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Patho 2 Exam 2 > Pathophysiology of the Digestive System > Flashcards

Pathophysiology of the Digestive System Flashcards

1
Q

Inflammatory Bowel Disease

A

Group of disorders that all have chronic inflammation and widespread ulceration in the GI tract

*Ulcerative Colitis and Crohn’s Disease –> Both as inflammatory disorders that cause intestinal ulcerations and both often present with bouts of painful bloody diarrhea and cramping

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2
Q

Ulcerative Colitis Site, Depth of Ulcers, and Pattern of Ulceration

A

Site: Only Colon

Depth of Ulcers: Shallow (mucosa), begin in the mucosa and don’t usually penetrate down into the muscle layers

Pattern of Ulceration: Continuous, the ulcers tend to begin in the rectum and sigmoid colon and the ulcers are continuous and tend to spread in an ascending way to affect more and more of the colon

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3
Q

Crohn’s Disease Site, Depth of Ulcers, and Pattern of Ulceration

A

Site: Entire GI tract (mouth to anus)

Depth of Ulcers: Deep, sometimes penetrating

Pattern of Ulceration: Patchy, skip lesions

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4
Q

Crohn’s Disease (3)

A
  1. Can cause ulcers to occur anywhere along the GI tract
    * Oral mucosa ulcers are fairly common
    * Perianal disease – ulcers around anal region
    * Stomach, small intestine, colon, etc. ulcers
  2. Pattern of ulceration: the ulcers are patchy along the GI tract; they are non-continuous
    * See scattered ulcers in a variety of places
  3. Depth of ulcers: ulcers begin in the sub-mucosa, spread in both directions, can become very deep and often penetrating
    * Can even form fistulas, where an ulcer penetrates the wall and continues to eat away at a neighboring hollow organ
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5
Q

Ulcerative Colitis (4)

A
  1. Ulcers begin in rectal/sigmoid colon and as the disease progresses the ulcers affect more and more of the colon, ascending upwards
  2. The most severe form will have ulcers extending all the way through the secum
  3. Site of inflammation begins in the mucosa
  4. As the ulcers progress, you get eating away of the lining and it moves inward
  5. May require surgery and the colon will be resected together
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6
Q

Ulcerative Colitis Definition

A

A chronic (reoccurring) inflammatory disease that causes ulceration of the colonic mucosa – usually the rectum and sigmoid colon

  • A disease of exacerbations and remissions
  • Reoccurring disorder
  • Can reduce frequency and severity but it will still happen
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7
Q

Ulcerative Colitis Clinical Manifestations (4)

A
  1. Diarrhea that may be associated with blood
  2. Bowel movements are frequent and in small volumes
  3. May also have colicky abdominal pain, urgency, tenesmus, and incontinence
  4. Patients with mainly distal disease may have constipation with frequent discharge of blood and mucus
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8
Q

Tenesmus

A

a continual or recurrent inclination to evacuate the bowels, caused by disorder of the rectum or other illness.

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9
Q

Ulcerative Colitis Characteristics of Symptoms (5)

A
  1. Onset of symptoms is gradual – progressive over several weeks
    - Can reoccur every few months
  2. Symptoms may be preceded by a self-limiting episode of rectal bleeding that occurred weeks or months earlier
  3. Most patients at first presentation of UC have mild symptoms, 27% first present with moderate symptoms, 1 % first present with severe disease.
  4. Sense of urgency and incontinence
  5. If disease is limited to rectum or lower part of sigmoid colon → can experience rectal bleeding and rebound constipation after the frequent episodes of diarrhea
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10
Q

Mild Ulcerative Colitis (6)

A
  1. Four or fewer stools per day with or without blood
  2. No signs f systemic toxicity
  3. No signs of anemia
  4. Physical examination often normal
  5. Ulcers confined to the rectum or rectosigmoid
  6. Intermittent rectal bleeding – mild diarrhea, mild cramping pain, some periods of constipation
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11
Q

Moderate Ulcerative Colitis (7)

A
  1. Involves more of the colon
  2. Frequent loose bloody stools (>4 per day)
  3. Abdominal tenderness to palpation
  4. Mild anemia not requiring blood transfusion
  5. Abdominal pain that is not severe
  6. Minimal signs of systemic toxicity such as low grade fever
  7. Adequate nutrition is maintained usually
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12
Q

Severe Ulcerative Colitis

A
  1. Extensive colon involvement that may extend to cecum
  2. Frequent loose stools (>6 per day)
  3. Severe cramps, fever > 37.5
  4. Hypotension
  5. Tachycardia
  6. Anemia
  7. Bleeding often necessitates transfusion
  8. May suffer rapid weight loss leading to poor nutritional state
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13
Q

Acute Complications of Ulcerative Colitis (4)

A
  1. Severe bleeding
  2. Fulminant Colis
  3. Toxic Megacolon
  4. Perforation
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14
Q

Ulcerative Colitis Complication: Severe Bleeding (4)

A
  1. Blood loss is a major complication
  2. Massive hemorrhage can happen to ~3% of patients
  3. May require immediate surgery
  4. Bleeding may be severe in up to 10 percent of patients. Massive hemorrhage occurs in up to 3 percent of patients with ulcerative colitis at some time in their disease course and may necessitate urgent colectomy
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15
Q

Ulcerative Colitis Complication: Fulminant Colis (3)

A
  1. Fulminant= extremely severe, happening quickly
  2. Patients with ulcerative colitis may develop fulminant colitis with more than 10 stools per day, continuous bleeding, abdominal pain, distension, and acute, severe toxic symptoms including fever and anorexia. Patients with fulminant colitis are at high risk of developing toxic megacolon.
    * This patient will look like have symptoms similar to sepsis
  3. High risk for toxic megacolon
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16
Q

Ulcerative Colitis Complication: Toxic Megacolon (6)

A

A type of intestinal obstruction

  1. Can occur when the ulcers start to get deep enough; if they are deep enough into the colon wall, they can begin to wear away at the muscle
  2. If they damage the muscle layer, then that area of the colon dilates
    - Lose muscle tone and the area dilates (becomes larger)
    - By dilating, it creates an obstruction so things can’t move past it
    - Feces accumulate in the dilated portion of the colon
    - Begin absorbing too much of the waste that is accumulating in the dilated area
  3. Inflammatory process extends beyond the mucosa to involve the muscle layers of the colon
  4. Characterized by colonic diameter ≥6 cm or cecal diameter >9 cm and the presence of systemic toxicity.
  5. Triggers significant inflammation and can lead to severe systemic toxicity
  6. Can be very life-threatening; requires immediate surgery
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17
Q

Ulcerative Colitis Complication: Perforation (3)

A
  1. Perforation of the colon most commonly occurs as a consequence of toxic megacolon
  2. Any perforation of the lower GI tract increases risk of major infection
  3. Perforation with peritonitis has been associated with 50 percent mortality in patients with ulcerative colitis
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18
Q

Crohn’s Disease (4)

A
  1. Autoimmune disorder involving chronic inflammation and ulceration of GI tract (from mouth to the perianal area)
    * The ulcers tend to be scattered and are not continuous
  2. Can see ulcers in multiple locations, that can be found anywhere along the GI tract from the mouth to the anus
  3. The ulcers can cause the portion of the GI tract to collapse down and form scar tissue/form a stricture
    * Narrow stricture causes obstruction
  4. An idiopathic disorder characterized by transmural inflammation of the GI tract
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19
Q

Clinical Manifestations of Crohn’s Disease (9)

A

Clinical manifestations of Crohn disease (CD) are more variable than those of ulcerative colitis.

  1. Fatigue
  2. Prolonged diarrhea
  3. Abdominal pain
  4. Weight loss
  5. Fever,
  6. With or without gross bleeding
  7. Malabsorption
  8. Perianal disease
  9. Fistula
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20
Q

Crohn’s Disease: Abdominal Pain (5)

A
  1. Crampy abdominal pain is a common manifestation of CD, regardless of disease distribution.
  2. Can cause muscle spasms in the abdomen
  3. The transmural nature of the inflammatory process results in fibrotic strictures.
    * These strictures often lead to repeated episodes of small bowel, or less commonly colonic, obstruction.
  4. A patient with disease limited to the distal ileum frequently presents with right lower quadrant pain.
  5. Occasionally, patients will have no clinical manifestations of CD until luminal narrowing causes constipation and early signs of obstruction with abdominal pain.
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21
Q

Crohn’s Disease Diarrhea (5)

A
  1. Diarrhea is a common presentation, but often fluctuates over a long period of time.
  2. Diarrhea associated with CD may have multiple causes, including:
  3. Excessive fluid secretion and impaired fluid absorption by inflamed small or large bowel
  4. Bile salt malabsorption due to an inflamed or resected terminal ileum
  5. Steatorrhea related to loss of bile salts
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22
Q

Crohn’s Disease Bleeding

A

Although stools frequently reveal the presence of microscopic levels of blood (eg, positive guaiac or immunochemical test), gross bleeding is less frequent than in ulcerative colitis.
*An exception to this are some patients with Crohn’s colitis.

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23
Q

Crohn’s Disease Malabsorption

A

Especially if duodenum/ileum/small intestine are involved

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24
Q

Crohn’s Disease Perianal Disease (2)

A
  1. Perianal pain and drainage from large skin tags, anal fissures, perirectal abscesses, and anorectal fistulas
  2. Fistula=channel between two structures; so rectum is forming fistula with anus and there is the draining of feces onto the surface of the skin
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25
Q

Crohn’s Disease Systemic Symptoms (2)

A
  1. Fatigue is common: fevers caused by chronic inflammation or perforation/peribowel infection.
  2. Weight loss due to obstruction induced loss of appetite or malabsorption
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26
Q

Crohn’s Disease Fistulas

A
  1. Tracts or communications that connect two epithelial lined organs.
  2. Common sites include intestine and bladder, skin, bowel, and vagina.
  3. Enteroenteric fistulas
  4. Enterovesical (bladder) fistulas that lead to recurrent UTIs
  5. Enterovaginal fistulas
  6. Enterocutaneous fistulas
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27
Q

Enterocenteric fistulas

A

Fistula between two loops of intestine that are adjacent to one another

  • Common
  • May be asymptomatic or present as a palpable mass
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28
Q

Enterovesical fistulas

A

Bladder; leads to recurrent UTIs

  • A loop between large intestine and bladder
  • Lead to recurrent UTIs due to leaking of feces into the bladder
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29
Q

Enterovaginal fistulas

A

may present with passage of gas or feces from the vagina

  • A loop between intestine and vagina
  • Passage of feces into vagina
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30
Q

Enterocutaneous fistulas

A

can cause bowel contents to drain to the surface of the skin

*Can cause bowel contents to drain onto the surface of the skin

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31
Q

Diverticuli Disease (6)

A
  1. A relatively common disease that is age dependent
  2. Excessive intra-colon pressure causes herniation of the colon mucosa at weak points along the colon wall
  3. Usually asymptomatic unless diverticuli become inflamed, infected, or rupture
  4. A condition that is nearly non-existent in anywhere other than the first world because the first world is the only place that you can get access to enough refined carbohydrates
  5. The pouches are asymptomatic
    * Usually found incidentally with colonoscopy
  6. If the pouches become inflamed, irritated, if material gets trapped in them, or if they rupture then you get → diverticulitis (inflammation of the diverticuli)
    * This will cause intense stomach pain, abdominal cramping
    * In the case of perforation, it can cause fever and peritonitis
    * Need antimicrobial drugs to prevent progression to sepsis
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32
Q

Diverticuli (5)

A

The individual pouches causing the disease

  1. The pouches are herniations of colonic mucosa
  2. Herniate along the points where there is slight vulnerability; where blood vessels or nerves move through
  3. The mucosa gets pushed through the vulnerability and creates the pouch
  4. Pouches are caused by increased intracolonic pressure brought about by age (narrowing of the colon with age) and a diet low in fiber and high in refined foods
  5. Chronic high intracolonic pressure → the pressure in the large intestine is high in a chronic way
    * Causes the herniations
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33
Q

Diverticuli Disease Risk Factors (2)

A
  1. Age
    *Mainly affects aging population (> 50 years old)
    *As we age, the motility in our large intestine decreases
    This also means that people over 50 are more vulnerable to constipation
  2. Diet
    *Low fiber and high refined carbohydrates tends to produce hard stools as well
    (Fiber = natural stool softener)

These two things cause pressure to be elevated
Hard stool and high intracolonic pressure

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34
Q

Diet if you have asymptomatic pouches (2)

A
  1. Avoid nuts or seeds, because they can increase likelihood of getting trapped in the pouch and trigger diverticulitis
  2. Also should incorporate fiber in diet and reduce any risk of constipation
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35
Q

Hepatitis (definition and 4 most common causes)

A

Inflammation of liver (liver disease)

  • The most common causes of liver injury leading to inflammation and chronic injury is normally:
    1. hepatitis caused by a chemical injury (ex: alcoholic hepatitis)
    2. hepatitis caused by exposure to high acetaminophen,
    3. hepatitis caused by exposure to certain organic solvents and environmental pollutants,
    4. multiple viruses that cause forms of hepatitis
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36
Q

Liver cirrhosis

A

When hepatitis becomes chronic and longstanding, it can lead to a state of liver failure known as cirrhosis
*A state of liver cirrhosis represents a fibrotic liver state, where overall liver function is very limited

37
Q

Most Common Clinical Manifestations of Liver Disease (4)

A
  1. Portal hypertension
  2. Ascites
  3. Hepatic Encephalopathy
  4. Jaundice
38
Q

Portal Hypertension

A
  1. Abnormally high BP is the portal circulation
  2. Caused by any diseases that obstruct or impede blood flow through any component of the portal venous system or the vena cava
  3. In portal circulation, the blood pressure is normally extremely low, so any increased pressure will be abnormally high for what it normally is
39
Q

Portal Hypertension Complications (4)

A
  1. Varices
  2. Acites
  3. Spleenomegaly
  4. Hepatic Encephalopathy
40
Q

Varices (6)

A
  1. Distended and tortuous collateral veins – prolonged elevation in pressure in collateral veins causes their transformation into varices are most common in esophagus and stomach
  2. Varicose veins are distended with blood flow; the valves have collapsed and are dilated and tortuous
  3. When you see varicose veins, it is because there is a sluggish movement of blood through it, there is a risk for thrombosis and the risk for rupture of the veins leading to bleeding
  4. We see these varices commonly in lower esophagus and upper stomach
  5. Patients who have this usually have profound cirrhosis/severe liver failure
  6. Reflects high portal hypertension
41
Q

Number 1 risk of varices (6)

A

Varices are dangerous because they can rupture and bleed

  1. When varices bleed, the bleeding can be acutely catastrophic or slower in nature but still leading to high mortality complications
  2. Rupture in one of these varices (especially lower esophageal) will lead to a massive hemorrhage and vomiting of a lot of blood
    * the person will lose a lot of blood very quickly
  3. Mortality rate of variceal bleeding is over 60%
  4. There may also be a slower bleed that leads downward, and causes a patient to pass black tarry stool
    * Still a significant amount of blood loss, but the blood loss is not as rapid

5 In most cases of rupture, emergency endoscopy will be performed
*Can repair the bands during endoscopy, but if it is in the stomach then banding is not as easy

  1. This is a direct consequence of portal HTN!!
42
Q

Spleenomegaly

A

Blood vessels draining from the spleen and leading to portal vein

  • As portal pressure rises, blood flow away from the spleen is reduced and the spleen becomes enlarged
  • In patients with cirrhosis, you can palpate the spleen
  • This is a direct consequence of portal HTN
43
Q

Portal Circulation (4)

A
  1. The liver is filtering all the blood coming from the GI tract
    * Blood drains to the liver and onto vena cava
  2. Splenic vein, gastric veins of the stomach, and esophageal vains of the esophagus also drain into portal circulation
  3. When pressure in portal circulation doubles or triples it creates increased pressure in all of these branches and interferes with the ability of blood to drain into the liver
  4. Portal HTN may be 10-12mmHg
    * Even if it is still small, the pressure has doubled, especially because these are veins, which are normally low pressure
44
Q

Hemorrhoids Associated with Portal Hypertension

A

Portal Hypotension leads to varices, and one type of varices is hemorrhoids (varicose veins in rectum)

45
Q

Portal Circulation Steps (4)

A

1st: As we consume food and liquids into our GI tract, and through process of digestion and absorption, etc., everything we consume enterally enters blood that then enters the portal circulation
2nd: Anything absorbed through our GI tract passes through the liver before going anywhere else (i.e. before entering general circulation)
3rd: Converges onto the portal vein and then the blood drains from the portal vein into the liver
4th: All of the portal blood flow passes through the liver and then drains into the hepatic vein, and then goes to the vena cava and then general circulation

46
Q

Cirrhotic Liver (4)

A
  1. Will have thick bands of fibrous scar tissue separating little nodules of regenerative liver
  2. Liver is trying to regenerate and recover, but instead there are islands of degenerative liver separating a lot of scar tissue
  3. There are also little blood vessels moving through and the scar tissue will surround those blood vessels
    * This impedes blood flow through the liver
    * Blood will have to squeeze through the liver, and the result is increased blood pressure in the portal circulation
  4. Diseased liver impedes blood flow through it → portal hypertension
47
Q

Sudden Rupture of Varices

A

Sudden: If varices break open you can get vomiting of massive amounts of blood and hemorrhagic shock

48
Q

Slow Rupture of Varices (5)

A
  1. Varices rupture and bleed into GI tract/stool
  2. When this happens you see black tarry stool
  3. Can lead to anemia and acute complications, because the person with these varices will have high protein blood going into GI tract
    * So body is being forced to digest this blood and liver is unable to detoxify the large amounts of protein → hepatic encephalopathy
  4. Being forced to digest your own blood can acutely raise your ammonia levels and lead to neurological manifestations
  5. Low level bleed turns into a very serious event, potentially leading to coma and death
49
Q

Complications of Rupture Varices (4)

A
  1. Vommiting of large volumes of blood
  2. Blood in stool
  3. Anemia
  4. Hemorrhagic shock
50
Q

Ascites

A
  1. The condition of pathologic fluid accumulation within the abdominal cavity.
  2. Ascites traps fluid in a “third space” from which it cannot escape
  3. Cirrhosis is most common cause
  4. Several factors contribute to the accumulation of fluid in the third space: Hypoalbunemia is the main factor for developing ascites
51
Q

Contributing Factors to Asictes (4)

A
  1. Portal HTN
  2. Hypoalbunemia
  3. Hepatorenal Sydnrome
  4. Impaired liver breakdown of ADH and Aldosterone
52
Q

How does portal HTN lead to ascites?

A

Increased blood pressure in messenteric circulation

*Contributes to ascites because there is an increase in pushing pressure promoting fluid movement into peritoneal cavity

53
Q

How does hypoalbunemia lead to ascites? (4)

A
  1. Decreased albumin / decreased plasma oncotic pressure
    * Someone with liver failure isn’t producing enough albumin (because the liver synthesizes albumin from protein)
  2. Albumin helps keep fluid in the blood vessels, it determines plasma oncotic pressure
    * So when albumin drops, plasma oncotic pressure drops (pulling pressure keeping fluid in bloodstream)
  3. Without albumin, the fluid leaks out and will leak into the interstitial spaces
    * Less of pulling pressure due to loss of albumin, increased pushing pressure from portal HTN = ASCITES
  4. Since the person has portal hypertension, the mesenteric pressures have increased (facing abdominal cavity); so there is increased capillary BP pushing fluid into the third space
54
Q

How does hepatorenal syndrome lead to ascites? (5)

A
  1. Not producing enough albumin, can’t keep fluid in blood vessels, so blood pressure drops
    * The patient looks like they have a lot of fluid volume because they can’t keep the fluid in their blood vessels
  2. When kidney sees low BP, it interprets that it should retain volume
    * Result: kidneys release renin and you get a significant sodium and water retention
  3. All this fluid doesn’t stay in the blood vessels due to the liver impairment, and it ends up in the peritoneal cavity (ascites) and contributes to peripheral edema
  4. The kidneys are working overtime to try and retain fluid, and this can be a common cause of death with end stage liver disease
  5. The person will look fluid congested, but their blood volume is depleted because they don’t have the albumin to keep it in the blood vessels
55
Q

How does Impaired liver breakdown of ADH and Aldosterone lead to ascites?

A

Leads to expansion of plasma volume and increased blood pressure
*The half life of these hormones gets extended when the liver isn’t working

56
Q

How to dx ascites

A

percussion and fluid wave (put one hand on belly and tap on other side, if you see a wave then you know the belly is mostly fluid)
*How you determine if it is fat or fluid, because fat wouldn’t make a wave

57
Q

Paracentesis

A

Draining of fluid from the peritoneal cavity

  • Can pull out ~10L/week of fluid
  • The only way to get the fluid out with ascites
58
Q

Paracentesis Major Complication

A

If you pull the fluid too quickly, the patient’s BP can crash

  • When they have excess fluid, they have reached an equilibrium → if you pull all the fluid out then there is a rapid shift of fluid out of the vessels and BP will crash
  • Hemodynamic/close monitoring of BP with this procedure is important
59
Q

Hepatic Encephalopathy (4)

A
  1. A complex neurological syndrome characterized by impaired cerebral function, flapping tremors, and EEG changes
  2. The neurotoxins causing the manifestations are also temporarily increasing the permeability of the blood brain barrier; Brain becomes more vulnerable to exposure of toxins
  3. May develop rapidly or slowly with chronic liver disease
  4. Caused by the diversion of blood away from the liver/the lack of liver detoxification of blood
60
Q

Hepatic Encephalopathy Clinical Manifestations (5)

A
  1. Flapping tremors of hands
  2. Emotionally labile
  3. Personality changes
  4. Intellectual impairment
  5. Depressed level of consciousness
61
Q

Pathophysiology of Hepatic Encephalopathy (4)

A
  1. Either the blood is getting diverted away from the liver or whatever blood goes through the liver isn’t getting appropriately detoxified
  2. One substance that liver usually detoxifies but isn’t with liver failure is ammonia
    * Another is GABA, which is an inhibitory NT
    * Any spillover of GABA in the blood should normally get removed by the liver
  3. An important prerequisite for the syndrome is diversion of portal blood into the systemic circulation through portosystemic collateral vessels
    * Ammonia hypothesis
    * GABA hypothesis
  4. Consuming large protein loads will make ammonia higher, GABA higher, and encephalopathy more severe worse
    * Including bleeding into the varices
62
Q

How does slowed GI tract lead to Hepatic Encephalopathy

A

1st: The more slowly feces moves through the colon, the more ammonia that is produced by the bacteria in colon

2nd: Bacteria produce a lot of ammonia but normally the liver would neutralize this
* So anything minor that can make the patient constipated will cause the encephalopathy to be more severe

This patients will be taking laxatives to minimize ammonia increasing!

63
Q

Acute Episode of Hepatic Encephalopathy

A

Going from grade 0-2 to grade 3-4 in acute period of time

*0-1 is usually where the patient will normally be

64
Q

Grade 0 Hepatic Encephalopathy

A

Clinically normal mental status but minimal changes in memory, concentration, intellectual function, and coordination

65
Q

Grade 1 Hepatic Encephalopathy

A

Mild confusion, euphoria, or depression; decreased attention; slowing of ability to perform mental tasks; irritability; and disordered sleep pattern, such as inverted sleep cycle

66
Q

Grade 2 Hepatic Encephalopathy

A

Drowsiness, lethargy, gross deficits in ability to perform mental tasks, obvious personality changes, inappropriate behavior, and intermittent disorientation, usually regarding time

67
Q

Grade 3 Hepatic Encephalopathy

A

Somnolent but can be aroused, unable to perform mental tasks, disorientation about time and place, marked confusion, amnesia, occasional fits of rage, present but incomprehensible speech

68
Q

Grade 4 Hepatic Encephalopathy

A

Coma with or without response to painful stimuli

69
Q

Jaundice

A

Elevated circulating bilirubin the blood, which comes from the breakdown of RBC by the spleen

70
Q

Bilirubin

A

Substance that is naturally lipid soluble, so it can easily deposit itself into tissues like the skin and create a discoloration

71
Q

Bilirubin breakdown (3 steps)

A

1st: RBC go to the spleen and the ones that are aging get trapped in the spleen and the spleen disassembles them and the protein and iron gets recycled, but the hemoglobin group gets converted into bilirubin (bilirubin comes form heme group)
2nd: Bilirubin leaves the spleen as unconjugated bilirubin; very fat soluble

3rd: Will go to liver to become conjugated, by having a sugar molecule be attached to it
* We conjugate bilirubin so we can control the movement of it by making it water soluble

72
Q

How does bilirubin get to the liver?

A

Traveled out of splenic vein, into portal vein, to liver

  • Had to be bound to albumin to get there because it’s lipid soluble
  • Once converted, it then leaves the liver and goes to gallbladder to get released with bile
73
Q

How does ACUTE liver disease lead to jaundice? (4)

A
  1. something is killing off/harming liver cells so the liver can’t conjugate bilirubin and you get a rise in circulating unconjugated bilirubin
    * Causes jaundice
  2. The acute liver damage that causes damage is happening because the liver cells are getting attacked and dying and not conjugating bilirubin
  3. Person will turn yellow, bilirubin will be in urine and high in blood
  4. But when acute damage subsides, everything goes back to normal
    * This doesn’t occur with end stage live disease
74
Q

How does END STAGE liver disease lead to jaundice? (4)

A

Bilirubin will always be high because…

  1. Limited amount of conjugation by liver
  2. There is portal hypertension
    * Impedance of blood from spleen into portal vein into liver
  3. Less albumin
    * Bilirubin can more easily get out of blood vessel because less albumin to keep it in there
  4. Movement of feces through colon has slowed, which slows the rate that the flora in the gut unconjugates bilirubin
    * Reduced gut motility enhances unjconjugated bilirubin
75
Q

Viral Hepatitis

A

Certain viruses attack hepatocytes, which results in chronic inflammation and progressive fibrosis of the liver
*Each virus has different lifecycle, types are listed below

*Incubation period varies, usually between 2-6 weeks depending on virus

76
Q

Hepatitis A

A

Causes acute illness, mode of transmission is predominately a fecal/oral route
*Shed virus in feces and through food contamination it gets spread

77
Q

Hepatitis B (4)

A
  1. Causes chronic disease
  2. Parenteral route, can be sexually transmitted
  3. Can eventually lead to end-stage liver failure, but not always
  4. Those who contract it early have less of a chance of progressing to failure
78
Q

Hepatitis D (3)

A
  1. This virus that can only come about if you are already infected with HepB
  2. Has a similar transmission as B, so you have to already have it
  3. Often times people who get D will go into acute liver failure
79
Q

Hepatitis C (2)

A
  1. causes chronic disease and is also parenteral transmission, usually do to exposure of contaminated blood
  2. Aggressive virus that will usually lead to end stage liver failure
80
Q

Hepatitis E

A

IDENTICAL TO HEPATITIS A:

Causes acute illness, mode of transmission is predominately a fecal/oral route
*Shed virus in feces and through food contamination it gets spread

81
Q

Portal Triads (3)

A

1 A branch of the portal vein, portal artery and bile duct

  1. Within portal triads, blood comes into liver and bile flows out
  2. With mile and moderate hepatitis, the inflammation is centered around the triads because it is the point through which blood enters the liver
    * The inflammation and the expanding fibrosis also originate at the triads
82
Q

Clinical Manifestations of Viral Hepatitis (3)

A
  1. Acute viral hepatitis causes abnormal liver function test results
  2. The serum aminotransferase values, aspartate transaminase (AST), and alanine transaminase (ALT) are elevated
  3. Viral hepatitis (especially HepC) can lead to post-necrotic cirrhosis
83
Q

Prodromal Phase of Viral Hepatitis (3)

A

STAGE 1
1. Begins about 2 weeks after exposure and ends with appearance of jaundice. Symptoms may include: fatigue, anorexia, malaise, nausea, vomiting, headache, hyperalgia, cough, and low-grade fever

  1. Also common is right upper abdominal pain and weight loss
  2. The virus is highly transmissible at this stage
84
Q

Icteric (jaundice) Phase of Viral Hepatitis (3)

A

STAGE 2
1. Begins about 1-2 weeks after prodromal phase and lasts anywhere from 2-6 weeks. Is the acute phase of illness.

  1. Hepatocellular damage and intrahepatic bile stasis causes jaundice.
  2. After jaundice phase there is a progression into a recovery phase or into a chronic phase if it is a chronic viral hepatitis type
85
Q

Recovery Phase or Chronic Phase of Viral Hepatitis (2)

A

STAGE 3
1. With chronic hepatitis, severity of symptoms go down dramatically by the virus continues to cause hepatocyte death, damage, inflammation, and fibrosis

  1. With the chronic diseases, your immune system can’t completely clear the virus and the virus persists at a much slower rate and you are not acutely ill
86
Q

Alcoholic Liver Cirrhosis

A

Caused by alcoholic hepatitis

  • Due to chronic hepatocellular damage caused by alcohol abuse
  • Acetoaldehyde causes this damage
87
Q

Bands associated with liver cirrhosis (3)

A

Very thick bands…

  1. Liver is trying very hard to regenerate itself but it is choked by fibrotic tissue
    * This is what causes portal HTN
  2. Liver goes from being soft and supple to shriveled and hard fibrotic organ
  3. Once you hit the cirrhotic stage it is completely non-reversible
    * Only curative treatment is transplantation
88
Q

Liver Cirrhosis (5)

A
  1. An irreversible inflammatory disease that disrupts structure and function.
  2. Not uncommon to see development of cancer within liver tissue at this point
    * The carcinoma will be secondary to the chronic damage/inflammation that has occurred
    * Will become more difficult to get a liver transplant
  3. Chronic inflammation that leads to bands of fibrosis in between nodules of regenerated liver tissue.
  4. develops slowly over a period of several years
  5. The severity and rate of progression depends on the cause
89
Q

Types of Liver Cirrhosis (2)

A
  1. Alcoholic cirrhosis (includes a reversible fatty liver phase)
  2. Postnecrotic cirrhosis (post viral hepatitis B, C, or D)

Patho 2 Exam 2 (8 decks)

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