower right colon
3. Lower abdomen: colon, uterus, bladder.

59
Q

What activates visceral pain and how is it interpreted by the brain?

A

Visceral pain is activated by stretch receptors following obstruction or distortion. It is felt in the midline because the fibers from these organs enter the spinal cord on both sides and the brain consequently interprets the pain as central, even though the impulses may originate in a very specific lateral area.

60
Q

What often accompanies visceral pain?

A

Visceral pain is often accompanied by autonomic effects such as sweating and nausea.

61
Q

What happens with appendicitis and how does it affect pain?

A

With appendicitis, eventually the inflammation spreads to the outer part of the wall of the appendix and irritates the parietal peritoneum. The resulting parietal pain is transmitted via somatic sensory nerves and is highly localized. It is intensified by moving.

62
Q

what is the treatment for appendicitis?

A

a combination of surgery and antibiotics, and intensive care if the appendix has
ruptured

63
Q

what is the prevention of appendicitis?

A

Appendicitis could be almost entirely prevented by an increase in dietary fiber in industrialized
countries.

64
Q

difference in impact of diarrhea in north America and other countries?

A

In North America, it is mostly an inconvenience but in other countries this is a major killer especially in
children; it kills millions of children every year, they can die very quickly.

65
Q

what are the inputs and outputs of fluid in the GI?

A
  • fluids in intestine are reabsorbed very efficiently
    9L/day entering GI tract and 98% is reabsorbed
    7L is secreted into GI tract
    2L is from food and drink
66
Q

what is the major cause of acute diarrhea (what percent) and what is it often accompanied by (what symptoms)?

A

Acute diarrhea is almost always due to microbial infections and is often accompanied by headache, fever,
anorexia and vomiting: 90% of the cases in North America are due to viral infections

67
Q

what are mechanisms that cause diarrhea?

A
  1. osmosis
  2. decrease absorption
  3. increase secretion
68
Q

how does osmosis cause diarrhea and what often causes this?

A
  • A non-absorbed solute will retain fluid within the
    intestine, thereby stimulating peristalsis.
  • Common problem is deficiency of lactase
    (enzyme found in the brush border of the
    intestine and breaks down lactose found in milk)
69
Q

what is the difference between primary and secondary lactase deficiency and how does it cause diarrhea?

A
  • In primary
    deficiency, the enzyme is gradually lost in later
    childhood (people with origins in Africa and Asia). Throughout evolution, humans could lose
    this enzyme because no one drank milk after early childhood. - Secondary deficiency can also
    occur due to damage to intestine during viral infections. This deficiency can last a couple of weeks.
  • lactose accumulates in the lumen of the
    intestine and by osmosis retains fluid and the increased volume in the intestine causes diarrhea.
70
Q

what can cause decreased absorption leading to diarrhea?

A
  • due to injury or destruction of intestinal epithelial cells by viral infections or other disease
  • villous atrophy: mucosal surface area is decreased which lowers the absorptive capacity
71
Q

what causes increased secretion leading to diarrhea?

A
  • bacteria may release enterotoxins that stimulate intestinal fluid secretion.
  • Two major bacteria
    producing enterotoxins are cholera and E. coli (traveller’s diarrhoea).
  • The enterotoxins bind to specific
    receptors on the epithelial cells and irreversibly activate enzymes producing cAMP.
  • This causes the cell to continuously secrete Cl, Na and H20 until it is shed and replaced.
  • Luckily there is a high turnover rate
    of intestinal epithelial cells, so we can recover rapidly with proper therapy.
72
Q

what is a misconception related to what causes diarrhea?

A

There is a misconception that diarrhoea is primarily due to increased motility of the intestine and this is
wrong. Diarrhea is due to one or more of the 3 mechanisms

73
Q

consequences of acute and chronic diarrhea?

A
  1. Severe fluid loss
    - 5-10% of body weight; not only water but electrolytes
    - drop in blood volume -> drop in blood pressure -> increase
    in heart rate (to try and compensate)-> shock (inadequate
    perfusion of tissues) -> kidney failure -> death
  2. Loss of potassium
    - leads to cardiac arrhythmias which can be fatal
  3. Metabolic acidosis
    - losing a lot of bicarbonate from the intestine
    - pH drops
    Chronic diarrhea will lead to malnutrition
74
Q

How is Cholera transmitted and where are the recent outbreaks?

A

Cholera is transmitted by ingesting water or food that is contaminated by faecal material. The current pandemic is due to a specific new bacterial strain that first appeared in South America in the early 1990’s. There have been recent epidemics in Africa and Haiti and in 2024, Africa has serious outbreaks.

75
Q

How does the cholera bacteria cause disease?

A

he motile bacteria burrow through the mucous layer, adhere to intestinal epithelial cells and release cholera toxin. The toxin binds to a receptor on the cell membrane which allows it to be endocytosed and the active unit of the toxin is released in the cytosol. It then permanently turns on cyclic AMP production which activates a chloride channel on the luminal surface of the epithelial cell. As the Cl is secreted, Na and H20 follow, causing severe watery diarrhea

76
Q

What is the mortality rate of Cholera with and without treatment?

A

Cholera kills very quickly, with a mortality rate of 60% without treatment and 1-2% with treatment.

77
Q

what is the treatment for cholera?

A
  • In underdeveloped countries, may not have adequate antibiotics or facilities for intravenous rehydration.
  • treat by increasing the absorption to balance the increased secretion. Absorption can be increased by
    drinking a solution of glucose and salt since intestinal absorption of glucose and sodium are coupled.
  • WHO
    provides an oral rehydration solution based on this concept. The person should drink a volume of this
    solution equal to the fluid being lost by the diarrhoea. It saves millions of lives as it is highly effective and
    inexpensive. An oral vaccine is now being used in areas where cholera is endemic.
78
Q

how is ACUTE VIRAL GASTROENTERITIS
spread?

A

Caused by contamination of objects, food, or the water supply by fecal matter.

79
Q

what virus can cause ACUTE VIRAL GASTROENTERITIS?

A

rotavirus

80
Q

What is Rotavirus and when is infection most common?

A

Rotavirus is a major cause of severe pediatric diarrhea. It is an RNA virus with many subgroups that can recombine. Infection is most common during early childhood from 6-24 months.

81
Q

How does Rotavirus infect cells?

A

Rotavirus attaches to and enters cells lining the intestinal villus by specific receptor attachment. The number of these receptors decreases with age.

82
Q

What mechanisms has Rotavirus evolved to overcome the host immune response?

A

Rotavirus has evolved multiple mechanisms to overcome the host immune response and the defence mechanisms of epithelial cells and the microbiome. A viral protein (non-structural protein 4) increases enterocyte secretion and disrupts tight junctions

83
Q

What are the symptoms of Rotavirus infection?

A

The virus causes injury and lysis of some enterocytes within 24 hours, with shedding of virus into the lumen, causing watery diarrhea, vomiting, fever and respiratory symptoms. Lactose intolerance can last for weeks afterwards.

84
Q

How common is Rotavirus diarrhea in Canada and how is it treated?

A

In Canada, 1 in 3 children under two years of age will have Rotavirus diarrhea each year. The virus is highly contagious and survives on objects for several days. Treatment involves rehydration.

85
Q

How are adults usually protected from Rotavirus?

A

Adults are usually protected by IgA, and fewer receptor sites for viral attachment.

86
Q

What is the impact of Rotavirus in underdeveloped countries and is there a vaccine available?

A

In underdeveloped countries, Rotavirus kills up to 1 million children per year, and they can die in 1 day. An effective and safe vaccine is now available and is used in Canada.

87
Q

what are the four major categories of food poisoning?

A
  1. norovirus
  2. salmonella
  3. Staphylococcus
  4. E. coli
88
Q

What is Norovirus and how does it spread?

A

Norovirus is responsible for mass outbreaks because it spreads quickly via water or food, and it is the most frequent cause of food poisoning. The source is other humans, the virus reproduces in intestinal epithelial cells, is shed in the stool, and infected food handlers can easily spread the pathogen.

89
Q

When and where are Norovirus outbreaks more likely to occur?

A

Norovirus outbreaks often occur after group activities, in institutions and on cruise ships, and are more frequent in winter.

90
Q

What are the symptoms of Norovirus and when do they begin?

A

Symptoms (diarrhea, nausea, vomiting, dehydration, anorexia, fever) begin 1 – 2 days after exposure and last for several days.

91
Q

Who does Norovirus attack and the symptoms resemble which other virus?

A

Norovirus attacks older children and adults, producing the same symptoms as rotavirus, but often less severe.

92
Q

What damage does Norovirus cause in the small intestine?

A

Norovirus causes villous injury in the small intestine and long-lasting disaccharidase damage (can’t break down lactose); milk intolerance can last 2-3 weeks.

93
Q

Why can infection with Norovirus occur many times?

A

There are multiple variants of the virus, and antigenic drift continually occurs; consequently, infection can occur many times

94
Q

How does Salmonella infect the intestine?

A

Salmonella targets epithelial cells of the intestine. The bacteria attach to surface epithelial cells and M cells with adhesins, then secrete virulence proteins into the host cytoplasm that allow them to be internalized and transported to the lamina propria where macrophages endocytose them into a vacule (SCV).

95
Q

What is Salmonella and who does it affect?

A

Salmonella is a bacterial infection that affects 1% of the population every year, causing severe diarrhea and nausea. It can be dangerous to young children, the elderly, and the immunosuppressed.

96
Q

What happens after Salmonella is endocytosed by macrophages?

A

The bacteria prevent lysosomal fusion with the vacule, allowing them to multiply and eventually destroy the macrophage and trigger an inflammatory response.

97
Q

What causes diarrhea in Salmonella infection?

A

Diarrhea is due to toxins released by the bacteria and cytokines released during inflammation that increase secretion and motility of the intestine.

98
Q

What is the usual source of Salmonella and how does it contaminate food?

A

Food is the usual source of this microbe, primarily animal sources, notably chicken. It is also present in eggs, milk, beef and even pet turtles, and can contaminate many types of food if the processing facility is inadequate.

99
Q

What are the symptoms of Salmonella infection and how long do they last?

A

symptoms are headache, nausea, vomiting, diarrhea and abdominal pain. They last for 2-3 days.

100
Q

hat can happen to immunocompromised patients with Salmonella infection?

A

Immunocompromised patients can develop septic shock and bacteremia.

101
Q

How is Salmonella infection treated?

A

The treatment involves drinking fluids, but antibiotics or anti-motility drugs should not be taken because they make the situation worse by damaging protective microflora and increasing the chance of bacteremia.

102
Q

What is Staphylococcus and how does it cause illness?

A

Staphylococcus is a non-motile organism that multiplies in contaminated food at room temperature and liberates a heat-resistant toxin. Ingestion of the preformed toxin causes subsequent illness.

103
Q

How can Staphylococcus be prevented from growing and forming toxins?

A

Refrigeration prevents staphylococcal growth and toxin formation.

104
Q

What is usually the source of Staphylococcus contamination?

A

The source of contamination is usually improper food handling by another human. Staphylococci are frequent residents in the nasopharynx and skin.

105
Q

What types of food are excellent growth media for Staphylococcus?

A

Meat, including salted meats, and foods containing mayonnaise are excellent growth media for Staphylococcus.

106
Q

When and where are Staphylococcus outbreaks more likely to occur?

A

Summer picnics and prolonged buffets are the perfect environment for Staphylococcus outbreaks.

107
Q

What are the symptoms of Staphylococcus infection and when do they begin?

A

Symptoms include rapid (few hours) onset of severe diarrhea, pain, and vomiting caused by the toxin acting on the intestine and on the CNS.

108
Q

Who does Staphylococcus affect?

A

Staphylococcus will affect everyone, in contrast to other types of food poisoning where effects are produced by a live microorganism and susceptibility is more variable.

109
Q

How is Staphylococcus infection treated?

A

Treatment for Staphylococcus infection is purely supportive, involving fluids. Recovery is usually rapid.

110
Q

What is Enterotoxigenic E. Coli and how is it transmitted?

A

Enterotoxigenic E. Coli causes Travellers’ Diarrhea and local infections via contaminated food. It is transmitted through fecal-oral transmission of pathogenic intestinal flora, often through contaminated water.

111
Q

What are the sources and symptoms of Enterotoxigenic E. Coli infection?

A

The sources include water, all raw foods, ice, and restaurants in underdeveloped countries. Symptoms include diarrhea, fatigue, fever, cramps, anorexia, nausea, vomiting, and can last 3-4 days and be severe.

112
Q

What is the mechanism of Enterotoxigenic E. Coli infection and how is it treated?

A

Enterotoxigenic E. Coli colonize the small intestine, then liberate a toxin (similar to cholera toxin in action) which causes increased secretion of fluid and electrolytes. Therapy involves oral rehydration solution, antibiotics, and codeine for severe cases

113
Q

What is Enteropathogenic E. Coli and what does it cause?

A

enteropathogenic strains of E. Coli cause infantile diarrhea. They bind to epithelial cells and damage microvilli.

114
Q

What is Enterohemorrhagic E. Coli and what does it produce?

A

Enterohemorrhagic strain - E coli 0157- is cytotoxic, produces Shiga toxins that cross the intestinal epithelium and reach the intestinal vasculature, where they target the vascular endothelial cells and block protein synthesis.

115
Q

What are the effects of the Shiga toxins produced by Enterohemorrhagic E. Coli?

A

The Shiga toxins kill the cells and trigger coagulation and microthrombi, causing tissue necrosis. The bacteria also directly damage intestinal epithelial cells, causing diarrhea, along with the hemorrhage and ulceration. The toxin also damages the kidney; infection can be fatal.

116
Q

what is the main source of Enterohemorrhagic E. Coli?

A

Animals are a main source of the
microbe and contaminated beef has been a problem in North America, but almost all types of foods can be
involved through contaminated water.

PATH 300 (9 decks)

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