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HLTH 341 - Pathobiology > Test 3 > Flashcards

Test 3 Flashcards

1
Q

in the GI system, what is the breakdown of food and fluids facilitated by?

general

A

enzyme

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2
Q

majority of molecular absorption into cells occurs where?

general

A

small intestine

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3
Q

what are the 5 roles of the GI system?

A
  1. mechanical processing and movement
  2. secretion
  3. digestion
  4. absorption of nutrients
  5. elimination
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4
Q

what are the accessory organs of the GI system?

A
  • salivary glands
  • liver
  • gallbladder
  • pancreas
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5
Q

the pancreas produces and secretes what two things?

general

A

enzymes
bicarbonate - neutralize stomach contents

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6
Q

identify and describe the layers of the GI system from innermost to outermost

A
  • innermost - mucosa - epithelial cells in direct contact with the lumen
  • submucosa - connective tissue containing blood vessels, lymph vessels and nerves
  • muscularis - smooth muscle responsible for movement and motility
  • outermost - serosa - connective tissue that provides anchorage of GI structures
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7
Q

what layer of the GI system contains the lamina propria?

A

mucosa

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8
Q

what layer of the GI system contains the peritoneum?

A

serosa

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9
Q

what are the 5 main GI hormones?

A
  1. gastrin
  2. cck - cholecystokinin
  3. secretin
  4. gip - gastric inhibitory peptide
  5. ghrelin
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10
Q

describe gastrin:
* secreted by
* secretion trigger
* what it causes

A
  • secreted by mucosal cells in stomach
  • secreted in response to stomach distrention or partially digested substances
  • causes increased gastric motility and relaxation of pyloric and ileocecal sphincters (promote stomach emptying)
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11
Q

describe CCK:
* secreted by
* secretion trigger
* what it causes

A
  • secreted by jejunum
  • secreted in response to fat
  • causes contraction of gallbladder and pancreatic secretions
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12
Q

describe secretin:
* what it causes

A
  • neutralizes gastric secretions
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13
Q

describe GIP:
* secreted by
* secretion trigger

A
  • secreted by upper portion of small intestine
  • secreted in response to fat in chyme and carbohydrates
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14
Q

describe ghrelin:
* secreted by
* secretion trigger
* what it is counteracted by

A
  • secreted by stomach
  • increases appetite, stimulates GH secretion, produces weight gain
  • counteracted by leptin
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15
Q

what are the 3 physiological characteristics of movement through the GI system?

A
  • peristalsis - progressive movement that propels material forwards
  • segmental contractions - to keep contents constantly moving and facilitate mechanical breakdown
  • sphincters - rings that separate sections to promote one way movement
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16
Q

identify and describe the defense mechanisms of the GI system

A
  • mucous - move pathogens and prevent direct contact with epithelial layers
  • muscular layer and peristalsis - move items down and prevent pathogens from stopping and invading
  • stomach acidity - antimicrobial effects to prevent tract colonization
  • GI bile - create a hostile environment
  • microbiome - add a protective layer, compete for nutrient resources, produce helpful components (i.e. vit K - coagulation)
  • GALT - adaptive response
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17
Q

define dysphagia

A

difficulty swallowing

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18
Q

define gastritis

A

inflammation of the stomach lining

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19
Q

define gastroenteritis

A

inflammation along the GI tract

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20
Q

define enteritis

A

inflammation of the colon and small intestine

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21
Q

define enterocolitis

A

inflammation of the colon and small intestine

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22
Q

define colitis

A

inflammation fo the colon

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23
Q

define hemmorhagic colitis

A

bloody diarrhea

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24
Q

describe constipation by:
* definition
* causes
* complications
* preventative things

A
  • definition: small, infrequent, or difficult bowel movments, less than 3 times a week
  • causes: low fiber, lack of exercise, aging (slowed peristalsis), motility impacting conditions (diverticulitis, obstruction)
  • complication: fecal impaction
  • preventative thing: cellulose
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25
Q

identify the 4 types of diarrhea

A
  1. osmotic
  2. secretory
  3. inflammatory/exudative
  4. motility related
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26
Q

describe osmotic diarrhea

A

diarrhea when nutrients are inadequately or poorly absorbed

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27
Q

describe secretory diarrhea

A

diarrhea caused by toxins that stimulate intestinal fluid secretion and impair absorptions
* can lose 1L or more a day
* i.e. cholera

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28
Q

describe inflammatory or exudative diarrhea

A

diarrhea caused by inflammation of the mucosal lining
* pus like formation can cause white flakes/patches

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29
Q

describe motility related diarrhea

A

rapid movement of food through tract - decreased transit time of chyme with absorptive surfaces

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30
Q

define dysentery

A

presence of blood in loose or liquid stools

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31
Q

what are some means of diagnosis, treatment, and prevention of GI pathologies?

A
  • diagnosis: S&S assesment, imaging, fecal samples
  • treatment: alleviate symptoms, oral rehydration therapy
  • prevention: eliminate aggravators, proper health and hygiene, sanitation and food handling
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32
Q

what function do antacids have in treating GI pathologies?

A

reduce excessie acidity

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33
Q

what function do antiemetics have in treating GI pathologies?

A

relieve vomiting from drugs, motion sickness, or other therapy

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34
Q

what function do laxatives/enemas have in treating GI pathologies?

A

facilitate bowel movement to treat acute constipation

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35
Q

what function do antidiarrheals have in treating GI pathologies?

A

reduce peristaltic activity (motility) and relieve cramps

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36
Q

what function do coating agents have in treating GI pathologies?

A

enhance gastric mucosal barrier against irritants such as NSAIDs

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37
Q

what function do anticholinergic drugs have in treating GI pathologies?

A

reduce pns activity, reduced secretions and motility

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38
Q

what function do histamine blockers have in treating GI pathologies?

A

useful in gastric reflux

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39
Q

what function do proton pump inhibitors have in treating GI pathologies?

A

reduce gastric secretion

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40
Q

describe gastric ulcers by:
* definition
* common sites
* potential causes
* variabiltiy (traits that can be variable)

A
  • definition: lesions in the mucosa
  • common sites: stomach, duodenum, esophagus
  • causes: stress, foods, meds, H. pylori
  • variable traits: number, size, location, severity, causes
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41
Q

severity of a peptic/gastric ulcer can vary based on what?

A

size and depth

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42
Q

a true ulcer is a lesion into what layer of the GI lining?

A

submucosa

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43
Q

a pentrating ulcer goes into what layer of the GI lining? what can possibly occur with this type of ulcer?

A
  • into the serosa
  • can cause pain and bleeding - indicative when blood in stool
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44
Q

describe H. pylori including:
* gram state: + or -
* motility
* spore forming?
* transmission
* other implications

A
  • gram negative
  • motile via multiple polar flagella
  • non spore forming
  • transmitted via fecal-oral or oral-oral
  • also implicated in stomach cancer and gastritis
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45
Q

what are some things that being H pylori positive increases risk of?

A
  • gastric cancer
  • MALT lymphoma
  • gastric ulcers
  • duodenal ulcers
  • functional dyspepsia (indigestion)
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46
Q

describe the pathogenesis of H. pylori

A
  • enabled by urease : neutralizes stomach pH
  • adheres to gastric epithelial cells
  • LPS and antigens stimulate immune response and inflammation
  • slowed ulcer healing
  • high recurrence rate
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47
Q

what are the 4 major virulence factors of peptic/gastric ulcers?

A
  1. LPS
  2. TFSS/T4SS
  3. Vac A
  4. Cag A
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48
Q

describe TFSS/T4SS

GI system

A
  • secretion system
  • allows pathogen to secrete virulence factors into host
  • decreases host function and may induce apoptosis (contribute to erosion)
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49
Q

describe Vac A

GI system

A
  • pore forming cytotoxin
  • targets mitochondria
  • reduces membrane potential and compromises ATP synthesis
  • cytochrome c leakage - caspase activation - proapoptotic
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50
Q

describe Cag A

GI system

A
  • activate of MMP that can facilitate erosion
  • alter cell-cell and cell-basement leakage
  • e-cadherin or beta-catenine disruption
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51
Q

what are some clinical manifestations of peptic and gastric ulcers?

A
  • localized abdominal pain and burning
  • nausea - vomiting and loss of apetite
  • sometimes bleeding
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52
Q

what are some potential complications of peptic/gastric ulcers?

A
  • hemorrhages: via erosion of blood vessels
  • perforation: complete erosion that allows chyme to enter peritoneal cavity
  • obstructon: via scar tissue formation (more likely in duodenum and esophagus)
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53
Q

what is GERD (gastroesophageal reflux disease)?

A

periodic reflux of gastric contents into the distal esophagus

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54
Q

what does the severity of GERD depend on? what can GERD cause?

A
  • severity depends on LES competense, frequency, and amount of acid
  • may cause erosion and inflammation
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55
Q

what are the clinical manifestations of GERD and some aggravating factors?

A
  • manifestations - heartburn, chest pain, dysphagia
  • aggravating factors - caffiene, spicy food, fatty food, alcohol, smoking, some meds
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56
Q

since some clinical manifestations of GERD include heartburn and chest pain it is often confused for what?

A

angina

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57
Q

what is GERD often seen in conjunction with?

A

hiatal hernia

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58
Q

what is a hiatal hernia?

A

when the uppermost portion of the stomach protrudes into the thoracic cavity through the hiatus (opening in the diaphragm)

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59
Q

what are some potential causes of a hiatal hernia?

A
  • incompetent sphincter
  • diaphragm tone
  • abdominal pressure - full stomach, obesity, pregnancy
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60
Q

what are some risks/complications associated with hiatal hernias?

A

perforation/rupture into thoracic cavity due to:
* contents (bacteria and food) within the sac causing aggravation
* feedforward mechanism of inflammation causing pressure on the sac

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61
Q

what are some things that impact the tone of the LES?

A
  • delayed gastric emptying
  • increased transient LES relaxations
  • loss of secondary peristalsis
  • increased acidity
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62
Q

what are some complication risks with esophageal reflux disease (6)?

A
  1. stricture - stiffness caused by scar tissue formation
  2. pain
  3. obstruction - food and inflammation preventing passage of food from the esophagus to stomach
  4. perforation
  5. hemorrhage - dependent on depth may be internal or external
  6. pneumonia - contents rise high enough that they go down the trachea into the lungs
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63
Q

what is barrett’s esophagus?

A

change in esophageal cell morphology from squamous to columnar epithelieum

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64
Q

how can barrett’s esophagus be diagnosed? can it be reversed?

A
  • diagnosis - via endoscope
  • reversible - yes with removal of irritant
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65
Q

what type of cancer does barrett’s esophagus increase the risk of?

A

adenocarcinoma (glandular epithelial cells)

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66
Q

what are the 2 diseases within IBD?

A
  1. ulcerative colitis (UC)
  2. crohn’s disease
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67
Q

define IBD by:
* typical diagnosis time
* disease course (general)
* cause

A
  • diagnosis time - childhood
  • disease course - variable periods of exacerbation and remission
  • cause - idiopathic (unknown because multifactoral)
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68
Q

compare/contrast IBD and food-borne infectious GI issues in terms of diagnosis and treatment

A

IBD:
* fecal culture - negative
* treatment - cant use antibiotics
infectious:
* fecal culture - positive
* treatment - can use antibiotics

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69
Q

ulcerative colitis is a chronic inflammatory disease of the mucosa of the ____ and ____.

A
  • rectum
  • colon
    ( distal GI tract )
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70
Q

in UC inflammation begins at the base of ____ causing damage and invasion with ____. this results in formation of an ____ within crypts and formation of large ____ in the mucosal layer

A

in UC inflammation begins at the base of intestinal crypts causing damage and invasion with leukocytes. this results in formation of an abcess within crypts and formation of large ulcers in the mucosal layer

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71
Q

in ulcerative colitis coalescence of abscesses results in large ulcerations through the ____.

A
  • epithelia barrier
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72
Q

what are the clinical manifestations of ulcerative colitis?

A
  • severe lower abdominal cramping
  • diarrhea
  • rectal bleeding
  • hallmark - bloody diarrhea
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73
Q

what causes the diarrhea experienced in ulcerative colitis?

A
  • mucosal destruction in colon ->
  • decreased ability to absorb water and sodium ->
  • excess fluid volume in intestinal contents ->
  • excessive fluid loss
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74
Q

ulcerative colitis can be related to ____ which can cause developmental delays in youth

A

low weight

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75
Q

is ulcerative colitis associated with an increase or decrease in lumenal diameter?

A

decrease

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76
Q

what are some other names for crohns?

A
  • regional enteritis
  • granulomatous colitis
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77
Q

in what areas of the GI tract does crohns normally occur (2)?

A
  • terminal ileum of SI
  • ascending colon
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78
Q

what is crohns and what does it involve (4)?

A
  • chronic inflammation of all layers of the intestinal wall
  • includes ulcerations, strictures, fibrosis, fistulas
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79
Q

what can crohn’s result in?

A

blockage and inflammation of lymphatic vessels

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80
Q

what are skip lesions seen in crohn’s

A
  • distribution of affected segments alternating with normal segements of bowel
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81
Q

what are fistulas seen in crohn’s?

A
  • abnormal opening between two structures
  • crohns - between the small and large intestine
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82
Q

what are some clinical manifestations of crohns?

A
  • intermittent fever,
  • soft or semi-formed stool (may or may not have blood - not as severe as UC when not bloody)
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83
Q

what comorbidities may be seen in people with crohns?

A
  • anorexia
  • weight loss
  • anemia
  • fatigue (malabsorption and malnutrition)
  • delayed growth and sexual maturation in kids
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84
Q

what are the main components of crohns disease (3)?

very broad

A
  • genomic
  • immune
  • microbiome
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85
Q

what are some potential triggering factors in crohns?

A
  • exercise
  • smoking
  • infection
  • envrionment
  • hygiene
  • diet
  • drugs
  • stress
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86
Q

what are some treatments for ulcerative colitis and crohn’s (6)?

A
  1. anti-inflammatory meds
  2. anti-motility agents (symptomatic relief)
  3. immunotherapeutic agents
  4. antimicrobials
  5. nutritional supplements
  6. surgical resection (extreme)
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87
Q

compare and contrast crohns and ulcerative colitis by:
* region affected
* distribution of lesions
* stool
* granuloma?
* fistula, fissure, abscess?
* stricture, obstruction?
* malabsorption, malnutrition?

A
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88
Q

what is the etiology of irritable bowel syndrome?

A

unclear or variable

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89
Q

what are some clinical manifestations of IBS

A
  • lower abdominal pain
  • diarrhea/constipation - abnormal bowel movements
  • gas, bloating, nausea
  • fecal urgency or incomplete evacuation
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90
Q

IBS pathogensis is associated with different types. describe abnormal gastrointestinal motility and secretion

A
  • diarrhea type: rapid transit time of feces throguh bowel
  • constipation/bloating type: delayed transit time of feces through bowel
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91
Q

IBS pathogensis is associated with different types. describe visceral hypersensitivity

A

immune system, involvement of activated mast cells and T lymphocytes

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92
Q

IBS pathogensis is associated with different types. describe post-infectious

A

low-grade inflammation associated with bacterial enteritis

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93
Q

IBS pathogensis is associated with different types. describe overgrowth of flora

A
  • causes constipation and bloating due to methane gas production
  • imbalance in microbial growth - i.e. with long term use of antibiotics
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94
Q

IBS pathogensis is associated with different types. describe food allergy or intolerance

A

certain food antigens may activate a hypersensitive immune response in the mucosa

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95
Q

IBS pathogensis is associated with different types. describe pyschosocial factors

A

emotional stress, affecting the nervous system and neuroendocrine pathway

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96
Q

what are some treatment techniques for IBS

A
  • laxatives
  • fiber supplements
  • antidiarrheal medication
  • antidepressants
  • analgesics for pain
  • antipasmodic medication
  • serotonin balancing medications
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97
Q

define diverticulum

A

outpouching of the mucosa through the musculature

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98
Q

define diverticulosis

A

symptomatic diverticular disease

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99
Q

define diverticulitis

A

inflammation usually due to diverticulitis stasis

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100
Q

what does diverticular disease result from?

A
  • low dietary fiber intake
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101
Q

what does diverticular disease result in?

A

high intraluminal pressure

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102
Q

what is diverticular disease associated with symptomatically?

A
  • cramping
  • tenderness
  • nausea
  • vomiting
  • slight fever
  • elevated white blood cell count
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103
Q

what is the primary location of secondary metastasis?

104
Q

kRas mutations can lead to what types of cancer?

A
  • pancreas
  • colon
  • billiary tract
  • small intestine
  • lung
  • ovary
  • endometrium
105
Q

nRas mutations can lead to what types of cancer?

A
  • skin
  • hematopoetic
  • autonomic ganglia
106
Q

hRas mutations can lead to what types of cancer?

A
  • savlivary gland
  • urinary tract
  • cervix
107
Q

32 Ras-GEF genes are associated with what Ras state?

A

active - bound to GTP

108
Q

14 Ras-GAP genes are associated with what Ras state?

A

inactive - GTP hydrolysis and GDP binding

109
Q

what is the pathway for the stimulation of grwoth factors and Ras leading to cancer?

A
  1. growth factors
  2. Ras
  3. Raf
  4. MEK
  5. ERK
  6. proliferation, differentiation, cell survival
110
Q

how can Ras activation be detected?

A

phosphorylation via immunoblotting

111
Q

what Ras mutation affected basal homeostasis is colonic epithelieum leading to excessive crypt depth?

A

K-Ras (G12D)

112
Q

polyps are outgrowths that grow into what area? what can they be assesed through?

A
  • grow into the lumenal cavity
  • assessed through endoscopy
113
Q

mutations in what genes are associated with colorectal cancer (4)?

A
  1. p53
  2. apc
  3. smad2
  4. smad4
114
Q

what do most colorectal malignancies develop from?

A

adenomatous polyps

115
Q

what are the two forms of colorectal cancer?

general

A
  1. sessile
  2. pedunculated
116
Q

what are sessile polyps?

A
  • raised protuberance with a broad base
  • more consistent size throughout
117
Q

what are pedunculated polyps?

A
  • attached to bowel wall by a stalk narrower than the body of the polyp
  • narrow base with longer/narrow head
118
Q

what are the general clinical manifestations of colorectal cancer?

A
  • change in bowel habits
  • bleeding
  • abdominal pain and discomfort
  • fatigue, weight loss, anemia
119
Q

what occurs with colorectal cancer in the transverse colon?

A
  • semisolid stool
  • anemia - occult blood in stool
  • change in bowel habits
120
Q

what occurs with colorectal cancer in the ascending colon?

A
  • liquid stool
  • occult blood in stool or melena
  • anemia, fatigue
  • late-palpable mass
121
Q

what occurs with colorectal cancer in the descending colon?

A
  • solid stool
  • constipation and discomfort
  • abdominal fullness and distention
  • red or dark blood in stool
  • black, tarry stool
122
Q

what occurs with colorectal cancer in the rectum?

A
  • solid stool
  • abdominal discomfort and cramps
  • ribbon or pellet stool
  • incomplete emptying
  • red blood on the surface of stool
123
Q

what type of restriction results due to circumferential growth in colorectal cancer?

124
Q

what are some risk factors for colorectal cancer (9)?

A
  1. genetics
  2. familial polyps (FAP)
  3. smoking
  4. alcohol
  5. western diet
  6. processed meats
  7. obesity
  8. sedentary lifestyle
  9. chronic irritation or inflammation
125
Q

colorectal cancer can be diagnosed through 3 ways - testing, visual imaging, and screening. identify some diagnosis techniques in each.

A
  • testing: biomarkers, blood tests, genetic tests
  • visual imaging: radiograph, ultrasound mri, ct
  • screening: endoscope and biopsy
126
Q

what are the major regions of the pancreas?

A
  • head
  • neck
  • body
  • tail
127
Q

what is the exocrine function of the pancreas?

A

digestive enzyme and bicarbonate secretion

128
Q

the pancrease secretes enzymes including ____ (3), which is stimulated by the hormones ____ (2) and the proteases ____ (3).

A
  • enzymes: amylase, lipase, proteases
  • hormones: cck, secretin
  • proteases: trypsin, chymotrypsin, carboxypeptidase
129
Q

briefly describe how zymogens are released from pancreatic acinar cells?

A

zymogen granules fuse with the apical side of the cell and they are released into the duct leading to the small intestine

130
Q

what is teh role of amylase in the pancreas?

A

split starch and glycogen into disaccharides

131
Q

what is the role of lipase in the pancreas?

A

split triglycerides into fatty acids and monoglycerides

132
Q

what is the role of trypsin, chymotrypsin, and carboxypeptidase in the pancreas?

A

split protein into peptides

133
Q

what is the role of nucleases in the pancreas?

A

split nucleic acids into nucleotides

134
Q

what are the mechanisms present that prevent auto-digestion?

A
  • pro-enzymes
  • trypsin activation (needed)
  • trypsin inhibitors (SPINK1)
  • trypsin inactivation
135
Q

what are the four potential consequences of pancreatic pathophysiology?

A
  1. insufficiency
  2. inflammation
  3. neoplasms
  4. obstruction
136
Q

what can pancreatic insufficiency lead to?

A

fatty stools (steatorrhea)

137
Q

what can pancreatic inflammation lead to?

A

autodigestion of the tissue

may be acute or chronic

138
Q

what can pancreatic neoplasm lead to?

A
  • ductal adenocarcinoma
  • neuroendocrine carcinoma
139
Q

what can pancreatic obstruction lead to?

A

stones or fibrosis

140
Q

what are some potential causes of acute pancreatitis?

A
  • alcohol
  • gallstone or biliary sludge
  • hypercalcemia ot triglyceridemia
  • vascular disease (ischemia)
  • iatrogenic causes
  • hereditary
  • structural abnormalities
141
Q

what are the 3 pathogenic mechanisms of acute pancreatitis?

A
  1. duct obstruction - leads to ischemia and acinar cell injury
  2. acinar cell injury - release of proenzymes and lysosomal hydrolases leading to acinar cell injury
  3. defective intracellular transport - metabolic injury causing intracellular enzyme activation
142
Q

what are the lesions of acute pancreatitis (think: causes of acinar cell injury and activated enzymes) (4)?

A
  1. interstitial inflammation and edema
  2. proteolysis
  3. fat necrosis
  4. hemorrhage
143
Q

what is the pathogenic mechanism in which acute pancreatitis can occur via blocked secretion?

A
  1. block apical secretion
  2. proteases activated within acinar cells
  3. digestive enzymes enter interstitial space through disrupted junctions or the basolateral membrane
144
Q

what are the three types of blockages in pancreatitis?

A
  1. blocking pancreatic outflow - backflow of digestive juices
  2. allows backflow of bile into pancreas - inflammation and acinar damage
  3. prevents bile and pancreatic secretions - fatty stool and pancreatic backflow
145
Q

based on IL and cytokine activation what can pancreatitis lead to?

A
  1. vascular leakage
  2. acute tubular necrosis
  3. acute respiratory distress syndrome
  4. shock
  5. hypovolemia
146
Q

acute pancreatitis can cause what type of hemorrhage (colour) and what type of necrosis (colour and type)?

A
  • hemorrhae - red-black
  • necrosis - yellow-white fat
147
Q

what are the clinical manifestations of acute pancreatitis?

A
  1. epigastric/abdomenal pain radiating to the back (band-like, not localized)
  2. abdominal distention
  3. low-grade fever
148
Q

what are 6 things that may come back elevated in a diagnostic test if you have acute pancreatitis?

A
  1. serum amylase
  2. serum lipase
  3. aminotransferases (AST, ALT)
  4. alkaline phosphatases
  5. bilirubin
  6. lipids
149
Q

apart from elevated levels, diagnostic tests for acute pancreatitis may also show what (2)?

A
  1. hypocalcemia (caclium sites of fat necrosis)
  2. leukocytosis
150
Q

apart from blood/serum tests what other diagnostic tests can be done?

A

abdominal x-rays, ultrasounds, or CT

151
Q

what are some treatments (4) for acute pancreatitis?

A
  1. stopping oral intake - reduce pancreatic secretions
  2. treatment of electrolyte imbalances
  3. analgesics - pain relief
  4. endoscopic treatment
152
Q

describe bacterial infection as a risk/complication of acute pancreatitis

A
  • antibiotic treatment
  • culture of aspirate fluid
  • indicative of poor prognosis
153
Q

describe abscess or hemorrhage surgical treatments as a risk/complication of acute pancreatitis

A
  • neurosectomy: debridement of devitalized tissue
  • pancreatectomy: major pancreatic resection, typically resulting in drains
154
Q

describe psuedocyst as a risk/complication of acute pancreatitis

A
  • collection of fluid within or adjacent to the pancreas
  • notable with abdominal fullness/dystention/mass/tenderness
  • managed through endoscopic or surgical drainage
155
Q

describe pancreatic ascites as a risk/complication of acute pancreatitis

A
  • persistent leak in pancreatic duct into pleural space and mediastinum
  • painless and massive
  • detected via imaging (ultrasound/ct) or aspirated fluid analysis
  • treated through prolonged parenteral nutrition or stent
156
Q

what are the two main causes of acute pancreatitis?

A

gallstones and alcohol

157
Q

describe interstitial pancreatitis’ progression

A
  1. diffused localized inflammation through pancreatic body and tail
  2. transient organ dysfunction, acute fluid collections, mortality (<2%)
  3. resolution of fluid infilration or pseudocyst
  4. resolution
158
Q

describe the progression of necrotizing pancreatitis

A
  1. persistent organ failure, severe acute pancreatitis, mortality (15-20%)
  2. sterile necrosis (10% mortality), infected necrosis (30% mortality)
  3. walled off pancreatic necrosis
159
Q

briefly describe chronic pancreatitis and it’s predisposing factors

A
  • chronic inflammatory lesions in pancreas associated with alcohol intake, does not increase risk for cancer
  • predisposing factors: alcohol consumption, idiopathic, hereditary
160
Q

describe the pathogenesis of chronic pancreatitis

A
  • necrosis of exocrine parenchyma (surrounding connective tissue) followed by fibrosis
  • leads to calcification and obstructed flow of pancreatic juices
  • persistent symptoms secondary to dysfunction over weeks and months
161
Q

describe the mechanism of chronic pancreatitis via hypersecretion

A
  • acinar hypersecretion
  • viscous pancreatic secretions
  • protein plug formation from inappropriate protein breakdown
162
Q

describe the mechanism of chronic pancreatitis via acinar atrophy

A
  • acinar cells without zymogen granules (unhealthy)
  • ductal stricture and fibrosis - no lumenal diameter
  • protein plug formation (intraductal)
  • may be due to ischemia
  • nothing flows out - may cause necrosis
163
Q

what are some clinical manifestations of chronic pancreatitis?

A
  1. diabetes - progressive loss of islets
  2. malabsorption - fat, vitamins A, D, E, and K
  3. weight loss - poor intake related to pain
  4. insidious onset of steady pain
  5. nausea
  6. 5 years of continual pain before decrease in symptoms
164
Q

what are some complications of chronic pancreatitis?

A
  • pseudocyst
  • pancreatic ascites
  • obstruction of common bile duct
  • portal and splenic vein thrombosis - may lead to GI hemorrhage
  • peptic ulcer disease
165
Q

what are some treatments for chronic pancreatitis?

A
  1. pancreatic sphincterotomy - manage stones
  2. endoscopic drains of pseudocysts
  3. biliary/pancreatic stents
  4. whipple procedure
166
Q

despite pancreatic cancer only being about ____% of cancer its ranks ____th among deaths due to malignancies

167
Q

what is the median survival rate and mortality % of pancreatic cancer?

A
  • 1 year median survival rate
  • 95% mortality
168
Q

is metastases in pancreatic cancer common or uncommon? when does it occur in cancer progression?

A
  • common
  • occurs early
169
Q

what are some clinical manifestations of pancreatic head tumors?

A
  • jaundice
  • malabsorption
  • weight loss
170
Q

what are some clinical manifestations of pancreatic tail tumors?

A
  • abdominal pain
  • nausea
171
Q

what percent of pancreatic carcinomas are located in the head of the pancreas?

172
Q

how does mutations with the PRSS1 gene lead to hereditary pancreatitis?

A

constitutively active trypsin leads to protein degradation, inflammation, abnormal phenotypes, and cancer progression

173
Q

what is the most commmon type of pancreatic cancer? what activation/inactivation occurs?

A
  • adenocarcinoma
  • KRAS activation, p53 inactivation
174
Q

what type of neoplasia occurs in pancreatic cancer?

A
  • low or high grade intraepithelial neoplasia
176
Q

what are some key mutations that occur in pancreatic cancer?

A
  • p16
  • tp53
  • SMAD4
  • BRCA2
177
Q

what are some fibrotic microenvironment features of pancreatic cancer (5)?

A
  1. abundance of ECM
  2. excessive active fibroblasts
  3. hypoxia
  4. low nutrients
  5. immune cells
178
Q

what are some metabolic reprogramming feature of pancreatic cancer?

A
  1. glucose and glutamine uptake
  2. lipid and protein uptake
179
Q

what are 2 factors that determine pancreatic cancer resectability?

A
  1. arterial/venous involvement
  2. metastases
180
Q

describe stage 1a pancreatic cancer by:
* tumor grade
* nodal status
* distant metastases
* median survival (months)

A
  • tumor grade: T1
  • nodal status: 0
  • distant metastases: 0
  • median survival (months): 24.1 months
181
Q

describe stage 1b pancreatic cancer by:
* tumor grade
* nodal status
* distant metastases
* median survival (months)

A
  • tumor grade: T2
  • nodal status: 0
  • distant metastases: 0
  • median survival (months): 20.6
182
Q

describe stage 2a pancreatic cancer by:
* tumor grade
* nodal status
* distant metastases
* median survival (months)

A
  • tumor grade: T3
  • nodal status: 0
  • distant metastases: 0
  • median survival (months): 15.4
183
Q

describe stage 2b pancreatic cancer by:
* tumor grade
* nodal status
* distant metastases
* median survival (months)

A
  • tumor grade: T1, T2, or T3
  • nodal status: 1
  • distant metastases: 0
  • median survival (months): 12.7
184
Q

describe stage 3 pancreatic cancer by:
* tumor grade
* nodal status
* distant metastases
* median survival (months)

A
  • tumor grade: T4
  • nodal status: 0 or 1
  • distant metastases: 0
  • median survival (months): 10.6
185
Q

describe stage 4 pancreatic cancer by:
* tumor grade
* nodal status
* distant metastases
* median survival (months)

A
  • tumor grade: T1, T2, T3, T4
  • nodal status: 0 or 1
  • distant metastases: 1
  • median survival (months): 4.5
186
Q

what are some clinical manifestations of pancreatic cancer (12)?

A
  1. abdominal pain
  2. anorexia
  3. weight loss
  4. jaundice
  5. diarrhea
  6. weakness
  7. palpable gallbladder
  8. constipation
  9. hematemesis/melena (dark feces)
  10. vomiting
  11. abdominal mass
  12. migratory thrombophlebitis
187
Q

what are some abnormal lab tests that may occur with pancreatic cancer?

A
  • increased: AST, bilirubin, amylase
  • decreased: albumin
188
Q

what does the liver produce? what is its function?

A
  • bile - emulsifies lipids
189
Q

what is the function of the hepatic portal system?

general

A

drain blood from the digestive tract to the liver

190
Q

where is the liver located in the body?

A

right quadrant of the abdomen

191
Q

what are the 3 components of the structure of the liver?

A
  1. hepatocytes
  2. lobules
  3. sinusoids
192
Q

what is characteristic of the structure of the liver that allows it to filter?

A

integrated vascular supply (all hepatocytes have contact with vasculature)

193
Q

what is the function of the hepatic vein?

A

transport blood from the liver through the inferior vena cava to the heart

194
Q

what is the function of the proper hepatic artery?

A

deliver oxygenated blood from the abdominal aorta to the liver

195
Q

what is the function of the hepatic portal vein?

A

deliver oxygenated blood from the GI tract to the liver

ingested nutrients and toxins undergo metabolism w/n hepatocytes

196
Q

what is the function of the hepatic ducts?

A

transport bile from the liver to the gallbladder

197
Q

what is the function of the common bile duct?

A

transport bile from the gallbladder to the duodenum (SI)

198
Q

describe bile by its:
* colour
* production site
* released into…
* contents
* function
* acidity

A
  • colour: yellow-green
  • production site: liver
  • released into: duodenum by sphincter of oddi
  • contents: bile salts, bilirubin, cholesterol, triglycerides, phospholipids
  • function: emulsifies fat and increase fat absorption (good for fat-soluble vitamins)
  • acidity: alkaline (no HCl)
199
Q

what percent of bile acids are recirculated? what percent are synthesized de novo?

A
  • recirculated: 90%
  • de novo: 10%
200
Q

what blood vessel carries blood from the digestive tract capillary beds to the liver capillary beds?

A

hepatic portal vein

201
Q

heptocyte failure can be attributable to what (3)?

A
  1. loss of hepatocyte function
  2. disruption of blood flow
  3. disruption of bile flow
202
Q

what are some clinical manifestations of hepatocyte failure? (8)

A
  1. jaundice
  2. ascites
  3. muscle wasting
  4. excess blood loss
  5. blood protein deficiency
  6. vitamin deficiency
  7. hormone deficiency
  8. glucose imbalances
203
Q

what is jaundice and what is it caused by?

A
  • yellowing of skin and whites of eyes, amber colour urine
  • caused by insufficient bilirubin metabolism
204
Q

what is the typical pathway of hemoglobin breakdown?

A

hemoglobin -> heme + globin
heme -> bilirubin
globin -> amino acids

205
Q

explain how red blood cell aging and destruction occurs

A
  1. enzymatic activity and membrane lipids of rbc decrease
  2. mononuclear phagocytes engulf rbc where they are digested by proteolytic and lipolytic enzymes
206
Q

where are the majority of old red blood cells processed?

A

spleen and liver

207
Q

describe the process of bilirubin metabolism (7 steps)

A
  1. heme - hemeoxygenase -> iron + heme (biliverdin)
  2. beiliverdin - biliverdin reductase -> bilirubin
  3. bilirubin and albumin transported to liver via plasma
  4. bilirubin uptake into liver
  5. bilirubin conjugation via UDP-GT
  6. at ER membrane: bilirubin monoglucuronide and diglucuronide generated
  7. bilirubin monoglucuronide and diglucuronide excreted through canaliculi
208
Q

within the intestine what does bacterial beta-glucuronidases generate?

A

urobilinogen

209
Q

describe pre-hepatic jaundice

A
  • excessive rbc destruction
  • elevated unconjugated bilirubin levels
210
Q

describe hepatic jaundice

A
  • when there is hepatocyte disease/dmg
  • elevated levels of conjugated and unconjugated bilirubin
  • liver unable to process bilirubin
211
Q

describe post-hepatic jaundice

A
  • liver unable to process bilirubin
  • build up of bile in liver due to obstructed bile flow into gallbladder or duodenum
  • elevated conjugated bilirubin
  • lightly colored stool (absence of bile)
212
Q

what are some syndromes that explain genetic mechanism of jaundice (5)?

A
  1. dubin-johnson
  2. rotor’s
  3. crigler-najar
  4. neonatal hyperbilirubinemia
  5. gilbert’s
213
Q

describe portal hypertension by its:
* definition
* cause
* result (varices in what locations)

A
  • definition: increased pressure due to impaired blood flow through the liver
  • causes: liver tissue degeneration, GI flow congestion
  • result: varices - esophageal, gastric, hemorrhoidal, periumbilical
214
Q

describe gastroesophageal varices and what it can lead to

A
  • venous network surrounding the proximal stomach and esophagus
  • can rupture and cause GI bleeding
215
Q

in gastroesophageal varices why does the venous pathway dilate?

A

in response to elevated portal pressure to try and transport blood from splanchnic bed around cirrhotic liver and back to heart

216
Q

describe GI ascites by:
* definition
* causes
* manifestation
* treatment

A
  • definition: accumularion of fluid within peritoneal cavity
  • causes: portal hypertension, plasma hypalbuminemia
  • manifestation: abdominal distention
  • treatment: paracentesis - relieve pressure and allow for assessment
217
Q

what are the two main pathologies of the liver?

A

hepatitis
cirrhosis

218
Q

what are the 5 main causes of hepatitis?

A
  1. idiopathic
  2. alcoholic
  3. viral
  4. infection elsewhere in the body
  5. chemical or drug toxicity
219
Q

describe chronic persistent hepatitis

A
  • chronic low-grade liver inflammation (any cause)
  • inflammation confined to portal triads
  • no destruction of normal liver structures
  • manifestations: asymptomatic or mild, non-specific
220
Q

describe chronic active hepatitis

A
  • progressive, destructive liver inflammation
  • lasts more than 6 months
  • extends to hepatic lobule (piecemeal necrosis)
  • may progress to cirrhosis
  • manifestations: fatigue, nausea, malaise, anorexia, ascites, heptomegaly, pain, jaundice
221
Q

what are some structural differences present in liver with chronic injury (ECM)?

A
  • loss of microvilli/fenestration of hepatocytes
  • increased fat cells (fatty liver disease) in ECM
  • increased rigidity of ECM
222
Q

describe cirrhosis by:
* characterization
* liver state
* result
* association
* testing

A
  • characterization: extensive diffusive fibrosis that causes bile to back up and interferes with blood supply
  • liver state: fibrotic, scarred, nodular
  • result: permanent alteration of hepatic blood flow and liver function
  • association: loss of lobular organization
  • testing: liver biopsy and serologic testing
223
Q

describe/define biliary cirrhosis

A
  • inflammation and scarring of liver
  • obliteration of bile ductules
  • diffuse, widespread fibrosis
  • nodule formation
224
Q

describe the 3 stages of cirrhosis (alcoholic liver disease)

A

1. intial - fatty liver
* liver enlargment
* asymptomatic and reversible
2. second - alcoholic hepatitis
* inflammation and cell necrosis
* fibrous tissue formation - irreversible
3. third - end stage cirrhosis
* fibrotic tissue replaces normal tissue
* little normal function

225
Q

describe alcoholic fatty liver

A
  • fat accumulation in liver cells
  • more fat delivered than can be metabolized by hepatocytes
  • mild, asymptomatic, liver enlargment, abdominal discomfort, portal hypertension
226
Q

describe alcoholic hepatitis

A
  • active inflammation of the centrilobular region of the liver
  • neutrophilic infiltration and intracellular inclusions (mallory bodies)
227
Q

what are some functional losses with cirrhosis

never gonna get them all - moreso for cntrl f

A
  • decreased removal/conjugation of bilirubin
  • decreased bile production
  • impaired digestion and absorption of nutrients
  • backup of bile in liver
  • decreased production of blood-clotting factors
  • imapired glucose/glycogen metabolism
  • impaired ammonia -> urea conversion
  • decreased inactivation of hormones and drugs
  • decreased removal of toxic substances
  • blockage of blood flow through liver = portal hypertension
  • spleen congestion = hemolysis
  • inadequate storage of iron and vitamin B12
  • esophageal varices and potential homorrhage
  • ascites causing abdominal distention and pressure
228
Q

what are some initial clinical manifestations of cirrhosis?

A
  • often mild/vague
  • fatigue, anorexia, weight loss, anemia, diarrhea
  • dull aching pain
229
Q

what are some clinical manifestations of advanced cirrhosis

A
  • ascites and periperhal edema
  • increased bruising
  • esophageal varices
  • jaundice
  • encephalopathy
230
Q

what is the general function of the gall bladder?

A

store concentrates and bile

231
Q

what is the composition of bile?

A
  • water
  • electrolytes
  • organic solutes
  • bile acids
  • pigment
  • cholesterol
  • phospholipids
232
Q

what are the primary bile acids?
where are they made?
what is their precursor?

A
  • cholic and chenodeoxycholic acids
  • made in the liver
  • cholesterol precursor
233
Q

what are the secondary bile acids?
where are they made (via what)?

A
  • deoxyhcolic acid, lithocholic aicd, ursodeoxycholic acid
  • made in intestinal tract via microbial metabolism
234
Q

define and describe cholelithiasis

A

formation of gallstones - calculi (solid material) that form in the bile

235
Q

define and describe cholecystitis

A

inflammation of the gallbladder wall and/or cystic duct

236
Q

define and describe acalculous cholecystitis

A

inflammation of the gallbladder wall and/or cytic duct in the absence of stones

237
Q

define cholangitis

A

inflammation usually related to infection of the bile ducts

238
Q

define choledocholithiasis

A

obstruction of the biliary tract by gallstones

239
Q

where can gallstones be present?

A

bile ducts, gall bladder, cystic duct

240
Q

what do gallstones typically consist of?

A

cholesterol aggregates and/or calcium

241
Q

describe gallstone formation

A
  • supersaturation of bile with cholesterol causing precipitation
  • nucleation of crystals
  • hypomotility (stasis of bile) or general movement of anatomy that allows formation
242
Q

pain associated with gallstones typically occurs when?

A

when stones move throughout the ductal system

243
Q

what are some risk factors for gallstones (3)?

A
  • high cholesterol in bile
  • high cholesterol intake
  • obesity
244
Q

what is the composition of pigment stones?

A

pigment polymers and calcium salts

245
Q

describe black pigment stones

A
  • most common
  • idiopathic or associated with cirrhosis or hemolysis
  • excess bilirubin, rbc degradation, hemolysis
246
Q

describe brown pigment stones

A
  • common is areas with greater risk of parasitic infection
  • associated with biliary parasitosis, bacterial colonization, and infection
247
Q

what are some clinical manifestations of gallstones

A
  • asymptomatic
  • obstruction of duct by large calculi causing radiating pain
  • epigastric pain in upper right abdomen
  • nausea and vomiting
  • bile back up to liver
  • risk of rupture
248
Q

describe chronic cholelithiasis by:
* biliary colic
* manifestations
* diagnosis
* treatment

A
  • biliary colic - intermittment obstruction of cystic duct
  • mani: worse with meal, persistent epigastric radiating pain, nausea/vomiting/sweating, increases steadily for 15 min, fatty food intolerance
  • diagnosis: ultrasound
  • treatment: cholecystectomy, chemical dissolution of stones, lithotripsy (mechanical breaking of stones)
249
Q

describe acute cholecystitis by:
* definition
* clinical manifestations
* diagnosis
* treatment

A
  • definition: acute inflammation of gallbladder wall, obstruction of cystic duct frequently (related to bile stasis)
  • manifestations: severe abdominal pain, radiates to back, fever, leukocytosis, mild elevations of bilirubin and serum transaminases
  • diagnosis: abdominal ultrasound
  • treatment: laparoscopic cholecystectomy, antibiotics
250
Q

describe acaclulous cholecystitis

A
  • occurs in patients without preexisting gallstones
  • males >50
  • typically occurs in major surgery, critical illness, trauma, burn-related injury, total parenteral nutrition
  • rapid development of gangrene, perforation, emphysematous cholecystitis , and empyema
251
Q

describe chronic cholecystitis

A
  • chronic inflammation of gallbladder wall
  • low-grade irritation from gallstone, recurrent acute attacks
  • predisposing factors: diabetes, obesity
  • clinical manifestations: asymptomatic / intermittement biliar colic or acute attacks
  • complications; biliary sepsis, porcelain gallbladder, higher risk of cancer
252
Q

provide an overview of the appendix and its functions

A
  • vermiform organ that protrudes from cecum
  • right quadrant of abdominal cavity
  • function - immunoprotective function, containment of good bacteria
253
Q

what are some causes of appendicitis?

A
  • appendicolith
  • fecalith
  • tumors that could be benign or malignant
  • intestinal parasites
  • hypertophied lymphatic tissue
  • unknown exact etiology
254
Q

what are some clinical manifestations of appendicitis?

A
  • intrluminal pressure build up
  • neutrophil buildup
  • lower right quadrant abdominal pain
  • localized, sharp, stabbing pain
  • fever
  • malaise
  • urinary frequency/urgency
255
Q

how is appendicitis diagnosed?

A
  • physical exam and clinical presentation
  • blood work with elevated leukocytes
  • imaging
257
Q

how is appendicitis treating?

A
  • surgical removal via appendectomy
  • ruptured - irrigation through abdominal cavity

HLTH 341 - Pathobiology (3 decks)

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