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4630 Final > Acute GI dysfunction > Flashcards

Acute GI dysfunction Flashcards

1
Q

upper GI type of bleeding?

A

arterial, hematemesis and melena

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2
Q

lower GI type of bleeding?

A

venous bleeding, hematochezia

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3
Q

Hematemesis bright and dark

A

bright: upper, higher updarker: old bleed from jejunum where bile is breaking it down

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4
Q

melena

A

-black tarry stool-foul smelling, black (can happen only with 50 cc of bleeding)-from small or ascending colon

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5
Q

hematochezia

A

-bright blood in stool=lower GI blood (from colon)

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6
Q

clinical manifestation of GI bleed

A

hematemesis, melena, hematochezia, fatigue, dyspnea, syncope, angina

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7
Q

Most common cause of upper GI bleeding

A

peptic ulcer disease

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8
Q

peptic ulcer disease

A

Causes: NSAIDS,H. Pylori, cigarette smokingTypes: Duodenal and gastricDx: H. pylori testing, visualization with endoscopy, barium x-ray, combination antibiotic (amoxy, clarithromycin, tetracycline, and metronidazole)Treatment: H2 blockers, PPI

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9
Q

Acute erosive or hemorrhagic gastritis

A

-Severe inflammation of the gastric mucosa (NSAID gastritis, alcohol gastritis, stress gastritis)-treatment: endoscopic sclerotherapy (inject something to make varices coagulate), vasopressin IV or intraarterial

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10
Q

esophageal and gastric varices

A

-associates with cirrhosis, portal htn, and portal or splenic vein thrombosis-massive bleeding-treatement: sclerotherapy or esophageal balloon (creates pressure to stop bleeding), can also band the verice or pollup-this is often how end stage hepatic pts die

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11
Q

mallory-weiss tears

A

-a small tear in the mucosal lining at the gastro-esophageal junction (often preceded by vomit, most bleeds stop without intervention)-DX with endoscopy-If bleeding is excessive may treat with vasopressin, usually stops on its own

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12
Q

acute lower GI bleeds

A

Causes: diverticular bleeding, ischemic bowel disease, inflammatory bowel disease, neoplasms

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13
Q

Diverticular bleeding

A

-only occurs in about 3% of those with diverticulosis-when occurs, may have massive loss of blood that is life threatening-artery ruptures to fill diverticula-dx with colonoscopy to determine reason for bleeding25% require surgical intervention to stop bleed

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14
Q

ischemic bowel disease

A

-interruption of colonic blood supply (bowel obstruction, occlusion of blood flow through vascular system)-risk factors: surgical procedure to vasculature and bowel resection, afib, atherosclerosis, hypotn, sickle cell, DM, lupus, pacreatitis, anticoagulant therapy-S/S:* intermittent bleeding*. A pt. who’s h&h is dropping and we don’t know why, mixed dark and bright red bleeding, fever, abd pain-DX: endoscopy shows purple color bowel, xray may show air sacks, barium contrast shows thumbprints-TX: fix blood flow to bowel (fluid resuscitation), Antibiotic tx for infection, bowel resection as needed to remove necrotic bowel*FINAL EXAM “THUMBPRINTS” PICTURE OF ISCHEMIC BOWEL DISEASE

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15
Q

inflammatory bowel disease

A

-S/S: bloody diarrhea, light to moderate bleeding-TX: Stop bleeding, administration of corticosteroids to control inflammation, anti-TNF tx (immune biologic therapy), surgical resection as needed

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16
Q

what is anti-TNF used for

A

helps with inflammation in IBS, it is an immune biologic therapy

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17
Q

neoplasms

A

-up to 20% benign and malignant tumors are associated with bleeding-slow, chronic, and self-limiting-DX: barium x-rays, ct scan, mri, pet scan, endoscopy-TX: dependent on type, stage, patient wishes

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18
Q

management of acute GI bleeding unstable pt.

A

-is the patient stable? (hypotn, tachy, altered LOC, cap refill delayed= unstable)-urgent interventions: hemodynamic resuscitation and oxygen delivery-establish cause of the bleeding once stabilized-Is it upper or lower?-Upper: hematoemesis and melana-Lower: hematochezia (bright)

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19
Q

management of acute GI bleeding stable pt.

A

-stable? (bloody diahrrea, bp normal, AO=stable)-Look at labs, get a really good history, meds (NSAIDS), alcohol consumption, cigarette smoking, sickle cell, clotting factor disorders-is it upper or lower

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20
Q

initial assessment of GI bleed

A

Laboratory changes-H&H-Platelets-Electrolytes-BUN/Creat (helps differentiate upper and lower. If greater than 35 think upper GI, less than 35 is probably lower GI)-PT/INR -liver functions test-cardiac enzymes (might be getting ischemic to heart muscle itself bc of blood loss)-every pt. who comes in with GI bleed should be typed and crossedFluid Volume Status-hypotension (SBP less than 90)-narrowed pulse pressure (MAP less than 60)-orthostatic hypotension (concerned with drop in BP 20mmhg or rise in HR of 20bp/min)-tachycardia-ST changes (only when the pt is becoming ischemic. Need tele monitor)-cap refill delayed-mucous membranes dry-UO dropping below 30cc/hr-mental status changes

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21
Q

interventions in GI bleed

A

-Maximized 02 carryping capacity, keep 02 sat above 92%-restore normovolemia: 2 large bore lvs, administer 2 liters of crystalloids (LR, normal saline, should see improvement in 20min), followed by PRBCs as needed, FFP, Platelets, Factor VIII-Patient positioning to maintain SBP-NG tube placement-Erythromycin 3mg/kg over 20 minutes one hour prior to procedures-PPI’s-Reglan 10 mg IV-Bowel Prep

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22
Q

what guage in a pt. going to surgery or hemodynamically unstable

A

18 gauge

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23
Q

if hemoglobin is less than 7, then?

A

give blood no matter what, even if they have had a fluid challenge

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24
Q

If they are anticoagulated, and their PT is going to be greater than 13, and INR greater than 1.5, you are going to give them?

A

-FFP or platelets (provider preference)

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25
Q

Platelets less than 5,000 or after 10 units of PRBCs?

A

platelets

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26
Q

patient may need what if they’re anticoagulated or on coummadin?

A

Vitamin K

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27
Q

PT positioning for systolic BP (will be on test)

A

patient is hypotensive, put them in supine or supine with legs elevated (head flat)

28
Q

NG tube placement bright blood, coffee ground,no blood or bile, or bile no blood means for each?

A

-if you get bright blood on your NG placement, think upper GI-coffee ground, upper GI but probably not active-No blood and no bile, GI bleed is below the pyloric sphyncter-bile but no blood, thinking no upper GI bleed at all

29
Q

What does erythromycin do?

A

helps gastric motility to clear out stuff in upper GI so they can actually see what’s happening

30
Q

bowel prep to clean out bowel, most used?

A

go lightly

31
Q

proceedures

A

endoscopy: colonoscopy, sigmoidoscopy, -injection therapy-thermal coagulation therapy (light that causes coagulation)-clip them

32
Q

Obstruction

A

a mechanical blockage arising from a structural abnormality that presents a physical barrier to the progresssion of gut contents-can be partial or complete, simple or strangulated

33
Q

Ileus

A

is a paralytic or functional variety of obstruction

34
Q

patho of obstruction

A

results in-initial overcoming of the obstruction by increased peristalsis-increased intraluminal pressure by fluid and gas-vomiting-sequestration of fluid into the lumen from the surrounding circulation-lymphatic and veous congestion resulting in oedematous tissue-factors 3,4,5 result in hypovolaemia and electrolyte imbalance-further: localized anoxia, mucosal depletion necrosis and perforation and peritonitis-bacterial overgrowth with translocation of bateria and toxins causeing bacteraemia and septicaemiaWhat do we do?-decomplress with NGT to low/intermittent suction-replace lost fluid-correction electrolyte abnormalities-recognize strangulation and perforation (strangulation no passage of flatulance, severe pain, fever, peritoneal tenderness and swelling rigidity, leukocytosis, increases in amylase levels as well)-systemic antibiotics

35
Q

partial obstruction

A

classic sign, loose watery stool (passing around the blocking fecal matter)

36
Q

a simple

A

obstruction that causes it to become ischemic

37
Q

Small bowel adhesions

A

-accounts for 60-70% of all SBO-results from peritoneal injury, platelet activation and givrin formation-associated with starch covered gloves, intraperitoneal sepsis, haemorrhage and wash with irritant solutions iodine and other foreign bodies.-As early as 4 weeks post laparotomy. The majority of patients present between 1-5 years-70% of patients had a single band-patient with complex bands are more likely to be readmitted-readmission in surgically treated patients is 35%-common surgeries you see them in: (25% colorectal surgery, 20% gynaecological, 14% in appendectomies)

38
Q

hernia

A

-accounts for 20% SBO-common: femoral, ID inguinal, umbilical, incisional and internal-the site of obstruction is the neck of the hernia-compromised viscus is with in the sac-ischemia occurs initially by venous occlusion followed by edema and arterial compromise-strangulation noted by: persistent pain, discoloration, tenderness, constitutional symptoms

39
Q

Large Bowel obstruction

A

-distinguishing ileus from mechanical obstruction is challenging-according to leplacs law: maximum pressure is at it’s maximum diameter. CECUM is at the greatest risk of PERFORATION-perforation resultes in release of feces with heavy bacterial contamination

40
Q

Role of CT

A

-used with IV contrast, oral and rectal contrast (tripple contrast: IV, oral, and rectal contrast)-able to demonstrate abnormallity in the bowel wall, mesentery, mesenteric vessels and peritoneum-can show: level of obstruction, degree, causes, degree of ischemia, free fluid and gas

41
Q

Barium bastrografin studies

A

-should not be used in pts with peritonitis-used in acute abdomen but is diluted-useful in recurrent and chronic obstruction

42
Q

Initial dagnostics for LBO

A

Lab-CBC-clotting-arterial blood gasses-U& CRT, na, K Amylase, LFT and glucose, LDH-group and save (x-match if needed)-optional (ESR< CRP< Hepatitis profile)Radiological-x-rays-USSECG (cardiac ischemia)

43
Q

Clinical finding BO high

A

-pain is rapid-vomiting copiuous and contains bile jejunal content-abdominal distention is limited or localized-rapid dehydration from vomiting

44
Q

Distal SBO

A

-pain: central and colicky-vomitous is feculunt-distension is severe-visible peristalsis-may continue to pass flatus and feacus before absolute constipation

45
Q

Colonic BO

A

-? pre-existing change in bowel habit-colicky in lower abdomen-vomiting is late (has to back all the way up)-distension prominent-cecum ? distended

46
Q

persistent pain may be a sign of

A

strangulation

47
Q

Clinical examination general, abdominal, and others

A

general-vital signs, P, BP, Sat, RR, T-dehydration-anemia, jaundice, LN-assessment of vomitus if possible-full lung and heart examAbdominal-abdominal distension and it’s pattern-hernial orifieces-visible peristalsis-cecal distention-tenderness, guarding and rebound-organomegaly-bowel sounds (high pitched, absent)-rectal examinationOthers-systemic examination-if deemed necessary (CNS, vascular, gynecological, musculoskeletal)

48
Q

Initial management of LBO

A

-resuscitate (60-100%), insert 2 lines, IVF (120ml and hour crystalloids), add K+ at 1mmmol/kg bc of vomiting (dropping K)-draw blood-inform senior member in team-NPO, NG placement, urinary cath-IV antibiotics -If concern exist about fluid overloading a central line should be inserted-follow-up lab results and correction of electrolyte imbalance-pt should be nursed in intermediate care-rectal tubes should only be used in Sigmoid volvulus

49
Q

Indications for surgery

A

-Evidence of strangulation-signs of peritonitis (bowel has ruptured)-if the obstruction won’t clear in 24-48 hours-not sure why there is an obstruction or what is going on -try to stabilize pt. before surgery

50
Q

Ileus

A

Associated with the following conditions:-postop and bowel resection-ischemia-infection inside and outside the stomach-endocrine-spinal and pelvic fractures-retro-peritoneal hematoma-metabolic abnormalities-bed ridden-drug induced (morphine, tryciclic meds)

51
Q

Ileus or obstruction?

A

Clinical features:-is there an underlying cause?-is the abdomen distended but tenderness is not marked-is the bowel sounds diffusely hypoactive Radiological features-is the bowel diffusely distended-is there gas in the rectum-are further investigations helpful in showing an obstructionDoes the pt. improve on conservative measures?

52
Q

Types of IAH/ACS primary, secondary, recurrent

A

-Primary: injury/disease of abdomino-pelvic region, “surgical”-Secondary: sepsis, cap leak, burns, “medical”-Recurrent: ACS develops despite surgical intervention

53
Q

IAP interpretation

A

Pressure Interpretation0-5 Normal5-10 Common in most ICU pts>12 (grade 1) Intra-abdominal HTN16-20 (grade 2) Dangerous IAH- begin non- invasive intervention>21-25 (grade 3) Impending, decompressive lappi

54
Q

patho

A

ischemia leads to inflammatory responses, cap leakage, coupled with our fluid resuscitation, tissue edema, increases abd pressure, leads back to more ischemia creating this cycle

55
Q

causes of IAP elevation and findings

A

-major abdominal/retroperitoneal problem-ischemic insult/SIRS requiring fluid resuscitation with a positive fluid balance of 5 OR MORE LITERS within 24 HOURS (10lb weight gain)-temp, HR, and resp increases, WBC .12,000 (elevates)

56
Q

physiologic sequelae cardiac

A

-increased ABD pressure cause compression of vena cava with reduced venous return-elevated intra-thoracic pressure with multiple negative cardiac effectsResult:-decreased cardiac output, increased SVR-increased cardiac work loads-decreased tissue perfusion-misleading elevations of CVP and PAWP-cardiac insufficiency, cardiac arrest

57
Q

physiologic sequalae pulmonary

A

incrased intra-abd pressure casuses-elevated diaphragm, reduced lung bolumes and alveolar inflation, stiff thoracic cage, increased intersitial fluidResults:-elevated intrathoracic pressure-incread peak pressure, reduced tidal volumes-Barotrauma-atelectasis, hypoxia, hypercarbia-ARDS

58
Q

physiologic sequalae gastrointestinal

A

increased intra abd pressure causes-compression and congestion of mesenteric veins and capillaries-reduced cardiac output to the gutresult-decreaes gut perfusion incresaed gut edema and leak-ischemia, necrosis-bacterial translocation-development and perpetuation of SIRS-further increase in IAP

59
Q

physiologic renal

A

elevated IAP causes-compression of renal veins, parenchyma-resuced cardiac output to kidneysresult-reduced BF to kidney-renal congestion and edema-dereaed glomerular filtration-renal failure, oliguria/anuria

60
Q

physiologic neuro

A

elevated IAP causes-increased intrathoracic pressure-increases in superior vena cava pressure with reduction in drainage of SVC into the thoraxresult:increaed central venous pressure and IJ pressure-increased ICP-decreaed CPF-cerebral edema, brain anoxia, brain injury

61
Q

APP

A

abdominal perfusion pressure = MAP-IAP-reflects actual gut perfusion bettter than IAP alone-optimizing APP.60 mm HG should probably be primary endpoint

62
Q

Decompressive laparotmy

A

-delay in abd compression may lead to intestinal ischemia, decompress early

63
Q

bladder pressure monitoring how to?

A

insert catheter to bladder, hook to transducer, read pressures off of the bladder-make sure transducer is level with the bladder

64
Q

patient meets one of the following criteria and has at least two risk factor for IAH:

A

-new intensive care until admission-evidence of clinical deterioration or new organ failurerisk factors:-Diminished abd wall compliance-increased intraluminal contents-increased abdominal contents-capillary leak/fluid resuscitation

65
Q

how you messure

A

-messure in expiration, pt. laying supine-put in 25 ml fluid to measure it against-wait 30 seconds and measure it

4630 Final (11 decks)

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