GI/Burns Flashcards
Jaundice occurs when
The flow of bile is obstructed or an excess of RBC destruction
Portal HTN is the result of
increased pressure throughout the portal resulting from obstruction of blood flow
What are two consequences of portal HTN
Ascities and varies
Ascities occurs as a result of failure of the liver to
Metabolize aldosterone which incrases Na and water retention
Na and water retention decrease
synthesis of albumin
Ascities may occur with
Cancer, kidney disease and HF
S/S of ascities
Increased abdominal girth Rapid weight gain SOB Straie Distended viens
Management of ascities
Avoid salty foods
diuretics (Spirinolactone)
Bed rest
Paracentesis
Hemorrhage from esophageal varices can result from
Lifting heavy objects straining Sneezing coughing vomiting
S/S of esophageal varices
Hematemesis
Melena
For esophageal varices hemorrhage what med is given to decrease bleeding
Ocetreotide
Characteristics of a superficial burn
Damage to the epidermis Caused by low intensity heat Red with mild edema Pain Heals w/in 3-6 days
Characteristics of a superficial partial thickness wound
Red, weeping surface Blister formation Blanch when pressure is applied Intense pain Heals w/in 10-21 days
Characteristics of a deep partial thickness burn
Less painful, more nerve endings destroyed
Red, dry, no blisters
Edema is moderate
Heals w/in 3-6 weeks
Characteristics of full thickness burns
Destruction of entire epidermis and dermis
Hard, dry, leathery
Would is white, red, yellow, brown or black
Sensation is reduced or absent
Characteristics of deep full thickness wounds
Extends beyond the skin into muscle, bone and tendons
Wound is black
Sensation completely absent
Healing takes month
Causes of burns: dry heat
Results from open flames. Stop, drop and roll
Causes of burns: moist heat
Contact with hot liquids or steam. Remove saturated clothes
Causes of burn injury: contact burns
Hot metal, tar or grease. Remove hot substance
Cardiac alterations that occur after burn injury
Decreasesd CO, perfusion and O2 delivery Drop in BP Increase in heart workload Hypovolemia Peripheral edema Release of catecholamines causing vasoconstriction RBCs may be destroyed causing anemia Elevated hematocrit Slow or absent cap refill
Fluid and electrolyte alterations that occur after burn injury
Edema forms
Hyperkalemia
Hyponatremia
Loss of capillary integrity and fluid localized causing blister formation
Pulmonary alterations that occur after a burn injury
ALveolar surfactant production decreases
Carbon monoxide combines with hemoglobin
Catcholamine release reducing the O2 delivery
Signs of possible inhalation injury
Smoky breath Hoarseness, stridor, wheezing Sooty sputum Injury occuring in enclosed space Burns to neck and face Dyspnea, tachypnea Drroling
Gi alterations that occur after burn injury
Risk for ACS Decreased peristalsis Decreased bowel sounds Formation of Curlings ulcer Elevated blood glucose N/V, abd distention
During a burn injury, if there is muscle damage, what is released from the muscle cells
Myoglobin
Myoglobin is excreted thru the
Kidneys
If there is inadequate blood flow thru the kidneys, the myoglobin occludes the renal arteries resulting in
Kidney failure
What are the priorities in the Emergent phase of a burn injury (onset of injury to 48hrs)
Establish an airway (100% humidified oxygen) Fluid replacement (LR) Encourage pt to cough up secretions Maintain body temp Prevent infection Indwelling cath NG tube (TBSA over 25%)
What information is obtained during a assessment following a burn injury
Time of injury Source of heat How did it happen? Interventions taken? Drugs/alcohol factor Events occuring from time of burn to admission
Signs of caron monoxide poisoning
Headache Confusion Tinnitus Nausea Absence of cyanosis or pallor
What is the ABA fluid resuscitation formula
4ml x pt weight kg x %TBSA
For fluid resuscitation, how is the infusion regulated
Half of the infusion within the first 8 hrs, the second half is given over the next 16hrs
What is the appropriate urinary output for thermal and chemical injuries
30-50ml/her
What is the appropriate urinary output for electrical injuries
75-100ml/hr
What are the priorities during the acute phase (48hrs- wound closure)
Maintenance of resp/cardio status F/E balance Infection prevention Pain management Splint and position client Perform ROM exercises Nutrition (up to 5000cal/day)
Complications that can occur during the acute phase include
Pneumonia
Malnutrition
Loss of musculoskeletal function
Infection and sepsis
How to perform wound cleaning
Mild soap, water and wash cloth to prevent infection. Hair in and around the burn area should be clipped short or shaved. Temp of water should be maintained at 100 degrees and room temp should be maintained at 80-85 degrees to prevent hypothermia
Mechanical debridement
Pt immersed in tub or has small areas of wound washed at bedside
Nonviable tissue is removed by forceps or scissors
Wet-to-dry dressing not encouraged
Natural debridement
The devitalized tissue separates from the underlying viable tissue spontaneously
Chemical/enzymatic debridement
Topical agent is applied directly to the burn wound. Enzymes digest collagen in necrotic tissues
What is the most important energy source for burn patients
Carbohydrates
When the oral route is used, what kin of diet should burn pt be on
High protein
High calorie
Examples of topical antimicrobial drugs used at every dressing change to prevent infection
Silver sulfadiazine
Rehabilitation phase (wound closure to when pt returns to highest possible level of functioning)
Psychosocial adjustment
Prevention of scars
Resumption of preburn activity
May take years
What are the 2 underlying alterations the development of hepatic encephalopathy
Inability of the liver to detoxify by products of metabolism. Portosystemic shunting
What is considered the major etiologic factor in te development of encephalopathy
Ammonia. It enters the brain and excites peripheral benzo type receptors stimulating GABA
Serum ammonia levels can be lowered by
Elimination of protein from diet
Antibiotics (neomycin sulfate) which reduces the number of intestinal bacteria capable of converting urea to ammonia
Other factors that unrelated to ammonia levels that can cause hepatic encephalopathy includes
Excessive diuresis Dehydration Infections Surgery Fever Meds (diuretics that cause K loss, tranquilizers, sedatives)
Early sx of hepatic encephalopathy
Confusion
Sleep during the day and restless at night
Asterixis
Simple tasks become difficult
In early stages, DTR are hyperactive with worsening of condition these reflexes disappear
What medication is given to reduce ammonia levels
Lactulose
Lactulose can be given with _____ to mask sweet taste
Fruit juice
For comatose pts, lactulose can be given
In NG tube or enema
Other nursing interventions for a pt with hepatic encephalopathy
IV glucose to minimize protein breakdown
Administration of vitamins
Correct electrolyte imbalance (especially K+)
Hepatitis A transmission and sx
Fecal-oral route. Ingestion of food or liquid that is infected. Anorexia is the most severe/common. No jaundice
Management of Hepatitis A
Bed rest, nutritious diet. During periods of anorexia the pt should receive frequent small meals eupplemented with IVF with glucose
Hepatitis B transmission and sx
Transmitted thru blood, saliva, semen and vaginal secretions. Sx include loss of appetiete, dyspepsia, aabdominal pain, malaise, generalized aching and weakness. The liver is tender and enlarged
