NURS 453 test 3 Flashcards
(251 cards)
1
Q
Addison’s Disease
A
Incurable disease controlled w/ hormone replacement
90% of adrenal cortex destroyed
2
Q
Primary cause of Addisons disease
A
Autoimmune (80%) and idiopathic
3
Q
Secondary cause of Addisons disease
A
Steroid withdrawal, pituitary tumor
4
Q
Adrenal glands produce
A
cortisol and aldosterone
5
Q
what does cortisol do
A
helps the body respond to stress, maintains BP, balance the effects of insulin…has hundreds of functions
6
Q
what does aldosterone do
A
helps maintain BP, H2O/Na+ balance
7
Q
cortisol is a
A
glucocorticoids
8
Q
aldosterone is a
A
mineralocorticoids
9
Q
androgens
A
Sex hormones in both men and women
10
Q
Patient Presentation in Addison’s Disease
A
Low BP, dizziness, orthostatic HoTN, hypoglycemia, fatigue, weight loss, hair loss, salt craving
11
Q
Addisonian crisis or Acute Adrenal Insufficiency also known as
A
acute adrenal failure
12
Q
what happens during acute adrenal failure
A
Adrenal glands STOP making hormones necessary for bodily functions = An acute deficiency of cortisol production
- Life threatening emergency!!!
13
Q
acute adrenal failure results in
A
Circulatory collapse and electrolyte imbalance
14
Q
signs and symptoms of acute adrenal failure
A
Non-specific
Will sometimes have fever
Hypovolemic Shock
Profound Hypoglycemia – lack of creating sugar and using it quick
Confusion, altered mental status – due to low MAPs/BP
Ventricular Dysrhythmias – V tach usually (potassium levels increase dramatically)
Vomiting, Diarrhea, Anorexia, Cramps
15
Q
causes acute adrenal failure
A
stress, Adrenal surgery/hemorrhage
16
Q
A patient’s circulatory collapse in an addisonian crisis is often refractory to fluids and vasopressors…. WHY???
A
we give them vasopressors during this crisis but the patient does not respond because they still lack the hormone needed to squeeze (increase their BP)
17
Q
Labs in acute adrenal failure
A
look at BP and sugar in ER, low Na and Cl-, increased K, decreased glucose, make sure to look at cortisol, ACTH levels, and adrenal antibodies later
18
Q
diagnostics in acute adrenal failure
A
ACTH stimulation test, Insulin-induced hypoglycemia test, CT, MRI
19
Q
ACTH stimulation test
A
measure cortisol before and after synthetic ACTRH
Normal response is rise in cortisol – normal person
Addisons: little to no response, and high ACTH levels`
20
Q
during acute adrenal failure there is Ongoing cortisol monitoring to monitor efficacy of steroid dosage. when do you take them?
A
Highest early in “morning” (0600 – 0800)
lower in the evening (1600 – 1800)
21
Q
Immediate treatment of acute adrenal failure is directed at
A
combating circulatory shock - Restoring circulating volume…dehydration
Administer fluids (0.9% NS) (hyponatremia)
Monitor VS
Administer Corticosteroids (usually high doses)
22
Q
nursing care plan of acute adrenal failure
A
VS…orthostatics
ECG monitoring
Bradycardia, heart block (due to the slowing of the SA and AV node conduction), peaked T waves, prolonged PR (due to the slower conduction)
Blood sugar
Electrolytes
Monitor and treat for hyperkalemia (at risk for V tach), hypoglycemia and hyponatremia
Neuro checks – seizures due to hyponatremia
Urine output (I & O)
Daily weights
23
Q
Assist patients to avoid what during acute adrenal failure
A
stress - Physical, Mental, Emotional, Spiritual
24
Q
Hydrocortisone
A
synthetic form of cortisol
25
what do we need to administer during acute adrenal failure
Corticosteroid administration
26
what do we want to maintain during acute adrenal failure
maintain perfusion with isotonic fluid and give vasopressors
27
education during acute adrenal failure
Importance to take cortisol replacement daily
↑ dose at times of stress (fever, flu, surgery, etc)
Double/triple doses!!!!!
Follow up with MD immediately
28
what concepts to think about during diabetic kept acidosis and HHS
Acid Base Balance - Directly linked to the cause/dehydration
Fluids and electrolytes (Key) - Dehydration!
Inflammation
Perfusion - Dehydration
29
DKA and insulin
Insulin Deficiency
| Insulin dependent diabetics (Type I & II)
30
DKA what happens
```
Break down of FAT & PROTEIN→Ketones
Rapid onset
Liver continues to produce glucose
Hyperglycemia (> 250)
Osmotic Diuresis
Severe Dehydration
```
31
HHS and insulin
```
Insulin Present (Only Type II)
Liver continues to produce glucose
```
32
HHS what happens
Neuro signs may be the first really noted
Slower, insidious onset
Break down of fatty acids minimal because of insulin facilitating glucose transport into cells
NO KETONES
Hyperglycemia (> 600)
Osmotic Diuresis
Severe Dehydration
33
DKA diagnostic criteria
pH < 7.30 (Typically) - pH in SEVERE cases can drop below 7.0
Metabolic Acidosis (due to build up of lactic acid) w/ respiratory compensation
Blood glucose greater than 250 mg/dL
+ Ketones in blood and urine
Serum bicarbonate less than 18 mEq/L
aka CO2 on BMP/CMP
34
HHS diagnostic criteria
```
Blood glucose ˃ 600 mg/dL
NO KETONES!!!!!
Serum bicarbonate can be ˃ 18 mEq/L
Serum osmolality can ˃ 320 mOsm/kg
pH ˃ 7.30
```
35
Causes of DKA and HHS
Infection! Most common cause!
Increase demand brought on by illness/stress
↓ or missed insulin dose
Undiagnosed & untreated DM
36
DKA presentation
```
Ketoacidosis
Insulin deficiency states
Fat is broken down
Brain is being fed to a degree with the ketones; lack of neuro changes
Tends to be rapid onset
```
37
HHS presentation
Slower onset - why? -
| Key: neuro changes
38
presentations that are seen in both DKA and HHS?
Hyperglycemia
Dehydration and electrolyte loss
Acidosis (lack of perfusion at the cellular level)
39
blood sugars in DKA
above 250
40
blood sugars HHS
above 600
41
why are there such high glucose levels during DKA and HHS?
Liver continues to produce glucose
Stress hormones induce more glucose production
Starving cells stressed – that is why we have polyphagia
42
Osmotic diuresis
↑ glucose causes ↑ serum osmolality
| H2O moves from interstitial to intravascular = cellular dehydration - occurs during DKA and HHS
43
Why is there such bad dehydration in DKA and HHS?
osmotic diuresis, polyuria - can loose up to 7 liters of fluid in 24 hours, blood viscosity increases
44
ketoacidosis =
metabolic acidosis
45
what occurs during ketoacidosis?
decreased perfusion causes +++ lactic acid release r/t anaerobic metabolism
FAT/PRO breakdown used for fuel
Free fatty acids convert to ketones
Brain cells are especially sensitive to loss of glucose for fuel and inability to use fatty acid fuel. Seen first as ↓ LOC.
overall buildup of ketones results in metabolic acidosis
46
DKA: Clinical manifestations
Keys: RAPID ONSET
Polyuria: excessive urination (increased BS pulling water out of cells)
Polydipsia: dehydration, dry mouth, excessive thirst
Polyphagia: excessive hunger (cells are starving)
Others:
GI effects: n/v/abd pain
Neuro effects: Not as profound, ketones allow brain to be fed; can be altered LOC
47
vital signs in DKA
Kussmaul respirations: fruity/acetone breath – compensation for metabolic acidosis
Tachycardia/HoTN/Orthostatic HoTN
Fever – why? – possible infection and increase stress response
48
HHS clinical manifestations
Gradual onset so it is important to do history
Will have similar symptoms to DKA
Polyuria, Polydipsia, Polyphagia
GI symptoms: fewer to none…remember no ketones
Neuro effects (are Key for HHS, NO KETONES): (nothing to feed the brain cells)
Profound dehydration (sunken eyes, poor turgor)
possible seizures, reversible paralysis, death- Directly related to increased glucose causing serum osmolality to rise and having more neurological manifestations
49
Labs for DKA and HHS
+ Ketones (serum and urine) are defining factor to determing if you have DKA or HHS
ABG: ↓ pH, ↓ bicarb
CMP(complete metabolic panel)/BMP:
↓CO2, ↓ Na+
K+ can be normal, depends on time frame; huge losses as it progresses
↑ BUN (30 mg/dL) and ↑ Creatinine (1.5 mg/dL)
Anion gap >12
Serum osmolality high (HIGH) – due to concentration of blood
50
anion gap
Difference between the cations and anions in the extra cellular fluid (ECF)
Normal levels: 10 – 14 mEq/L
51
Initial Interventions DKA and HHS
ABCs..
Ensure patent airway
Administer oxygen
FLUIDS!!!!...
IV access – hydration!
Begin fluid resuscitation then give them regular insulin
Electrolyte replacement once partial glucose correction
52
treatment for DKA/HHS
Utilization of standing orders/protocols – ensures we are not overcorrecting the patient too fast (can cause cerebral edema)
Reversing dehydration
Reverse ketoacidosis (DKA)
Replacing insulin (once you have established rehydration)
53
fluids during DKA/HHS
0.9% NS (if Na+ high give 0.45%) until glucose is about 300 to 250; then switch to fluids with Dextrose like D5 0.45%NS or D5 0.9% NS. What does this prevent? – preventing cerebral edema
54
when do you know that you should switch to D5 in DKA/HHS treatment?
u/o ˃ 0.5ml /kg/hr and B/P normal
55
DKA/HHS and potassium
pts can be either hyperkalemic or hypokalemic – hyperkalemic why? – renal compromise and cannot excrete
56
Aim for BG reduction in reversing acidosis
36 – 54 mg/dL/hour (45 an hour is what we are hoping for)
| Hourly evaluation of BG
57
Acidosis as a result of ketosis is primarily reversed with
insulin (and fluids)
58
Nursing Diagnosis for DKA and HHS
Deficient fluid volume r/t absolute loss
59
what hormones does the anterior pituitary secrete?
Growth hormone - controls growth
Prolactin - stimulates production of milk after childbirth
ACTH (adrenocorticotrophic hormone) - stimulates production of hormones from the adrenal glands
TSH (thyroid stimulating hormone) - stimulates production of hormones from thyroid gland
FSH (follicle stimulating hormone) and LSH (luteinizing stimulating hormone) - stimulate activity in the ovaries of women and the testes in men.
60
The posterior pituitary secretes
ADH (anti-diuretic hormone) - controls the concentration of urine
Oxytocin - stimulates the contraction of the womb during childbirth and the secretion of milk for breast feeding.
61
how would you fix a pituitary tumor?
Transphenoidal hypophesectomy or
| Laproscopic surgery through nose or through the upper lip
62
post op care after removal of a pituitary hormone?
no nose blowing or deep breathe and cough. may need dressing depending one where the incision was, oral care, monitor for diabetes encipitus – will cause issues with fluids and electrolytes
63
DI
Deficiency of antidiuretic hormone (ADH, vasopressin) results in inability to conserve water
64
SIADH
Excessive amounts of ADH secreted from posterior pituitary and other ectopic sources. – body not producing urine
65
commonality between DI and SIADH
ADH – key component that we see between the two
66
DI causes
unknown, idiopathic, tumors
67
SIADH causes
80% r/t small cell carcinoma
68
risk factors for DI
head injury, neurosurgery, tumor
69
SIADH risk factors
increased ICP, malignant conditions
70
what happens in DI
Permeability of water is diminished, resulting in excretion of large volumes of hypotonic fluid.
71
what happens in SIADH
Water Retention
Hyponatremia (dilutional)
Hypo-osmolality - A continual release of ADH causes water retention from renal tubules and collecting ducts.
72
DI physical exam
```
Mucous Membranes - Dry
Skin - Dry, cool skin
Cardiovascular (more acute) - Tachycardia to respond to fluid loss
Electrolyte Problems (acute)
weight loss
decreased level of consciousness
faucet pee
```
73
SIADH physical exam
```
R/T Hyponatremia - Decreased deep tendon reflexes, confusion, seizures, fatigue, H/A, anorexia, nausea, decreased mental status, seizures, coma.
R/T Fluid Vol. Excess
- Wt. gain w/o edema
- JVD
- Tachycardia
- Tachypnea
- Rales (crackles)
GI - decreased motility
```
74
complications of DI
Electrolyte Imbalance
Hypovolemia
Hypotension
Shock
75
complications of SIADH
Seizures
Coma
Permanent brain damage
Further complications of existing disease processes.
76
diagnostics of DI
```
Urinary OutPut- A few liters to 18L/d
Serum Osmo ↑ >290
Serum Na+ ↑ >150
Sp. Gravity < 1.005
Water deprivation study
```
77
diagnostics of SIADH
Serum Na+ ↓ < 130
Urine Na+ ↑
BUN ↓
urinary output low – urine will be concentrated
78
management of DI
Surgical:
Hypophysectomy
Medical:
IV Fluids – quarter saline – remember they are holding onto sodium
79
management of SIADH
```
Surgical:
None
Medical:
Hypertonic Flds.
Demeclocycline (antibiotic) to facilitate free water clearance (side effect)
Sodium restriction
Diuretics due to low plasma osmo
Treat underlying cause.
```
80
nursing management for DI/SIADH
monitor Daily Wt. & I/O
| What do you do for a thirsty pt? – hard candy if they can swallow safely
81
functions of the kidney
filtration, reabsorption, secretion, production of erythropoietin, production of renin (important for regulation of BP
82
nutrition and renal failure
too much protein can cause kidneys to shut down. renal failure causes altered Ca and phosphorous.
83
kidney and aging
starts to shrink, decrease in GFR, increase in BUN and creatinine
84
lab studies in kidney patients
```
U/A
Culture & Sensitivity
Specific Gravity
Ketones, Protein, Glucose
BUN/Cr 10:1
Electrolytes
Calcium/Phosphorus
Bicarbonate
CBC
Osmolality
```
85
diagnostics in renal patients
```
KUB
IVP
Ultrasound
CT/MRI
Cystoscopy
Urethrogram
Renal Bx
Cystogram
```
86
Acute Renal Failure
A clinical syndrome characterized by a rapid loss of renal function with progressive azotemia (an accumulation of waste products [BUN & Cr]. Also includes changes in electrolytes and fluid status.
Uremia: (Literally, urine in the blood).
Oliguria: decreased UOP <400ml/d
87
AKI development
Usually develops over hours to days with progressive elevations of BUN, Cr & K+
60% of ICU pts with 70% -80% Mortality
88
AKI prerenal
factors external to kidney (Hypovol., Dehydration, Hemorrhage, Burns, Cardiac issues, Anaphylaxis, Neuro Injury, Septic Shock, Thrombosis)
Low UOP, rise BUN & Cr 10:1, inability to conserve Na.
Usually Reversible shock – effecting kidney at prerenal status
89
infrarenal AKI
Direct damage to parenchyma resulting in impaired nephron fxn ( prolonged ischemia, nephrotoxins, myoglobin)
ATN (Acute Tubular Necrosis) 90% of all AKI
90
post renal AKI
Mechanical obstruction of urinary outflow (BPH, prostate CA, calculi, trauma) < 10% of AKI
91
initiating phase AKI
This begins at the time of the insult and continues until the signs and symptoms become apparent.
Lasting hours to days.
92
Oliguric Phase AKI
Reduction in GFR
Occurs within 1-7 days of causative event
Duration 10-14 days, but can last months
The longer in this phase the poorer the prognosis for recovery of complete renal function.
Urinary Changes, Fluid Vol. Excess, Metabolic Acidosis, Sodium Balance Loss, Potassium Excess
93
diuretic phase AKI
Begins with gradual increase in dly UOP secondary to high urea concentration in the urine and the inability of the tubules to concentrate the urine.
Can excrete waste, but not concentrate
Must monitor lytes and hydration levels
Lasts 1-3 weeks
Patients lab values begin to normalize near the end of this phase
94
recovery phase AKI
Begins with increasing GFR
BUN and CR levels plateau and then decrease
Improvements occur in first 1-2 weeks of this phase, but renal function may take up to 12 months to stabilize
Outcome influenced by the patient’s overall health, severity of renal failure and the number and type of complications
Some will progress to CRF
Older adults less likely to recover full function
Those who recover achieve clinically normal function without complications.
95
Acute renal failure diagnostics
H&P, UA, Chemistry, US, CT, MRI
96
care for ARF
```
Adequate Perfusion
Diuretics
Fluids
K+
Nutrition – protein, potassium, sodium, calcium, phosphorous
Dialysis
```
97
Rhabdomyolysis Patho
the breakdown of muscle fibers resulting in the release of muscle fiber contents (myoglobin) into the circulation. Some of these are toxic to the kidney and frequently result in kidney damage.
98
causes of rhabdo
Traumatic Injury (Burns, Crush Injury, Electrocution, Blunt Force, Lightening Strike)
Excessive Exertion
Ingestion of Toxic Substances inclusive of Drugs and ETOH (inhibits ADH secretion)
Status Epilepticus
Shock Induced Hypoxia
Hypothermia/Hyperthermia
99
s/s of rhabdo
tea colored urine, Muscle Weakness, Gen. Fatigue
100
hallmark of rhabdo
increase in serum Creatine kinase
101
normal CK
45-260 units/L
102
labs for rhabdo
CK, ABGs- possible acidosis, BUN/Cr, potassium/phos, calcium, clotting, too screen, U/A - positive protein, brown casts, uric acid
103
early complications from rhabdo
```
Hyperkalemia – can lead to arrythmias and death
Hypocalcemia
Hepatic inflammation
Cardiac arrhythmia
Cardiac arrest
```
104
late complications of rhabdo
multisystem organ failure
Acute renal failure
Disseminated intravascular coagulation
105
nursing management for rhabdo
monitor!
106
treatment for rhabdo
```
Removal of Tight Clothing
Fasciotomy or Escharatomy
NS @ to 1000-1500ml/hr to maintain UOP @ 300ml/hr
diuretic
dialysis
```
107
diffusion
greater to lesser
108
osmosis
lesser to greater
109
Continuous Renal Replacement Therapy (CRRT)
Used for hemodynamically unstable pts.
| Artificial kidney support.
110
Heparin Induced Thrombocytopenia (HIT)
immun reaction to heparin. lowers platelet count, and causes thromboses
111
acute pyelonephritis
considered intrarenal - inflammation cause from bacteria
112
acute pyelonephritis manifestations
flank pain, fatigue, chills, fever, dysuria
113
urosepsis
systemic infection with a urinary source. seen a lot in geriatric population
114
nephrotic syndrome marked by:
very high levels of protein in the urine, a condition called proteinuria
low levels of protein in the blood
swelling, especially around the eyes, feet, and hands
high cholesterol → high triglycerides
115
what is nephrotic syndrome
immune response that leads to damage of the glomeruli and third spacing of fluids (fluid accumulates into the tissues rather than circulating)
116
kidney's glomeruli do what
they keep protein in the blood from leaking into the urine
| the damaged glomeruli allow 3-10 grams or more of protein to leak into the urine during a 24-hour period.
117
Anasarca
weeping of the skin- protein leaking from skin
118
What’s Causing Nephrotic Syndrome?
infection, allergens, drugs
119
Diagnosing Nephrotic Syndrome
blood and urine samples (Protein)
| may order a 24-hour collection of urine
120
Treatment and Care for nephrotic syndrome
focuses on reducing high cholesterol, blood pressure, and protein in urine
Symptom Mgt -> Relieve edema, Control primary disease, Reduced Na & low to mod Protein Diet
121
Nursing Care for nephrotic syndrome
Assessment of edema, I/O, Weigh dly, Measure abd. girth, hygiene, monitor dietary intake
122
Renal trauma occurs most commonly from
blunt force. usually in men under 30
123
diagnostics for renal trauma
U/A, US, cystogram, CT, MRI
124
risk factors of renal cancer
2 X more often in men than women, cigarette smoking most common risk factor.
125
s/s of renal cancer
Undetected due to lack of symptoms. Either found incidentally or when tumor becomes large and invasive. Hematuria, flank pain and palpable mass in flank or abdomen
126
what usually occurs with renal cancer
Usually have mets before dx made.
127
bladder cancer risk factors
Hematuria (painless), bladder irritability, dysuria, frequency, urgency
128
Carcinomas
Cancers that begin in the skin or in the tissue that line or cover internal organs
129
Sarcomas
Start in the connective tissue including bones, cartilage, tendons, and fibrous tissue
130
Leukemia
Bone marrow makes too many white blood cells, and they do not form correctly, but continue to build up in the blood
131
Lymphomas and Myelomas
cancer in the lymphatic system – system that filters bodily fluid and fights infection
132
Brain and Spinal Cord Cancer
Most common start from glial cells
133
Melanoma
Most dangerous type of skin cancer
Risk factors include:
Have fair skin, blue or green eyes, or red or blond hair
Live in sunny climates or at high altitudes
134
Liver Cancer
```
common causes
Cirrhosis (alcohol abuse)
Autoimmune disease
Hep B or C
Chronic inflammation
```
135
Pancreatic Cancer common causes
Diabetics
Chronic pancreatitis
Smokers
136
Clinical manifestations of pancreatic cancer:
Clinical manifestations
Dark urine & clay stools
Fatigue & weakness
Jaundice
137
only tru way to diagnose cancer
biopsy
138
grading system for cancer shows
how much the cells resemble the original tissue
139
TNM staging system
T - tumor
N - nodes
M - metastasis
Once staging is complete is does NOT change
140
treatment options for cancer
surgery, radiation, chemo, biotherapy, immunotherapy
141
factors that affect the response to chemo
rate of tumor growth, genetics, hormones
142
different chemos affect
different phases of cell growth
143
immunotherapy
uses the body's immune system but there us a chance for immune response side effects
144
complications of central lines
extravasation, hypersensitivity, flare reaction
145
flare reaction
distinguishable from extravasation by lack of pain or swelling, presence of good blood return
146
sign of extravasation
Redness, swelling
Stinging, burning, pain at the site
Loss of blood return
147
side effects of chemo
Blood-Related Side Effects
Nausea and Vomiting
Hair Loss
Mouth and Sore Throat
148
nadir
Point at which the lowest blood-cell count is reached
Usually 7-10 days after treatment
Onset and duration depends on agent used
WBC & platelets are usually 1st to drop
Anemia is seen later
149
life span of a neutrophil
7-12 hours
150
life span of platelets
7-8 days
151
life span of erythrocytes
90-120 days
152
mild neutropenic absolute neutrophil count
1000-1500
153
moderate neutropenic absolute neutrophil count
500-1000
154
severe neutropenic absolute neutrophil count
0-500
155
how to calculate Absolute Neutrophil Count (ANC)
ANC = Total WBC × (% Segmented Neutrophils + % Bands)
156
Leading cause of morbidity in chemo patients
infection leading to sepsis leading to septic shock
157
often the only sign of infection
fever above 100.4
158
infection prevention
good hand hygiene!!!
159
what meds can we give a chemo patient for infection prevention
colony-stimulating factors - Neupogen andNeulasta
160
Thrombocytopenia
Nadir 8-14 days after chemotherapy
| risk for bleeding
161
Thrombocytopenia – Assessment
```
Petechiae, bruising and hemorrhage
GI bleeding
Neurological signs of bleeding
Hypotension
Tachycardia
```
162
Thrombocytopenia - Management
risk for bleeding to no blowing nose, use of electric razor, decrease activity, maintain SBP less than 140, prevent constipation, avoid NSAIDs
163
anemia clinical manifestations
fatigue, tachycardia, dizziness, cold intolerance
164
mouth and sore throat medication
MBX - magic mouthwash, nystatin, Stanford mouthwash
165
UC/Crohns concept
concept of inflammation that causes manifestations of fluid and electrolytes
166
both UC and Crohn's are characterized by
chronic inflammation of the intestine w/ periods of remission & exacerbation
167
UC
inflammation beginning in the rectum and spreading up the COLON (only) in a continuous pattern
168
what occurs in UC
Ulcerations destroy the mucosal epithelium, causing bleeding and diarrhea
Fluid and electrolyte losses
Protein loss
Pseudo polyps
169
Clinical manifestations of UC
```
Major:
Bloody diarrhea
Abdominal pain
Other:
fever
Tenesmus
rectal bleeding
Rare malabsorption/ nutritional problems
```
170
Tenesmus
painful spasm of the anal sphincter along with an urgent desire to defecate without the significant production of feces
171
crohns
Can affect any part of the GI tract from the lips to the anus
Most often seen in the terminal ileum and colon
172
Hallmark sign of crohns
skip lesions: Segments of normal bowel occurring between diseased portions causing classic cobblestone appearance
173
Crohns manifestation
Major: Diarrhea
Major: Abdominal cramping
Fever
Weight loss- severe if small intestine involved
Common Malabsorption/ nutritional problems-if small intestine involved
174
fistulas are seen more in
crohns - leaks out all the way to skin
175
strictures and UC/crohns
occasional in UC and common in chrons
176
Perforation and UC/Crohns
UC - Common d/t toxic mega colon
| Crohns- Common d/t bowel wall destruction
177
surgery and UC/Crohns
UC - Usually cured with colectomy
| Crohns - Common reoccurrence at site of anastomosis
178
cancer and UC/Crohns
UC - Significantly ↑ incidence after 10 years
| Crohns - ↑ incidence w/ small intestine & colon but not as much colon CA as w/ UC
179
what other reactions can occur with crohns
```
Systemic Complications Triggered by circulating products of inflammation. Can cause:
Arthritis
Eye inflammation
Skin lesions
Liver failure
```
180
management for UC/Crohns
drug therapy, surgery, nutrition
181
nutrition with UC/Crohns
```
High-calorie, High-protein
Low-residue diet- helps control diarrhea
Vitamin and iron supplements
Elemental diets: Enteral feedings for bowel rest
Parenteral nutrition: during bowel rest
```
182
drugs for UC/Crohns
Aminosalicylates, Antimicrobials, Corticosteroids, Immunosuppressants, Biologic therapy, Antidepressants
183
Aminosalicylates:
Sulfasalazine (Azulfidine)
184
Antimicrobials
Flagyl, Cipro, Biaxin (more effective w/ Crohn’s)
185
Corticosteroids:
Prednisone help to attain remission
186
Immunosuppressants:
taken 3-6 mo (more effective for Crohn’s)
187
Biologic therapy:
Remicade, given IV, to induce and maintain remission
| Humira – monoclonal antibody blocks TNF-alpha
188
IBD nursing diagnoses
Diarrhea r/t bowel inflammation and intestinal hyperactivity
Imbalanced nutrition: less than body requirements r/t decreased absorption and increased nutrient loss through diarrhea
Ineffective coping r/t chronic disease, lifestyle changes, inadequate confidence in ability to cope
189
Solid organs
liver, spleen, kidneys and pancreas; bleed profusely
190
Hollow organs
stomach, intestines, bladder, gallbladder; peritonitis/sepsis leakage after injury
191
regions of the abdomen
Peritoneal
Retroperitoneal
Pelvis
192
Two categories of trauma
blunt and penetrating
193
________ are a frequent cause of trauma deaths
missed ABD injuries
194
blunt trauma is associated with:
increase fatalities
195
Blunt Abdominal Trauma
Leading cause of morbidity and mortality among all age trauma victims
Injury secondary to compressive, shearing, crushing, and deceleration forces
196
most common cause of blunt abdominal trauma
MVCs
197
Blunt Abdominal Trauma causes
serious damage to solid organs
198
hollow organs can collapse
and absorb force
199
why would you suspect visceral damage
if you see any of the below in an ABD trauma case
Abd tenderness or guarding
Abd or flank ecchymosis (cullens sign/grey turners)
Hemodynamic instability
Lumbar spine injury/lower rib fx
Pelvic fx
200
Cullen’s Sign
bruising around the umbilicus - Intra-peritoneal hemorrhage
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Grey Turner’s sign
flanks- Retro-peritoneal hemorrhage
202
what type of organs are more prone to injury in Penetrating Abdominal Trauma
hollow organs - can lead to sepsis and infection
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what do you not want to do to during penetrating abdominal trauma?
do not remove the weapon! - the weapon may be holding the pt from bleeding
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Nursing Management ABD Trauma
indwelling urinary cath, oxygen, NG, 2 large bore IVs
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diagnostics for ABD trauma
Focused Abd Sonogram for Trauma (FAST) US or CT (sometimes both)
Surgery: Exploratory laparotomy
Unstable penetrating trauma, OR regardless of what FAST shows
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what is used with ABD trauma in rural areas when CT is not available
Diagnostic Peritoneal Lavage DPL - old technique
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Intra-abdominal pressure (IAP) in a normal adult
0-5
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Intra-abdominal Hypertension (IAH)
elevation in IAP ≥ 12 mmHg
209
Causes of IAH
Surgical:
ruptured AAA, blunt/penetrating trauma, post op bleed
Medical:
pancreatitis, ileus, sepsis, burns, infection, fluid resuscitation
Recurrent: comes back
210
Abdominal Compartment Syndrome
Defined as sustained IAP > 20 mmHg with new organ dysfunction or failure
Painful condition occurring when pressure within the abdomen builds to dangerous levels
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what happens during abdominal compartment syndrome
Pressure ↓ the blood flow, prevents nourishment and O2 from reaching nerves, cells and organs
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patients at risk for abdominal compartment syndrome
Abdomen related: Abdominal surgery: distended abdomens: intra- abdominal infection/abscess/ tumors
Systemic related: Major trauma, burns, shock states, acidosis, sepsis
Other: Prone positioning; Mechanical ventilation/Peep greater than 10 cm, Age, obesity
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What does ACS mean for your patient?
```
50% of IAP is reflected into the thoracic cavity…causing ⇩ CO
Atelectasis, PNA
decrease PaO2 increase PaCO2
decrease GFR; AKI
increase ICP
decrease wound healing
```
Complication of Abdominal Trauma!!!
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Intra-abdominal Pressure indirect Monitoring
- Urinary bladder pressure monitoring
- NG tubes
- Rectal tubes
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Gold standard for indirect intermittent pressures
Urinary bladder pressure monitoring
| Utilizes a foley catheter for monitoring
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Nursing Interventions for Abdominal compartment syndrome
evacuate intraluminal contents (NG tube to suction), Monitor for daily BM/prevent constipation, Optimize fluid resuscitation, Optimize systemic and regional perfusion
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Acute Pancreatitis
An inflammatory disorder of the pancreas characterized by severe upper abdominal pain and increased serum concentration of pancreatic enzymes
218
Most common prognostic systems Acute Pancreatitis
Ranson’s Criteria
219
Ranson Criteria
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Estimating the severity of acute pancreatitis
Morality rates:
0 to 2 factors: 2%
3 to 4 factors: 15%
5 to 6 factors: 40%
7 to 8 factors: 100%
```
220
Acute pancreatitis causes
Most Common (80% of cases):
Gallbladder Disease
Excessive ETOH
221
clinical manifestations of Acute pancreatitis
```
Hallmark symptoms: abdominal pain, n/v
LUQ/mid epigastric radiating to the back
Report twisting/knife like sensation
Can be aggravated by eating….why?
fever
ABD distention
```
222
labs for Acute pancreatitis
```
Serum lipase
≥ 3 x the upper limit of normal
more specific to pancreas
more accurate marker for acute pancreatitis
Amylase (will be increased as well)
Elevations in:
Triglycerides, CRP, glucose, WBCs, bilirubin, LFTs, PT
Urine amylase
Reductions in:
Calcium, magnesium, potassium, albumin
```
223
gold standard for diagnostics for acute pancreatitis
CT of abdomen
Gold standard for diagnosis, pancreatitis inflammation and necrosis
can also get ABD US, MRI, CXR
224
pulmonary complications in acute pancreatitis
Backup of pancreatic enzymes cause auto-digestion of pancreas – pancreatic edema and necrosis can occur
Cytokines, macrophages, WBCs = ↑ vascular permeability, tissue edema
Diaphragm becomes inflamed causing reduced movement
Lungs have ↓ expansion, Atelectasis
Pleural effusions form, further impact ventilation and gas exchange
ARDS – lung compliance markedly ↓
Death
225
complications seen from acute pancreatitis other than pulmonary
```
Cardiovascular:
Hypotension and shock
Renal:
oliguria
Hematologic:
DIC
GI/Hepatic:
hepatic dysfunction
bowel infarction
```
226
Collaborative Management for Acute Pancreatitis
Ensure Hemodynamic Stability…remember this is C of your ABCs
Pain & N/V management
Antibiotics: ONLY if SEPSIS or abscess are present
NPO & NG
Enteral or parental support within 5 to 7 days
Evidences shows safe, cost effective, fewer septic, metabolic, complications
NG suction: ONLY if patient has persistent vomiting obstruction or gastric distention
227
Chronic Pancreatitis
Main features are abdominal pain, malabsorption, weight loss and diabetes
228
Classic triad of chronic pancreatitis
calcification, steatorrhea, and diabetes
| history of heavy ETOH use
229
gold standard for dx for chronic pancreatitis
Surgical biopsy of pancreas
230
Labs for chronic pancreatitis
```
Pancreatic enzymes (amylase and lipase)
CBC w/ diff (WBCs and diff)
CMP/BMP (electrolytes are usually Ok unless obstruction or severe n/v/d)
```
231
causes of upper GI bleeds
55% peptic ulcer disease
| others can be from Stomach cancer; Erosive gastritis...
232
Variceal bleeding
Most often associated with ETOH use; large veins under increased pressure; rupture/hemorrhage
233
What do I see during a GI bleed
```
Severe ABD pain
Metabolic acidosis
Lactic acidosis
Anoxia
Hematemesis (Upper)
Hematochezia (lower)
Melena (Upper)
```
234
Collaborative Care for GI bleed
```
Correct the labs:
Hbg/hct (1/3 ratio), platelets
CMP: BUN/CR, LFTs, Electrolytes
Coags
ABG (metabolic acidosis)
```
235
Anticipate medications for GI bleed
```
Vasopressors:
- norepinephrine, vasopressin, phenylephrine
Acid Reduction:
- PPIs: pantoprazole sodium (Protonix) IV drip
- Give IV bolus then ~ 8 mg/hr IV
- NOT Titrated!
Octreotide IV drip (Sandostatin)
- Give an IV bolus then ~ 50 mcg/hr IV
- NOT Titrated!
- ↓ bleeding of varices
May need to give blood products
```
236
acute liver failure causes
```
Drugs are #1 cause
#1: Tylenol (acetaminophen), NSAIDs (all types), INH, mushrooms
#2: Hepatitis B & C
```
237
outcomes for acute liver failure
75 - 90% DIE!; 10-25% “SURVIVE”…W/ INTENSIVE CARE!
| NEED A LIVER
238
Collaborative CareAcute Liver Failure
Lower the AMMONIA LEVEL!
Neomycin, metronidazole, rifaximin or LACTULOSE (gold standard)
↓ ammonia formation by decreasing bacterial action on the protein in feces by can cause renal toxicity and hearing impairment
Correction of coagulopathies: best through PREVENTION!
239
cirrhosis cause
alcohol - number 1 cause
240
Liver DiseaseMnemonic: ABCDEFGHIJ
A Asterixis (liver flap)/Ascites/Ankle edema/Atrophy of testicles/Angiomas
B Bruising/BP changes
C Confusion/Clubbing/Color change of nails
D Dupuytren's contracture
E Erythema(palmar)/Encephalopathy/Esophageal Varices
F Fetor hepaticus…”breath of the dead”
G Gynecomastia
H Hepatitis (B & C), Hepato-splenomegaly/renal/portal HTN
I Itching/↑ in size of parotids
J Jaundice
241
TIPS
Trans jugular intrahepatic porto systemic shunt
| Manage complications of portal HTN
242
Bariatric Surgery
```
to qualify: BMI>40 or >35 with comorbidities
5+ years
Understand risks/benefits
Tried and failed at weight loss
No serious endocrine disorders
```
243
Restrictive bariatric Surgeries
gastric banding - ↓ stomach to 30 mL, feeling fuller faster
244
malabsorption bariatric surgeries
Various lengths of the small intestine bypassed ↓ absorption of nutrients
Less food is absorbed – DOES alter digestion
245
Roux-en-Y Gastric bypass
```
Stomach size is ↓ w/ gastric pouch
Most common bariatric procedure in US
Considered gold standard
Low complication rates
Excellent patient tolerance
```
246
what can occur with Roux-en-Y Gastric bypass
DM II
247
Preoperative Concerns with bariatric surgeries
Liquid Diet for up to 6 wks preop
| Detailed health hx, address comorbidities; interdisciplinary team approach required
248
post op complications in bariatric surgeries
Dehiscence or leaking
- First sign is tachycardia
Anemia: malabsorption of Iron and Vit B
Increased risk of Infection
249
Long term bariatric surgery complications:
bowel obstruction, dumping syndrome, n/v/d, gallstones, hernias, hypoglycemia, malnutrition, stomach perforation, ulcers, death (rare)
250
Post-operative bariatric Concerns
Assessment & intervention for complications
- Anastomosis leaks
- Thrombus formation
Airway management!!
251
Nutritional Goals: after bariatric surgery
```
PREVENT MALABSORPTION
DUMPING SYNDROME
SPEED HEALING
Meals:
6 to 8 small @ 30 mL
Don’t skip!!!
High PRO/low FAT/low CHO/low roughage
Fluids: NOT w/ meals; limited to 1000 mL/day
Avoid concentrated sweets
Supplements
Length of time to advance diet varies
```
