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Med-Surg I > Exam 2 shortened > Flashcards

Exam 2 shortened Flashcards

1
Q

primary HTN

A

no known cause
associated with risk factors

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2
Q

secondary HTN

A

specific disease states
medications such as estrogen, steroids, immunosuppressants

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3
Q

malignant HTN

A

severe with rapid progression
individuals 30-50 years old

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4
Q

pulmonary HTN

A

vasoconstriction
increased vascular resistance
poor tissue perfusion
right sided HF
hypoxemia

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5
Q

rebound HTN

A

abrupt d/c of meds

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6
Q

white coat HTN

A

in clinical setting

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7
Q

isolated systolic HTN

A

elderly
structural and functional change associated with age
decrease in elasticity of everything including blood vessels
not able to handle blood, increased stroke volume
cerebrovascular morbidity and mortality

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8
Q

normal BP

A

systolic <120
AND
diastolic <60

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9
Q

elevated BP (pre HTN)

A

systolic: 120-129
AND
diastolic: <80

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10
Q

stage 1 HTN

A

systolic: 130-139
OR
diastolic 80-89

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11
Q

stage 2 HTN

A

systolic: >140
OR
diastolic >90

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12
Q

hypertensive urgency (BP, organ damage, treatment)

A

very high BP
no organ damage
fast acting agents (ACE, BB)
normalize BP within 24-48 hours

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13
Q

hypertensive emergency (BP, organ damage, med, treatment)

A

BP >180/120
organ damage
IV vasodilators
reduce BP by 25% within one hour
gradual reduction over 6 hours
not too fast, can cause organ failure from sudden decrease in perfusion

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14
Q

signs and symptoms of PVD

A

claudication of the foot arch, hands, and/or lower limbs
pain may occur at rest
increased sensitivity to cold with numbness
diminished distal pulses
cool extremities

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15
Q

nursing care for PVD

A

monitor every 15, 30, 60 minutes
assess extremity and compare:
-pulse
-BP
-infection
-bleeding
limited ROM with bed rest for 24 hours
avoid crossing legs, standing still, trauma to extremities, constriction
wear closed toe shoes and white socks
night light and skid-free rugs
no smoking
legs lower than heart
avoid cold temps

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16
Q

arterial vs venous pain

A

arterial: claudication, numbness, and tingling
venous: feeling of fullness with prolonged standing or sitting

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17
Q

arterial vs venous pulse

A

arterial: decreased or absent bilaterally
venous: difficult to find or full

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18
Q

arterial vs venous color

A

arterial: pale, elevated leg; dusky/red, dependent leg
venous: cyanotic on dependency

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19
Q

arterial vs venous temperature

A

arterial: cool
venous: warm

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20
Q

arterial vs venous edema

A

arterial: absent or mild
venous: present

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21
Q

arterial vs venous skin

A

arterial: dry
venous: moist

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22
Q

arterial vs venous ulcers

A

arterial: toes and gangrene
venous: superficial with gangrene

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23
Q

raynaud’s

A

vasospasms of hands/feet
affects 17-50 years old
more common in women
worse in cold and stress
connective tissue, autoimmune disorder
blanching/cyanosis
numbness
throbbing pain

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24
Q

raynaud’s treatment

A

calcium channel or adrenergic blockers
sympathectomy
decrease cold temp
no smoking
wear gloves
avoid drugs that increase vasospasm (OTC decongestants)

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25
Q

what can raynaud’s lead to

A

ulcers and gangrene

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26
Q

buerger’s

A

occlusive disease
affects upper and lower extremities
young adult male smokers
causes fibrosis and scarring
small vessels too big

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27
Q

buerger’s manifestations

A

same as PVD
claudication of foot arch, hands, and/or lower limbs
pain may occur at rest
increased sensitivity to cold with numbness
diminished distal pulses
cool extremities

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28
Q

buerger’s treatment

A

smoking cessation
avoid triggers
meds for vasodilation
treat ulcer and gangrene
may need amputation

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29
Q

DVT risk factors

A

surgery, HRT estrogen, pregnancy, trauma, obesity, prolonged standing, personal/family history

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30
Q

signs and symptoms of DVT

A

calf or groin tenderness
positive homans (dorsiflexion of foot causes pain)
redness
sudden onset of unilateral swelling of leg
warmth
induration (hardening) along blood vessel
SOB if progresses to PE

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31
Q

treatment of DVT

A

compression stockings
bedrest
elevation of extremity
avoid knee gatch
warm soaks (prescription needed)
no massage or ROM to affected extremity
monitor changes

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32
Q

heparin (what is it, therapeutic range, given to who, antidote)

A

low grade molecular weight
INR: 2-3
given to low risk pts at home
antidote: protamine sulfate

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33
Q

warfarin (do not take with what, and antidote)

A

ASA and vitamin K (antidote)

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34
Q

PE risk factors

A

venous stasis
HRT
fracture (fat embolism, can’t use anticoag, use steroids instead)

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35
Q

PE s&s

A

chest pain
tachy
dyspnea
dry cough
blood tinged sputum
petechiae
hypotension
low grade fever

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36
Q

treatment of PE

A

anticoags
complete bed rest
monitor
antidote for anticoags
surgery

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37
Q

varicose veins

A

protruding veins
feeling of fullness and pain when standing
vein wall thickens and dilates
valves are affected
veins become tortuous

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38
Q

varicose veins risk factors

A

obesity, pregnancy, occupations that require standing, heart disease, family history

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39
Q

varicose veins treatment

A

elastic stockings
walk
elevation
sclerotherapy
surgical removal of vein
laser surgery

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40
Q

intermittent claudication develops when

A

after a fixed amount of activity
certain distance causes cramping and burning in toes, heels, and foot, and muscle discomfort

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41
Q

claudication distance

A

denotes severity of the disease
predictable

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42
Q

what does rest pain mean in claudication

A

disease is advancing

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43
Q

complication of claudication

A

leg ulcers

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44
Q

stage 1 of claudication

A

asymptomatic
reduced pulses

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45
Q

stage 2 of claudication

A

claudication
pain while walking or exercising
relieved with rest
intermittent claudication

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46
Q

stage 3 of claudication

A

claudication with rest pain
when feet are in dependent position the pain is relieved (bc of blood flow), dependent rubor
most likely will progress

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47
Q

stage 4 of claudication

A

necrosis and gangrene
CLI (critical limb ischemia)
ulcers
tissue near obstruction is so damaged

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48
Q

arterial ulcers (what is it, effects where, characteristics, pain, depth, exudate)

A

decreased arterial blood flow
usually effects toes and lateral malleolus
sharp edges
no granulation tissue
pale base
nail beds yellow, gray, necrotic, and rigid
atrophy in nearby tissue
LOTS of pain bc lack of oxygen (ischemic)
deep or superficial
minimal exudate

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49
Q

venous ulcers (characteristics, effects where, pain, exudate, depth)

A

irregular shape
healthy base
warm foot
distal pulse palpable
edema around ankle (backup of venous blood)
eczema (scaly)
develops in ankle area and medial malleoli
minimal pain
heavy exudate
not very deep

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50
Q

foot care of PVD

A

no creams or ointments esp between toes

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51
Q

care after bypass surgery

A

broad spectrum abx 48h prior
assess the site

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52
Q

iron deficiency anemia (microcytic)

A

most common type
total body iron content decreased
iron stores depleted (<3g)
1 mg absorbed for every 10-20 ingested
ferritin <12 G/L

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53
Q

risk factors of iron deficiency anemia

A

blood loss
menstruating and pregnant women
adolescents
children
infants
GI tumors
malabsorption
high fiber diet
chronic alcoholism

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54
Q

diagnosis of iron deficiency anemia

A

GI series (barium studies)
occult blood
upper endoscopy
colonoscopy

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55
Q

management of iron deficiency anemia

A

diet rich in iron (christmas! and avoid foods that block iron absorption [milk])
supplemental iron
-compliance
-dark tarry stools
-with juice/water (straw, rinse mouth)
-observe for toxicity
-vitamin C
-avoid antacids
-injections (z-trak)

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56
Q

folate deficiency anemia (megaloblastic)

A

folic acid (b vitamin)
small amount stored
nervous system not effected

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57
Q

vitamin B12 deficiency (pernicious) (diagnosed how, what it is)

A

diagnosed by schilling test
decreased absorption of vitamin B12
abnormal structure and function
-megaloblastic
-macrocytic
erythropoiesis
nerve function
myelin production

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58
Q

risk factors of pernicious anemia

A

family history
european
chronic gastritis
meds
vegetarian diet
gastric surgery

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59
Q

S&S of pernicious anemia

A

SOB
brain fog, lack of focus/coordination
dry skin
premature gray hair
vision problems
infertility
menstrual changes
incontinence
mouth ulcers
swollen or cracked tongue

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60
Q

management of pernicious anemia

A

monthly B12 injections
IM or nasal cyanocobalamin
iron supplements
folic acid
monitor cardiac rhythm
integumentary
daily weight
dizziness
oxygen
energy conservation
blood transfusion
erythropoietin
-hemoglobin and hct 2x/week

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61
Q

aplastic anemia

A

normocytic, normochromic
bone marrow hypoplasia or aplasia
RBCs are normal size and content but low in number
alteration of stem cell and marrow (replaced by fat)

62
Q

risk factors of aplastic anemia

A

congenital
idiopathic
acquired
-myelotoxins
-autoimmune
-infections

63
Q

S&S of aplastic anemia

A

pancytopenia
lassitude (lack of energy)
anorexia
infection
petechiae
purpura
retinal hemorrhage

64
Q

management of aplastic anemia

A

immediate withdrawal of offending agent
pharmacologic
transfusion
radiotherapy
bone marrow transplant

65
Q

nursing management of aplastic anemia

A

explain bone marrow aspiration/biopsy
risk for infection
gas exchange impaired
ineffective tissue perfusion

66
Q

posterior iliac crest aspiration

A

most frequent
prone or lateral position, knees flexed, pillow under head, eyes away

67
Q

anterior iliac crest

A

supine position, hips and knees flexed, eyes away, light towel over face
vertebrae
ribs
sternum

68
Q

sickle cell anemia

A

both parents have trait (recessive, 25% chance of inheritance)
partial or complete replacement of abnormal hgb S for normal hgb A
deformed cell changes from round to sickle cell shape
asymptomatic until 4-6 months bc of fetal hemoglobin

69
Q

diagnosis of sickle cell

A

hgb electrophoresis
sickle-turbidity test (sickledex)

70
Q

assessment of sickle cell

A

health history and physical exam
pain
lab data (s-shaped hemoglobin)
presence of symptoms
swelling, fever, pain
sickle cell crisis
blood loss (menses, GI)
cardio
neuro

71
Q

clinical manifestations of sickle cell

A

anemia
hemolysis
hgb 5-11 g/dl
jaundice
bone expansion
cardio
organ involvement

72
Q

medical management of sickle cell

A

pain management
hydration
aggressive treatment of infection (prophylactic abx for 2 months-5 years)
chemo
corticosteroids
bone marrow function (reticulocyte count)
stem cell transplant

73
Q

nursing diagnosis of sickle cell

A

ineffective coping
fluid volume
fatigue
acute pain
risk for infection and powerlessness
deficient knowledge

74
Q

Collaborative problems and potential complications of anemia

A

Hypoxia
Ischemia
Infection
Dehydration
CVA
Anemia
Acute and chronic renal failure
Heart failure
Impotence
Poor compliance
Substance abuse
Polycythemia

75
Q

complications of sickle cell

A

Vaso-occlusive crisis
-Most common type of crisis
Severe pain
-Ischemia
-Infarction
-Fever, pain, tissue engorgement
Aplastic crisis
-Paravirus B19
-Invades RBC precursors
-Destroys RBC
Splenic sequestration crisis
-Life threatening
-Death can occur within hours
-Blood pools in the spleen
-Profound anemia, hypovolemia, shock
acute chest syndrome
CVA
emotional and behavioral problems

76
Q

when to discard blood for transfusion

A

after 4 hours

77
Q

care for blood transfusion

A

given early in crisis, might reduce ischemic pain
treated with hydration and opioids- taught deep breathing and incentive spirometer

78
Q

pneumonia nursing care

A

supplemental oxygen (nasal cannula 1-3L, non rebreather if osat less than 90, watch for oxygen toxicity)
elevate head of the bed to semi or high fowlers
splint chest with folded hands or pillow while coughing to reduce pain
fluids (2-3000mL of fluids to thin the mucus [unless kidney or cardiac pt], no dairy)
postural drainage (relies on gravity, position head down to give more space for lungs to expand
reposition q2 hours
controlled breathing and coughing q1h
avoid large crowds, get flu vaccine (unless egg allergy or Guillain barre), and avoid allergies (frequent asthma leads to PNA)
INCENTIVE SPIROMETRY AVOIDS ATELECTASIS

79
Q

oxygen toxicity S&S

A

fatigue, irritability, LOC changes

80
Q

S&S of PNA

A

dyspnea
hypoxemia (cyanosis, nail bed clubbing)
high temp
cough
tachy
resp distress
productive cough
stabbing chest pain
tachypnea
orthopnea
NVD
anorexia
cerebral hypoxia (changes in LOC, agitation, CONFUSION, coma)

81
Q

patho of PNA

A

bacteria enters bronchus, fluid develops, blood enters, infected blood goes through capillaries bc alveolar membrane is fragile and broken, sepsis!

82
Q

consolidation

A

lungs full of liquid and mucus, oxygen can’t get through, ineffective air exchange (pleural effusion)
decreased lung capacity

83
Q

assessment of PNA

A

breath sounds (crackles, expiratory wheeze, tactile fremitus increased, areas of consolidation [risk for atelectasis])
chest x-rays for areas of consolidation
pulse oximetry
blood culture
ABG
CBC (elevated WBC)
PFT (tidal volume, vital capacity, total lung capacity)

84
Q

complications of PNA

A

atelectasis
pleural effusion
lung abscess (localized collection of bacteria caused by aspiration)
pleurisy
peri/endocarditis

85
Q

nursing care of asthma

A

bronchodilators (short acting like albuterol; long acting like salmeterol)
anti-inflammatory, mast cell stabilizers, antihistamines
methylxanthines (theophylline) last resort
anticholinergic (decrease secretions)
low dose oxygen
hydration
PT and postural drainage
controlled breathing and coughing every hour
INCENTIVE SPIROMETRY
semi fowlers
reduce panic and anxiety

86
Q

S&S of asthma

A

bilateral wheezing (expiratory)
chest tightness
SOB
dyspnea
coughing
overuse of accessory muscles leading to barrel chest
acute resp distress syndrome (airway too constricted to let air out [asthma attack])
anxiety and panic
hyperventilation

87
Q

patho of asthma

A

hyperresponsiveness from immune system causes bronchospasm and bronchoconstriction releasing histamine, prostanoids, cytokinins causing vasoconstriction causing bronchial edema causing increased secretions causing mucus plug

88
Q

mild intermittent asthma

A

<2 attacks/week and normal life between exasperations

89
Q

mild persistent asthma

A

> 2 attacks/week but <1 per day
ADLs interrupted

90
Q

moderate persistent asthma

A

daily symptoms and use of short acting inhaler to get through the day
affects activity

91
Q

severe persistent asthma

A

continuous symptoms with limited activity

92
Q

assessment of asthma

A

chest xray
ABG
PFT
breath sounds

93
Q

complications of asthma

A

Pneumonia bc of inability to get rif of secretions
Atelectasis
Hypoxemia
Respiratory acidosis
Emphysema
Chronic bronchitis
Status asthmaticus (life threatening)

94
Q

status asthmaticus nursing care

A

intubation
bronchodilators, steroids, epinephrine IV
oxygen
management of asthma attacks after stabilized

95
Q

S&S of status asthmaticus

A

Labored breathing
Wheezing that is worse on inspiration and expiration
Nonproductive cough
Overuse of accessory muscles → barrel chest
Cyanosis
Respiratory acidosis

96
Q

patho of status asthmaticus

A

Severe persistent asthma attacks caused from hypersensitivity related to NSAIDS
Complication of asthma when people don’t respond to treatment

97
Q

assessment of status asthmaticus

A

count respirations

98
Q

complication of status asthmaticus

A

pneumothorax (lung can’t inflate bc of air in pleural space)

99
Q

pt teaching of TB including diet and supplements

A

drug regime
importance of compliance
preventing spread to others
no special precautions of personal articles
mask until meds suppress infection
well balanced diet (high protein, calorie, calcium)
supplements (iron, vit B6)

100
Q

foods to avoid with TB

A

tuna
aged cheese
soy sauce
yeast extract
red wine

causes SE (HA, diaphoresis, HTN, palpitations) and decreases absorption. contains tyramine and histamine

101
Q

meds for TB

A

INH and rifampin (combination abx)
pyrazinamide (for active TB)
ethambutol (myambutol)

102
Q

how long is TB treatment

A

6-12 months

103
Q

TB skin test interpretation and contraindications

A

Area of indurations read within 48-72 hours
10 mm or more: positive
5-9 mm: doubtful (usually repeated)
For HIV: 5 or more is positive

BCG vaccine or HIV

104
Q

Chest radiography (CXR) for TB

A

not specific

105
Q

QuantiFERON-TB gold test

A

Results within 24-36 hours and are not affected by prior vaccination with BCG

106
Q

TB convertor

A

newly infected
negative to positive
+ skin does not mean active disease (cellular immunity developed)

107
Q

tidal volume (what is it, amount, and what effects it)

A

The amount of air inspired and expired in a normal breath
500 mL
May not vary

108
Q

total lung capacity (what is it, amount, and what effects it)

A

the maximum amount the lungs can expand
TV+IRV+ERV+RV (5800 mL)
decreased with atelectasis and pneumonia
increased in COPD

109
Q

vital capacity (what is it, amount, and what effects it)

A

the maximum amount of air exhaled after maximal inhalation
TV+IRV+ERV (4600 mL)
decrease in neuromuscular disease, generalized fatigue, atelectasis, pulmonary edema, COPD, and obesity

110
Q

inspiratory reserve volume (what is it and amount)

A

the maximum amount of air inhaled after a normal inhalation
3000 mL

111
Q

expiratory reserve volume (what is it, amount, and what effects it)

A

maximum amount of air that can be exhaled forcibly after normal exhalation
1100 mL
decreased with obesity, ascites, pregnancy

112
Q

residual volume (what is it, amount, and what effects it)

A

volume of air remaining in lungs after maximum exhalation
1200 mL
may be increased with obstructive disease

113
Q

inspiratory capacity (what is it, amount, and what effects it)

A

maximum amount of air inhaled after normal expiration
TV+IRV (3500 mL)
decrease in restrictive disease or obesity

114
Q

functional residual capacity (what is it, amount, and what effects it)

A

amount of air remaining in lungs after normal expiration
ERV+RV (2300 mL)
may be increased in COPD
decreased in ARDS and obesity

115
Q

cholecystitis

A

Inflammation of the gallbladder
Usually caused by stones that irritate the gallbladder, causes obstruction of cystic duct
Over 90% of cases due to calculous

116
Q

cholelithiasis

A

Calculi in gallbladder
Gallstones block cystic duct
Leads to cholecystitis

117
Q

choledocholithiasis

A

Stones in the common bile duct
Cholesterol stones or pigmented

118
Q

bile

A

stored in gallbladder
made and secreted in liver
food enters duodenum and digests food by bile
emulsifies fats
excretes RBCs
gives stool dark color

119
Q

gallbladder

A

Storage depot for bile
Release bile
CBD (common bile duct) connects gallbladder and duodenum

120
Q

incidence of cholecystitis

A

Obesity
Native americans
Increases with age (40+)
Women nearly 70% of cases
Hormone therapies (BC)
Mortality rate higher among men
Frequent changes in weight (rapid loss)
Diseases (diabetes, crohn’s, cystic fibrosis, ileal resection increases risk for cholelithiasis → cholecystitis)
Frequent surgeries
Anything that causes us to lose fluid causes crystallization leading to stones
Way to remember: fair, female, fat, over fourty

121
Q

cholecystitis causes what

A

high fat triggers attacks
calculus big cause
calculi make gallbladder inflamed, pain in RUQ, and edema. infection causes pus to leak in blood causing peritonitis
edema may cut off blood supply

122
Q

cholecystitis in elderly

A

may not show S&S until oliguria and septic shock

123
Q

acalculous

A

no gallstones

major surgery
trauma
severe burns
cysts
primary infection
blood transfusions
causes in fluid and electrolyte balance (dehydration)

124
Q

biliary colic

A

Spasm of biliary duct as it tries to push stone out
Severe pain RUQ
Radiate around to back and right shoulder
Triggered by large, rich meals

125
Q

clinical manifestations of cholecystitis

A

biliary colic (hallmark)
Rebound tenderness and rigidity at RUQ
N/V
Feeling of fullness
Fever
Exacerbations
Jaundice with CBD (common bile duct) obstruction; must be cholelithiasis
Pruritus (itching)
Clay colored stools
Steatorrhea (from lack of emulsification of stools, when there is obstructive jaundice)
Tea colored urine

126
Q

cholelithiasis

A

may go unnoticed until biliary colic with obstruction of cystic duct
As gallbladder becomes distended, pain intensifies
Blood tests show increase in bilirubin
Stone may retreat or pass

127
Q

pigment gallstone

A

from backup of bile

128
Q

cholesterol gallstone

A

Bile supersaturated with cholesterol bc of:
Decrease in bile acids dissolving cholesterol
OR
Increase in cholesterol

129
Q

diagnostics of cholelithiasis

A

Ultrasonography (NPO after midnight)
Cholecystography
ERCP (Diagnostic and treatment)
PCT (Treatment and diagnosis, looks at structures of the gallbladder and liver)
MRI (shows calcified stones)
Blood test (Non specific, to rule out other conditions, high WBC shows inflammatory process, + cholesterol can cause cholesterol stones, liver enzymes, pancreatic enzymes)
Abdominal x-ray (calcified stones)

130
Q

treatment of cholelithiasis

A

ERCP, PTC
Removing stones
Non surgical, endoscope in duodenum, wire snare placed in gallbladder, removes stone (complication is bleeding)
Extracorporeal lithotripsy (crushing of the stone)
Dissolve stones
Lies in cushion filled with water and high energy
sound waves, shatters the stone
Only if the stones are <4 in amount or <3 cm in
diameter
Drink 2-3 quarts of water a day to get rid of any
stone fragments
NG tube
low fat
avoid alcohol
avoid gas forming foods
avoid fried foods
eat high carbs and protein

131
Q

surgeries for cholelithiasis (once symptoms subside)

A

Laparoscopic cholecystectomy (fewer risks)
Camera used
Fine after 3-4 days
May complain of shoulder pain bc of injected air into
abdomen (tell pt that they can use heat applications
for 15-20 min every hour and ambulate to promote
CO2 absorption)
Bile duct injury serious side effect
Report abdominal symptoms
Open cholecystectomy
Can be delayed for 6 weeks until symptoms subside
Actual incision

132
Q

drug therapy for cholelithiasis

A

abx
lipid lowering agents
antispasmodics
analgesics (demerol NOT morphine unless severe)

133
Q

post op care for cholelithiasis

A

Assess
Monitor VS
Skin care around biliary drainage (some bile may leak out)
T-tube (300-400mL in first 24h, serosanguineous in the beginning, bile color after 24 hours, tube clamped during meals and 1-2 hours after meals, kept below gallbladder to prevent reflux and infection, emptied every 8 hours, pts may have diarrhea after cholecystectomy, but stool should be brown after a week, physician removes tube)
NG tube to relieve distension and vomiting
Pain control
I&O
Encourage activity
low fat diet, limit weight and pregnancies
cough and deep breathe

134
Q

what to report after cholelithiasis surgery

A

Fever (leads to cholecystitis)
Jaundice
Pruritus (itching can mean blockage with backup of bilirubin)
Dark color urine
Pale color stools
Rigidity of abdomen (peritonitis)
Sudden drop in BP (shock)
Gangrene of gallbladder and peritonitis r/t perforation
Resp problems (frequent problem, hard to deep breathe bc of place of incision)

135
Q

dumping syndrome

A

Food rapidly enters jejunum without the benefit of normal digestive process
If a pt is getting tube feedings, they might get dumping syndrome
Can occur in anyone who had a surgery removing part of the stomach
Rapid gastric emptying or sudden influx of hypertonic fluid triggers a shift of fluid into the abdomen as the small intestines pull fluid from the EC space to try to dilute hypertonic fluid
Decrease in circulating volume causes vasomotor disturbances
Occurs within 10-30 mins after eating

136
Q

S&S of dumping syndrome

A

Vertigo
Tachycardia
Syncope
Sweating
Pallor
Palpitation
Diarrhea
Nausea
Weakness, they want to lie down
Happens after surgery and during tube feedings (dilute)
Symptoms resolve within an hour or from bowel movement
Hypoglycemia

137
Q

intestinal manifestation of dumping syndrome

A

Can occur 2-3 hours after a meal
Epigastric fullness
Distention of jejunum with food and fluid
Abdominal discomfort
Cramping
Nausea
Borborygmi (stomach rumbling)

138
Q

teaching for dumping syndrome

A

Small feeding
High protein and fat
Low CHO, fiber
Dry diet
Provide antispasmodic

139
Q

interventions for dumping syndrome

A

dry diet
low carb (stays in stomach longer)
lying down after eating to slow passage
high fat and protein
low fiber
small, frequent meals

140
Q

post-op for dumping syndrome

A

increased risk of hemorrhage
Bile reflux from removal of pylorus
Dysphagia
Bowel obstruction from adhesions

141
Q

GERD

A

Backflow of gastric content into esophagus as it goes past a weak or lower LES without belching or vomiting
results in esophagitis

142
Q

3 aggressive factors

A

HCl
bile
pancreatic enzymes

143
Q

2 protective factors

A

saliva
mucus

144
Q

GERD risk factors

A

Weight gain
Obesity
Pregnancy
Lying flat after meals
Medications (Ca+ channel blockers, BB, high levels of estrogen and progesterone, NSAIDS, stress cause reflux)
Hiatal hernia
Smoking
Weakened LES tone
Foods: tomatoes, citrus, spicy
Alcohol
Caffeine
Chocolate
Chewing tobacco
High fat foods
Carbonation
Elderly

145
Q

patho of GERD

A

Change in the pressure zone of gastroesophageal sphincter
Normally, high pressure prevents reflux but permits passage of food
Displacement of angle of gastroesophageal junction
Incompetent LES
Inflamed esophageal mucosa
Esophagitis from backflow of aggressive factors which puts pts at high risk for esophageal cancer

146
Q

Degree of GERD depends on

A

Frequency of reflux
Contents of reflux
Buffering ability of saliva and mucus
Rate of gastric emptying

147
Q

GERD clinical manifestations

A

dyspepsia (moves up and down, relieved with antacid)
pain (occurs after activity, supine or distended abdomen makes it worse, radiates to back of neck or jaw and penetrates to back, take nitroglycerin, worse when bending over or recumbent, don’t do strenuous exercise after eating, sit after meals, walk)
esophageal spasm
odynophagia (pain during swallowing)
intermittent dysphagia (worse in beginning of meal)
acid regurgitation (SOUR AND BITTER)
water brash (hypersalivation SALTY)
eructation (belching)
distended abdomen

148
Q

GERD diagnosis

A

barium swallow
esophagoscopy
Esophageal biopsy
Cytology (looking at cells)
Gastric secretions
Acid perfusion tests

149
Q

complications of esophagoscopy

A

Aspiration
Perforation
Oversedation
Hemorrhage from perforation

150
Q

post op for esophagoscopy

A

Assess airway if pt not arousable
Check VS
Check for breathing
Check gag reflex!
Eating before it returns causes choking

151
Q

med management of mild GERD

A

Antacids (Al or Mg hydroxide), calcium carbonate
Maalox, mylanta (brand names)
Increase gastric pH
Reduce pepsin activity
Buffers/neutralize gastric acid to soothe mucosa
Works in 30 min
Should be taken AFTER a meal, not before
Neutralizing acid that forms after meals
Mg can cause diarrhea

Med-Surg I (6 decks)

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