Vol.3-Ch.6 "Gastroenterology" Flashcards

1
Q

What are 5 risk factors for Gastrointestinal disease?

A
  • Excessive alcohol consumption
  • Excessive smoking
  • Increased stress
  • Ingestion of caustic substances
  • Poor bowel habits
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2
Q

What are the three main types of abdominal pain classifications?

A
  • Visceral
  • Somatic
  • Referred
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3
Q

What are the 3 main mechanisms of visceral pain?

A

The 3 main mechanisms of visceral pain in the abdomen are:

  • inflammation
  • distention (stretched or inflated)
  • ischemia (inadequate blood supply)
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4
Q

Where is visceral pain typically originating from?

What is the pain usually described as and why?

A

Visceral pain originates in the walls of hollow organs, capsules of solid organs, or the visceral peritoneum.

It is usually described as a vague or poorly localized dull or crampy pain ; b/c inflammation, distention, and ischemia all transmit pain signals from visceral afferent neural fibers back to the spinal column at various levels (not a specific entrance)

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5
Q

How does the body react to vague, not localized pain?(4)

A

With nausea, vomiting, diaphoresis, and tachycardia

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6
Q

What might cause a hollow organ to shift from generating visceral pain to somatic pain?

A

Tearing or rupture and the spilling of it’s contents, causing bacterial or chemical irritation in the abdominal cavity

(example: appendicitis starts as a dull achy pain but once it ruptures it becomes a specific and sharp pain)

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7
Q

What typically causes somatic pain and what type of pain is felt? Why?

A

Typically chemical or bacterial irritation in the abdomen causes somatic pain which is felt as a localized and sharp pain.
This is because somatic pain is generated along specific neural fibers that have specific entrance points in the spinal column.

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8
Q

What is the pathological reason that referred pain is pain that is felt at a different location than where the pain is originating from?

A

B/c many neural pathways from various organs pass through or over regions where the organ was formed during embryonic development.

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9
Q

Before palpating the abdomen, auscultating the abdomen, or moving the Pt you should first?

A

Visually inspect the abdomen

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10
Q

The abdomen can hold how much fluid (like blood) before it is visually distended?

A

4-6L

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11
Q

What is Cullen’s sign?

Grey Turner’s sign?

A

Cullen’s sign = periumbilical ecchymosis

Grey Tuner’s sign = ecchymosis in the flank

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12
Q

What form of inspection is of little help when dealing with the abdomen and why?

A

Auscultating and or percussion offers little help as it often requires a quite environment and an experienced clinician as well as most of the bowel sounds are heard throughout the whole area.

If it is to be done though it must be done before palpating and for at least 2 minutes in each quadrant starting form the furthest from affected area moving towards the affected area.

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13
Q

When palpating, what should you palpate first to last?

Also, what can be felt that will immediately tell you to stop palpating and why?

A

You should have the PT point to the area of most discomfort and then move backwards inspecting that place last.

If you palpate a pulsating mass then STOP immediately, as additional pressure may cause the mass to rupture

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14
Q

Persistent abdominal pain lasting longer than ___ hours is considered a surgical emergency and always requires _____?

A

Persistent abdominal pain lasting longer than 6 hours is considered a surgical emergency and always requires transport?

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15
Q

What are the 5 organs that make up the Gastrointestinal system?

A
  • GI tract
  • Liver
  • Gallbladder
  • Pancreas
  • Vermiform Appendix
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16
Q

What makes up the Upper GI Tract? (4)

A
  • Mouth
  • Esophagus
  • Stomach
  • Duodenum (end of the stomach and the first part of the small intestine)
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17
Q

6 major causes of Upper GI Hemorrhaging?

A
  • Peptic Ulcer Disease
  • Gastritis
  • Varix Rupture
  • Mallory-Weiss syndrome
  • Esophagitis
  • Duodenitis
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18
Q

5 Upper GI Diseases?

A
  • Esophageal Varices
  • Acute or Chronic Gastroenteritis (either/or)
  • Peptic Ulcers
  • Cyclical vomiting syndrome
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19
Q

What is the main functional difference between the upper and lower GI tracts?

A

The upper is most the physical digestion of the food and some chemical.

The lower is where the nutrients are absorbed into the blood and solid wastes are formed and excreted

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20
Q

What is the cut off line that defines hemorrhaging as either upper or lower GI hemorrhaing?

A

The Ligament of Treitz ; this is the ligament that support the duodenojejunal junction (the point where the first two sections of the small intestine meet)

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21
Q

What 2 factors are major contributors to the fatality % of GI bleed?

A

1: the rising ability for people to self medicate with over the counter meds which causes them to not go to the doctors till the problem is advanced
2: the age of the pts with GI problems is rising which increases the likelihood of additional health problems being present

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22
Q

What sign/symptom might be different if the bleed originates in the upper vs lower tract?

A

If it is in the upper it might cause Hematemesis and could be bright red if fresh or look like “coffee grounds” if old

If it is in the lower it might cause melena; if melena is present there must have been at least 150ml of blood in the GI tract for at least 5-8 hours

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23
Q

What are the 2 most common signs and symptoms of hemorrhage in the GI system and why?

A

Most often it will cause nausea and vomiting b/c blood is highly irritating to the GI system.

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24
Q

What is Mallory-Weiss Syndrome?

A

An esophageal rupture secondary to vomiting

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25
Q

What is the tilt test? What sign and symptoms are you watching for?

A

The Tilt-Test is when you test for orthostatic hypotension by having a Pt stand up and you watch for a 10mmHg drop in BP or a 20bpm drop in HR. This is testing for volume deficiency that may be caused by hemorrhaging.

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26
Q

How much circulating volume can the body loose approximately before clinical indicators start to arise?

A

Approximately 15%

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27
Q

How much fluids can you start with in general for a hemorrhagic hypovolemic Pt?

A

20ml/kg

28
Q

What is an Esophageal Varice?
What causes it?
(Upper GI disease)

A

It is a swollen vein in the esophagus (rupture causes a 35% mortality rate)

Ultimately they are caused by an increase in portal pressure. After the blood from the abdominal organs drops off the nutrient rich blood at the liver the blood then flows from the Liver to the Inferior Vena Cava via the Hepatic vein. If there is Liver Damage then that blood flowing out of the liver might meet high resistant causing a back up of blood into the Left Gastric Vein and into the Esophageal Veins.

Causing them to Evaginate or “outpocket”, and it is these evaginations that are Esophageal Varices

29
Q

What is Cirrhosis and how is it connected to Esophageal Varices? What causes it?

A

Cirrhosis of the liver is caused by high alcohol (or other caustic substance) that results in fatty deposits and fibrosis (scarring) in the liver parenchymal tissue, thus obstructing portal blood flow. This obstruction to flow is what can create the back up of blood leading to the formation of Esophageal Varices

(Not unlike atherosclerosis in the heart)

**alcohol liver cirrhosis accounts for 2/3 the cases of esophageal varices

30
Q

Why might clotting time be diminished with a large Esophageal Varices rupture?

A

Because the high portal pressure backs up blood into the spleen which destroys platelets stored there. Also, the damaged liver that caused the increase portal pressure is not capable of creating clotting elements (like prothrombin) as well as a healthy one.

31
Q

What is Acute Gastroenteritis?
(Upper GI disease)

What is the pathology of it?

A

It is an inflammation of the stomach and intestines with associated sudden onset of vomiting and diarrhea.

The inflammation causes hemorrhaging and erosion of the mucosa (deepest) and submucosal (2nd deepest) layers (inner most layers of the intestines) which can lead to the destruction of the Villi that help to absorb water and nutrients. The water that the villi would normally absorb is now just being wasted out of the body at an increased rate, hence the diarrhea.

32
Q

Gastritis Vs Gastroenteritis

Who is susceptible?

A

Gastritis = inflammation of the stomach

Gastroenteritis = inflammation of the stomach AND
intestines

Alcohol and tobacco abusers, as well as frequent NSAIDs (like aspirin )use are at high risk for this. (they all have the same ability to break down the mucosal surfaces of the stomach and intestines)

33
Q

Aside from the related severe diarrhea and vomiting caused by Acute Gastroenteritis, what other life threatening problems can happen with this disease?

A

The first major issue that will happen next is hypovolemia from the loss of fluids through the vomiting and diarrhea, this can lead to hypovolemic shock but even a step further can take effect. If there is enough electrolyte loss associated with the hypovolemia, the Pt can also develop chest pain and cardiac arrhythmias may form.

34
Q

What is Chronic Gastroenteritis?

Upper GI disease

A

Chronic Gastroenteritis (not acute) involves long term mucosal changes or permanent damage. Unlike the acute version; chronic gastroenteritis is usually attributed to a microbial infection.

35
Q

What is the most prevalent pathogen that causes Chronic Gastroenteritis in the US?

How are all the microbes that cause this usually spread?

How does the common US pathogen differ in signs and symptoms from the other pathogens that cause this?

A

Helicobacter Pylori (H. Pylori)

They are transmitted by the fecal-oral route or by infected food or water

Most of the bacteria that cause chronic gastroenteritis cause nausea, vomiting, diarrhea, fever, abdomin cramping, lethargy, or anorexia ; but H. Pylori causes heartburn, abdomen pain, and gastric ulcers

36
Q

What are peptic ulcers?
Where can they occur?
(Upper GI disease)

A

Erosions caused by gastric acid.

They can occur anywhere in the GI tract.

37
Q

The main two types of peptic ulcers are Gastric Ulcers and Duodenal Ulcers.
Who are more likely to get Gastric and who are more likely to get Duodenal

(Gastric = stomach ulcer ; duodenal = ulcer in the duodenum)

A

Gastric Pts are usually:

  • over 50
  • work physical jobs
  • have pain after eating (no pain at night)

Duodenal Pts are usually:

  • executives/leaders under high stress
  • pain at night or on an empty stomach
  • (possibly genetic, not proven yet)
38
Q

Explain the pathology of how a peptic ulcer forms.

Pay attention to what causes the irritation as those are the risk factors for peptic ulcers

A

To break down food boluses the body produces hydrochloric acid. HCL acid also converts pepsinogen (an enzyme) into its active form, pepsin. The two together can become offensive to the mucosal layers of the GI tract (they’re very acidic). To combat this, there are usually glands in the mucosa to help protect it, however, NSAIDs/Acid stimulators/or H. Pylori (H.P. accounts for almost 80%) damage the mucosa and it’s glands, leaving the mucosa susceptible to the highly acidic HCL and pepsin. This causes the peptic ulcers.

39
Q

Other than NSAIDs, acid stimulators, or H. Pylori; what other 2 things may cause peptic ulcers?

A

A blocked pancreatic duct; as chyme moves from the stomach and into the duodenum via the pyloric sphincter, the pancreas will secrete an alkalotic solution to neutralize the chyme. But if that duct is blocked then that highly acidic chyme doesn’t get neutralized.

The other is Zollinger-Ellison Syndrome which involves an acid-secreting tumor that provokes ulcerations

40
Q

What is Cyclical Vomiting Syndrome and what are the 4 distinct phases? (Upper GI disease)

A

It is a repetitive sudden attack or episode of severe nausea, vomiting, and physical exhaustion without apparent cause. The exact cause is unknown but it does appear to affect children more.

  • Prodrome Phase: Feels nausea and vomiting are about to begin, accompanied with diaphoresis that can last minutes to hours.
  • Vomiting Phase: 20-30 minutes of intense nausea, vomiting, and retching. phase can last for hours to days
  • Recovery Phase: Over time the symptoms fade and the Pt is able to eat and return to normal
  • Well Phase: the Pt is asymptomatic
41
Q

What 5 things make up the Lower GI Tract?

A
  • Jejunum (after the duodenum)
  • Ileum
  • Large Intestine (Ascending, transverse, descending, sigmoid colon)
  • Rectum
  • Anus
42
Q

4 major causes of lower GI bleeds?

A
  • Diverticulosis
  • Colon lesions
  • Rectal lesions
  • Inflammatory Bowel disorder

(small intestine = app. 6m long ; long = app. 1.5m long)

**Lower GI bleeds are usually chronic and rarely fatal

43
Q

What are the main 6 Lower GI diseases?

Of the 6 which is the most common, and what is the main risk factor for it?

A
  • Ulcerative Colitis
  • Crohn’s disease
  • Diverticulitis
  • Hemorrhoids
  • Irritable bowel syndrome
  • Bowel Obstruction

Diverticulitis is the most common b/c the elderly are the most prevalent in lower GI bleeds and diverticulitis is common amongst the elderly

44
Q

What is Ulcerative Colitis?
(Lower GI disease)

Pancolitis VS Proctitis

A

It is an inflammatory (ulcerative) process that creates a continuous length of chronic ulcers in the mucosal layer of the colon (doesn’t usually do deeper to hit the submucosa). As the ulcers heal, granular tissue replaces them, thickening the mucosa

It is of unknown origin (idiopathic inflammatory bowel disorder or IBD) but it is noted that a large release of cytokines can cause an overwhelming inflammatory response in the submucosa kind of like histamines

75% involve the rectum or rectosigmoid portion.

Pancolitis = if it spreads to entire colon
Proctitis = if it is limited to the rectum
45
Q

What are the 2 big idiopathic inflammatory bowel disorders or IBD (it is of unknown origin)?
Who are susceptible to which one?

A

Ulcerative Colitis; ages b/w 20-40

Crohn’s Disease ; white females, under frequent stress, and in the Jewish population

The big differences between the two is that Ulcerative colitis typically doesn’t affect the submucosal layer, just the mucosa and is confined to just the rectum/large intestine.

Crohn’s can happen anywhere from mouth to anus and will affect the mucosa and submucosa, making it a more damaging and serious version of Ulcerative colitis

46
Q

What is Crohn’s disease?

Lower GI disease

A

This is also an idiopathic inflammatory bowel disorder or IBD (it is of unknown origin).

As inflammation begins it damages the innermost layer of the mucosa which then forms Granulomas that further break down the mucosal and submucosal layers. The affected section of intestinal wall then becomes rubbery and nondistensible due to hypertrophy and fibrosis of the muscles underlying the submucosa (there is a circular layer and a straight layer.

The patchwork-quilt formation of granulomas (small area of inflammation), fibrosis, and hypertrophy also decrease the intestines’ internal diameter, resulting in fissure (incomplete tears) in the mucosa and possibly submucosa as food passes through.

This pattern of ulceration and then scarring can also lead to fistulas (an abnormal connection between organs) which can progress to an obstruction of the small bowel.

47
Q

What is diverticulitis?

Lower GI disease

A

It is a common complication of diverticulosis, which is a condition were there are diverticula present in the intestine. Diverticula are small outpouchings of mucosa and submucosal tissue that pushed through the outer most layer of the intestine, the muscle.

Diverticulitis is an inflammation of the diverticula, secondary to infection.

Pts with diverticulosis will not be symptomatic. Not until they develop diverticulitis (inflammation of the diverticula) in which case they will have pain in the lower left side

48
Q

How does one form a diverticula?

A

2 things happen.

1: when one has a low fiber diet it forces the muscle layers of the colon to spasm and push harder to move the contents.
2: the outermost layers of the colon are made of 2 different layers of muscle, and among the different layers are smaller muscles called Teniae Coli, through which nerves and blood vessels run. Well as people get older and those muscle weaken, if the colon muscle spasms and pushes to hard to move fecal matter it can can an outpouching of the mucosa and submucosa through the Teniae Coli which in term can trap small amounts of fecal matter that leads to infection and eventually inflammation (Diverticulitis)

49
Q

What does diverticulitis usually present with and what could it lead to that may be more serious?

A

Usually presents with lower left sided colicky pain (b/c most diverticula are in the sigmoid colon, almost 95% in fact and it got it nick names “left sided appendicitis”) as well as a low grade fever (b/c it started as an infection), with the usual nausea, vomiting, and pain on palpation

This could lead to possible hemorrhaging or larger perforation of the colon wall leading to spillage of colon contents in to the peritoneal cavity causing peritonitis

50
Q

What are hemorrhoids and what can usually cause them?

Lower GI disease

A

They are small masses of swollen veins that occur in the anus (external) or rectum (internal)

Heavy lifting, pregnancy, portal hypertension, straining during deification, and a lower fiber diet can cause these.

51
Q

Are hemorrhoids typical a viable emergency call?

A

Not really. They do not typically cause any major hemorrhaging. Straining during deification can cause them to open and bleed bright red with stool, alerting the PT and causing them to call EMS. The biggest worry is infection if they rupture frequently but for the most part they may open during heavy lifting or deification with straining but will usually thrombose into a closed state again.

52
Q

What is irritable bowel syndrome? (aka Spastic Colon)

Lower GI disease

A

It is unknown what exactly causes it but it is defined at a functional issue rather than a structural problem. It is commonly associated with abdominal pain/cramping, increased gas, altered bowel habits, food intolerance, abdominal distention

53
Q

What is a bowel obstruction?

Lower GI disease

A

It is a blockage of the hollow space within the small and large intestine. It usually occurs in the small intestine due to its smaller diameter, greater length, flexibility, and mobility.

54
Q

What are the 4 main causes of a bowel obstruction?

What is the most identifiable sign of an obstructed bowel?

A

1: Inguinal Hernia (loop of small bowel in inguinal canal)
2: Intestinal Intussusception (adjoining bowel tissue telescopes into bowel lumen
3: Intestinal Volvulus (twisting of small bowel till it becomes shut off like a knot)
4: Intestinal adhesion (other organs adhere to the colon)

The most identifiable sign of a bowel obstruction is if the Pt is frequently vomiting high amounts of bile or contents that look and smell like feces.

55
Q

What is mesenteric Ischemia?

A

It is the occlusion or narrowing of either of the 2 mesenteric arteries. The Superior or Inferior Mesenteric Arteries.

Often will induce abdominal pain, nausea, vomiting, and diarrhea.

Can be acute or chronic and often chronic will turn into acute suddenly and without warning. Usually occurs in people 60 or older or heavy smokers

56
Q

What do the two mesenteric arteries supply?

A

Superior Mesenteric Artery (SMA): supplies the intestine from the lower part of the duodenum through 2/3rds of the transverse colon and the pancreas

Inferior Mesenteric Artery (IMA): supplies the large intestine from the splenic flexure to the upper part of the rectum, which includes the descending and sigmoid colon, and part of the rectum.

57
Q

Where is the appendix?

How does it become inflamed causing appendicitis? (which is the most common emergency surgical call we will get)

A

It is at the junction of the small and large colon. It is inferior to the ileocecal valve and is the first section of the ascending colon.

It is susceptible to being obstructed by fecal matter because of its location and shape, once obstructed it can inflame the lymphoid tissue (which is mostly what it is made of) and then lead to a bacterial or viral infection that ulcerates the mucosa.

The inflammation also causes the size of the appendix to grow and can shut off flow of the appendicular artery and cause thrombosis. This shutting off of its own artery causes the appendix to become ischemic and infarction and necrosis follow. At this point the walls of the organ are dead and weak and ready to rupture, spilling its contents into the peritoneal cavity.

58
Q

What signs and symptoms are associated with appendicitis?

Where is McBurney’s Point?

A

At early stages the Pt will have colicky pain associated with nausea and vomiting and sometimes a low grade fever.

As it progresses and the appendix grows the pain will localize to the right lower quadrant. Typically at McBurney’s Point, which is 1-2 inches above the anterior iliac crest along a direct line from the anterior crest to the umbilicus.

59
Q

What is Cholecystitis?
What is the high majority of cases caused by?

What will a pt with Cholecystitis present with?

A

It is inflammation of the gall bladder.
Usually caused by Cholelithiasis (the formation of gall stones)

Often the pt will present with acute right upper quadrant pain. Sometimes it may irritate the diaphragm causing right shoulder pain or the pain may cause pale cool or diaphoretic skin.

Murphey’s sign may be present ; a positive Murphey’s sign would be point tenderness under the right costal margin.

60
Q

What are the two types of gall stones and which is more common?

A

There are cholesterol based or bilirubin based gall stones.

Cholesterol is much more common and is seen with a specific risk profile: obese, middle aged women with more than one biological children.

61
Q

How are gallstones formed?

usually cholesterol based

A

As the liver produces bile it travels down the common bile duct to empty into the small intestine through the sphincter of Oddi. The sphincter of Oddi opens when chyme leaves the stomach through the Pyloric Sphincter. When the Sphincter of Oddi closes the bile backs up into the gall bladder through the cystic duct.

Here the bile waits till the Sphincter of Oddi opens again but it can become supersaturated while waiting and form Calculi (gall stones made of bilirubin and or cholesterol) which can obstruct the bile trying to leave the next time the sphincter opens. This causes the bile to to back up and sit longer than it should which breaks down the mucosal membrane of the gall bladder. Further irritating the epithelial membrane of the gall bladder, prostaglandins are released and over time the inflammation progressing raises the pressure in the gall bladder to the point that blood flow is reduced to the epithelium.

62
Q

What is Pancreatitis?
What are the 4 main causes?
Overall, what is the main thing that gives Pancreatitis its high mortality rate?

A

It is inflammation of the Pancreas.

  • Metabolic: caused by alcoholism
  • Mechanical: obstructions via gallstones or elevated serum lipids
  • Vascular: caused by thromboembolisms or shock
  • Infections

All ultimately can cause a high mortality because of the accompanying sepsis and shock (septic shock)

63
Q

How does the pancreas become inflamed and cause acute Pancreatitis?

A

Most of the pancreas tissue is arranged in glandular structures called Acini. These produce digestive enzymes that empty into duodenum at the ampulla of Vader. The other function of the pancreas is to produce insulin and glucagon at specific islets (this is a small total area of the pancreas). Sometimes gall stones leaving through the common bile duct can obstruct the ampulla of Vader can cause a back of of the digestive enzymes. This like other caustic fluids in other organs causes inflammation and edema, and the edema over time increases pressure in the organ enough that it cuts off blood flow to the organ.

Once death of tissue begins, the death of the Acinar tissue (the Acini tissue that the pancreas is mostly comprised of) begins to deteriorate and often this causes sudden acute pain which is why this is also called “Acute Pancreatitis)

64
Q

What causes chronic pancreatitis?

Post Acute pancreatitis

A

This occurs post acute pancreatitis. After the damage to the Acini tissue occurs in Acute Pancreatitis, which usually occurs because of heavy alcohol consumption, the alcohol results in fatty deposits on the platelet plugs in the acinar tissue formed to try to heal the damage. This makes the plugs bigger and the plugs in general disrupt the flow of enzymes from the pancreas. When the enzymes back up behind the ampulla of Vader, it causes the enzymes to begin to digest the tissues of the pancreas causing lesions. This lesions can eventually lead to hemorrhaging if they worsen.

65
Q

What is Hepatitis?

What are the different versions and how are they contracted?

A

It involves damage to hepatocytes (liver cells) associated with inflammation or infection.

HepA (HAV): (AKA Infectious Hep) Most well known, spreads through oral-fecal route. Self-limiting and lasts 2-8 wks

HepB (HBV): (AKA Serum Hep) transmitted as a bloode borne pathogen and can last in body fluids outside the body for days. Effects can be minimal or lead to ischemia and necrosis

HepC (HCV): Transmitted through blood transfusions and often causes debilitating damage to the liver

HepD (HDV): Less common and stays dormant until acivated by HBV

HepE (HEV): is a waterborne infection and has a high mortality rate with pregnant women

HepG (HGV): can cause superinfection of Hep A,B,&C but alone is seen in people who develop hep after a transfusion and its long term affects are unknown

66
Q

What is the classic sign of a Hep patient?

What causes it?

A

Jaundice of the skin and or eyes is trademark and is caused by increased bilirubin retention

67
Q

What is the classic referred pain for an agitated diaphragm?

A

Pain in the upper right hand shoulder.

Therefore infection or inflammation of organs adjacent like the pancreas, liver, gallbladder, etc can cause an irritated diaphragm and cause this pain.