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Pathology > Chaptr 17 Part 2 > Flashcards

Chaptr 17 Part 2 Flashcards

1
Q

Symptoms and signs of general obstruction of the small intestine and colon

A

Abdominal distention, vomiting, pain, constipation, tympanic by percussion

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2
Q

What causes 80% of SI and colon obstruction

A

Hernias, adhesions, intussusceptions, and volvulus

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3
Q

What causes 10-15% of SI and colon obstruction

A

Tumors, infarction, and other causes of structures

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4
Q

Hernias

A

Protrusion of a serosa lined pouch of peritoneum that can trap bowel segments externally, usually small bowel

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5
Q

What is the most frequent cause of intestinal obstruction worldwide and 3rd most common USA

A

Hernia

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6
Q

Acquired hernia

A

Occur anteriorly via inguinal and femoral canals, umbilicus or surgical scars
(External herniation)

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7
Q

Incarceration hernia

A

Permanent entrapment due to venous stasis+edema

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8
Q

Hernia strangulation

A

Due to arterial and venous compromise due to pressure at the neck of the pouch

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9
Q

Infarction and hernia

A

Sure

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10
Q

What is the most common cause of obstruction in USA

A

Adhesions

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11
Q

What is an adhesion

A

Localized inflammation due to surgery, trauma, infection, endometriosis or radiation;rarely congenital

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12
Q

How does adhesion form

A

Healing of inflammation-leads to fibrous bridges creating closed loop through which viscera may slide and become entrapped -internal herniation

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13
Q

Obstruction and strangulation from adhesion

A

Yup as viscera slide and become trapped

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14
Q

Volvulus

A

Complete twisting of a bowel loop about its mesenteric vascular base

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15
Q

What happens when volvulus compromise vascular and luminal

A

Infarction and obstruction

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16
Q

Where is volvulus most common

A

In redundant loops of sigmoid colon

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17
Q

What is the biggest concern with colculus

A

Can lead to toxic megacolon

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18
Q

Intussusception

A

Intestinal segment telescopes into the immediately distal segment

Peristalsis propels th invaginated segment with its attached mesentery

Obstruction, vessel compression and infarction

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19
Q

Intussusception is the most common cause of what

A

Intestinal obstruction in children <2 yrs

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20
Q

Causes of intussusception in young kids

A

Spontaneous or associated with viral infection, rotavirus vaccine
-get reactive hyperplasia of peyer patches and other lymphoid tissue acting as a leading edge

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21
Q

Intussusception older children

A

Due to intraluminal mass or tumor

-surgical intervention is necessary

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22
Q

Diagnosis intussusception

A

Via contrast enemas

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23
Q

Treat intussusception children

A

Contrast enema, air enema

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24
Q

Treat intussusception older

A

Surgery

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25
Q

Ischemic bowel disease

A

Collateral blood supple allows slow, progressive loss of blood supply to be tolerated

Abrupt compromise of a vessel leads to infarction of several meters of intestine

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26
Q

What areas are at risk for ischemic bowel disease

A

Mucosal infarction to transmural

Watershed zones=most vulnerable

Epithelial cells at tips of villi(bc end of capillary network)

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27
Q

What are watershed regions of bowel

A

Splenic flexure

Sigmoid colon and rectum

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28
Q

Splenic flexure

A

Between superior and inferior mesenteric arteries

Marginal artery of Drummond

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29
Q

Sigmoid colon and rectum

A

Where inferior mesenteric, pudendal and iliac arterial circulations end

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30
Q

Acute causes of ischemic bowel disease-vascular etiology

A

Severe atherosclerosis (at origin of mesenteric vessels)

AAA

Hypercoagulatioble states
Embolization due to cardiac vegetation’s or aortic atheromas

Hypoperfusion due to cardiac failure, shock, dehydration or wegener granulomatosis

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31
Q

Morphology ischemic bowel disease

A

Patchy

Mucosa is hemorrhagic and ulcerated

Bowel wall is thickened with edema

Transmural infarction: large portions of bowel are affected and there is a sharp line between infarct and healthy tissue

Coagulation necrosis: 1-4 DAYS AFTER, MAY LEAD TO PERFORATION, SEROSTITIS WITH PURLUENT EXUDATES AND FIBRIN DEPOSIT

Epithelial surface sloughs off(CHARACTERISTIC), HYPERPROLIFERATION IN CRYPTS

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32
Q

Chronic ischemic bowel disease

A

Fibrous scarring of lamina propria

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33
Q

Who gets ischemic bowel disease

A

70 or older

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34
Q

Ischemic bowel disease

Can be caused by cocaine (___)or from CMV/E-coli (O157-H7) or trauma (___)

A

Vasoconstrictor use

Epithelial damage

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35
Q

Prognosis ischemic bowel disease

A

Unlikely fatal

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36
Q

Presentation of ischemic bowel disease

A

Acute: sudden onset of cramping, LLQ pain, desire to defecate, passage of blood or bloody diarrhea

Progresses to school and vascular collapse in hours if severe

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37
Q

Prognosis infarct ischemic bowel disease

A

10% of transmural infarct die first 30 days

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38
Q

Death fro ischemic bowel disease in doubled in who

A

Patients with right sided colonic disease

-right side of colon is supplied by superior mesenteric artery, which also supplies small intestine

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39
Q

Worse prognosis ischemic bowel disease

A

COPD or signs and symptoms lasting longer than 2 weeks

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40
Q

Does ischemic bowel disease recur

A

No

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41
Q

Treatment ischemic bowel disease

A

Surgery if bowel sounds are absent (paralytic ileus) or if guarding, rebound develop

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42
Q

Chronic ischemia

A

Can masquerade IBD

Episodes of bloody diarrhea interspersed with periods of healing

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43
Q

__ infection causes ischemic GI disease due to viral tropism for endothelial cells

A

CMV

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44
Q

Radiation enterocolitis and ischemic bowel disease

A

Epithelial damage+vascular injury

Radiation fibroblasts in stroma

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45
Q

Acute radiation enterocolitis: ischemic bowel disease

A

Anorexia, abdominal cramps, malabsorption diarrhea

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46
Q

Chronic radiation enterocolitis ischemic bowel disease

A

More indolent, may present as inflammatory enterocolitis

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47
Q

Ischemic bowel disease : necrotizing enterocolitis

A

Most common acquired GI emergency of neonate*

Prematureinfants or low birth weight babies are at high risk

Present when oral feeding is initiated

Acute disorder ofsmall and large intestines leading to transmural necrosis

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48
Q

Angiodysplasia

A

Malformed tortuous, ectatic dilation of veins, venues and capillaries in mucosa and submucosa

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49
Q

Where is angiodysplasia most common

A

In cecum or ascending colon

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50
Q

What percent of adult population patients older than 60 have angiodysplasia

A

1%

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51
Q

Angiodysplasia causes _% of major lower GI bleeds

A

20

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52
Q

Morphology angiodysplasia

A

Only vascular wall and a layer of attenuated epithelial cells separate vascular channels from the intestinal lumen, limited injury=significant bleeding

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53
Q

Diagnose angiodysplasia

A

Diagnosis of exclusion

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54
Q

Malabsorption

A

Defective absorption of fats, proteins, carbohydrates, electrolytes, minerals, water, and vitamin (fat and water soluble)

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55
Q

Presentation of malabsorption

A

Chronic diarrhea

Hallmark=steatorrhea*

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56
Q

Accompanying symptoms malabsorption

A

Weight loss, anorexia, abdominal distention, borborygmi(gurgling), muscle wasting

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57
Q

More common causes malabsorption

A

Pancreatic insuffiency, celiac disease, Crohn’s disease and intestinal GVHD following allogenic hematopoietic stem cell transplantation

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58
Q

What are the 4 processes of nutrient absorption

A

Interruption of intraluminal digestion

Terminal digestion

Transepithelial transport

Lymphatic transport of absorbed lipids

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59
Q

Interruption of intraluminal digestion

A

Emulsification and break down of nutrients into absorbable forms

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60
Q

Terminal digestion

A

Hydrolysis of carbs and proteins in enterocyte brush border

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61
Q

Transepithelial transport

A

Nutrients, fluid, electrolytes transported across and processed in the small intestinal epithelium

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62
Q

Consequences of malabsorption

A

Anemia, mucositis

Pyridoxine (B6) folate, b12 defiency

Bleeding

Vitamin k defiency

Osteopenia and tetany

Ca, mg or vit d defiency

Endocrine or skin disturbances

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63
Q

What are main categories of diarrhea

A

Secretory

Osmotic

Malabsorptive

Exudative

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64
Q

Secretory diarrhea

A

Isotonic (to plasma) stool

Persists during fasting

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65
Q

Osmotic diarrhea

A

Due to excessive osmotic forces exerted by unabsorbed luminal solutes

Fluid is >50 mosm more concentrated than plasma
Seen with lactase defiency

Abates with fasting

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66
Q

Malabsorptive diarrhea

A

Generalized failure of nutrient absorption

Associated with steatorrhea

Relieved by fasting

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67
Q

Exudative diarrhea

A

Due to inflammatory disease

Purple NT, bloody stools

Persists during fasting

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68
Q

What aer the 2 diseases that only have issues with intraluminal digestion

A

Chronic pancreatitis

Cystic fibrosis (->pancreatitis)

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69
Q

What is the diseases that only has a problem with terminal digestion

A

Disaccharidase defiency

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70
Q

What is the only disease that only has a problem with the lymphatic transport

A

Whipple disease

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71
Q

What is the only disease that only has a problem with transepithelial transport

A

Abetalipoproteinemia

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72
Q

Cystic fibrosis

A

Formation of pancreatic intraductal concretions leads to duct obstruction, low grease chronic autodigestion of pancreas, and exocrine pancreatic insuffiency

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73
Q

Absorption and CF

A

Failure of intraluminal nutrient absorption

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74
Q

Treat absorption i CF

A

Supplemental oral enzymes

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75
Q

Genes cf

A

CFTR absence

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76
Q

Celiac disease

A

Celiac sprue

Immune mediated diarrheal disorder due to ingestion of gluten-containing foods
Wheat, rye, barley

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77
Q

Genetics celiac disease

A

Class II HLADQ2, HLAD!8

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78
Q

Gluten and celiac disease

A

Usually broken down by brush borer into a-gliadin (alcohol soluble fraction): disease producing component. Resistant to degradation by protease

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79
Q

Gliadin induced damage

A

Il15 activation of cd8 lymphocytes that express NKGD2 which attack MIC-A on enterocytes (apoptosis) leading to enhanced gliadin transport into cells

Deamination by transglutaminase

De-aminated peptide bind MHC of susceptible patients (specific HLA) activating CD4 cells and leads to more tissue damage

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80
Q

Where is celiac disease anatomically

A

2nd part of the duodenum to the proximal jejunum

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81
Q

Villi in celiac disease

A

Diffusely flattened(atrophic)

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82
Q

Crypts celiac disease

A

Elongated regenerative crypts associated with intraepithelial CD8 T cells

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83
Q

Villa us atrophy celiac

A

Loss of mucosal and brush border surface

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84
Q

Lamina propria celiac

A

Exuberant lamina propria chronic inflammation

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85
Q

How diagnose celiac disease

A

Biopsy of second part of duodenum or proximal jejunum increased numbers of CD8 T cells, crypt hyperplasia and villous atrophy

Increase in the number of intraepithelial lymphocytes, particularly within the villus, is a sensitive marker of celiac disease, even in the absence of epithelial damage and villous atrophy

Lymphocytosis and villous atrophy are not specific; may be present in viral enteritis

Need histology and serology

IgA antibodies to tissue transglutimnase or anti endomysial

May also be detected in IgA defiency

HLADQ2/8 absence is highly predictive ; presence is not diagnostic

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86
Q

Dermatitis hepetiformis is found in 10% of celiac

A

Micro abscess: papillae

Subepidermal-blister

Granular IgA deposits

Extremely pruritis small vesicles

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87
Q

Why get dermatitis herpetiformic with celiac

A

Anti-gluten antibodies cross reacting with BM proteins

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88
Q

Adult celiac disease

A

30-60
Can be clinically silent or symptomatic

Chronic diarrhea, bloating, chronic fatigue, anemia (iron and vitamin malabsorption)

Dermatitis herpetiformis: itchy, blistering skin lesion(10%)

Females 2:1 may be due to monthly menstrual bleeding impairing absorption

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89
Q

Pediatric celiac disease classic

A

6-24 months

-irritability, abdominal distention, anorexia, chronic diarrhea, failure to thrive, weight loss, msucle wasting

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90
Q

Pediatric celiac non classic

A

Later onset
Abdominal pain, nausea, vomiting, bloating, constipation, arthritis, aphthous stomatitis, iron deficient anemia, deflated puberty, short

No gender preference

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91
Q

Treat celiac

A

Gluten free

Decrease risk of long term complications: anemia, female infertility, osteoporosis, and cancer

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92
Q

Considerations is symptoms return

A

Adhering to diet

Development of enteropathy associated T cell lymphoma or small intestine adenocarcinoma

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93
Q

Environmental enteropathy/tropical sprue

A

Prevelance in areas and populations with poor sanitation and hygiene

Distal bowel is most severely affected (young)

Malabsorption, malnutrition, stunted growth, and defective intestinal mucosal immune function

Defective intestinal barrier function, chronic exposure to fecal pathogens, and othe microbial contaminants and repeated bouts of diarrhea within the first 2-3 years of life are likely involved

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94
Q

Environmental enteropathy and oral antibiotics or nutritional supplementation

A

Not correlated

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95
Q

Environmental enteropathy cognitive

A

Associated uncorrectable cognitive effects

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96
Q

Autoimmune enteropathy

A

Severe, persistent diarrhea and autoimmune disease affecting young kids

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97
Q

IPEX

A

Immune dysregulaion, polyendocrinopathy, enteropathy, X linked

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98
Q

IPEX genetic

A

FOXP3 mutation=defective CD4

Treg cells

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99
Q

In autoimmune enteropathy, what are there autoantibodies to

A

Enterocyte and goblet cells

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100
Q

What else do we see with autoimmune enteropathy

A

Neutrophils and intraepithelial lymphocytes

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101
Q

Treatment autoimmune enteropathy

A

Immunosuppression (cyclosporine) and HSC transplant in rare cases

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102
Q

Lactase defiency

A

Enzyme located in brush borer of villus absorptive epithelial cells

Biopsy is unremarkable bc the defect is biochemical

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103
Q

Congenital lactase defiency

A

Explosive diarrhea with water, frothy stools and abdominal distention following dairy ingestion

Rare AR mutation in lactase gene

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104
Q

Acquired lactase defiency

A

Abdominal fullness, diarrhea, flatulence, following ingestion of lactose products

Due to fermentation of unabsorbed surgery by colonic bacteria

Downregulation of lactase gene expression often following a viral or bacterial infection

May resolve over time

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105
Q

Who gets acquired lactase defiency

A

Common in Native American, african American, and Chinese populations

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106
Q

Abetalipoproteinemia

A

Inability to secrete triglyceride rich lipoproteins

AR mutation of microcomal triglyceride transfer protein (MTP) that presents in infancy

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107
Q

What happens when u don’t have TMP

A

Enterocyte cant assemble or export lipoproteins —>intracellular lipid accumulations

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108
Q

Pathogenesis abetalipoproteinemia

A

Microsomal TG transfer protein normally transfers lipids to rough ER, promoting TG production

Complete absence of all plasma lipoproteins containing APO B (though gene is not affected)=inability to assemble and export lipoproteins causing intracellular accumulation

Vacuolization of intestinal epithelial cells seen with oil red-O stain, espicially after fatty meal

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109
Q

Clinical abetalipoprotenemia

A

Failure to thrive, diarrhea, steatorrhea

Acanthocytic red cells (burr cells) in peripheral blood smears due to inability to absorb essential FA

Defiency of fat soluble vitamins ADEK

Lipid membrane defects

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110
Q

Infectious enterocolitis symptoms

A

Diarrhea, abdominal pain, urgency, perinatal discomfort, incontinence, hemorrhage

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111
Q

What causes 10% of all death in children <5 worldwide

A

Infectious entercolitis

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112
Q

Infectious entercolitis: enteric viruses commonly cause pediatric infectious diarrhea leading to what

A

Severe dehydration and metabolic acidosis

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113
Q

Vibrio cholera

A

Comma-shaped

Gram -ve

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114
Q

Epidemiology vibrio cholera

A

Endemic to Ganges valley (India) and Bangladesh

Seasonal variation , rapid growth in warm temperatures

Primarily transmitted in contaminated drinking H2O (fecal-oral)

Rampant in areas of natural disasters where supplies may be compromised

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115
Q

Clinical vibrio cholera symptoms

A

Most asymptomatic or mild diarrhea

Severe-rice water diarrhea fishy odor

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116
Q

Incubation period vibrio cholera

A

1-5 days

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117
Q

Severe vibrio cholera

A

Dehydration, hypotension, muscle cramping, anuria, shock, loss of consciousness, and death in 24 hours

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118
Q

Treat vibrio cholera

A

Oral rehydration=99% success

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119
Q

If don’t treat vibrio cholera

A

50% mortality

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120
Q

Campylobacter enterocolitis cause

A

Campylobacter jejuni

Improperly cooked chicken, unpasteurized milk, or contaminated water

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121
Q

What is the most common bacterial enteric pathogen in developed countries

A

Campylobacter

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122
Q

Travels diarrhea and food poisoning

A

Campylobacter enterocolitis

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123
Q

Campylobacter

A

Gram -, comma shaped, flagellated

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124
Q

Morphology campylobacter enterocolitis

A

Neutrophils in the submucosa and cryptos may cause crypt abscess

Crypt architecture is preserved

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125
Q

Sequelae campylobacter

A

HLAB27=reactive arthritis

Erythema nodosum

Guillain-Barré syndrome-ascending flaccid paralysis due to immune mediated inflammation of peripheral nerves due to molecular mimicry due to LOPS cross reactivity

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126
Q

Clinical campylobacter

A

Acute watery diarrhea or may follow influenza-like prodrome

Dysentery in 15% adults, 50% kids

Only 500 organisms necessary for NF1 toon

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127
Q

Incubation campylobacter

A

8 days

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128
Q

How long after campylobacter enterocolitis do u shed bacteria

A

1 month after resolution

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129
Q

Diagnosis campylobacter enterocolitis

A

Stool culture

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130
Q

Treatment campylobacter

A

Antibiotics are not usually necessary

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131
Q

Shigella

A

Non encapsulated, non motile, facultative anaerobe

Closely related to the enteroinvasive strain of E. coli

Resistant to acidic environment of stomach-> low infective dose

Taken up by M cells in the intestine

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132
Q

What is the most common cause of bloody diarrhea

A

Shigella

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133
Q

How get shigella

A

Fecal oral transmission or contaminated food.water

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134
Q

Kids and shigella USA

A

Children in daycare, migrant workers, travelers to developing countries, nursing home population

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135
Q

Virluence of shigella

A

Infective dose,several hundred organisms

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136
Q

Who dies rom shigella

A

Kids <5

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137
Q

Shigella is responsible for _% of all pediatric deaths and _% of all diarrheal deaths

A

10

75

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138
Q

Morphology shigella

A

Most common in the left colon

Hemorrhagic and ulcerated mucosa

Often with pseudomembranes

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139
Q

Incubation shigella

A

1 week

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140
Q

Treat shigella

A

Self limited diarrhea, fever, abdominal pain

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141
Q

Dysenteric phase shigella

A

50%, up to a month

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142
Q

Subacute shigella phase

A

Patients have waxing and waning diarrhea

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143
Q

Children shigella

A

Shorter duration, more severe

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144
Q

Complication triad of shigella

A

Sterile reactivation arthritis, urethritis, conjunctivitis in HLAB27 + males 20-40

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145
Q

Shigella serotype 1 complication

A

Leads to toxin causing hemolytic uremic syndrome

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146
Q

Complication shigella

A

Toxic megacolon and intestinal obstruction are uncommon

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147
Q

Diagnosis shigella

A

Confirm via stool culture

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148
Q

Treat shigella

A

Antibiotics shorten duration of signs and symptoms

Anti diarrheal medications are CONTRAINDICATED because they delay clearance

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149
Q

Salmonella enteritidis

A

Gram - bacillus

Member of the enterobacteriaceae family

-TLR=LPS
TLR5=flagellin

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150
Q

Who is at risk for salmonella

A

Small$ necessary, even less in patients on acid suppression therapy

Incidence peaks in summer and fall

Commonly in young children and older adults

Food poisoning due to ingestion of contaminated food (raw/undercooked meat, poultry, eggs milk)

Large outbreaks in centralized food processing

TH17 genetic defect=increased susceptibility

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151
Q

Vaccination salmonella

A

Got human and farm animals

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152
Q

Clinical salmonella

A

Signs and symptoms similar to other enteric pathogens

Range from loose stool to profuse diarrhea to dysentery

Stool cultures essential for diagnosis

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153
Q

Complications salmonella

A

Severe illness more likely in patients with malignancy, immunosuppression, alcoholism, CV, dysfunction, sickle cell disease, and hemolytic anemia

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154
Q

Diagnose salmonella

A

Stool

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155
Q

Treat salmonella enteritidis

A

Most infections are self limited and last 1 week

Antibiotics are not recommended, prolong airier state, no effect on duration fo diarrhea

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156
Q

Typhoid fever (enteric fever)

A

Salmonella enterica (typhi and paratyphi)

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157
Q

Endemic areas typhoid fever-who gets it

A

(Typhi) Children and adolescents most affected

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158
Q

Developed counties-who gets typhoid fever

A

No age preference

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159
Q

Typhoid fever associated with

A

Travel (paratyphi0: India, Mexico, Philippines, Pakistan, El Salvador, haiti

-travelers most likely to be vaccinated

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160
Q

Transmission typhoid fever

A

Transmitted human human or via food/contaminated H2O

Taken up by M cells

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161
Q

Morphology typhoid fever

A

Infection causes plateau-like elevations of Peters patches in terminal ileum

Enlargement of draining mesenteric lymph nodes

Acute and chronic inflammatory cell recruitment to the lamina proporia leads to necrotic debris’s and overlying mucosal ulcers that orient along the axis of the ileum (may perforate)

Spleen is enlarged and soft with uniform pale red pulp and obliterated follicular markings

Typhoid nodules: focal hepatocyte necrosis int he liver with macrophage aggregates

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162
Q

Typhoid fever symptoms

A

Anorexia, abdominal pain, bloating, nausea, vomiting, bloody diarrhea

Followed by asymptomatic phase that leads to bacteremia and fever with flu like symptoms

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163
Q

90% of typhoid fever patients have + blood cultures during __ phase

A

Febrile

-antibiotics can prevent further disease progression

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164
Q

Gallbladder typhoid fever

A

Colonization can be associated with gallstones and the chronic carrier state

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165
Q

Rose spots typhoid fever

A

Small erythematous maculopapular lesion on chest and abdomen

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166
Q

Typhoid fever extra intestinal

A

Osteomyelitis (espicially in sickle cell), encephalopathy, meningitis, seizures, endocarditis, myocarditis, pneumonia, cholecystitis

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167
Q

Treat typhoid fever

A

Antibiotics to prevent progression

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168
Q

What is no antibiotics with typhoid fever

A

Initial febrile phase lasts 2 weeks have sustained high fever and abdominal tenderness mimicking appendicitis

Symptoms abate after several weeks in surviving patients

Can get relapse

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169
Q

How get yer Sinai enterocolitica

A

Ingestion of pork, raw milk and contaminated H2O

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170
Q

Yersinia enterocolitica mimics appendicitis?

A

Tropism for ileum, appendix and right colon

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171
Q

In yersinia enterocolitica where do organisms proliferate

A

Extracellularly in lymphoid tissue leading to lymph node and peyer patch hyperplasia

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172
Q

Morphology yersinia enterocolitica-mimic crohns

A

Bowel was thicking

Overlying mucosa can become hemorrhagic and ulcerated with neutrophilic infiltrates and granulomas

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173
Q

Yersinia enterocolitica clinical

A

Abdominal pain +/- fever, diarrhea, nausea, vomiting

Teens/young adults: mimic appendicitis

Younger children: enteritis and colitis predominate

Extra-intestinal: pharyngitis, arthralgia, erythema nodosum

Lymph node or blood cultures may be +

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174
Q

How detect yersinia enterocolitica

A

Stool

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175
Q

Iron enhances yersinia enterocolitica virluence

A

Stimulates systemic dissemination
-individuals with increased non heme iron (chronic forms of anemia o hemochromatosis) are at increased risk to develop sepsis and die

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176
Q

Post infectious complications yersinia enterocolitica

A

Reactive arthritis, urethritis, conjunctivitis, myocarditis, erythema nodosum, and kidney disease

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177
Q

E. coli

A

Gram - bacilli that colonize healthy GI tract

Most onpathogenic

Some can cause human disease

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178
Q

Anterotoxigenic E. coli

A

Travelers diarrhea (could also be campylobacter)

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179
Q

Symptoms diarrhea with enterotoxigenic E. coli

A

Secretory, non inflammatory diarhea, dehydration and if severe, shock

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180
Q

How does enterotoxigenic E. coli spread

A

Contaminated food or water

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181
Q

Who is particularly susceptible to enterotoxigenic E. coli

A

Children less than 2

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182
Q

What does enterotoxigenic E. coli cause

A

Cl and H2O secretion and inhibit absorption

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183
Q

Enterotoxigenic E. coli heat label toxin

A

Similar to cholera toxin

Activates AC=increased cAMP, increased Cl secretion

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184
Q

Enterotoxigenic E. coli heat stable toxin

A

Increased cGMP

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185
Q

Enteropathy E. coli

A

Causes endemic diarrhea and diarrheal outbreaks in patients less than 2 years old

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186
Q

Enteropathy E. coli Tir

A

A receptor for intimin allows detection and diagnosis of infection by EPEC

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187
Q

Enteropathy E. coli produce attaching and effacing lesions

A

In which bacteria attach tightly to the enterocyte apical membranes and cause local loss (effacement of the microvilli)
-proteins (Tir) necessary for creating A/E lesions are all encoded in the locus of enterocyte effacement (LEE) which is also present in many EHEC strains

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188
Q

In enteropathy E. coli, bacteria attach to enterocyte __ membrane, cause local loss of microvilli (effacement)

A

Apical

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189
Q

Tir and other proteins are necessary for what (enteropathy E. coli)

A

Creating A/E lesions all encoded int he locus of enterocyte effacement which is also present in many ehec strains

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190
Q

When enteropathy E. coli attach to enterocyte apical membrane, what happens

A

Cause loss of microvilli (effacement)

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191
Q

Do enteropathy E. coli produce shiga toxin

A

NO

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192
Q

Enterohemorrhagic E. coli

A

O157:H7 and non-O157:H7

From consumption of undercooked need (cows are reservoir), milk and vegetables

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193
Q

Do enterohemorrhagic E. coli produce shiga like toxins

A

Yup and clinically resemble shigella dysenteriae

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194
Q

O157:H7

A

More likely to produce outbreaks, bloody diarrhea, hemolytic uremic syndrome (HUS) and ischemic colitis

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195
Q

Why are antibiotics contraindicated in patients with enterohemorrhagic E. coli

A

Killing bacteria increases the amount of toxin released and enhances HUS
Espicially in kids

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196
Q

Enteroinvasive E. coli

A

Do not produce toxins

Invade epithelial cells causing nonspecific, acute self limited colitis

Transmitted via food, water or human contact

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197
Q

Where is enteroinvasive E. coli most common

A

Infects young children in developing countries

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198
Q

Enteroaggregative E. coli

A

Can also cause travelers diarrhea

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199
Q

Describe enteroaggregative E. coli diarrhea

A

Non bloody diarrhea that is prolonged in AIDS patients

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200
Q

How does enteroaggregative E. coli cause diarrhea

A

Attach to epithelial via fimbriae and are aided by dispersion, bacterial protein which neutralizes the - surface of LPS

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201
Q

Enteroaggregative E. coli and shiga

A

Do make shiga like toxin but causes minimal histologic damage

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202
Q

Enteroaggregative E. coli characteristic

A

Adherence lesions only visible with electron microscope

203
Q

Pseudomembranous collitis

A

Caused by overgrowth of clostridium difficult due to antibiotic use

Formation of adherent inflammatory pseudomembranes overlying sites of mucosal injury

Also due to immunosuppression

204
Q

Describe the pseudomembrane

A

Made up of an adherent layer of inflammatory cells and debris at sites of colonic mucosal injury

205
Q

Are pseudomembranes specific for pseudomembranous colitis

A

No may occur with ischemia of necrotizing infections

206
Q

Morphology pseudomembranous colitis

A

Surface epithelial is denuded and the lamina propria contains a dense infiltrate of neutrophils and occasional fibrin thrombi within capillaries

207
Q

Damaged crypts pseudomembranous colitis

A

Distended by a mucopurluent exudate that form an eruption like a volcano that leads to the formation of the membrane
-histology is pathognomonic

208
Q

Risk factors pseudomembranous colitis

A

Advanced age, hospitalization and antibiotic use

209
Q

Clinical presentation pseudomembranous colitis

A

Fever, leukocytes, abdominal pain, cramps, watery diarrhea, dehydration

But most are asymptomatic

Peripheral edema
Fecal leukocytes and occult blood , but grossly bloody diarrhea uncommon

210
Q

Pseudomembranous colitis why peripheral edema

A

Protein loss leads to hypoalbuminemia

211
Q

Diagnosis pseudomembranous colitis

A

Detect toxin in stool

212
Q

Treat pseudomembranous colitis

A

Metronidazole, oral vancomycin (stays in GIT, is not absorbed)

213
Q

Recurrence in up to _% of patients with pseudomembranous colitis

A

40

214
Q

Whipple disease

A

Rare, systemic condition due to actinomycete tropheryma whippelii

Accumulation of organism laden macrophages accumulate in laminae propria of small intestine and in mesenteric lymph nodes leading to lymphatic obstruction

215
Q

Who gest whipple disease

A

Caucasian males (farmers, occupational exposure)

216
Q

Characteristics of whipple

A

Gram+ bacillus

217
Q

Who gest whipple disease

A

Caucasian males, particularly farmers and others with occupational exposure to soil or animals

218
Q

Morphology whipple disease

A

Dense accumulation of distended foamy macrophages in small intestine lamina propria

Stuffed with PAS positive bacteria in lysosomes

Also seen in lymphatics, lymph nodes, synovial membranes of joints, cardiac valves, and brain

Marked villous expansion in small intestine

Lymphatic dilation and mucosal lipid deposition lead to shaggy white yellow mucosal plaques

219
Q

Triad of whipple disease

A

Diarrhea, weight loss, arthralgia

220
Q

Why get malabsorptive diarrhea with whipple disease

A

Impaired lymphatic transport

221
Q

Complications of whipple disease

A

Malabsorption, arthritis, fever, LAD, neurological, cardiovascular, or pulmonary disease

222
Q

What causes 1/2 of all gastroenteritis outbreaks worldwide, is a common cause of sporadic gastroenteritis in developed nations, most common cause of acute gastroenteritis requiring medical attention, and 2nd most common cause of severe diarrhea in infants and young kids

A

Norovirus

223
Q

Cruise ship virus

A

Norovirus

224
Q

What is the most common virus causing diarrhea in kids and infants

A

Rotavirus

But norovirus will become one as toravirus vaccination becomes widespread

225
Q

Characteristics norovirus

A

Icosahedral, ssRNA virus

Calciviridae family
-the cruise ship departing from California

226
Q

Transmission norovirus outbreaks

A

Transmission via contaminated food or H2O

227
Q

Treanmission sporadic cases norovirus

A

Human human transmission

228
Q

Transmission norovirus places

A

Schools, nursing homes, cruise ships

229
Q

How is norovirus spread

A

Airborne droplets, environmental surfaces and forties

230
Q

Incubation period norovirus

A

Short

231
Q

Symptoms norovirus

A

Nausea, vomiting, watery diarrhea, abdominal pain—nonspecific abdominal complaints

232
Q

Treat norovirus

A

Self limited in immunocompetend

233
Q

Morphology norovirus

A

Villous shortening, loss of brush border, crypt hypertrophy, lymphocytic infiltration

234
Q

Immunocompromised norovirus

A

Persists up to 9 months, patients experience intermittent diarrhea, malnutrition and dehydration that can exacerbate their underlying disease

235
Q

Rotavirus characteristics

A

Encapsulated virus with segmented dsRNA

236
Q

What is the most common cause of severe childhood diarrhea and diarrheal mortality worldwide

A

Rotavirus

237
Q

Who is most susceptible to rotavirus

A

Children 6-24 months —-daycare

238
Q

Do children 0-6 months get rotavirus

A

No passive immunity from mom , but less effective in India

239
Q

Rotavirus 2 year olds and on

A

Immunity that develops following the first or second infection

240
Q

Where are rotavirus outbreaks

A

Hospitals and daycare centers

241
Q

Infective load rotavirus

A

<10 particles and has short incubation time

242
Q

Vaccine rotavirus

A

Associated with intussusception

243
Q

Rotavirus pathogenesis

A

Net secretion of H2O/electrolytes, malabsorption, osmotic diarrhea

244
Q

Adenovirus

A

Nonspecific signs and symptoms after 1 week incubation period

245
Q

Symptoms adenovirus

A

Diarrhea, vomiting, abdominal pain maybe fever and weight loss

246
Q

Adenovirus is the _ leading cause of pediatric diarrhea

A

3rd

247
Q

Who besides children is effected by adenovirus

A

Immunocompromised patients

248
Q

Epithelium adenovirus

A

Epithelial degeneration

249
Q

Villi adenovirus

A

Villous atrophy and compensatory crypt hyperplasia

250
Q

Ascaris lumbricoidrs

A

Ingested eggs hatch in intestint->larvae penetrate the intestinal mucosa->migrate from splanchnic to systemic circulation->enter the lungs to grow within the alveoli ->coughed up swallowed ->larvae mature into worms->eosinophilic rich inflammatory reaction->physical obstruction or the intestine or biliary tree

251
Q

How does ascaris lumbricoides spread

A

Fecal oral

252
Q

Diagnose ascaris lumbricoides

A

Eggs in stool

253
Q

Strongyloides

A

Larvae penetrate unbroken skin ->migrate through the lungs->induce inflammatory infiltrates->reside in the intestines maturing into adult worms

254
Q

Strongyloides autoinfection

A

Eggs of strongyloides can hatch within the intestine and release larvase that penetrate the mucosa
Infection can persist for life

255
Q

Strongyloides larva stage inside or outside the human host

A

Outside

256
Q

Tissue reaction to strongyloides

A

Strong and induce peripheral eosinophilia

257
Q

Nectar dupdenale and ancylostoma dupdenale

A

Hookworms—larvae penetrate through he skin, develop int he lungs, migrate up the trachea and are swallowed

258
Q

What do necator dupdenale and ancylostoma duodenale do in the duodenum

A

Suck blood and reproduce-multiple superficial erosions, focal hemorrhage and inflammatory infiltrates

259
Q

Chronic infection of necator dupdenale and ancylostoma dupdenale is associated with

A

Iron defiency anemia

260
Q

Enterobius vermicularis

A

Pinworm/parasites

261
Q

Do enterobius vermicularis invade host tissue

A

No

262
Q

Where do enterobius vermicularis live life cycle

A

In intestinal lumen

263
Q

Symptoms enterobius

A

Rarely

264
Q

Transmission enterobius vermicularis

A

Fecal oral

265
Q

Diagnose enterobius vermicularis

A

Scotch tape test

266
Q

Trichuris trichiura

A

Whipworms

267
Q

Who gets trichuris trichiura

A

Young kids

268
Q

Heavy infections of trichuris trichiura

A

Can lead to bloody diarrhea and rectal prolapse

269
Q

Trichuris trichiura does _ penetrate intestinal mucosa and rarely causes serious disease

A

Not

270
Q

Schistosomiasis

A

Adult worms residing within mesenteric veins

271
Q

Symptoms schistosomiasis

A

Trapping of eggs within the mucosa and submucosa

272
Q

Schistosomiasis causes a __- immune reaction that can cause bleeding and obstruction

A

Granulomatous

273
Q

Intestinal cestodes

A

Tapeworms that reside in the intestinal lumen but do not penetrate the intestinal mucosa==peripheral eosinophilia does not occue

274
Q

Treanmission intestinal cestodes (tapeworm)

A

Raw meat that contains encrypted larvae

-proglottids and eggs are shed in the feces

275
Q

Symptoms intestinal cestodes

A

Diarrhea, abdominal pain, nausea

276
Q

What are the three primary species of intestinal cestodes

A

Diphyllobothrium latum (fish tapeworm)=causes B12 defiency and megaloblastic anemis because it competes with the host for dietary B12

Taenia solium (pork)

Hymenolepis nana (dwarf tapeworm)

277
Q

Entamoeba histolytica treanmission

A

Fecal oral

278
Q

Symptoms of entamoeba histolytica

A

Abdominal pain, bloody diarrhea, or weight loss causes liver abscesses and dysentery

279
Q

What can entamoeba histolytica cause that is associated with significant mortality

A

Acute necrotizing colitis and megacolon

280
Q

Describe entamoeba cysts

A

Have chitin wall and 4 nuclei and resistant to gastric acid

281
Q

Describe entamoeba histolytica

A

Flask shaped upcer with a narrow neck and broad base

282
Q

Pathogenesis entamoeba histolytica

A

Penetrate splanchnic vessels and embolism to liver producing abscesses

283
Q

Entamoeba histolytica __ mitochondria or Karen’s cycles enzymes=obligate fermenters of glucose.

A

Lack

284
Q

Treat entamoeba histolytica

A

Metronidazole takes advantage of this and is an effective treatment (lacking mitochondria)

285
Q

Giardia lamblia

A

Most common parasitic pathogen in human and spread recalls contaminated water or food

286
Q

Giardia lamblia form ___ that are resistant to ___

A

Cysts

Chlorine

287
Q

Describe giardia lamblia

A

Flagellate protozoan that decrease expression of brush border enzymes, including lactase

288
Q

How do clear giardia lamblia

A

IgA and mucosal IL-6

289
Q

Giardia

A

Continuous modification of the major surface antigen

290
Q

How get giardia lamblia

A

Ingested from fecally contaminated for or H2O

291
Q

Trophozites giardia lamblia

A

Characteristics pear shape with two equal size nuclei

292
Q

Does giardia lamblia invade tissue

A

No

293
Q

How does giardia work

A

Secretes products that damage crush border=malabsorption

294
Q

Cryptospordium

A

Chronic diarrhea in AIDS patients
Oocytes are resistant to chlorine-need to freeze or filter

Entire life cycle in a single host

295
Q

Cryptospordium malabsorption of what

A

Na, Cl secretion, an increased tight junction permeability-nonbloody watery diarrhea

296
Q

Where is cryptosporidium concentrated

A

In terminal ileum and proximal colon

Present through the GIT, biliary tree and even the respiratory tract of immunodeficiency hosts

297
Q

How diagnose cryptosporidium

A

Oocytes in stool

298
Q

IBS

A

Non pathological , chronic relapsing abdominal pain, bloating and changes in bowel habits representing multiple illnesses

299
Q

Who gets IBS

A

20-40 years old, significant female

300
Q

Causes of IBS

A

Psychological stressors, diet ,abnormal GI motility, disrupted brain gut axis, immune activation or altered gut microbiome

301
Q

Diagnose IBS

A

Clinical criteria: gross and microscopic evaluation is normal in most patients

302
Q

Symptoms IBS

A

Abdominal pain 3 days/month over three months

303
Q

When does pain from IBS improve

A

Following defecation

304
Q

What does longer duration of IBS mean

A

Decreased likelihood of improvement

305
Q

Issues with IBS

A

No serious long term sequelae

May undergo unnecessary abdominal surgery due to chronic pain

Ability to function may be compromised

306
Q

Treat IBS

A

Depends on signs and symptoms: 5HT2 antagonists, opoids, anticholinergics or fecal transplant

307
Q

IBD

A

Chronic condition due to inappropriate mucosal immune responses to normal gut flora

Classified as either crohn disease or ulcerative colitis

308
Q

Who gets IBD

A

Teens-early 20s
Caucasions
Ashkenazi jews

Hygiene hypothesis

309
Q

Hygiene hypothesis

A

Increasing incidence is due to improved food storage condition, decreased food contamination, and changes in gut microbiome composition

310
Q

Why do people with IBD have reduced frequency of enteric infection

A

Inadequate development of mucosal immune regulation

311
Q

IBD helminth

A

Helminth infections may prevent development

312
Q

Pathogenesis IBD

A

Altered host integration with intestinal microbiota

Intestinal epithelial dysfunction

Aberrant mucosal responses

Altered composition of gut microbiome

Genetic influences are stronger in Crohn’s disease than in ulcerative colitis

313
Q

IBD mucosal immune response

A

T helper cells polarized to TH1 types

TH17 cells with IL23 receptor polymorphisms have a reduced risk of crohns and ulcerative colitis

Mutations or proinflammatory cytokines: TNF, IFNy, IL13

Mutations of immunoregulatory molecules leads to severe, early onset of disease: IL10, TGFb

Antibodies against flagellin==Crohn’s disease
-uncommon in ulcerative colitis

314
Q

Crohn’s disease

A

Transmural inflammation that involves any area of the GI tract

With intermittent signs and symptoms that may be brought on by social or environmental factors (smoking)

315
Q

Genetics crohns

A

Genes related tot he response of mycobacterium

NOD2 polymorphism: NFKB activation affected

ATG23l2 and IRGM can also be involved

316
Q

Epithelial defects crohns

A

Epithelial tight junction Barriers are defective due to NOD2 polymorphism

317
Q

Crohn’s disease: _% involve small intestine, _% colon, _% both

A

40
30
30

318
Q

Skip lesions crohns

A

Separate, sharply delineated disease areas with granular and inflamed serose and adherent creeping mesenteric fat

319
Q

Bowel crohns

A

Wall is thick and rubbery

320
Q

Crohns strictures

A

Present in crohns and not in ulcerative colitis

321
Q

Crohns punched out aphthous ulcers

A

That coalesce into axilla oriented serpentine ulcers

322
Q

Crohns cobblestone appearance

A

Sparing of interspersed mucosa with disease tissue that is depressed

323
Q

Fissures and fistula crohns

A

Yup

324
Q

Microscopic morphology crohns

A

Mucosal inflammation and ulceration with intraepithelial neutrophils and crypt abscesses

Creeping fat

Chronic mucosal damage with villus blunting , atrophy, pseudo-pyloric or paneth cell metaplasia and architectural disarray
-paneth cell metaplasia may occur in the left colon where paneth cells are normally absent

Transmural inflammation with lymphoid aggregates in submucosa, muscle wall and subserosal fat

Noncaseating granulomas throughout the gut, even in uninvolved segments

Cutaneous granulomas misnamed metastatic crohns

325
Q

Presentation crohns

A

Present with intermittent attacks of diarrhea, fever, and abdominal pain (may be rlQ like appendix)

With asymptomatic periods that may last weeks-months

Malabsorption, malnutrition, hypoalbuminemia, iron deficient anemia, +/- B12 defiency may occur

326
Q

Disease onset of Crohns is associated with initiation

A

Smoking

327
Q

With Crohns, __ _ are common and need to be respected

A

Fibrosis strictures

328
Q

Crohns extra intestinal

A

Migratory polyarthritis, sacrolitis, ankylosis spondylitis, erythema nodosum, uveitis, cholangitis, amyloidosis, finger clubbing

329
Q

Crohns have increased risk of developing what

A

Adenocarcinoma in patients with longstanding colon involvement

330
Q

Why can crohns lead to obstruction

A

From strictures

331
Q

Crohns have antibodies to what

A

Saccharomyces cerevisiae***

332
Q

Treat crohns

A

Immunosuppression

Surgical resection of fibrotic strictures/fistulae to adjacent viscera, abdominal or perineal skin, bladder or vagina and can recur at site of anastomsis

333
Q

Ulcerative colitis

A

Inflammatory disease limited to the colon and rectum

Affects only the mucosa and submucosa

334
Q

Epithelial defects in ulcerative colitis

A

ECM1 normally inhibits MMP9 to reduce severity of disease

HNFA associated with reduced intestinala barrier function

335
Q

Skip lesions ulcerative colitis

A

No

336
Q

What does ulcerative colitis involve

A

Left colon and rectum (retrograde involvement: pancoliitis)

Distal ileum may show some inflammation (backwash ileitis)

337
Q

In ulcerative colitis, extensive broad based ulcers that are aligned along the long axis of the ___

A

Colon

338
Q

Mucosa in ulcerative colitis

A

Reddened, granular, and friable with inflammatory pseudopolyps and easy bleeding

339
Q

Ulcerative colitis pseudopolyp

A

Isolated islands of regenerating mucosa that often bulge into the lumen

Tips can touch each other and create mucosal bridges

340
Q

Ulcerative colitis morphology

A

Crypt abscess, ulceration, chronic mucosal damage, glandular architectural distortion and atrophy

No thickening, strictures, fissures, or granulomas

341
Q

Complication ulcerative colitis

A

Inflammation can lead to damage in the muscularis propria and disturb neuromuscular function which leads to colonic dilation and toxic megacolon (high risk perforation)

-

342
Q

30% ulcerative colitis require __ within 3 years which cures intestinal disease but extra GI symptoms remain

A

Colectomy

343
Q

Ulcerative colitis have increased risk of what

A

Colonic adenocarcinoma

344
Q

Clinical presentation ulcerative colitis

A

Intermittent attacks of bloody diarrhea with stringy, mu oil material and abdominal pain that persists days-months before subsiding

345
Q

What may trigger initial onset of ulcerative colitis

A

Infectious enteritis, psychological stress,or cessation of smoking

346
Q

___ may partially relieve symptoms ofof UC

A

Smoking

347
Q

Extra-intestinal UC

A

Migratory polyarthritis, sacrolitis, ankylosis spondylitis, uveitis, skin lesions, primary sclerosis cholangitis

348
Q

Indeterminate colitis diagnosis

A

Definitive diagnosis is not possible in 10% of patients due to clinical overlap
-used for cases of IBD without definitive features of either ulcerative colitis or crohn disease

349
Q

Indeterminate colitis do not involve the small bowel and have colonic disease in a continuous pattern (__)

A

UC

350
Q

Risk of interminate colitis

A

Patchy histologic disease, fissures, family history of crohns, perinatal lesions, onset after initiating use of cigarettes

351
Q

Peri-nuclear anti-neutrophil cytoplasmic antibodies

A

75% of individuals with ulcerative colitis

11% with crohns

352
Q

Overlap of clinical management of UC vs crohns is __ therefore these people will be just fine

A

Minimal

353
Q

Colitis associated neoplasia (carcinoma)

A

Long term complication of IBD that depend on

Duration>8-10 yrs
Extend of disease: pancolitis>those with only left sided disease
Greater frequency and severity of active infalmmation (presence of neutrophils)

354
Q

Surveillance colitis associated neoplasia

A

8 years after diagnosis, immediately if co diagnosed with primary sclerosing cholangitis

355
Q

Colitis associated neoplasia classification

A

Low or high grade

356
Q

High grade colitis associated neoplasia

A

Prompt colectomy because associated with invasive carcinoma at the same site or elsewhere in the colon

357
Q

Low grade colitis associated neoplasia

A

May be treated with colectomy of closely followed based on age, foci

358
Q

Diversion colitis

A

Complication of ostomy and blind distal segment of colon from which normal fecal flow is diverted

Develops in the diverted segment , particularly in UC patients

359
Q

Morphology diversion colitis

A

Development of numerous mucosal lymphoid follicles

360
Q

Diversion colitis treat

A

Enemas containing short chain fatty acids (product of bacterial digestion int he colon and an important energy source for colonic epithelial cells) promotes mucosal recovery

361
Q

Cure diversion colitis

A

Re-anastomosis

362
Q

Microscopic colitis

A

Chronic, nonbloody, watery diarrhea without weight loss

363
Q

What are the two types of microscopic colitis

A

Collagenous colitis

Lymphocytic collitis

364
Q

Demographic and characteristic of collagenous colitis

A

Middle aged and older women

Dense, subepithelial collagen layer, increased numbers of intraepithelial lymphocytes and mixed inflammatory infiltrate within the lamina propria

365
Q

Lymphocytic colitis characteristic and associated

A

Subepithelial layer is of normal thickness and the increase in intraepithelial lymphocytes is greater, frequently exceeding ont T cell per five colonocytes

Celiac disease and autoimmune disease (graves, RA, autoimmune or lymphocytic gastritis

366
Q

GVHD occurs after what

A

Following hematopoietic stem cell transplantation

Why does GVHD occur

367
Q

Why does GVHD occur

A

Donor T cells targeting antigens on the recipients GI epithelial cells

368
Q

GVHD lamina propria lamina propria lymphocytic infiltrate is sparse

A

Ok

369
Q

What is the most common histological feature of GVHD

A

Epithelial apoptosis of crypts cells

370
Q

GVHD most common symptoms

A

Watery diarrhea but also may be bloods

371
Q

Sigmoid diverticulum disease

A

Refers to small acquired

372
Q

Sigmoid diverticulum disease

A

Small, acquired pseudo-diverticulum, flask like outpouchings of the colonic mucosa and submucosa

373
Q

Where does sigmoid diverticula occur

A

Along taeniae coli

Most common in the sigmoid colon

374
Q

Colonic diverticula are often multiple and the condition of having them is called ___

A

Diverticulosis

375
Q

Diverticulitis

A

When they become inflamed and irritated

376
Q

Where are sigmoid diverticulum uncommon

A

Japan and developing coutnries due to diet

377
Q

Where do sigmoid diverticula occur

A

Western coutnries

378
Q

Pathogenesis sigmoid diverticula

A

Inherent structure of colonic muscularis propria+elevated intraluminal pressure in the sigmoid colon
-most often, the muscularis proporia is absent

Increased intraluminal pressure due to exaggerated peristaltic contractions, with spasmodic sequesteration of bowel segments

379
Q

Manage sigmoid diverticula

A

Eat more fiber->increased stool bulk

Resolves spontaneously and few patients require intervention

380
Q

Clinical sigmoid diverticula

A

Intermittent cramping
Continuous lower abdominal discomfort
Constipation
Distention
Sensation of never being able to completely empty rectum
Alternating constipation and diarrhea that can mimic IBS

381
Q

Treat sigmoid diverticula

A

High fiber

382
Q

Polyps

A

Masses that protrude into the colorectal region (or esophagus, stomach, SI)

383
Q

How do polyps begin

A

As elevationsof mucosa

384
Q

Sessile

A

Lacking a stalk

385
Q

Pedunculated

A

Has a stalk

386
Q

Non neoplastic

A

Inflammatory, hamartin atoms, hyperplastic

387
Q

Most common polyp

A

Neoplastic adenoma

388
Q

Hyperplastic polyps

A

Bening epithelial proliferation’s with no malignant potential

389
Q

Why get hyperplastic polyps

A

Piling up of goblet and absorptive cells due to decreased epithelial cell turnover and delayed shedding

Can also occur adjacent to or overlying other lesions tat may be clinically important

390
Q

When get hyperplastic polyps

A

6th-7th decade

391
Q

Hyperplastic polyps are histologically similar to __ __ __ but are not potentially malignant

A

Sessile serrated adenomas

392
Q

Morphology hyperplastic polyps

A

Most common left colon
Multiple
Smooth, nodular protraction often on crests of mucosal folds

Mature goblet+absorptive cells

Serrated surface architecture typically restricted to the upper 1/3 of the crypt

393
Q

Inflammatory polyps triad

A

Rectal bleeding, mucus discharge, inflammatory lesion on the anterior rectal wall

394
Q

Inflammatory polys are from

A

Chronic injury and healing

395
Q

Inflammatory polys: how damage rectal mucosa

A

Sharp angle of the anterior rectal shelf with impaired relaxation of the anorectal sphincter

396
Q

Mucosal prolapse : inflammatory polyps

A

Entrapment by fecal stream

397
Q

Morphology inflammatory polyps

A

Mixed inflammatory infiltrates, erosiona nd epithelial hyperplasia+lamina propria fibromuscular hyperplasia

398
Q

Hamartomatous polyps

A

Occur sporadically or as a component of a genetic syndrome

Many are due to germline mutation in tumor suppressor genes or Porto oncogenes

399
Q

Risk of what with hamartomatous polyps

A

Cancer, so many are considered precancerous lesions

400
Q

Symptoms hamartomatous polyps

A

Extra intestinal symptoms

401
Q

Genetics hamartomatous polyps

A

Yea family members effected

402
Q

Juvenile polyps

A

Focal hamartomatous malformations of small intestine and colon mucosa

403
Q

Who gets juvenile polyps

A

Children <5 who present with rectal bleeding

404
Q

Where are most juvenile polyps

A

Rectum

405
Q

Genetics juvenile polyps

A

Sporadic:solitary lesion

AD-3-100 polyps may require colectomy to limit hemorrhage

406
Q

Juvenile polyps sequelae

A

Polyps in stomach and small bowel that can undergo malignant transformation which may lead to clubbing

407
Q

Morphology juvenile polyps

A

Pedunculated, smooth surfaced, reading lesions with cystic spaces

Cysts are dilated and filled with mucin and inflammatory debris

Mucosal hyperplasia may be initiating event
Most common mutation is in SMAD4 which affects TGFb signaling

30-50% develop colonic adenocarcinoma by age 45 if they have juvenile polyposis syndrome

408
Q

What is juveniles polyposis syndrome

A

Dysplasia is present -extremely rare if sporadic

409
Q

What are people with juvenile polyposis syndrome at risk for

A

30-50% get colonic adenocarcinoma by 45

410
Q

Peutz-jeghers syndrome inheritance

A

Rare AD pattern of inheritance is common between peutz jeghers syndrome and familial adenomatous polyposis

411
Q

What is peutz jeghers syndrome

A

Multiple GI hamartomatous polyps and mucocutansous hyperpigmentation

Dark blue brown macules onthe lips, nostrils, buccal mucosa, palmar hand, genitalia and perinatal region
-similar to freckles but no freckles on buccal mucosa

412
Q

Age peutz jeghers syndrome

A

11

413
Q

Risk of peutz jeghers syndrome

A

Several malignancies

414
Q

Sequelae peutz jeghers syndrome

A

40% increased lifetime risk of malignancies
-100% guarantee to get malignancy in FAP-prophylactic colectomy

Screen neonates for sex cord tumors of testes

Screen in late childhood for gastric and small intestine cancers

Screen in 2-3 decades for colon, pancreatic, breast, lung, ovarian and uterine cancers

May initiate intussusception

415
Q

Morphology peutz jeghers syndrome

A

50% have heterozygous STK11 loss of function mutation
-lack of STK11 mutations does not exclude the diagnosis of peutz jeghers syndrome

Arborizing polyps:small bowel.colon, stomach

Polyps are large, pedunculated and lobulated with arborizing smooth msucle, CT, glands and lamina propria lined by normal epithelium

416
Q

Diagnosis peutz

A

Multiple polyps in small intestine, mucocutaneous hyperpigmentation, and a positive family history

Detection of STK11 mutations can be helpful in patients without mucocutaneous hyperpigmentation
The pigment is melanin

417
Q

Neoplastic polyps

A

Any cancer in he GI tract can produce a polyp

418
Q

Most common neoplastic polyps

A

Colonic adenomas which are precursors to colorectal adenomas which are precursor to colorectal adenocarcinomas

419
Q

Name some other neoplastic polyps

A

Adenocarcinoma, neuroendocrine, stromal, lymphomas, etastatic

420
Q

Adenomas

A

Intraepithelial neoplasm ranging from small, pedunculated polyps to large, sessile lesions

421
Q

Adenomas are found in 30% of adults at age ___ in western world

A

60

422
Q

Symptoms adenoma

A

Usually silent

423
Q

Adenomas are associated with __ diet

A

Western

424
Q

Characterization colorectal adenoma

A

Presence of epithelial dysplasia

425
Q

Adenoma: what is epithelial dysplasia

A

Benign precursor lesions

426
Q

Do adenomas always progress to adenocarcinoma

A

No

427
Q

How can you tell whether an adenoma will progress to adenocarcinoma

A

No markers to tell

428
Q

What are large adenomas associated with

A

Occult bleeding and anemia

429
Q

What are villous adenomas associated with

A

Cause hypo proteinemic hypokalemia due to secretion of protein and potassium

430
Q

Morphology adenoma

A

Pedunculated or sessile with a velvet or raspberry surface

Hallmark of epithelial dysplasia=hyperplasia, nuclear hyper-chromasia, loss of polarity-epithelial cells fail to mature as they migrate from crypt to surface

Tubular, tubulovillous, villous

431
Q

Adenomas are connected to submucosa by what

A

Thin vascular wall

432
Q

What is the most important characteristic correlating with risk of malignancy of adenomas

A

Larger size=cancer

Higher degree of dysplasia=cancer

433
Q

Sessile serrated adenomas

A

Full length exhibits serrated architecture, with crypt dilation and lateral growth
Despite malignant potential, typical dysplastic changes seen in other adenomas is absent-similar to hyperplastic polyps

Found more commonly in the right colon

434
Q

Where are sessile serrated adenomas most commonly found

A

Right colon

435
Q

Intramucosal carcinoma

A

Occurs when dysplastic cells invade the lamina proporia or muscularis mucosa

Little or no metastatic potential due to lack of lymphatic channels in colonic mucosa

Complete polpectomy==curative

436
Q

Invasive adenocarcinoma

A

Crosses into the submucosa and accesses lymphatics

Risk of metastases is

437
Q

Familial adematous polyposis (FAP)

A

Autosomal dominant , APC mutation (negative regulator of WNT)

Numerous colorectal adenomas develop as a teenager
-morphologically indistinguishable from sporadic adenomas except in terms of number

438
Q

Colorectal adenocarcinomas develop in __% of untreated FAP patients, often at <30 years and always by 50

A

100

439
Q

Prophylactics FAP

A

Prophylactic colectomy to prevent colorectal cancer

440
Q

FAP associated with what

A

Increased risk of neoplasia at other sites (ampulla of vater, stomach)

Gardner and turcot syndromes

441
Q

FAP is morphologically indistinguishable from __ __

A

Sporadic adenomas

442
Q

FAP extra intestinal

A

Congenital hypertrophy of retinal pigment epithelium (detected at birth)

443
Q

FAP with no APC mutation

A

Biallelic mutations of MYH( base excision repair gene)-MYH associated polyposis:polyps develop later, have <100 adenomas and acquire colonic aner at <50 years

Serrated polyps with KRAS mutations are often present

444
Q

Which characteristic of an adenoma is the most oimportant that correlated with risk of malignancy

A

Polyp size -4cm is thresholds

445
Q

Hereditary non polyposis colorectal cancer

A

AD
Most common syndromic form of colon cancer

Get clusters of cancer that develop at different sites throughout the body
-colorectal, endometrium, stomach, ovary, ureters, brain, small bowel, hepatobiliary tract, pancreas and skin

446
Q

Age hereditary polyposis

A

Under 50

447
Q

Location of hereditary non polyposis colorectal cancer

A

Right colon

448
Q

Genetics HNPCC

A

Inherited mutation in genes that encode proteins responsible for the detection, excision and repair of errors that occur during DNA replication

Mutations in MSH2 or MLH1 (mismatch repair)

449
Q

Colonic adenocarcinoma

A

Most common malignancy of the GI tract

450
Q

Colonic adenocarcinoma is responsible fo r_% of all cancer deaths

A

10

451
Q

In the USA colonic adenocarcinoma is the _ most common cause of cancer death

A

2nd

452
Q

Age colonic adenocarcinoma

A

60-70

Younger in HNPCC and FAP

453
Q

Risk factors colonic adenocarcinoma

A

Diet: change of GI flora and synthesis of carcinogenic byproducts which have prolonged contact with intestinal mucosa due to decreased stool bulk

Decreased vegetable fiber

Increased refined carb diet

NSAIDS: protective effect via COX2

454
Q

Colonic adenocarcinoma COX2

A

COX2 is overexpressed in 90% of colorectal carcinomas and 40-90% of adenomas

COX2 expression is regulated by TLR4; TLR4 is also overexpressed in adenomas and carcinomas

455
Q

Genetics colonic adenocarcinoma genetics

A

APC/B catenin pathway

Microsatellite instability due to defects in DNA mismatch repair

CpG island hypermethylation phenotype

Increased CpG is all methylation int he absence of microsatellite instability

456
Q

APC/B catenin pathway

A

80% sporadic colon tumors

Key - regulator of B catenin, a component of WNT signaling

Loss of APC-> B catenin accumulates->translocates to the nucleus->does gene transcription (MYC and cyclin D1)->cell proliferation->cancer

Can still have cancer in the presence of wild type APC when B catenin is constituitively active

Chromosomal instability is a hallmark of APC/B catenin pathways

457
Q

Colonic adenocarcinoma microsatellite instability due to defects in DNA mismatch repair

A

TGF-B:inhibits colonic epithelial cell proliferation

BAX: pro apoptotic

458
Q

Colonic adenocarcinoma CpG island hypermethylation phenotype

A

Microsatellite instability
MLH1 is hypermethylated

Activating mutations of BRAF oncogene

KRAS and TP53 are not mutated

459
Q

Colonic adenocarcinoma increased CpG island methylation in the sbsence of microsatellite instability

A

KRAS is mutated

TP53 and BRAF mutations are uncommon

460
Q

Colonic adenocarcinoma __ distribution throughout colon

A

Equal

461
Q

Colonic adenocarcinoma proximal colon

A

Polypoid, exophytic masses that rarely cause obstruction

462
Q

Colonic adenocarcinoma distal colon

A

Annular masses with napkin ring obstruction, lumen narrows , often to the point of obstruction

463
Q

Morphology colonic adenocarcinoma

A

Tall, columnar cells resembling adenomatous neoplastic epithelium with invasion into usubmucosa, muscularis propria or beyond

Strong desmoplastic response which makes them firm

Penetrate the bowel wall over the course of many years

Glands may be scarce or abundant, producing excess mucin
(Worse prognosis)

Tumors may have signet ring cells or show neuroendocrine differentiation

464
Q

Prognosis colonic adenocarcinoma

A

Depth of invasion==histological feature that most significantly affects prognosis w

465
Q

Righ sided colonic adenocarcinoma presentation

A

Fatigue and weakness due to iron deficient anemia

Older males or postmenopausal females with iron deficient anemia have this diagnosis until proven otherwise

466
Q

Left sided colorectal adenocarcinoma presentation

A

Can produce occult bleeding, changes in bowel habits or cramping and LLQ discomfort

467
Q

What is the most important prognostic factor of colonic adenocarcinoma

A

Depth of invasion and presence of lymph node metastases

468
Q

Colonic adenocarcinoma and muscularis proporia invasion

A

Decreased survival

469
Q

With colonic adenocarcinoma, metastases is most common to where

A

Liver, then lymph nodes ,lung, bone

Not rectum which does not drain via portal circulation

470
Q

Prognosis colonic adenocarcinoma

A

5 year survival 65%

471
Q

Patient with what presentation have colorectal cancer until proven otherwise

A

Older populations with blood loss/anemia and unintentional weight loss

472
Q

Anal canal: upper 1/3

A

Columnar rectal epithelium

Glandular carcinoma

473
Q

Anal canal: middle 1/3

A

Transitional epithelium

Cloacogenic carcinoma=basaloid tumors populated with immature cells from the basal layer of transitional epithelium
-basaloid pattern may be mixed with squamous or mucinous differentiation

474
Q

Anal canal lower 1/3

A

Stratified squamous epithelium

Squamous carcinoma

Pure squamous cell carcinoma of this region is often associated with HPV infection which can cause precursor lesions (condylomata acuminatum ‘anal warts’)

475
Q

Hemorrhoids

A

Not a medical emergency

Varices dilation of anal canal and perinatal submucosal venous plexuses
Associated with constipation (straining), venous stasis in pregnancy and cirrhosis (portal HTN)

Secondary thrombosis (with recanalization), strangulation or ulceration with fissure formation can occur

476
Q

Treat hemorrhoids

A

Sclerotherapy, rubber band ligation, infrared coagulation, surgery

477
Q

External hemorrhoids

A

Occur with ectasia of the inferior hemorrhoids plexus below the anorectal line

Extremely painful

These are portal-canal anastomoses, indicative of hepatic pathology

478
Q

Internal hemorrhoids

A

Occur with actasia of superior hemorrhoids plexus above the anorectal line

Generally painless

These are from staining

479
Q

Acute appendicitis

A

Initiated by progressive increases in intraluminal pressure that compromise venous outflow

Usually due to obstruction of the lumen by stool, tumor, or worms that increase intraluminal pressure

480
Q

What does acute appendicitis cause

A

Bacterial proliferation, ischemia, and inflammatory response leads to tissue edema and neutrophilic infiltration of the lumen , muscle wall and peri-appendiceal soft tissues

481
Q

Morphology acute appendicitis

A

Serosa is dull, granular and red neutrophilic infiltration of the muscularis propria-suppurative

Severe neutrophilic infiltration: fibrniopurulent esrosal exudate, luminal abscess formation, ulceration and suppuratove necrosis

Can progress to acute gangrenous appendicitis followed by perforation (suppurative peritonitis)

482
Q

Clinical acute appendicitis

A

Periumbilical pain migrating to RLQ , nausea, vomiting, abdominal tenderness (Mcburney), mild fever, leukocytosis

Children and elderly more likely to have abnormal presentation

483
Q

Complications acute appendicitis

A

Pyelophlebitis, portal vein thrombosis, liver abscess, bacteremia

Perforation has high morbidity

484
Q

Carcinoid tumor

A

Well differented neuroendocrine tumor

Most common tumor of the appendix

Usually benign often incidental finding

485
Q

Morphology carcinoid tumor

A

Solid bulbous swelling at the distal tip of the appendix that can reach 2-3 cm in diameter

Nodal metastases are infrequent
Distal spread is extremely rare

486
Q

Mucocele

A

Dilated appendix filled with mucin

487
Q

Mucocele presntation

A

May simply represent an obstructed appendix containing inpissaated mucin or be a consequence of:
Mucinous cystadenoma
Mucinous cystadenocarcinoma->invasion through appendices wall->intraperitoneal seeding->pseudomyxoma peritonei

488
Q

Peritonitis

A

Inflammation of the membrane lining the abdominal wall and covering the abdominal organs

May be due to bacterial infection or chemical irritation or perforation of abdominal viscera

489
Q

Sterile peritonitis

A

Irritation of the peritoneum due to leakage of bile or pancreatic enzymes

Perforation or rupture leads to highly irritating peritonitis that is often complicated by bacterial superinfection

490
Q

Acute hemorrhagic pancreatitis-peritonitis

A

Leakage of pancreatic enzymes and fat necrosis allows bacterial to spread to the peritoneal cavity

491
Q

Foreign material-peritonitis

A

Irritation of the peritoneum due to objects introduced surgically (talc, sutures, watches) that can induce a foreign body type granuloma and fibrous scarring

492
Q

Endometriosis-peritonitis

A

Irritation of the peritoneum due o hemorrhage into the peritoneal cavity

493
Q

Ruptured dermoid cyst-peritonitis

A

Irritation of the peritoneum due to release of keratinize which induce an intense granulomatous reaction

494
Q

Peritoneal infection

A

Perforation of GI structures releases bacteria into the peritoneal cavity

Spontaneous bacterial peritonitis develops in the absence of an obvious source of contamination

  • seen most often in patients with cirrhosis and ascites
  • seen less frequently in children with nephrotic syndrome
495
Q

Common bugs of peritoneal infection

A 
E. coli
Streptococci
Staph aureus
Enterococci
Clostridium perfringens
496
Q

Morphology peritoneal infection

A

Peritoneal membranes become dull and grey, followed by exudative and frank suppurations

Localized abscesses can develop

Inflammation tends to remain superficial

497
Q

Sclerosing retroperitonitis (idiopathic retroperitoneal fibrosis, or Mongolian disease)

A

Characterized by dense fibrosis that may extend to involve the mesentery

Cause is unknown (idiopathic)

Frequently compresses the ureters

498
Q

Peritoneal tumors

A

Primary are rare

499
Q

Meothelioma

A

Asbestos exposure

500
Q

Desmoplastic round cell tumor

A

Kids and young adults
-aggressive tumor
-bears resemblance o Ewing sarcoma and other small found cell tumors
Characterized by a reciprocal translocation t(11;220(p13;q12) resulting in fusion gene EWS-WT1

501
Q

Secondary peritoneal tumor

A

Secondary from direct spread or seeding leads to peritoneal carcinomatosis

502
Q

Mucinous carcinoma (of appendix)

A

Can cause pseudomyxoma peritonei

503
Q

All peritoneal tumors prognosis

A

All malignant and have poor prognosis

Pathology (28 decks)

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