GI/Burns Flashcards

1
Q

Jaundice occurs when

A

The flow of bile is obstructed or an excess of RBC destruction

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2
Q

Portal HTN is the result of

A

increased pressure throughout the portal resulting from obstruction of blood flow

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3
Q

What are two consequences of portal HTN

A

Ascities and varies

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4
Q

Ascities occurs as a result of failure of the liver to

A

Metabolize aldosterone which incrases Na and water retention

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5
Q

Na and water retention decrease

A

synthesis of albumin

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6
Q

Ascities may occur with

A

Cancer, kidney disease and HF

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7
Q

S/S of ascities

A
Increased abdominal girth
Rapid weight gain 
SOB
Straie
Distended viens
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8
Q

Management of ascities

A

Avoid salty foods
diuretics (Spirinolactone)
Bed rest
Paracentesis

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9
Q

Hemorrhage from esophageal varices can result from

A
Lifting heavy objects
straining
Sneezing
coughing 
vomiting
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10
Q

S/S of esophageal varices

A

Hematemesis

Melena

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11
Q

For esophageal varices hemorrhage what med is given to decrease bleeding

A

Ocetreotide

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12
Q

Characteristics of a superficial burn

A
Damage to the epidermis
Caused by low intensity heat
Red with mild edema
Pain
Heals w/in 3-6 days
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13
Q

Characteristics of a superficial partial thickness wound

A
Red, weeping surface
Blister formation
Blanch when pressure is applied
Intense pain 
Heals w/in 10-21 days
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14
Q

Characteristics of a deep partial thickness burn

A

Less painful, more nerve endings destroyed
Red, dry, no blisters
Edema is moderate
Heals w/in 3-6 weeks

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15
Q

Characteristics of full thickness burns

A

Destruction of entire epidermis and dermis
Hard, dry, leathery
Would is white, red, yellow, brown or black
Sensation is reduced or absent

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16
Q

Characteristics of deep full thickness wounds

A

Extends beyond the skin into muscle, bone and tendons
Wound is black
Sensation completely absent
Healing takes month

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17
Q

Causes of burns: dry heat

A

Results from open flames. Stop, drop and roll

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18
Q

Causes of burns: moist heat

A

Contact with hot liquids or steam. Remove saturated clothes

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19
Q

Causes of burn injury: contact burns

A

Hot metal, tar or grease. Remove hot substance

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20
Q

Cardiac alterations that occur after burn injury

A
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
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21
Q

Fluid and electrolyte alterations that occur after burn injury

A

Edema forms
Hyperkalemia
Hyponatremia
Loss of capillary integrity and fluid localized causing blister formation

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22
Q

Pulmonary alterations that occur after a burn injury

A

ALveolar surfactant production decreases
Carbon monoxide combines with hemoglobin
Catcholamine release reducing the O2 delivery

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23
Q

Signs of possible inhalation injury

A
Smoky breath
Hoarseness, stridor, wheezing 
Sooty sputum 
Injury occuring in enclosed space
Burns to neck and face 
Dyspnea, tachypnea 
Drroling
24
Q

Gi alterations that occur after burn injury

A
Risk for ACS
Decreased peristalsis 
Decreased bowel sounds
Formation of Curlings ulcer 
Elevated blood glucose
N/V, abd distention
25
Q

During a burn injury, if there is muscle damage, what is released from the muscle cells

A

Myoglobin

26
Q

Myoglobin is excreted thru the

A

Kidneys

27
Q

If there is inadequate blood flow thru the kidneys, the myoglobin occludes the renal arteries resulting in

A

Kidney failure

28
Q

What are the priorities in the Emergent phase of a burn injury (onset of injury to 48hrs)

A
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%)
29
Q

What information is obtained during a assessment following a burn injury

A
Time of injury
Source of heat
How did it happen?
Interventions taken? 
Drugs/alcohol factor
Events occuring from time of burn to admission
30
Q

Signs of caron monoxide poisoning

A
Headache
Confusion
Tinnitus
Nausea
Absence of cyanosis or pallor
31
Q

What is the ABA fluid resuscitation formula

A

4ml x pt weight kg x %TBSA

32
Q

For fluid resuscitation, how is the infusion regulated

A

Half of the infusion within the first 8 hrs, the second half is given over the next 16hrs

33
Q

What is the appropriate urinary output for thermal and chemical injuries

A

30-50ml/her

34
Q

What is the appropriate urinary output for electrical injuries

A

75-100ml/hr

35
Q

What are the priorities during the acute phase (48hrs- wound closure)

A
Maintenance of resp/cardio status 
F/E balance
Infection prevention 
Pain management 
Splint and position client 
Perform ROM exercises 
Nutrition (up to 5000cal/day)
36
Q

Complications that can occur during the acute phase include

A

Pneumonia
Malnutrition
Loss of musculoskeletal function
Infection and sepsis

37
Q

How to perform wound cleaning

A

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

38
Q

Mechanical debridement

A

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

39
Q

Natural debridement

A

The devitalized tissue separates from the underlying viable tissue spontaneously

40
Q

Chemical/enzymatic debridement

A

Topical agent is applied directly to the burn wound. Enzymes digest collagen in necrotic tissues

41
Q

What is the most important energy source for burn patients

A

Carbohydrates

42
Q

When the oral route is used, what kin of diet should burn pt be on

A

High protein

High calorie

43
Q

Examples of topical antimicrobial drugs used at every dressing change to prevent infection

A

Silver sulfadiazine

44
Q

Rehabilitation phase (wound closure to when pt returns to highest possible level of functioning)

A

Psychosocial adjustment
Prevention of scars
Resumption of preburn activity
May take years

45
Q

What are the 2 underlying alterations the development of hepatic encephalopathy

A

Inability of the liver to detoxify by products of metabolism. Portosystemic shunting

46
Q

What is considered the major etiologic factor in te development of encephalopathy

A

Ammonia. It enters the brain and excites peripheral benzo type receptors stimulating GABA

47
Q

Serum ammonia levels can be lowered by

A

Elimination of protein from diet

Antibiotics (neomycin sulfate) which reduces the number of intestinal bacteria capable of converting urea to ammonia

48
Q

Other factors that unrelated to ammonia levels that can cause hepatic encephalopathy includes

A
Excessive diuresis
Dehydration
Infections
Surgery 
Fever 
Meds (diuretics that cause K loss, tranquilizers, sedatives)
49
Q

Early sx of hepatic encephalopathy

A

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

50
Q

What medication is given to reduce ammonia levels

A

Lactulose

51
Q

Lactulose can be given with _____ to mask sweet taste

A

Fruit juice

52
Q

For comatose pts, lactulose can be given

A

In NG tube or enema

53
Q

Other nursing interventions for a pt with hepatic encephalopathy

A

IV glucose to minimize protein breakdown
Administration of vitamins
Correct electrolyte imbalance (especially K+)

54
Q

Hepatitis A transmission and sx

A

Fecal-oral route. Ingestion of food or liquid that is infected. Anorexia is the most severe/common. No jaundice

55
Q

Management of Hepatitis A

A

Bed rest, nutritious diet. During periods of anorexia the pt should receive frequent small meals eupplemented with IVF with glucose

56
Q

Hepatitis B transmission and sx

A

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