U8 Flashcards

1
Q

ACHALASIA

A

Achalasia

Pathophysiology: Impaired innervation decreased peristalsis and esophageal sphincter doesn’t relax so food bolus accumulates and cannot enter the stomach  esophagus distends

S/S: Pain minutes after swallowing, chest fullness, vomiting and complete esophageal obstruction.

Rx: Modified eating, medications, esophageal dilation/surgery - BOTOX Injections to paralyze the sphincter (so it will stay open).

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2
Q

GERD

A

Gastroesophageal Reflux Disease (GERD)

Pathophysiology: The esophageal sphincter is weak and does not close completely after
food enters the stomach, which allows the backflow of gastric juices from the stomach to enter the esophagus. Throat tissue is not the same as stomach tissue and cannot handle the acid from
the stomach. Many patients develop this condition as they get older after a lifetime of “bearing down” to have bowel movements because of the internal pressure pushing against the closed
sphincter. Also, weight lifters who hold their breath when training will have the same problem.
Heartburn is caused as chyme and gastric acid regurgitates into the esophagus about 1- 2
hour after meals causing inflammation of esophageal mucosa and tissue erosion (causing
ESOPHAGTIS). When this tissue heals it causes fibrosis (scar tissue) that does not stretch as well as the original esophageal tissue. Over time GERD causes the tissue of the throat to develop precancerous dysplasia (Barrett’s
Esophagitis) and could develop into esophageal cancer – so advise your patients, “DO NOT IGNORE HEARTBURN –
it can lead to throat cancer”.

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3
Q

GERD

JUST READ

A

S/S: Pain is worse when lying down or bending over. Patients will complain of having to sleep in a recliner
or with the head of the bed elevated to relieve the pain. NOTE: This pain can mimic a heart attack because the stomach is so close to the heart – or – patients with heart problems tell themselves they are just “having heartburn” and delay going
to the ER for a cardiac workup. (NOTE: Teach patients not to assume their chest pain is heartburn!)
Rx: Stop Smoking and avoid 2nd hand smoke (increases gastric irritation and causes
vasoconstriction which decreases healing); stop caffeine; check for gluten intolerance; Acid-suppressing medications. If coming to the ER with CHEST PAIN, a patient may be given a “cardiac cocktail” which contains an acid suppressing liquid medication and usually a numbing medication like lidocaine. If the pain goes away after drinking this “cocktail” then the problem
can be diagnosed as GI and not cardiac. Also, if the pain is worse when the patient lies down, it is caused by GERD and not a cardiac problem. If the reflux is severe enough, a surgery can be done (a Nissen Wrap/ fundoplication – say that fast 5 times!) this surgery wraps the top part of the stomach around the esophagus to make a tighter sphincter. Once this is done, the patient will not be able to vomit or belch air from the stomach.

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4
Q

MELENA

A

Black and tarry stool (lower GI bleed)

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5
Q

HEMATOCHEZIA

A

Bright red blood from anus- usually hemorrhoids

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6
Q

CROHNS

A

Crohn’s Disease
This painful autoimmune disorder (no medical cure) results in inflammatory lesions that may occur anywhere in the G.I. tract (from mouth to anus) but more often in the ascending colon and terminal ileum. Lesions involve all layers of the bowel wall and can cause fistulas (tunnels) to other organs or other parts of the body. Because of these fistulas and the colon not absorbing properly, the patient is prone to fluid and electrolyte imbalances as well as malabsorption of vitamins/minerals. Characteristic “skip lesions” = involve some areas of the bowel but not all - “Cobblestone” appearance of intestinal lining.

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7
Q

CROHNS

READ

A

Complications of Crohn’s Disease: Chronic inflammatory condition of the bowel. The bowel wall becomes congested, thickened, leading development of abscesses and fistulas. Scar tissue interferes with movement of chyme through the intestine and perforation or obstruction can occur. The chronic inflammation can lead to significant problems such as -

  1. Malabsorption: folic acid ( anemia), calcium/vitamin D (bone weakness) 2. Fluid and electrolyte imbalance 3. Diarrhea and dehydration 4. Anal fissures
       Acute Complications:
  2. Intestinal obstruction or perforation 2. Perianal abscesses, fistulas 3. May require removal of the inflamed intestine requiring an “ostomy”
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8
Q

ULCERATIVE COLITIS

A

Ulcerative Colitis - Also an autoimmune disease -
- Lesions only occur in the colon (the primary site of water reabsorption)  chronic dehydration and malnutrition - Ulcerative lesions only involve the mucosal layer- May lead to cavity formation with small hemorrhages and abscesses - Wall of bowel thickens and ulcerations are fibrotic in later stages

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9
Q

ULCERATIVE COLITIS

READ ONLY

A

Complications of Ulcerative Colitis:
 Intestinal obstruction  Dehydration, Fluid and electrolyte imbalances  Malabsorption, Iron deficiency anemia  Chronic bloody diarrhea mixed with mucus  Fever
 Weight loss  Abdominal cramping and pain  Nausea vomiting and the urge to defecate
 Acute complications = hemorrhage, toxic megacolon* and possible colon perforation.

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10
Q

IBS

A

Irritable Bowel Syndrome (IBS)
Pathophysiology: a functional gastrointestinal (GI) disorder, meaning symptoms are caused by changes in how the GI tract works; but without damage to the GI tract (as does occur with Ulcerative Colitis and Crohn’s Disease). IBS is a group of symptoms that occur together, not a disease. In the past, IBS was called colitis, mucous colitis, spastic colon, nervous colon, and spastic bowel. The name was changed to reflect the understanding that the disorder has both physical and mental causes and is not a product of a person’s imagination.

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11
Q

IBS

READ ONLY

A

IBS and Mental Health Problems:

Mental health or psychological problems such as panic disorder, anxiety, depression, and post-traumatic stress disorder are common in people with IBS. The link between these disorders and development of IBS is unclear. GI disorders, including IBS, are often found in people who have reported past physical or sexual abuse. Researchers believe people who have been abused tend to express psychological stress through physical symptoms.
IBS and Other Potential Contributing Factors:

Other contributing factors which may play a part in IBS have been suggested (see http://www.niddk.nih.gov/health-information/health-topics/digestive-diseases/ibs/Pages/facts.aspx for more information). Some possibilities under study include: Genetics, brain-gut signal problems, hypersensitivity to bowel stretching, bacterial gastroenteritis, overgrowth of normal gut flora, altered levels of neurotransmitters, etc. IBS is diagnosed when a person has had abdominal pain or discomfort at least three times a month for the last 3 months without other disease or injury that could explain the pain. The pain or discomfort of IBS may occur with a change in stool frequency or consistency or be relieved by a bowel movement.
S/S: Persistent or recurrent symptoms of abdominal pain, altered bowel function w/o GI damage, and varying complaints of flatulence, bloating, nausea, anorexia, constipation or diarrhea. Accompanies anxiety or depression. RX: Dietary management (smaller, more frequent meals, reduce fat content, avoid dairy/alcohol/caffeine, avoid gas producing foods); stress management; medications (laxatives or antidiarrheal medications as needed; Antidepressants).

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12
Q

LIVER PRODUCES (ABC)

A

Produces ABC: Albumin – The primary plasma protein in charge of oncotic/osmotic pressure in blood veins is synthesized in the liver
 Not enough protein in the plasma means body fluid is stuck in 3rd space because there is no protein in
blood veins available to PULL it out  Which will cause ASCITES and PORTAL HTN

 Bile - transports Bilirubin [blood breakdown byproduct], and cholesterol  If liver is not producing enough bile, there is transport system for getting the bilirubin and cholesterol out of the body which will cause. . . o Buildup of bilirubin in the tissues  jaundice (yellow) in skin and sclera, and o Buildup of Cholesterol (hyperlipidemia)

 Coagulation Factors  Not enough coag factors will cause bleeding problems.  (Recall from the Hematological System Unit that the “Associated Organ” for Platelets is the Liver)
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13
Q

LIVER ALSO DSM’S

A

Detoxes: Especially ETOH (med-speak for “ethyl alcohol”) and drugs

Storage: Glycogen [a “glucose package” – stored in the liver for release as needed by the body].

Metabolism of protein. Protein digested in Small Intestine  Ammonia byproduct  liver and metabolized into urea  sent to kidney for removal in urine.

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14
Q

CIRRHOSIS

A

Cirrhosis
Cirrhosis is scarred liver tissue that does not function normally. The most common cause of cirrhosis is chronic alcohol use. Ethyl alcohol (ETOH) is oxidized by the liver to acetaldehyde which damages hepatocytes). Cirrhosis can also be caused by viral hepatitis or hepatotoxic drugs

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15
Q

PORTAL HYPERTENSION

A

Obstructed flow in liver causes backup of fluid in Portal Veins 
vein & organ engorgement. Most often due to cirrhosis. Increased vein
pressure causes fluid to back up into vital organs causing those organs to stop functioning (i.e., splenomegaly). Portal HTN also causes the veins in the esophagus to engorge with blood, causing the veins to distend (esophageal varices) and possibly to burst – Bright red blood vomit (hematemesis) is a sign this has happened - Emergency action necessary. Pressure in the portal vein forces fluid out of the vein into the abdomenwhich contributes to ascites.

MANIFESTATION:
Esophageal / stomach varices, splenomegaly, ascites, hemorrhoids

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16
Q

ASCITES

A
Ascites Free Fluid in the abdomen caused by two problems: 
 #1- Portal hypertension increases capillary hydrostatic pressure(“PUSHES” fluid out of vessels into the gut) and,#2 – damaged liver does not synthesize serum protein  decreased oncotic pressure (no protein in vessels to “PULL” the fluid out of the gut back into the veins).
Abdominal distension, displaced diaphragm leading to dyspnea, peritonitis.
17
Q

HEPATIC ENCEPHALO-PATHY

A

Hepatic Encephalo-pathy
Damaged liver will not break down or synthesize protein which results in elevated ammonia levels. Ammonia is brain-toxic and high levels will cause changes in LOC. Increased ammonia and toxins unable to be processed by the liver are shunted from the GI tract into the circulation. Many toxinsfreely cross the blood-brain barrier causing neurologic S/S.
Confusion, asterixis*(see next page), apraxia, stupor, seizures, coma

18
Q

JAUNDICE

A

Jaundice:

Damaged liver cannot break down the bilirubin found in RBCs. The bilirubin deposits in the skin and sclera of the eyes – turning the skin and sclera “yellowish orange.” Causes intense pruritis (itching).
-Hemolysis of RBC’s increases Bilirubin levels. -Obstruction of bile flow from liver increases reabsorption -Intrahepatic disease inhibits Bilirubin conjugation and excretion
Jaundice – aka, “Icterus,” S/S = Yellow orangesclera/skin, dark urine “coke syrup”, light color stools “clay colored”, anorexia, fatigue, pruritus

19
Q

HEPATORENAL SYNDROME

A

Hepatorenalsyndrome
Decreased circulating blood volume leads to decreased renal perfusion triggering the renin-angiotensin system  HIGH BLOOD PRESSURE. Hepatic failure prevents removal of excess Angiotensin so the process is not
reversed and HTN gets worse.
In a complex chemical feedback system, renal failure occurs because of
vasoconstriction of the renal circulation and opposing systemic arteriolar vasodilatation resulting in reduced systemic vascular resistance andarterial hypotension. Following the kidney damage, less urine is removed from the body, so waste products that contain nitrogen build up in the bloodstream (azotemia). HR Syndrome occurs in up to 40% of patients with liver failure. Prognosis is poor because renal failure is irreversible unless liver transplantation is performed.
Oliguria, Na+ and H2O retention, hypotension, increased BUN and Creatinine levels

20
Q

LABS FOR LIVER FX

A

LFTs (Liver Function Tests) [specifically the liver enzymes ALT and AST] increase when liver tissue
has been damaged allowing the enzymes to escape into the blood.

 CBC is also done to check RBCs and platelet status.

 Ammonia levels are monitored due to the liver’s decreased ability to break down protein. High
ammonia levels cause encephalopathy (brain damage).

 Bilirubin if liver does not make bile, bilirubin [blood breakdown byproduct] is not cleared from the blood

 PT, PTT, INR will be drawn to test for bleeding problems.

 Occult Blood smear (aka, Hemoccult or Guaiac) tests stool samples for occult blood

21
Q

HEPATITIS

READ

A

Chronic hepatitis virus slowly attacks the liver over many years
without causing symptoms. When s/s do appear, they are vague and nonspecific, so Hepatitis
can go undetected until significant liver damage is present. An estimated 4.4 million Americans are living with chronic (lifelong) hepatitis. Most do not know they are infected.
Hepatitis and Liver Cancer
The major cause of liver cancer is HEPATITIS B AND C, and can develop silently as the liver becomes cirrhotic. Blood tests, ultrasound examinations, CT and MRI scans can identify the cancers. Biopsy of the liver is needed to definitely make a diagnosis of cancer. Liver CA is LETHAL. If the cancer is found early, only a small proportion of patients can be cured.

22
Q

TYPES OF HEPATITIS

A

TYPES OF HEPATITIS (NOTE: All are caused by viruses)

o Hepatitis A - Oral-fecal (food borne) - most common type of Hepatitis in the US. Havrix vaccine* (must be
given 3 weeks prior to exposure); IgG immunoglobulin is given after an exposure to unvaccinated patient.
Hepatitis A is spread from person to person via fecal contamination because the virus is present in the stool. It is spread via contaminated food or water by an infected person who gets small amounts of stool on his or her hands, does not wash his or her hands, and passes the stool onto food that is eaten by others. An example of this is outbreaks of hepatitis A in daycare centers for young children when employees don’t wash their hands after changing diapers, and they then pass the
viruses to the next child they feed.

o Hepatitis B – Blood/body fluid borne. Most common cause in US is through unprotected sex, but can also be spread by needle sticks, Mom-to-baby, etc. - Heptavax vaccine* (must complete series of 3); IgG immunoglobulin and Interferon (Intron-A) can be given to unvaccinated patient. If a chronically infected mother
gives birth, 90% of the time her infant will be infected and develop chronic hepatitis B, usually for life. This may give rise to
serious complications of liver disease later in life such as liver damage, liver failure, and liver cancer.

o Hepatitis C - Blood, sex, needle sticks, etc. – No Vaccine available. Treated with antiviral med - Interferon (Intron A). With acute hepatitis C, the virus is eliminated in 25% of people. The other 75% become chronically infected
and later may develop serious complications such as liver failure and liver cancer. Progress is being made on cures for Hepatitis C Virus through the use of antiviral medications but the drugs are a very costly option for treating this chronic and
debilitating disease.

o Others: Hepatitis D, E, F, G

23
Q

S/S OF HEPATITIS

A

Hepatitis: Signs & symptoms
 Can be either Acute or Chronic  Fatigue, weakness, loss of stamina  Nausea, vomiting, diarrhea, anorexia
 Fever and flu-like symptoms  Dark colored urine
 Jaundice of skin and sclera (aka, icterus)*
 Intense Pruritis due to icterus*

24
Q

PANCREATITIS

READ

A

Pancreatic disease (Pancreatitis) See pg. 748 of textbook

Pathophysiology: Injury or obstruction of pancreas causing digestive enzymes to leak into pancreatic tissue –> auto- digestion of tissue OR formation of cysts. PRIMARY CAUSE IS ALCOHOL ABUSE, followed by blockages caused by gallstones.

S/S: PPPPAAAAIIIIIINNNNNN !!!! Especially epigastric pain, fever, leukocytosis, nausea and vomiting, abdominal distention, increased bowel sounds, hypotensionand shock (look up “WHY” in textbook). Can mimic a heart attack, so it is necessary to rule out cardiac causes for pain (just like for GERD and Ulcers, etc.) because the pancreas is so near to the heart. Pancreatic Stools: “Foamy floaters” – bulky unformed stools, unusually foul-smelling, greasy stools (steatorrhea). The stool is light-colored and may even contain oil droplets. This is caused because pancreas enzymes are not breaking down fat in the intestines. Rx: GI rest (nothing by mouth or NG tube until condition is controlled because food causes the pancreas to try excreting digestive enzymes which increases the patient’s pain. Primary goal is pain control, and treat underlying cause (possibly with antibiotics). If patient is without food for a week, may consider giving nutrients via an IV.

25
Q

CHOLECYSTITIS

A

(Gallbladder)

Etiology: Associated with cholelithiasis (gallbladder stones composed of cholesterol and bile) and may be “superimposed” on chronic Cholecystitis (inflammation of the gallbladder). In the majority of cases, acute cholecystitis is caused by gallstones or biliary sludge getting trapped at the gallbladder’s opening. Can also be caused by infection, injury, or tumor.

26
Q

RISK FACTORS CHOLECYSTITIS

A

RISK FACTORS for Cholecystitis are classically called the “SIX F’s of Cholecystitis”: fair, fat,
female, fertile, forty, family history. Other risk factors include Crohn’s Disease, diabetes, hyperlipidemia, pregnancy, long labor (causes damage to gallbladder) or RAPID weight loss.

27
Q

S/S OF PAIN FOR CHOLECYSTITIS

A

S/S: PAIN - especially when eating food containing any fat. The duodenum signals the gallbladder when there is
fat present so the GB will release bile into the intestine and begin breaking down the fat. If the GB or bile duct is blocked by a stone, “sludge”, or an
infection, the GB contracts harder trying to overcome the obstruction to squeeze out some bile which results in severe
pain. Pain can starts within a few minutes after eating anything with fat in it. (NOTE: this is different than ulcer pain that is relieved with eating food). Pain can mimic heart attack (severe, radiating to between shoulder blades and up neck, unrelenting and non-reproducible just like cardiac pain). Other S/S of Cholecystitis are nausea, vomiting, fever, leukocytosis, jaundice (with obstruction) and Light color or Clay-colored stools because bile is being blocked from entering the intestine. Bile (bilirubin in the bile) gives stool a brown color, so without bile the stools will lack color.

Rx: Dietary modification (a no-fat diet), or Surgery - a laparoscopy procedure
called a cholecystectomy or “Lap Chole” for short, if the gallbladder is not
swollen/infected, otherwise will need to have a traditional gallbladder surgery.