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Patho 2nd Semester > GI Disorders > Flashcards

GI Disorders Flashcards

1
Q

Diverticulosis…

A

entry to out pouch is patent, asymptomatic

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2
Q

Why would a fever occur without the presence of exogenous pyrogens?

A

Injured or abnormal cells induce production of endogenous pyrogens

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3
Q

Tx for diverticular disease

A

address etiologic/risk factors, if complications occur tx, inflammation, sx. for obstruction or perforation

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4
Q

Irritable Bowel Syndrome (IBS) is what kind of GI disorder

A

MOTILITY

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5
Q

Are there abnormal structural or functional components in IBS?

A

None obvious.

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6
Q

What layers are involved in diverticular disease?

A

Mucosa herniates through muscular externa

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7
Q

Etiologic factors for IBS

A

Usually triggers (diet, stress, smoking, lactose, etc)

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8
Q

1st Patho theory for IBS (re: malabsorption)

A

Malabsorption of fermentable CHO & polyols. These are processed by gut flora, and the by product is gas, which leads to flatulence experienced by those w IBS

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9
Q

2nd Patho theory for IBS (re: serotonin)

A
  • Altered CNS regulation of GI sensory & motor fx
  • Molecular signalling defect for serotonin (in its synthesis, binding, transmission, etc) which leads to effects linked to serotonins functions (pain on peristalsis, etc)
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10
Q

Serotonin’s fx within the GIT

A

facilitates motility, secretion, perfusion, and pain

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11
Q

What must be excluded when diagnosing IBS?

A

Organic disease.

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12
Q

What 2 factors contribute to an out pouching to occur?

A

Increased intraluminal pressure & a weakened entry point

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14
Q

Etiology/Risk factors for diverticular disease

A

Poor diet (low fibre), inactivity, poor bowel habits (constipation, aging

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15
Q

Pharma Tx for IBS

A

antispasmodic drugs (to address peristalsis problem) EG. MODULON
antidiarrheals/laxatives
Abx (to lower normal gut flora causing flatulence)

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16
Q

Where can outpuchings occur in Diverticular Disease? Usually where?

A

Anywhere in the GIT. Sigmoid colon

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17
Q

How do the etiologic factors work within the peritoneum?

A

Must enter the peritoneal cavity via

  • PERFORATED ULCER
  • RUPTURED APPENDIX
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18
Q

Peritoneum is highly vascularized. This leads to…

A

Rapid absorption of bacterial toxins

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19
Q

What causes ileus in peritonitis?

A

SNS compensation to limit GI motility

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20
Q

Mnfts of diverticulitis

A

dull pain, nausea, vomiting, low grade fever

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21
Q

Diverticulitis…

A

entry to out pouch is strangulated. Inflammation and mnfts

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22
Q

Fluid shift from peritoneal cavity into bowels leads to…

A

Mucoid stools and increased intraluminal pressure

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23
Q

What leads to hyperemia in peritonitis?

A

Altered perfusion, vasodilation, and blood shunting d/t serious inflammation

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24
Q

What mainly leads to fluid shifts and the potential for hypovolemia in peritonitis?

A

Fluid shifting into the bowels and the peritoneal cavity (as exudate)

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25
Q

Tx for peritonitis

A

IV Abx
fluids and electrolytes
pain management
sx if indicated

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26
Q

Appendicitis is…

A

inflammation of the appendix WALL

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27
Q

Etiologic factors of appendicitis

A

Entry to appendix obstructed by:

  • fecalith
  • twisted appendix/bowel
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28
Q

Non Pharma Tx for IBS

A

Eliminate trigger, decrease stress.

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28
Q

Ethology of Peritonitis

A

Bacterial (E.Coli)

Chemical (HCl, bile, pancreatic juice)

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29
Q

When drainage of cecum is blocked in appendicitis, this leads immediately to…

A

Mucous secretion, which increases intraluminal pressure

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30
Q

Increased intraluminal pressure by blocked cecum/mucous secretion leads to…

A

Venous pressure is overcome by IL pressure, cutting off venous supply, then arterial supply. This leads to ischemia and necrosis

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31
Q

Once necrosis of the appendix wall occurs…

A

Bacteria within the appendix enter the wall, causing inflammation and infection

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32
Q

How does the course of pain look in appendicitis

A 
PERIUMBILICAL PAIN ~12 hrs (pain increases, colicky, dull pain)
LRQ PAIN (rebound pain)
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33
Q

Tx for appendicitis

A

IV fluids, Abx, analgesics, appendectomy (w/i 24-48 hrs, or perforation and sub sequential peritonitis can occur)

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34
Q

Thick exudate formed in peritonitis is good because..

A

Limits Spread

Seals up perforation

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35
Q

Inflammatory Bowel Disease (IBD) includes which 2 diseases?

A

Crohn’s Disease & Ulcerative Colitis

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36
Q

Ethology for IBD

A

environmental trigger (bacterial infection) & genetic susceptibility

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37
Q

Which area of the GIT is most affected in Crohns?

A

Ileum of small intestine

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38
Q

Which area of the GIT is most affected in UC?

A

Colon & rectum

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39
Q

manifestations of IBS

A

abdominal discomfort, pain, diarrhea/constipation, flatulence, nausea, mucoid stool

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41
Q

Which layer of the GIT is affected in UC?

A

mucosa

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42
Q

Granulomatous skip lesions are characteristic of…

A

Crohn’s disease

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43
Q

Which kinds of lesions are present in UC?

A

Continuous ulcerative lesions

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44
Q

Diarrhea is present in both UC and C? T/F?

A

T

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45
Q

Bleeding occurs in UC/C?

A

UC

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46
Q

Are those with Crohns or UC more likely to develop strictures/fistulas?

A

Crohns

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47
Q

Development of CA is most common in which IBD?

A

Ulcerative Colitis

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48
Q

What happens to the ulcerations in UC?

A

They harden and thicken.

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49
Q

Inflammation in UC leads to what in the lumen?

A

Exudate moving into the bowel, leading to edema/congestion.

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50
Q

What direction of spread do the lesions in UC follow?

A

Proximal to distal (anus to gut)

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51
Q

Why does dyspnea occur in peritonitis?

A

Pt is in ++ pain, will not want to irritate abdomen further by breathing

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52
Q

Why does weight loss occur in UC?

A

There is an impediment in the bowel

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53
Q

First line tx for IBD

A

SULFASALAZINE (antiinflammatory) & ABX

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54
Q

What other pharmacologic interventions are given if IBD not responsive to first line tx?

A 
Steroids
Immunomodulatory drugs (METHOTREXATE)
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55
Q

What 2 factors must be in place for a hernia to occur? Some examples of each?

A

Increased intraluminal pressure (pregnancy, obesity) and a weakened retaining structure (trauma, aging, congenital defects)

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56
Q

Sliding Haitial Hernia

  • What enters the thoracic cavity?
  • mnfts?
A
  • GEJ & upper part of stomach

- pain, heartburn, reflux

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57
Q

Rolling Haitial Hernia

  • What enters the thoracic cavity?
  • Where is the GEJ?
  • mnfts?
A
  • non-upper part of stomach
  • below the diaphragm
  • dyspnea (lung impacted), fullness after meals (lowered volume of stomach)
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58
Q

Fundoplication

  • for what disorder?
  • what 2 benefits?
A
  • Haitial hernias

- increases GEJ size (lowers chance of moving) and fortifies cardiac sphincter (to decrease reflux)

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59
Q

Inguinal Hernia

  • organs protrude through what?
  • usually contains…
  • what forms hernial sac?
A
  • Inguinal ring into scrotum
  • intestines & momentum
  • peritoneum
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60
Q

What other mnfs besides pain accompany appendicitis?

A

Nausea, vomiting, increased WBCs

61
Q

What happens at the cellular level in IBD?

A

IR targets normal gut flora, as well as the lining of the GIT the flora is attached to. There is a loss of tolerance towards the normal gut flora, causing inflammatory damage

62
Q

Indirect Hernia…

A

Herniation through existing aperture

63
Q

Peptic ulcer disease usually affects which area and layer …

A

Duodenum & Stomach, mucosa layer

64
Q

Etiology of PUD

A

Helicobacter pylori infection.

  • attach via adhesion proteins, release urease = bicarbonate = neutralizing acid to live
  • mechanism to create ulcer unclear, but bacterial infection = inflammation, and increased acid secretion = tissue damage
  • HP stimulates host cell to secrete gastrin = increase HCl sec = hypergastrinemia
65
Q

Risk factors for PUD

A

Stress, HCl/biliary acids, NSAIDS, smoking, chronic gastritis

66
Q

What defences does the body have against gastric secretion?

A
  • regulates HCl sec
  • perfusions takes away toxins and brings defence
  • epithelial lining regenerates itself
67
Q

Why will there be nutritional deficiency and weight loss in Crohns?

A

Loss of absorptive area d/t inflammatory damage (S.I.) = decreased absorption.

68
Q

Manifestations of PUD?

A

abd pain, nausea/vomiting

69
Q

Potential complications of PUD

A

perforation = peritonitis
damaged BVs = hemorrhaging
gut obstruction from scar tissue/edema/spasm

70
Q

3 unique tests for PUD

A

Serology (for Abs against HP)
UBT
Fecal Ag (surface markers on HP)

71
Q

Etiology for hepatitis

A

Microbial infection (usually virus)
Hepatotoxins
Autoimmunity

72
Q

Which layer of the GIT is affected in Crohns?

A

submucosa

73
Q

Tx for PUD

Why these drugs

A

Triple regimen
- PPI/H2RA + 2 Abx

PPIs block H sec
H2RA block histamine, needed for HCl sec

74
Q

HEPATITIS B

  • severity
  • MOT
  • incubation period
  • carrier state?
A
  • more severe, some chronic cases
  • saliva/serum
  • 28- 160 days
  • carrier state possible
75
Q

3 Main Patho points for Viral Hepatitis

A

IR & viral damage = damage/necrosis = decreased hepatocyte fx

Vasculature & ducts = inflammatory damage

Healing in ~4 months for acute forms (for complete hepatocyte regeneration)

76
Q

Etiologic factors for cirrhosis

A 
chemicals (ETOH abuse)
viral damage (Hep C)
drugs (Methotrexate)
Biliary disease
Metabolic disorders (hemochromatosis = overload of Fe, deposit in liver = toxicity)
cryptogenic (=idiopathic)
77
Q

Examples of drugs used for PUD

A

PPI: Losec
H2RA: Zantac
Abx: Amoxil & Biaxin

78
Q

Why is there no reflux in a rolling hiatial hernia?

A

Content is going and staying within stomach

79
Q

Mnfts during Prodromal Stage of Viral Hepatitis

WHY ABD PAIN?

A

Lethargy, myalgia, fever, anorexia, nausea, vominting, abd pain.

Liver swells = liver capsule stretched = pain

80
Q

Direct Hernia…

A

Herniation through retaining structure

81
Q

Tx for viral hepatitis?

A

rest, eliminate hepatotoxic drugs, diet changes, pain/pruritis relief, post exposure prophylaxis

82
Q

Prophylaxis for Hep A/B

A

gamma globulins/vaccine

83
Q

HEPATITIS C

  • severity
  • MOT
  • incubation period
  • carrier state?
A
  • worst, most severe, almost all cases become chronic
  • blood & sexually transmitted
  • 15-160 days
  • frequent carrier states
84
Q

Prophylaxis for Hep C

A

no vaccine, antiviral drugs

85
Q

Etiology for Autoimmune Hepatitis

A

complex trait, gene mutations of HLA on Chr 6, environmental trigger (viral infection/chemicals)

86
Q

Type 1 Autoimmune Hepatitis

A

affects women
Antinuclear Abs (target nuclear cell components)
Anti-smooth-muscle Abs (target SM of ducts and vessels)

87
Q

Stage 4 CR CA

A

metastatic tumors penetrate serosa and adjacent organs

88
Q

HEPATITIS A

  • severity
  • MOT
  • incubation period
  • carrier state?
A
  • mild, self limiting, acute
  • oral fecal
  • 15-50 days
  • NO
89
Q

Type 2 Autoimmune Hepatitis

A 
young kids (2-14)
Anticytosol and Antimicrosome Abs
90
Q

Dx for Autoimmune Hepatitis

A

exclude viral hep and other liver disease

there will be increased serum gamma globulins

91
Q

Colorectal Cancer
Etiology
Risk Factors

A

Idiopathic

increased age, family hx, IBD, high dietary fat and refined sugars, and inadequate intake of protective macronutrients

92
Q

High levels of dietary fat contribute to colorectal CA how?

A

High fat = high synth bile

Bile is converted by bacterial flora into potential carcinogens

93
Q

Aspirins role in protecting against colorectal CA?

A

Decreases synthesis of prostaglandin, which can influence cell proliferation and tutor growth

94
Q

When do manifestations subside? What is this stage called in viral hepatitis?

A

~3 weeks. Recovery stage

95
Q

Stage 1 CR CA

A

tutor limited to invasion of mucosal and submucosal layers

96
Q

Stage 2 CR CA

A

tutors goes into but not through muscular externa

97
Q

When do mnfts occur in CR CA?

A

CA present for long time before any presentations. Early = bleeding

98
Q

MNFTS of CR CA

A

changes in bowel habits, urgency, incomplete emptying.

99
Q

Tx of CR CA

A

sx removal
preoperative radiation
postoperative chemotherapy

100
Q

Cirrhosis is..

A

end stage liver disease

101
Q

In a nutshell, what happens that leads to cirrhosis. What primary problems do we encounter?

A

hepatocytes = necrosis = formation of scar tissue (fibrosis) = nodular liver

decreased liver fx and portal HTN

102
Q

3 Main points for Patho of Cirrhosis

A
  • hepatocytes destroyed and are replaced w non fx fibrinous scar tissue = puts pressure on vessels and become constricted = impeded perfusion
  • duct constrictions = impeded bile flow = bile stasis
  • decreased metabolic waste clearance = toxicity
103
Q

Complications of cirrhosis

What is their chance of occurring?

A

portal HTN, ascites, varices, GI bleeds, splenomegaly

They will always occur

104
Q

Tx for cirrhosis

A

maximize hepatocyte regeneration by…

  • modifying diet (decrease fat)
  • eliminating hepatotoxins
  • managing comps as they arise
105
Q

Portal HTN = ? in mmHg?

A

> 12 mmHg

106
Q

Complications of portal HTN

A 
Ruptured varix (eg. esophageal vein)
ascites, portosystemic shunts, splenomegaly
107
Q

Ascites is…

A

ACCUMULATION of fluid in the abdominal cavity

108
Q

Stage 3 CR CA

A

tumor invades serosal layer, regional lymph node involvement

109
Q

Why dyspnea in ascites?

A

Fluid opposes movement of diaphragm

110
Q

Protective macronutrients against colorectal CA

A

Vit A, C, E.

Free radical scavengers

110
Q

Dx of CR CA

A

digital rectal exam, FOBT, barium enema, sigmoidoscopy, colonoscopy

111
Q

Tx for small volume ascites (

A 
Diuretics
Dec. BV = Dec HP 
HP in cavity > HP in vessel
fluid -> vessel
Can be excreted
112
Q

Tx for large volume ascites (>5L)

A

paracentesis and volume expander (eg. albumin)

113
Q

Is liver failure acute or chronic?

A

Can be both

114
Q

Etiologic factors leading to acute liver failure

A

toxic liver damage, fulmiant hepatitis

115
Q

Etiologic factor leading to chronic liver failure

A

cirrhosis

116
Q

How is hematology impacted in liver failure?

A

impaired protein synth = impaired haemostats & anemia

depressed marrow fx (liver cannot supply resources) = leukopenia and thrombocytopenia

inadequate clearance of activated CFs = disseminated intravascular coagulation DIC (liver isn’t removing CFs = remain active = clotting w/i BVs)

GI Bleeds

117
Q

How is metabolism affected in liver failure?

A

inadequate bilirubin clearance = JAUNDICE
hypoalbuminemia = EDEMA/ASCITES
defective urea cycle = HYPERAMMONEMIA
decreased estrogen catabolism = HYPERESTROGENSIM

118
Q

What is hepatorenal syndrome? In which disease does it occur?

A

Severe decrease in renal perfusion. Portal HTN = blood shunting = decreased perfusion to kidneys = low renal perfusion.

Leads to OLIGURIA (low urine volume) and AZOTEMIA (build up of nitrogenous products in blood)

Liver failure

119
Q

Why does hepatic encephalopathy occur in liver failure?

A

Toxic compounds are not detoxified by liver d/t liver failure and portosystemic shunts. This leads to a build up of these toxins and their entrance into the systemic circuit out of the hepatic venous circuit.

120
Q

Mnfts during Clinical Stage of Viral Hepatitis

WHY PRURITIS?

A

manifestations during prodromal persist and worsen, jaundice, hepatomegaly, tender liver, pruritus

bile salts deposit in skin

121
Q

What does hepatic encephalopathy present with?

A

ASTERIXIS (hand tremors)
HYPERREFLEXIA
confusion, coma, death

122
Q

Walk me through ammonia conversion in hepatic encephalopathy

A

ammonia converted to glutamate
increased levels of glutamate = increased solute concentration/altered osmolarity = cellular dehydration/death of brain

increased glutamate also alters neurotransmission (why those with HE present with hyperreflexia, etc)

123
Q

Why are purgatives used in liver failure?

A

potent laxatives = clearance of gut of proteins

no protein = no protein catabolism = no ammonia = aversion of azotemia

124
Q

Why are non absorbable Abx used in liver failure?

A

move through gut and are not absorbed, kill bacteria involved in protein breakdown

125
Q

Etiologic factors contributing to cholelithiasis

A

abnormal bile composition ( eg. inc cholesterol and dec bile salts)
bile stasis (gives rise to precipitation)
inflammatory debris (nuclei for stone formation)
genetics

126
Q

What bacteria contribute to cholelithiasis?

A

E. Coli and Strep Faecalis

Alter composition of bile and give rise to inflammatory debris for stone formation

127
Q

Cholesterol Stones

A

bile components + cholesterol

128
Q

Pigment Stones

A

bilirubin + Ca salts

129
Q

Mixed Stones

A

made of many different components

130
Q

What complications can occur in cholelithiasis

A

cholecystitis, pancreatitis, perforation

131
Q

Et for portal HTN

A

pre-hepatic, intra-hepatic, or post-hepatic issue that increases resistance to blood flow in portal system. Mostly d/t cirrhosis

132
Q

Is pancreatitis self limiting?

A

Yes

133
Q

What is the main problem in pancreatitis?

A

INflm of pancreas and auto digestion of structural components of it

134
Q

Etiologic factors pancreatitis

A

ETOH, gall stones, idiopathic, pancreatic trauma, drugs that inflict injury on the panc

135
Q

Patho pancreatitis

A

bile flow obstructed = pre mature activation of pancreatic enzymes = enzymes damage pancreas via autodigestion

136
Q

When do the mnfts present in pancreatitis

A

following alcohol binge or a large meal

137
Q

Where does the pain occur in pancreatitis

A

epigastric => back and chest

138
Q

Et/patho of ascites

A

R sided HF, portal HTN, severe changes in OP/HP, cirrhosis, Na/H20 retention

139
Q

What tx for mild pancreatitis

A

NPO, correct metabolic props (insulin/glucagon)

140
Q

Why does hyperammonemia occur in liver failure?

A

Usually, liver combined ammonia with CO2 to form urea to be excreted as waste. Since the liver is non functional, ammonia cannot be combined into urea, so there is a build up of it in the blood

141
Q

What is the best diagnostic test to determine pancreatitis?

A

measure pancreatic lipase in blood

142
Q

What tx for cholelithiasis

A 
pain management
dissolving agents (contain bile acid. e.g.. ACTIGALL. only if NO obstruction/complications)
sx (retrograde endoscopy)
143
Q

How does alcohol contribute to pancreatitis?

A

It increases pancreatic secretion and constricts the sphincter in pancreatic duct = bile and pancreas secretions accumulate in the ducts = Es activated = congestion = secretions into pancreas = auto digestion and inflam = hemorrhage and necrosis

144
Q

What are the risks for Diverticular disease?

A

ageing, poor diet, inactivity, constipation

145
Q

What layers herniate in diverticular disease?

A

mucosa herniates through muscular external

Patho 2nd Semester (6 decks)

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