GI Alterations ppt (chap 21, 22, 23) Flashcards

1
Q

What are the causes of upper GI bleeding?

A

The usual causes are peptic ulcers (most common!), erosive gastritis, esophagogastric varices, mallory-weiss tear, AV malformation (arteries and veins bundled together), tumors, stress ulcer

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2
Q

What are s/s of upper GI bleeding?

A

Anemia, syncope, orthostatic changes, angina, dyspepsia, weakness, fatigue, dyspnea. May worsen CAD, HTN, DM, pulm dx, RF which all lead to SHOCK

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3
Q

How do you measure orthostatic BP? What should you be careful of?

A

Have the patient lie down for 5 minutes. Measure blood pressure and pulse rate. Have the patient stand (dangle if too weak/dizzy).
Repeat blood pressure and pulse rate measurements after standing 1 and 3 minutes.

A drop in SBP of ≥20 mm Hg, or in DBP of ≥10 mm Hg, or an increase in HR >20 beats per minute or more, or experiencing lightheadedness or dizziness is considered abnormal (intravascular volume loss).

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4
Q

What are the s/s of lower GI bleeding?

A

Hematochezia which resolves spontaneously, but may rebleed or require sx

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5
Q

What are the s/s of acute GI bleeding?

A

Acute: occult blood, hematemesis, melena, hematochezia

Chronic: anemia, fatigue, dyspnea, lightheadedness or syncope, low RBC count and hemoglobin, typically iron deficient, positive occult blood

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6
Q

What are the risk factors for developing an ulcer?

A

H. Pylori infection, NSAIDs (ibuprofen, naproxen sodium, ASA), antipletlet drugs (ASA/extended release dipyridamole, ASA extended release, cilostazol, clopidogrel)

H. Pylori releases releases cytotoxins and mucolytic enzymes that break down mucosa barriers causing inflammation making mucosa more susceptible to damage.

NSAIDs inhibits production of prostaglandins (help repair and maintain stomach mucosa) which leads to loss of integrity of the stomach which leads to bleeding.

Antiplatelet drugs – reduce blood clotting when bleeding occurs but can INCREASE THE RISK OF BLEEDING.

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7
Q

What are the s/s of an ulcer?

A

Pain (increases 1-2 hrs after eating and at gets worse at night), N/V, anorexia, weight loss

If in pyloric canal: bloating, nausea, vomiting

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8
Q

What is the treatment of an ulcer and how do these work?

A

Antibiotics
PPIs - end in azole (Nexium, Prilosec, etc.), decrease gastric acid production
Prostaglandins - Misoprostol (Cytotec), synthetic prostaglandin to replace what was lost with NSAIDs, be aware that these can cause miscarriage!
H2 receptor blockers - end in tidine (Zantac, Pepcid), create a protective coating on gastric mucosa by reducing gastric acid secretion and increasing gastric mucus/bicarb production
Cytoprotective agent - Sucralfate (Carafate), forms protective coating on injured mucosal surface, inhibiting gastric acid secretion, pepsin, and bile salts
Antacids - Aluminum carbonate (Gaviscon) & Calcium carbonate (Caltrate), neutralize excessive gastric acid

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9
Q

What are the causes of an ulcer?

A

Stress, gastritis, varices, Mallory-Weiss tears

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10
Q

What is considered a lower GI bleed?

A

Bleeding that happens beyond the ligament of Treitz (lower part of duodenum)

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11
Q

Name some examples of lower GI bleeds.

A

Diverticulosis, AV malformation, neoplasms, inflammatory bowel dx, ischemic bowel dx

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12
Q

How does the nurse manage a GI bleed?

A

Assess: if pt is hemodynamically unstable (↓BP or orthostatic hypotension, altered LOC, ↓UO; if unstable + hematemesis, hematochezia, or melena which means the pt needs to go to the ICU!!!)

Resuscitate: by drawing labs to type & crossmatch, CBC, clotting, chemistries; O2 and monitor LOC, VS, UO; crystalloids (NS, LR), PRBCs or whole blood; FFP if ↑ PT or PTT, platelets if thombocytopenia; vasopressin, Sengstaken-Blakemore tube, surgery (TIPS)

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13
Q

What are the types of acute intestinal obstruction and name the s/s of both.

A

Acute small-bowel obstruction and acute paralytic ileus. Signs and symptoms are: Abd distention, cramping/pain, vomiting, electrolyte imbalances → dehydration, abnormal lab values

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14
Q

What is the most common site for large bowel obstruction? What causes large bowel obstruction?

A

Sigmoid colon. Causes: carcinoma, diverticulitis, benign tumors, inflammatory bowel disorders, volvulus of sigmoid colon

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15
Q

What is the treatment of acute intestinal obstruction?

A

Fluid resuscitation to treat dehydration (use UO or CVP monitoring as a guide), NPO— NGT to low, intermittent suction, colonoscopy, electrolyte replacement, antibiotics if strangulation (see board-like abdominal distention with severe pain)

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16
Q

How many mmHg characterizes intraabdominal HTN and abdominal compartment syndrome? How is intraabdominal pressure measured? What is a complication of abdominal compartment syndrome and how is it improved?

A

> 12 mmHg for intraabdominal HTN and 20 mmHg for abdominal compartment syndrome. Intraabdominal pressure is measured indirectly by abdominal decompression (AbViser). A complication of abdominal compartment syndrome is end-organ dysfunction that is improved by abdominal decompression

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17
Q

What is the treatment of intraabdominal HTN and abdominal compartment syndrome? What is a complication of ACS?

A

@ 10-15 mm Hg: ↑ HOB, pulmonary hygiene
@ 16-25 mm Hg: ICU, sedation, fluid resus if unstable (↓ CO or BP), surgical decompression?
@ >25 mm Hg: surgical decompression

Reperfusion asystole and PE are complications of ACS

18
Q

Define acute liver failure. What causes acute liver failure?

A

Coagulation abnormalities with INR >1.5 and encephalopathy. Lasts

19
Q

Define Wilson’s disease.

A

A rare inherited disorder that causes too much copper to accumulate in the liver, brain and other vital organs.

*Pneumonic - Mr. Wilson loves to drink Moscow Mule in his cooper mug.

20
Q

How do you diagnose acute liver failure? How do you treat liver failure caused by acetaminophen toxicity and mushroom toxicity?

A

Dx: LFTs (ALT, AST, bilirubin, albumin, PT/INR), amylase, lipase, CBC, ammonia. If liver failure is caused by acetaminophen toxicity treat with activated charcoal via NG tube, N-acetylcysteine (PO/PT/IV). If liver failure is caused by mushroom toxicity (Amanita phalloides) treat with Penicillin G IV.

21
Q

What are the complications of acute liver failure?

A

Hepatic encephalopathy (characterized by asterixis, high levels of ammonia, and lactulose), cerebral edema, coagulopathy, hypoglycemia & electrolyte abnormalities, infection, cardiopulmonary abnormalities, AKI

22
Q

What are s/s of chronic liver disease?

A
Hepatic encephalopathy (lactulose - gas and diarrhea), esophageal variceal bleeding (tx: fluids, endoscopy, Sengstake-Blakemore tube, TIPS), ascites (tx: paracentesis, albumin)
coagulopathy, electrolyte abnormalities, infection, AKI
23
Q

Describe the patho of ascites.

A

Increased ADH secretion causes body to hold unto Na and water. Liver is messed up so there is low lvls of albumin which causes fluid to build up. Portal HTN. Increased lymph flow due to liver damage.

24
Q

What are s/s of hepatic insufficiency?

A

Coma, jaundice, spider nevi, pectoral alopecia, gynecomastia, esophageal varices, liver damage, splenomegaly, distention of abdominal veins, ascites, palmar erythema, altered hair distribution, testicular atrophy, hemorrhagic tendency, ankle edema, bone marrow changes

25
Q

What does drinking like a fish do to your liver?! :D

A

CIRRHOSIS.

26
Q

What is the function of the pancreas?

A

To secrete enzymes that help break down food so nutrients can be absorbed

27
Q

What happens when the pancreas messes up?

A

Pancreatic ducts become obstructed → hypersecretion of exocrine enzymes of pancreas → enzymes to enter bile ducts → bile backs up into pancreatic duct → pancreas is blocked the eff off → pancreatitis

28
Q

Define acute pancreatitis, what does it lead to, and what causes it?

A

Inflammation of the pancreas which leads to SIRS. Most often caused by gallstones and alcohol abuse

29
Q

How do you diagnose acute pancreatitis?

A

Pt needs at least 2 or 3 of the following symptoms: abdominal pain, serum amylase and/or lipase >3x upper limit of normal, CT scan findings.Labs: amylase and lipase (increased), glucose, calcium, WBC, BUN

30
Q

What s/s does the nurse for when assessing the pt for acute pancreatitis?

A

Pain, GI, systemic inflammation, inspect skin for cullen’s sign (brusing around the umblicus) or grey turner’s sign (brusing of the flanks that happens 24-48 before acute pancreatitis), CV, pulm, neuro, renal, heme, endo, electrolyte symptoms such as hypocalcemia - chvostek’s and troussesu’s sign

31
Q

What are the local and systemic complications of acute pancreatitis?

A

Local: necrosis, abscess, pseudocyst, abdominal compartment syndrome (ACS).

Systemic: Pulmonary (hypoxia, ARF, pneumonia, pleural effusion, atelectasis, ARDS), CV (hemorrhage, ↓ BP, shock, pericardial effusion, pericardial tamponade), renal (ARF), neurologic (encephalopathy), hematologic (vascular thrombosis, DIC), metabolic (hyperglycemia, metabolic acidosis, hypocalcemia), infectious (peritonitis, sepsis)

32
Q

How does the nurse manage acute pancreatitis?

A

Provide hemodynamic stability, pain management, reduced pancreas stimulation, social support, problem correction, prevention/treatment of complications

33
Q

Describe the nursing care of acute pancreatitis.

A

Optimize CO, respiratory status, balance f/e, control/relieve pain, relieve N/V, optimize nutrition

34
Q

Name the two types, cause, and prophylaxis/treatment of upper GI bleeding in relation to stress

A

Two types: superficial diffuse erosions and stress ulcers, caused by an imbalance of hostile and protective factors in stomach and duodenum, prophylaxis & treat with PPI and H2-blockers

35
Q

Define, list causes, manifestations, dx, prevention/tx of upper GI bleeding d/t to gastritis.

A

Transient inflammation of gastric mucosa, caused by NSAIDs, ETOH, acute stress, manifestations: coffee ground emesis (hematemesis), bloody aspirate if on NG tube or given melena, slow loss of blood indicated by low Hct and Hgb lvls, may be asymptomatic but can cause epigastric pain, N/V, bleeding which is a problem in critically ill pts, dx: direct visualization w/ endoscopy, prevent/treat: w/ PPI & H2 blockers, endoscopic sclerothrapy, IV vasopressin if diffuse bleed, if caused by NSAID stop or reduce dose and give misoprostol or switch to cox-2 inhibitor, if caused by ETOH stop ETOH and antiulcer therapy

36
Q

List causes and complications of upper GI bleeding d/t to varices.

A

Associated with cirrhosis (due to ETOH abuse), portal hypertension (causes varices), and portal or splenic vein thrombosis which leads to massive bleeding without warning

37
Q

Define, list causes, who is at risk, manefistations, dx, and tx of upper GI bleeding d/t to mallory-weiss tears.

A

tears that occur in the lower part of the esophagus and upper portion of esophagus (gastroesophageal junction) due to portal HTN, retching (vomiting sounds) or vomiting, ETOHics have high risk of this, manifestations: mild to massive hematemesis, stops on its own and rebleeding is rare, dx: upper GI endoscopy, tx: thermocoagulation and sclerosing injection

38
Q

Define, risk factors, complications, of lower GI bleeding w/ diverticulosis.

A

Small outpouchings of bowel wall caused by weakness, risk factors: >60 and chronic constipation, complications: diverticulitis – same thing as diverticulosis but w/ inflammation and infection (can rupture), 25% of cases can rebleed requiring surgery or angiography w/ vasopressin

39
Q

What are colorecal cancers primarily associated with, how does bleeding occur, what happens when acute blood loss happens, what happens when polyps are removed with lower GI bleeding w/ neoplasms.

A

Colorectal cancers primarily associated w/ occult bleeding but massive bleeding can occur, bleeding usually is slow, chorionic, and self limiting, acute blood loss is rare but if it happens bowel resection and tumor excision are indicated, when removing polyps bleeding continuous for a month

40
Q

Two types, difference, dx, complciation, tx of lower GI bleeding w/ inflammatory bowel disease.

A

Consist of ulcerative colitis and chron’s disease, ulcerative colitis is confined to mucosa/submucosa while chron’s extends through intestinal well from mucosa to serosa, dx both: colonoscopy/biopsy, life threatening bleeding can occur, tx: aminosalicylates & corticosteroids, surgery if nothing else works

41
Q

Define, what is it associated with, how does bleeding occur, manifestations, and tx of lower GI bleeding w/ AV malformation

A

Angiodysplastic lesions that are usually small, superficial, multiple, and located in the right colon, although lesions can occur throughout the intestinal tract and are often numerous, associated with cardiac disease, low flow states, and aging, the bleeding is slow and chronic but can be occult, manifestations: weakness, fatigue, dyspnea on exertion, guaiac positive stools, tx: minimal blood transfusion (2-4 U or less), if bleeding doesn’t stop on its own tx w/ arterial embolization with intraarterial infusion vasopressin, gelatin, sponge, microcoils, and polyvinyl ETOH particles, use vasopressin cautiously

42
Q

Define, causes, manifestations, dx, tx of lower GI bleeding w/ ischemic bowel disease.

A

Ischemia of the colon caused by interruption of clonic blood supply, causes: occlusion of major artery, small vessel disease, venous obstruction, low flow states (cardiogenic shock), intestinal obstruction, bleeding can occur from anticoagulant use if ischemic bowel is present, manifestations: intermittent dark and bright red blood and clots may be visible from the rectum, fever, abd pain, dx: GI endoscopy w/ purple discoloration of bowel, x-ray w/ air pockets, barium contrast w/ thumbprints, tx: restore blood flow – fluid resuscitation, optimization of CO, treat underlying disease, antibiotics, resection of bowel if indicated