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Complex > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

hepatitis

A

inflammation of the liver

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2
Q

non-infectious hepatitis: how long does it last

A

can be acute, less than 6 months

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3
Q

causes of non-infectious hepatitis (6)

A

-ETOH
-Other toxins: Bacterial, fungal, or parasitic toxic exposure
-Autoimmune diseases - primarily biliary atresia cirrhosis, -hemochromatosis
-Congenital wilson’s disease
-R-sided HF - d/t back up of fluid
-non-ETOH fatty liver (NASH)

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4
Q

infectious hepatitis causes

A

can be acute or chronic d/t:
-Hep viruses
-Herpes
-Epstein Barr
-Coxsackievirus
-Varicella-zoster

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5
Q

signs and symptoms of hepatitis (beginning) (8)

A

Yellowing skin and eyes
Extreme fatigue
Low grade fever
Loss of appetite
N/V
Dark urine
Light colored stool
Diarrhea

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6
Q

s/s that hepatitis is progressing towards cirrhosis

A

-jaundice d/t cirrhosis and portal HTN
-hepatomegaly d/t HTN or extra fluid
-ascites
-muscle wasting
-hypoalbuminemia
-Na retention
-vitamin deficiencies
-bruising and bleeding
-sparse body hair
-caput medusa
-dark amber urine d/t bilirubin
-clay colored stool b/c of bilirubin
-palmer erythema

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7
Q

why does hypoalbuminemia occur in patients with hepatitis

A

d/t liver’s impaired ability to synthesize proteins
Edema/third spacing d/t decreased oncotic pressure
Skin is shiny, soft and pitting

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8
Q

signs of hepatomegaly

A

RUQ tenderness
Can palpate borders - will feel lumpy due to nodules

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9
Q

what is cheilosis

A

happens to lips - swelling / fissures on lips
Vit B2 deficiency, sign of hepatitis

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10
Q

glossitis (what is it and how do you tx?)

A

inflammation of the tongue
happens with vit deficiences in hepatitis
tx: antibiotics , avoid spicy/hot food, good oral care

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11
Q

why do patients with hepatitis bruise and bleed more

A

Impaired clotting factors
sequestration of platelets in the spleen

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12
Q

what is caput medusa and what causes it

A

superficial varicose veins on abdomen
May have arterial bruit
d/t portal htn and congestion

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13
Q

when do patients with hepatitis start showing s/s?

A

65-75% of hepatocytes are destroyed or dysfunctioning

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14
Q

when does liver failure occur

A

when there is a loss of 60% or greater hepatocytes

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15
Q

what would you include in an assessment for hepatitis

A

ask about
Alcohol use, ecstasy, needle sharing (IV drug abuse)
Transfusion history
OTC drugs
Occupation and travel exposure
Safe sex

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16
Q

what lab values do you draw for the synthetic functions of the liver

A

albumin, PT

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17
Q

what is albumin responsible for

A

colloid/osmotic pressure, keeps intravascular volume in vessels

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18
Q

normal albumin level

A

3.5-5.3 gm/dl

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19
Q

what is PT

A

measures liver’s ability to synthesize clotting factors

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20
Q

normal PT / INR

A

Normal PT 11-13
Normal INR - 0.8-1.1
Dysfunctional liver → PT increases, at risk for bleeding

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21
Q

what values of albumin and PT/INR will happen in liver failure

A

decrease albumin and increase PT/INR (longer to clot, more bleeding)

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22
Q

what are the hepatocellular damage markers

A

AST
ALT

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23
Q

what is AST and normal values

A

aspartate transaminase
Normal: 6-40 iu/l
enzyme that usually helps metabolize amino acids
Go up when there is damage

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24
Q

what is ALT and normal values

A

alanine transaminase
Normal: 30-120 units/L
Helps metabolize proteins
Go up when liver is damaged

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25
Q

when are AST and ALT released

A

released when hepatocytes are injured or die
Numbers should come down if treated and working

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26
Q

how do you evaluate cholestasis (excretory function, slowing or stalling of bile flow through your biliary system)

A

alkaline phosphatase
bilirubin

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27
Q

what is alkaline phosphatase + normal levels

A

Increased when bile duct is damaged or obstruction so bile can’t get out
Normal: 44-147 iu/L
Later marker than AST and ALT

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28
Q

what is bilirubin

A

Made during normal breakdown of blood cells
Can increase with liver dysfunction or bile duct issues

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29
Q

total bili normal levels + jaundice levels

A

Normal 0.1-1.2 mg/dL
Become jaundice when bili > 2.5 mg/dL

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30
Q

direct bili normal levels

A

< 0.3 mg/dL

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31
Q

what is nursing mgmt for hepatitis?

A

supportive care (rest, nutrition, avoiding further liver injury)
daily weights, measure abdominal girth

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32
Q

when does a patient with hepatitis need to be hospitalized

A

-unstable hemodyanmics
-encephalopathy
-poor fluid/food intake
-ascites
-respiratory issues

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33
Q

what diet should a pt with hepatitis have

A

High calorie low protein diet, small frequent meals

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34
Q

how do you treat ammonia

A

Lactulose for ammonia - acidifies the colon to prevent absorption of ammonia
draws ammonia from the blood into the colon where it is removed from the body

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35
Q

how are you going to treat pt with hepatitis

A

-Lactulose for ammonia - acidifies the colon to prevent absorption of ammonia
-Antibiotics to clear colon of bacteria that produces ammonia
-cholestyramine to treat pruritus
-Need antiemetics to combat N/V
-IV fluid - has to be saline - Can’t metabolize ringers → makes ph imbalance worse

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36
Q

what causes hepatic encephalopathy

A

increased ammonia
tx with lactulose

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37
Q

pt teaching for hepatitis

A

Infection
Modes of transmission
diet/fluid restrictions
Total cessation of alcohol (if alcohol related)

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38
Q

what are the 4 categories of cirrhosis

A

Laennec’s (portal)
Post necrotic cirrhosis
biliary
cardiac

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39
Q

Laennec’s (portal) cirrhosis

A

Seen in alcoholic cirrhosis or severe malnutrition
Middle aged males 40-60 years

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40
Q

post necrotic cirrhosis

A

cirrhosis following submassive necrosis of the liver (subacute yellowatrophy) due to toxic or viral hepatitis

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41
Q

biliary cirrhosis (what causes it and what are the characteristics)

A

Caused by obstruction or infection of major extra or intrahepatic bile ducts
characteristics: Jaundice, abdominal pain, steatorrhea, enlargement of liver and spleen

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42
Q

cardiac cirrhosis

A

d/t intractable heart failure

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43
Q

what causes cirrhosis (6)

A

chronic Hepatitis Virus,
alcohol abuse,
nonalcoholic steatohepatitis,
hereditary hemochromatosis,
Wilson’s disease, and
alpha1-antitrypsin deficiency

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44
Q

how does cirrhosis occur

A

Inflammation, fibrotic changes, and increased intrahepatic vascular resistance cause compression of the liver lobule, leading to increased resistance or obstruction of normal blood flow through the liver, which is normally a low-pressure system

Leads to splenomegaly, varices, hemorrhoids, cardiac dysfunction, fatigue, unstable glucose levels

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45
Q

s/s of cirrhosis

A

Lower extremity edema, ascites and hypotension
decreased synthesis of albumin leads to interstitial edema and deceased plasma volume
Clotting dysfunction-bruising to hemorrhage low-grade DIC

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46
Q

physical findings of cirrhosis (3)

A

LE edema
Ascites
hypotension

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47
Q

lab data for cirrhosis (albumin, bili, Na/H2O)

A

decreased albumin
increased bili
Liver can’t eliminate solute free water → decrease in sodium concentration in serum –> more retention of water –> more edema

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48
Q

tx for cirrhosis

A

Antibiotics to clear colon of bacteria that produces ammonia
Hepatic encephalopathy: Tx: lactulose
IV lasix for ascites -Normal saline!
antihypertensives to prevent rupture of varices
Beta blockers and nitrates
If bleeding —> will need packed RBCs

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49
Q

is there a cure for cirrhosis

A

no

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50
Q

what is supportive care for cirrhosis

A

Treat symptoms
Daily weights, strict Is and Os
Measure abdominal girth with ascites everyday
Check urine output to make sure it is adequate
Blood tests everyday - electrolytes, plts, H&H, coags
Neuro assessment
Monitor nutrition
Ascites will lead to resp issues

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51
Q

how can you manage ascites

A

paracentesis

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52
Q

when is a VP Shunt used in ascites

A

when resistant to other therapies
drains peritoneal fluid from the peritoneum into veins, usually the internal jugular vein or the superior vena cava

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53
Q

what is TIPs

A

transjugular intrahepatic portosystemic shunt
Used to decompress portal venous system
Portal vein → bypass liver circulation to hepatic vein → can lead to metabolic encephalopathy
Point is to reduce portal HTN → decrease size of varices and decrease bleeding

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54
Q

how to manage ascites (3)

A

first step - IV lasix
second - paracentesis
third - VP Shunt

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55
Q

complications of VP shunt

A

infection, occlusion of tube - can thrombose, can make esophageal varices more engorged and cause hemorrhaging

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56
Q

normal ammonia levels

A

9.5 - 49 mcg/dl

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57
Q

if blood ammonia increases, what happens?

A

Decreased LOC
Neuromuscular disturbances
Asterixis - push back/ flex hand and it flaps
Hyperreflexia
Impaired thinking
Changes in memory, personality, concentration, reaction times

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58
Q

what can cause hepatic encephalopathy

A

Can be d/t use of TIPS,VP shunt, GI bleed from esophageal varices → create nitrogen load → leads to bacterial deamination = amino acids break down → converted to ammonia

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59
Q

how to tx hepatic encephalopathy

A

Low protein diet
Medications -
-Lactulose: Decreases colonic pH to decrease absorption of ammonia by facilitating BM
-Neomycin (antibiotic)
-Metronidazole (flagyl) - 500mg q8 (IV, PO)
—All 3 focus on clearing nitrogen out of gut

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60
Q

Asterixis

A

very early sign of hepatic encephalopathy - ask patient to hold hand out and like stopping traffic and watch for involuntary flapping motion

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61
Q

balloon tamponade

A

usually refers to the use of balloons inserted into the esophagus, stomach or uterus, and inflated to alleviate or stop refractory bleeding

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62
Q

nursing care for balloon tamponade

A

Can only be inflated for 24-48 hours, bc can cause necrosis, perforation, ulcerations, 12-24 after hemostasis
Pressure to 25-39mmHg
HOB > 30 degrees to prevent reflux

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63
Q

why is respiratory assessment so important with balloon tamponade

A

tube can move and obstruct airway-if this happens cut tube to deflate gastric balloon quickly, bleeding assessment-can cause perf or esophageal rupture

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64
Q

what are the exocrine cells of the pancreas

A

Aciner cells - synthesize and secrete digestive enzymes to assist in the breakdown of starch, fat and proteins
empty secretions into pancreatic ductal system → joins common bile duct

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65
Q

what are the endocrine cells of the pancreas

A

Islets of langerhans: secrete insulin, glucagon, and somatostatin

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66
Q

causes of acute pancreatitis

A

-heavy alcohol use (40%)
-gallstones (40%)
-others (10%) - trauma, infection, shock, medications, biliary tract disease, cancer, atresia

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67
Q

how do gallstones cause acute pancreatitis

A

blocks pancreatic secretions from emptying into duodenum → reflux of bile initiates inflammatory process
More common in women (Fat, Female, Forty, Farting)

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68
Q

what are the two types of acute pancreatitis

A

Interstitial: mild form, lasts 1-2 weeks, no organ dysfunction, reversible, no serious complications
Necrotizing: 10-20% of cases progress to this

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69
Q

necrotizing acute pancreatitis

A

Causes irreversible damage to pancreas and surrounding tissues
Poor prognosis for patient → sepsis, MODs, high mortality rate
Ill from every system standpoint
Cellular necrosis and hemorrhage inside the pancreas

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70
Q

what are the results of the inflammatory response in acute pancreatitis (necrotizing)

A

Hypovolemia from capillary permeability,
acute respiratory distress syndrome, DIC,
renal failure,
cardiovascular failure,
GI hemorrhage

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71
Q

what will you ask your patient about when it comes to history for acute pancreatitis

A

Ask about alcohol and gallbladder disease
Diabetes
Medications
Any biliary tract disease?
Any jaundice?
Anorexia
N/V
Abdominal distension

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72
Q

what is the hallmark sign of pancreatitis

A

Present with epigastric to LUQ pain
Pain = deep, sharp, constant, radiating through to the back and up to the chest
Increases within minutes of eating food high in fat content
pain is worst lying down (do not lay them in supine)
Nonspecific
10/10, severe

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73
Q

additional signs of pancreatitis

A

abdominal guarding on exam
low grade fever, jaundice
Diarrhea
Bleeding
Foul smelling bowel movement
Dehydrated quickly
decreased BP → increased HR
If islets of langerhans are damaged during necrosis → patient will develop diabetes

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74
Q

amylase + normal levels

A

convert starch and glycogen into simple sugars
Normal 23-85 (up to 140) u/L

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75
Q

will amylase increase or decrease in pancreatitis

A

elevation 3x normal

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76
Q

lipase

A

fats → fatty acids and glycerol
Normal: 0-160 u/l

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77
Q

what is the most sensitive indicator for acute pancreatitis

A

lipase

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78
Q

will BUN increase or decrease with pancreatitis

A

increase - suggests hypovolemia

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79
Q

will AST increase or decrease with pancreatitis

A

increase indicates damage to liver cells

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80
Q

will ALT increase or decrease with pancreatitis

A

indicative of gallstone pancreatitis
Increase

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81
Q

will WBC increase or decrease with pancreatitis

A

increase d/t inflammation

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82
Q

what do you need for diagnosis pancreatitis

A

Amylase and/or lipase are 3x normal
Characteristic pain
Abdominal imaging

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83
Q

what is the priority in the ED for pancreatitis

A

Priority = Volume resuscitation - a lot of NS and electrolyte (esp hypocalcemia)

then…
-pain relief
-stabilization of VS
-anticholinergics to decreases GI motility and pancreatic enzyme release
-Antispasmodics – relaxes the smooth muscle, relaxes sphincter of Oddi
-H2 blockers/PPI – decrease GI acid secretions
-When being fed, need pancreatic enzymes to aid in digestion of fats and proteins
-Antibiotics – if have necrotizing pancreatitis

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84
Q

priorities for pancreatitis in the ICU

A

Fluid resuscitation
Inotropic support
Respiratory support
Renal therapy
Nutritional support - Not TPN
Pharm therapy
Surgical intervention

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85
Q

what is MRCP and what is it used for

A

magnetic resonance cholangiopancreatography
Can detect gallstones down to 3mm in diameter and remove them
High quality

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86
Q

what does hypocalcemia indicate in pancreatitis

A

can indicate presence of pancreatic fat necrosis
Calcium binds with fatty acids during necrosis process

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87
Q

why would a patient with pancreatitis be hyperglycemic

A

decreased release from damaged beta cells → increase glucagon release + increased stress response from inflammation

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88
Q

will TGLs increase or decrease with pancreatitis

A

elevate - over 1000 mg/dl

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89
Q

3 pain control methods for pancreatitis

A

High fowlers
IV narcotics
NG tube to decompress belly

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90
Q

pancreatic rest for pancreatitis

A

NGT on low intermittent to decompress the stomach and to decrease stimulation of secretin which stimulates production of pancreatic secretions

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91
Q

signs of severe hemorrhagic pancreatitis

A

Turner’s Sign – bruising of the flanks, retroperitoneal hemorrhage
Cullen’s Sign – edema and bruising around the umbilicus

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92
Q

signs of hypocalcemia

A

Chvosteks & Trousseaus

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93
Q

Chvostek’s Sign

A

twitching of the facial muscles in response to tapping over the area of the facial nerve
hypocalcemia

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94
Q

Trousseau’s sign

A

carpopedal spasm caused by inflating the BP cuff to a level above the systolic pressure for 3 minutes

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95
Q

type 1 DM

A

no production of insulin

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96
Q

type 2 DM

A

insulin resistance, which is hyperglycemia, hyperinsulinemia, and consequent Beta cell exhaustion

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97
Q

complications of diabetes

A

Blindness - retinopathy, cataracts
Stroke
Premature CAD
HTN - Atherosclerotic changes in heart, brain, kidneys
Gastroparesis
Diarrhea (especially due to medications like metformin)
Fertility issues, impotence
Increased risk of infections
Peripheral Vascular disease - Poor wound healing, Amputation
Peripheral neuropathy

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98
Q

3 hallmarks of DKA

A

hyperglycemia that causes hyperosmolarity
metabolic acidosis
fluid/electrolyte disturbance / volume depletion from osmotic diuresis

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99
Q

most common cause of DKA

A

infection (30-50%, UTIs, pneumonias in older adults)

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100
Q

why are ketones produced in DKA

A

Ketones are produced when body is forced to use fat to create energy because lack of insulin that is converting glucose to energy
Fat is turned into ketones = acids → accumulate in bloodstream

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101
Q

other causes of DKA

A

Inadequate insulin therapy
Stroke, MI, pancreatitis
Alcohol/drug abuse
Trauma
Meds: diuretics, corticosteroids, beta blockers, some antipsychotics/anti seizures

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102
Q

is DKA more common with type 1 or 2

A

type 1

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103
Q

DKA nursing care assessment: history

A

Diabetic regime
Weight loss
Thirst
Urinary frequency
Bloating
Any anorexia?

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104
Q

s/s of DKA

A

kussmaul respirations
fruity breath d/t acetone
abdominal pain with N/V
Polyuria
Polydipsia
Abdominal distension
Dry mucous membranes - dehydration
Decreased perfusion
Hypotension
Tachycardia = compensatory
Altered mental status - somnolence, stupor, coma
Fever = sign of underlying problem being an infection

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105
Q

BG level in DKA

A

> 250 - 1200 mg/dl
average = 600

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106
Q

anion gap

A

specialized blood tests that lets us know about metabolic acidosis
Look at difference b/w sodium + potassium on one side and Cl and HCO3 on the other
Less than 11 = normal

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107
Q

how to improve circulatory volume and perfusion in DKA

A

NS 1L/hr in ED and ICU
Until HR and BP returns to normal
BP over 90/100
HR to come down

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108
Q

correcting electrolyte imbalances with DKA

A

potassium phosphate (once you get lab values)
bicarb (if ph is less than 7)

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109
Q

how to decrease serum glucose in DKA

A

Only regular insulin via IV
Will be on continuous insulin drip with q1 hr glucose checks
Want slow steady decline of blood glucose
Best to give low dose regular insulin IV gtt, 0.15U/kg initial, then 0.1U/kg/hour which is about 5-10U/hour. This produces a steady decline. Don’t want to go fast, for fear of water moving into cell and causing vascular collapse.
Once down to 250, add D5W to avoid hypoglycemia

110
Q

what do you want UA to be in DKA

A

20-30 ml/hr

111
Q

patient education in DKA

A

Monitoring
Correct diet
Hydration
Take insulin
know signs of hypoglycemia

112
Q

signs of hypoglycemia

A

Hypothermia
Tachypnea
Tachycardia
Dysrhythmias
Hyptertensive
Diaphoresis
Hunger
Nausea
Headache, altered mental status
Personality change
Blurred vision
Confusion
Severe: coma, convulsions

113
Q

hyperosmolar hyperglycemic state (HHS)

A

Acute illness of the pancreas
Marked hyperglycemia
Hyperosmolality
No ketoacidosis

114
Q

most common cause of HHS

A

Infections are most common cause
UTIs
Pneumonia
Cellulitis
Diverticulitis

115
Q

what population is HHS more common with

A

More common in type II
More common in older adults

116
Q

is dehydration worse in HHS or DKA

A

HHS

117
Q

nursing care assessment of HHS: history

A

Diabetes
Medications
Signs of recent infection
Change in LOC
Any decrease in activity
Difficult to wake up?
Profound weakness

118
Q

s/s of HHS

A

Weakness
Polyuria
Polydipsia
Impaired mental state → all the way to coma
s/s of dehydration (low BP, high HR)
NOT kussmaul’s breathing

119
Q

BG in HHS

A

Blood glucose can be 400-4000 mg/dL with an average of 1100

120
Q

will sodium be high or low in HHS

A

high d/t dehydration

121
Q

will serum osmolality be high or low in HHS

A

high d/t dehyrdation
Normal range - 275-299
Number will increase with dehydration r/t ADH being secreted
Will decrease when someone is volume overloaded/overhydrated

122
Q

do you have an anion gap in HHS

A

no - bicarb will be normal, ph will be relatively normal

123
Q

1 nursing care priority for HHS

A

1 IV fluid resuscitation to correct volume depletion

124
Q

hemodynamic monitoring in HHS

A

Would be concerned about pulmonary edema due to rapid volume repletion and can’t handle that amt of fluid
Looking for fluid returning to right side of heart (CVP) - hook up central line to monitoring
Want it over 12 but not over 14

125
Q

when do you add d5w in HHS

A

when BG is back in 200s

126
Q

teaching for HHS

A

Monitor glucose
Knowing side effects of medications
s/s of hypo and hyper glycemia
Understanding any kind of infection can propel them in to HHS

127
Q

DKA priority

A

control glucose so body stops making ketones, then fluid replacement

128
Q

functions of the skin (6)

A

Protects against infection
Prevents loss of body fluids
Controls body temp
Functions as a sensory and excretory organ
Produces vitamin D
Determines identity

129
Q

superficial (1st degree burn)

A

only affects the epidermis, or outer layer of skin. The burn site appears red, painful, dry, and absent of blisters. Scarring is rare or minimal.

130
Q

partial thickness (2nd degree burn)

A

Pink, mottled red
Hair follicles and sweat glands are preserved
Blisters
Wet, weeping with serous exudate
Extremely painful
Can have waxy white appearance
Firm but not leathery
Same causes as 1st degree but can have longer or greater exposure to cause
21-28 days of healing
Often require hospitalization

131
Q

full thickness 3rd degree burn

A

Epidermis, dermis, hair follicles, sebaceous glands are destroyed
Thrombosed vessels in dermis
Nerve endings are destroyed so they are painless
Degree of burn depends on intensity and duration of exposure
Do not heal from them spontaneously - only by grafting - has to be donor skin → pain returns

132
Q

fourth degree burn

A

If muscle and bone are involved
Can be different colors

133
Q

rule of nines: head and neck

A

9%

134
Q

rule of 9s: arms

A

each arm = 9%

135
Q

rule of 9s: anterior trunk

A

18%

136
Q

rule of 9s: posterior trunk

A

18%

137
Q

rule of 9s: legs

A

18% each!

138
Q

rule of 9s: perineum

A

1%

139
Q

quick estimate of burns

A

look at palms of victims hands

140
Q

burns based on body part

A

Upper part of the body - increased mortality
Head, neck, chest - pulmonary complications
Perineum - prone to infection

141
Q

what determines severity and outcome of burn

A

age
-Mortality is increased in adults over age 60 and in children over 2
-Poor antibody response
-Translucent nature of skin

142
Q

causes of burns

A

Thermal -flame, hot liquid, hot object
Chemical - tissue destructions secondary to chemical, liquid, or acid
Alkaline are worse than acid
Electrical - contact with an electrical current, only entrance and exit wounds are apparent
Radiation - localized d/t high radiation doses

143
Q

major to life threatening burns

A

Greater than 25% TBSAB adult, greater than 20% TBSAB child
Full thickness greater than 10%
Burn of face, hands, eyes, ears, perineum
Inhalation, electrical burn
Burn with extenuating circumstances: Chemical burn, electrical burn

144
Q

thermal burns tx

A

Irrigate burn with water for at least 20 minutes - will halt burning in tissues
Remove wet clothing, don’t put other clothing on - just cover with blankets
Remove all jewelry
Transport
High o2 concentration if the fire was in a closed space

145
Q

chemical burns tx

A

Dilute the chemical when appropriate
Remove contaminated clothing
Flush for at least 20-30 minutes

146
Q

electrical burns tx

A

Turn off source of current
Use non-conductive materials to remove electricity source
Immobilize and efficiently

147
Q

3 phases of burns

A

emergent
acute/reparative
rehabilitative

148
Q

emergent phase

A

Begins with the injury and lasts 24-48 hours or, in the critically ill patient, up to two weeks
Hyperkalemia → injured tissue and RBCs releases K+
Will look like systemic inflammatory response

149
Q

acute / reparative phase

A

Begins when initial fluid replacement is complete and fluid shifts from interstitial back to vascular space

150
Q

rehabilitative phase

A

from hospital admission to resumption of functioning level in society

151
Q

priorities in emergent phase (8)

A

ABCs
Institute and maintain strict isolation
Institute fluid resuscitation - cornerstone of emergent phase
Gastric intubation - NG tube
Foley catheter
Tetanus
Wound cultures
Tubbing

152
Q

parkland burn formula

A

4cc. X Kg. Body weight X TBSAB

*Fluids must be calculated from the time of burn occurrence as most of the fluid is lost in the initial 8 hours

*1/2 of the calculated fluid for the first 24 hours is given in that initial 8 hours

153
Q

what indicates you can move to acute phase

A

adaptive fluid level
Lucid Mental Status
Adaptive Vital Signs - 90 systolic and HR < 100 bpm
Adequate Peripheral Perfusion - Cap refill, color, temperature
Adequate Urinary Output - Minimum 50 cc
Return to Normal Weight
Pulse Rate Less than 120
Normal CVP
Clear Lungs

154
Q

Allograft/homograph

A

taken from a person other than the patient (most common = cadaver)

155
Q

xenograft

A

temporary tissue taken from another species (most common = pigs)

156
Q

autograph

A

skin taken from one area of one’s body transplanted to another, permanent

157
Q

Physiologic dressing

A

temporary biological dressing

158
Q

Escharotomy

A

surgical procedure where an incision is made through eschar to present healthy skin

159
Q

complications of burns (6)

A

**hypovolemic shock
wound infection
resp complications
curlings ulcer
electrolyte alterations
CV problems

160
Q

signs of hypovolemic shock

A

Compensated signs: increase HR and decreased BP, decreased urinary output, tachypnea, cyanosis

161
Q

most common bacteria with burns

A

Usually gram negative - pseudomonas

162
Q

signs of wound infection with burns

A

Dark discolorations around wound, edema on unburned area (margin), unexplained eschar separation

163
Q

burns: respiratory complications

A

Mortality rate - 20-84% (depends on comorbidities, early intervention)
From inhaling chemicals, fires, electric shock, burns of face, neck, chest, present with pulmonary insufficiency and pulmonary edema (ARDS)

164
Q

curlings ulcer

A

stress ulcer
50% of burn patients develop
Causes necrosis of gastric wall
As soon as 24 hours after burn
Mortality rate = 70%
Early signs - gastric distension, pallor, sweat, blood in NG residual (guaiac), If blood is in fluid, test burns blue, Also a heme test

165
Q

electrolytes in burns

A

Increase in hematocrit because RBC destruction
Leukocytes increase
Coag problems because of hemoconcentration
K+ is increased initially because of blood cell injury - Decreases when patient begins to diuresis
BUN increased because of protein catabolism

166
Q

what causes CV problems with burns

A

decreased CO

167
Q

priority in acute phase of burns

A

Fluid
Replaced with maintenance fluid to replace evaporated loss
Usually D5W with K+ in it (because patient is now voiding)
Signs its enough - edema is reabsorbed, return to pre burn weight 8-10 days post burn, voiding

168
Q

other priorities in acute phase of burns

A

Wound care - debridement, dressings, medications
Hydrotherapy
Nutrition

169
Q

nutrition in acute phase of burns

A

Need 5000-7000 calories a day to heal
Need food with carbohydrates, proteins, fats, vitamins
Wilmore formula - exact number of calories a burn patient needs in a day

170
Q

what must occur immediately and frequently with burns

A

debridement

171
Q

what are burns covered with temporarily

A

allografts/xenografts
Last 3-5 days
Monitor and care for graft
Stimulates healthy new growth
Stimulate growth, protect granulating tissue
Temporary wound cover

172
Q

when do you change allografts/xenografts

A

When you see purulence under the temporary cover
4-6 are usually needed

173
Q

when is a pt ready for an autograph

A

When healing and pink, vascularized tissue
Take small piece of skin and it gets stretched out and puts holes in it (so it can breathe)
Needs to be covered and kept moist with antimicrobial solution for at least 72 hours

174
Q

burn medications

A

silvadene
mafenide acetate

175
Q

silvadene

A

Creamy white ointment that spreads easily over the burn
Gram Negative, gram positive antimicrobial properties
Softens eschar
AE: Can cause leukopenia

176
Q

Mafenide acetate

A

second choice for burns
can interfere with electrolyte imbalance

177
Q

tubbing/tanking

A

At least once a day
Removes topical agents and cleanses
Softens the eschar, increasing range of motion –> debridement is done during tubbing
Loss of body heat
Painful, Stressful
Loss of Sodium
Possibility of cross contamination

178
Q

psychological impact of burns

A

Emergent Phase: Psychological “shutdown” - Major Concern: Physiological delirium
Acute Phase: Pain, depression, regression
Recuperative Phase: Apprehension
Intervention: Burn Support Group

179
Q

priorities in recuperative phase

A

jobst garments
splinting

180
Q

jobst garments

A

Treatment that covers entire surface of the burn, fits like a second skin
Prevents scarring
Can only take off for shower

181
Q

what does splinting do?

A

prevents contracture

182
Q

rule of 9s: chest

A

9%

183
Q

major risk factor for head trauma

A

alcohol consumption

184
Q

primary prevention for head trauma

A

helmets, seatbelts

185
Q

is there secondary prevention for head trauma

A

not really

186
Q

tertiary prevention for head trauma

A

golden hour, treat and care asap

187
Q

Acceleration

A

moving object strikes a stationary force
Ex: Head is hit with a bat

188
Q

deceleration

A

head in motion hits a stationary force
Motor vehicle crash - head hits steering wheel

189
Q

deformation

A

causes brain to twist in the head
Usually under physical assault

190
Q

countercoup

A

Brain is rotated inside the head from one side to another
ex: shaken baby syndrome

191
Q

blunt trauma

A

damage to the brain without penetration to the skull
Usually results from acceleration and deceleration injuries
On initial assessment, you don’t know what is going on
Seen more often than penetrating

192
Q

penetrating trauma

A

object disrupts integrity of skull and penetrates brain
Gunshot wound to the head

193
Q

shearing injuries

A

results from rotational force, affects white matter in the brain stem

194
Q

contusion

A

concussion with bruising to the brain

195
Q

skull fracture

A

common form of injury
Linear
Depressed
Compound

196
Q

subdural hematoma

A

Bleeding between sub dura and arachnoid membrane

197
Q

sub arachnoid hemorrhage: what causes it?

A

Not usually result of head trauma but can be d/t rupture aneurysms

198
Q

intracerebral hemorrhage

A

Direct bleeding in to brain itself
Not usually as a result of head trauma

199
Q

nursing goals for acute head trauma (3)

A

Reduce the risk of secondary damage
1. Stabilize vital signs
2. Prevent further Injury
3. **REDUCE ICP

200
Q

how to stabilize airway during primary survey

A

Airway: stabilize head → jaw thrust maneuver

201
Q

order of assessment (to see if patient is alert)

A

Squeeze trapezius on both sites
Sternal rub
Suborbital pressure
Nail bed pressure

202
Q

what does DERM stand for (after ABC)

A

depth of coma
eyes
respirations
motor mvmt

203
Q

lethargic

A

Drowsy but will follow simple commands and makes sense

204
Q

obtunded

A

Arousable with stimulation, can follow simple commands

205
Q

stuporous

A

Hard to arouse, inconsistently following commands, limited spontaneous movements

206
Q

semi comatose

A

Movements are purposeful when stimulated but not following commands or speaking coherently

207
Q

comatose

A

Patient may respond with reflexive posturing
Can still be breathing on their own and maintain BP and HR
Light vs deep coma

208
Q

Decorticate Posturing - what is it and what does it indicate

A

flexion and internal rotation of extremities.
Lesion above mid-brain.

209
Q

Decerebrate Posturing - what is it and what does it indicate

A

Abnormal extension- an extension and internal rotation of the upper and lower extremities.
Can indicate Brain herniation
More severe

210
Q

ICP - intracranial pressure

A

pressure exerted by CSF in the ventricles

211
Q

Monro-Kellie hypothesis

A

the sum of volumes of brain, cerebrospinal fluid (CSF) and intracerebral blood is constant. An increase in one should cause a reciprocal decrease in either one or both of the remaining two.

212
Q

normal ICP

A

4-15 mm Hg

213
Q

moderately elevated ICP

A

15-40 mm hg

214
Q

severe/life threatening ICP value

A

greater than 40 mm Hg

215
Q

what is cerebral perfusion pressure

A

pressure required to perfuse the brain cells

216
Q

how do you calculate CPP

A

MAP - ICP

217
Q

normal CPP

A

60-90 mm hg

218
Q

how do you measure CPP

A

Catheter placed through the skull into the subarachnoid space or cerebral ventricle (preferred method)
Changes in pressure are monitored, via a transducer, directly and continuously

219
Q

what is the number 1 diagnostic tool in head trauma

A

CT scan

220
Q

what should CSF look like

A

Fluid = clear, colorless, should not be bloody or cloudy

221
Q

when will a stroke show up on a CT scan

A

24-48 hours after stroke

222
Q

what can an MRI show

A

stroke bed + bleeding within 5 minutes of someone having stroke
gold standard for ischemic stroke

223
Q

early clinical manifestations of increased ICP

A

**Change in Level of Consciousness (Make sure you can wake them up)
Headache
Nausea and Projectile Vomiting
Cri-du-Ca (“cry of the cat” in infants/pediatric patients)

224
Q

late clinical manifestations of increased ICP

A

Loss of motor and sensory functions
Pupillary changes
Cushing’s triad

225
Q

cushings triad

A

Widening pulse pressure
Bradycardia
Irregular respirations
*Indicates herniation!

226
Q

what HOB degree promotes venous return

A

30 degrees

227
Q

what do you want the CO2 levels to be for patient with head trauma and why

A

want it between 30-35
> 45 = increased ICP
Hyperventilate pt to blow off CO2 to decrease PCO2 and decrease ICP

228
Q

what level of PO2 will increase ICP

A

< 60
need to increase oxygen setting on ventilator!

229
Q

diuretic of choice for increased ICP

A

mannitol

230
Q

s/s of impending herniation (6)

A

-Decreased LOC (Coma)
-PupillaryAbnormalities
-Motor dysfunction (hemiplegia, decortication, decerebration)
-Impaired brain stem reflexes (corneal, gag, swallowing)
-Alterations in Vital signs
-cushing’s triad

231
Q

complications of head trauma (9)

A

-Increased ICP
-post traumatic seizures
-cushing’s stress ulcer
-intracerebral CSF fistula
-diabetes insipidus
-acute hydrocephalus
-AV aneurysms
-carotid artery occlusion
-Psychiatric disturbances, personality alterations

232
Q

what causes cushing’s stress ulcer and how do you treat it

A

Major complication
All caused by GI irritation from psychological and physiological stress on human body
Tx with prophylactic therapy

233
Q

brain death

A

Cessation of all CBF and all vital stem functions
Different from clinical death - absence of breathing and circulation
Can be treated within 4 minutes of cessation of both activities
Guidelines established in 1981
Once established, ventilator can be removed and organs donated

234
Q

what is the biggest cause of spinal cord injury

A

MVA (50%)

235
Q

what should you expect with spinal cord injury

A

head trauma

236
Q

flexion

A

ruptures supporting ligaments, fractures vertebrae, damages vasculature → ischemia to spinal cord
Seen most frequently in MVA

237
Q

extension

A

stretches the spinal cord, complete transection as a result of injury
Patient loses voluntary movement below level of injury
ex : falling down stairs

238
Q

axial loading

A

impacts vertebrae by compressing the cord

239
Q

rotational forces

A

Injury that results from counter clockwise turning of body
Head turns one way, torso turns the other

240
Q

penetrating trauma (spine)

A

penetrating the spinal cord with some sort of object (missile, knife, gunshot wound)

241
Q

relationship between magnitude of force and damage to spinal cord

A

THE GREATER THE MAGNITUDE OF THE FORCE APPLIED TO THE SPINAL CORD, THE GREATER THE ASSOCIATED DAMAGE

242
Q

tetraplegia

A

(sometimes referred to as quadriplegia) is a term used to describe the inability to voluntarily move the upper and lower parts of the body.

243
Q

paraplegia

A

paralysis of the legs and lower body, typically caused by spinal injury or disease

244
Q

nursing interventions during critical phase of spinal cord injury

A

-respiratory support
-treatment of life threatening rhythm disturbances
-mgmt of paralytic ileus (with bowel and bladder programs)
-mgmt of atonic bladder
-drug therapy
-invasive and non invasive monitoring
-cervical immobilization with halo frame
-turning frame
-patient, family support

245
Q

drug therapy for spinal cord injury

A

Within 8 hours of injury
Drug: methylprednisolone in ED- corticosteroid and anti-inflammatory agent

246
Q

spinal shock

A

Immediate Response to spinal cord injury
Temporary Suppression of Reflexes controlled below level of injury
Input of Impulses from Higher Centers Ceases

247
Q

how long can spinal shock last

A

hours to months

248
Q

sign spinal shock is over

A

return of Bulbocavernosus (pulling on foley and there is puckering), Peri-Anal Reflexes (stretching or touching buttocks and anus contracts)

249
Q

autonomic hyperreflexia

A

Serious Emergency
Patient goes into hypertensive crisis
Caused by Noxious Stimuli that create exaggerated sympathetic response
risk after spinal shock

250
Q

examples of noxious stimuli that can cause hyperreflexia

A

distended bladder
tight clothing

251
Q

characteristics of pt in hyperreflexia

A

Cold skin
Goose bumps
Increase in BP - 300/160
Bradycardia
Severe headache
Very anxious

252
Q

goal in hyperreflexia

A

To Remove Noxious stimuli and Lower the Blood Pressure
how? 2 nurse job: foley, hydralazine, CCB IV to control BP

253
Q

what causes neurogenic shock

A

SNS loses ability to stimulate nerve impulses
SNS can’t regulate diameter of vessels → Massive vasodilation occur → Vessels relax → decreased tissue perfusion

254
Q

what kind of shock is neurogenic shock

A

distributive

255
Q

which patients are at risk for neurogenic shock

A

Spinal cord injury (above T6 thoracic or cervical)
Spinal anesthesia
Taking drugs that affect ANS or SNS

256
Q

are preload/afterload increased or decreased in neurogenic shock

A

decreased

257
Q

will patient in neurogenic shock be hypothermic or hyperthermic

A

hypothermia (warm dry extremities because of venous pooling, cold core body temp)

258
Q

will patient in neurogenic shock have tachy or bradycardia

A

bradycardia

259
Q

MAP goal for patient in neurogenic shock

A

85-90 mm hg

260
Q

do patients in neurogenic shock usually have normal, high, or low fluid volume

A

usually normal so need to be careful with IVF

261
Q

signs of fluid volume overload

A

dyspnea, crackles, edema, high CVP/PAWP

262
Q

in neurogenic shock - if fluids do not work to increase BP, what might you use?

A

Use vasopressors to cause vasoconstriction –>Increases SVR, blood pressure, CO
ex: Dopamine = positive inotrope - vasoconstriction and increased HR

263
Q

how do you increase HR in patient with neurogenic shock and how does it work?

A

Atropine to increase HR
Blocks PSNS effects on heart that is causing slow heart rate

264
Q

how do you prevent DVT in patient with neurogenic shock

A

ROM daily, compression stockings, anticoagulation

265
Q

what is gold standard for brain herniation

A

cushings triad

266
Q

priority assessment for burns

A

size because you need to know for fluid resuscitation

267
Q

CO2/ apnea test

A

remove from ventilator, monitor CO2 rising
If they don’t breathe by PaCO2 at 65 → back on vent
Must be negative 3x in a row
Never do when hypo or hyper thermic or sedated

268
Q

Partial thickness: superficial

A

Destroys epidermis and top layer of dermis

269
Q

Partial thickness: deep

A

Epidermis and dermis destroyed

270
Q

Widening pulse pressure

A

Systolic increases
Diastolic decreases

271
Q

what will a critically ill patient with cirrhosis present as?

A

unconscious, jaundiced skin and sclera, bleeding

Complex (3 decks)

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