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Nursing school level 4 > NURS 453 test 3 > Flashcards

NURS 453 test 3 Flashcards

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1
Q

Addison’s Disease

A

Incurable disease controlled w/ hormone replacement

90% of adrenal cortex destroyed

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2
Q

Primary cause of Addisons disease

A

Autoimmune (80%) and idiopathic

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3
Q

Secondary cause of Addisons disease

A

Steroid withdrawal, pituitary tumor

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4
Q

Adrenal glands produce

A

cortisol and aldosterone

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5
Q

what does cortisol do

A

helps the body respond to stress, maintains BP, balance the effects of insulin…has hundreds of functions

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6
Q

what does aldosterone do

A

helps maintain BP, H2O/Na+ balance

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7
Q

cortisol is a

A

glucocorticoids

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8
Q

aldosterone is a

A

mineralocorticoids

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9
Q

androgens

A

Sex hormones in both men and women

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10
Q

Patient Presentation in Addison’s Disease

A

Low BP, dizziness, orthostatic HoTN, hypoglycemia, fatigue, weight loss, hair loss, salt craving

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11
Q

Addisonian crisis or Acute Adrenal Insufficiency also known as

A

acute adrenal failure

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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!!!

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13
Q

acute adrenal failure results in

A

Circulatory collapse and electrolyte imbalance

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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

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15
Q

causes acute adrenal failure

A

stress, Adrenal surgery/hemorrhage

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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)

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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

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18
Q

diagnostics in acute adrenal failure

A

ACTH stimulation test, Insulin-induced hypoglycemia test, CT, MRI

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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`

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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)

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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)

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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

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23
Q

Assist patients to avoid what during acute adrenal failure

A

stress - Physical, Mental, Emotional, Spiritual

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24
Q

Hydrocortisone

A

synthetic form of cortisol

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25
Q

what do we need to administer during acute adrenal failure

A

Corticosteroid administration

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26
Q

what do we want to maintain during acute adrenal failure

A

maintain perfusion with isotonic fluid and give vasopressors

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27
Q

education during acute adrenal failure

A

Importance to take cortisol replacement daily
↑ dose at times of stress (fever, flu, surgery, etc)
Double/triple doses!!!!!
Follow up with MD immediately

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28
Q

what concepts to think about during diabetic kept acidosis and HHS

A

Acid Base Balance - Directly linked to the cause/dehydration
Fluids and electrolytes (Key) - Dehydration!
Inflammation
Perfusion - Dehydration

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29
Q

DKA and insulin

A

Insulin Deficiency

Insulin dependent diabetics (Type I & II)

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30
Q

DKA what happens

A 
Break down of FAT & PROTEIN→Ketones
Rapid onset
Liver continues to produce glucose
Hyperglycemia (> 250)
Osmotic Diuresis
Severe Dehydration
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31
Q

HHS and insulin

A 
Insulin Present (Only Type II)
Liver continues to produce glucose
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32
Q

HHS what happens

A

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

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33
Q

DKA diagnostic criteria

A

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

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34
Q

HHS diagnostic criteria

A 
Blood glucose ˃ 600  mg/dL
NO KETONES!!!!! 
Serum bicarbonate can be ˃ 18 mEq/L
Serum osmolality can ˃ 320 mOsm/kg
pH ˃ 7.30
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35
Q

Causes of DKA and HHS

A

Infection! Most common cause!
Increase demand brought on by illness/stress
↓ or missed insulin dose
Undiagnosed & untreated DM

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36
Q

DKA presentation

A 
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
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37
Q

HHS presentation

A

Slower onset - why? -

Key: neuro changes

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38
Q

presentations that are seen in both DKA and HHS?

A

Hyperglycemia
Dehydration and electrolyte loss
Acidosis (lack of perfusion at the cellular level)

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39
Q

blood sugars in DKA

A

above 250

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40
Q

blood sugars HHS

A

above 600

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41
Q

why are there such high glucose levels during DKA and HHS?

A

Liver continues to produce glucose
Stress hormones induce more glucose production
Starving cells stressed – that is why we have polyphagia

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42
Q

Osmotic diuresis

A

↑ glucose causes ↑ serum osmolality

H2O moves from interstitial to intravascular = cellular dehydration - occurs during DKA and HHS

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43
Q

Why is there such bad dehydration in DKA and HHS?

A

osmotic diuresis, polyuria - can loose up to 7 liters of fluid in 24 hours, blood viscosity increases

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44
Q

ketoacidosis =

A

metabolic acidosis

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45
Q

what occurs during ketoacidosis?

A

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

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46
Q

DKA: Clinical manifestations

A

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

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47
Q

vital signs in DKA

A

Kussmaul respirations: fruity/acetone breath – compensation for metabolic acidosis
Tachycardia/HoTN/Orthostatic HoTN
Fever – why? – possible infection and increase stress response

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48
Q

HHS clinical manifestations

A

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

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49
Q

Labs for DKA and HHS

A

+ 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

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50
Q

anion gap

A

Difference between the cations and anions in the extra cellular fluid (ECF)
Normal levels: 10 – 14 mEq/L

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51
Q

Initial Interventions DKA and HHS

A

ABCs..
Ensure patent airway
Administer oxygen
FLUIDS!!!!…
IV access – hydration!
Begin fluid resuscitation then give them regular insulin
Electrolyte replacement once partial glucose correction

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52
Q

treatment for DKA/HHS

A

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)

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53
Q

fluids during DKA/HHS

A

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

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54
Q

when do you know that you should switch to D5 in DKA/HHS treatment?

A

u/o ˃ 0.5ml /kg/hr and B/P normal

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55
Q

DKA/HHS and potassium

A

pts can be either hyperkalemic or hypokalemic – hyperkalemic why? – renal compromise and cannot excrete

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56
Q

Aim for BG reduction in reversing acidosis

A

36 – 54 mg/dL/hour (45 an hour is what we are hoping for)

Hourly evaluation of BG

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57
Q

Acidosis as a result of ketosis is primarily reversed with

A

insulin (and fluids)

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58
Q

Nursing Diagnosis for DKA and HHS

A

Deficient fluid volume r/t absolute loss

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59
Q

what hormones does the anterior pituitary secrete?

A

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.

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60
Q

The posterior pituitary secretes

A

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.

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61
Q

how would you fix a pituitary tumor?

A

Transphenoidal hypophesectomy or

Laproscopic surgery through nose or through the upper lip

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62
Q

post op care after removal of a pituitary hormone?

A

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

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63
Q

DI

A

Deficiency of antidiuretic hormone (ADH, vasopressin) results in inability to conserve water

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64
Q

SIADH

A

Excessive amounts of ADH secreted from posterior pituitary and other ectopic sources. – body not producing urine

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65
Q

commonality between DI and SIADH

A

ADH – key component that we see between the two

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66
Q

DI causes

A

unknown, idiopathic, tumors

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67
Q

SIADH causes

A

80% r/t small cell carcinoma

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68
Q

risk factors for DI

A

head injury, neurosurgery, tumor

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69
Q

SIADH risk factors

A

increased ICP, malignant conditions

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70
Q

what happens in DI

A

Permeability of water is diminished, resulting in excretion of large volumes of hypotonic fluid.

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71
Q

what happens in SIADH

A

Water Retention
Hyponatremia (dilutional)
Hypo-osmolality - A continual release of ADH causes water retention from renal tubules and collecting ducts.

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72
Q

DI physical exam

A 
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
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73
Q

SIADH physical exam

A 
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
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74
Q

complications of DI

A

Electrolyte Imbalance
Hypovolemia
Hypotension
Shock

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75
Q

complications of SIADH

A

Seizures
Coma
Permanent brain damage
Further complications of existing disease processes.

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76
Q

diagnostics of DI

A 
Urinary OutPut- A few liters to 18L/d
Serum Osmo ↑ >290
Serum Na+ ↑ >150
Sp. Gravity < 1.005
Water deprivation study
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77
Q

diagnostics of SIADH

A

Serum Na+ ↓ < 130
Urine Na+ ↑
BUN ↓
urinary output low – urine will be concentrated

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78
Q

management of DI

A

Surgical:
Hypophysectomy
Medical:
IV Fluids – quarter saline – remember they are holding onto sodium

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79
Q

management of SIADH

A 
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.
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80
Q

nursing management for DI/SIADH

A

monitor Daily Wt. & I/O

What do you do for a thirsty pt? – hard candy if they can swallow safely

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81
Q

functions of the kidney

A

filtration, reabsorption, secretion, production of erythropoietin, production of renin (important for regulation of BP

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82
Q

nutrition and renal failure

A

too much protein can cause kidneys to shut down. renal failure causes altered Ca and phosphorous.

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83
Q

kidney and aging

A

starts to shrink, decrease in GFR, increase in BUN and creatinine

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84
Q

lab studies in kidney patients

A 
U/A
Culture &amp; Sensitivity
Specific Gravity
Ketones, Protein, Glucose
BUN/Cr 10:1
Electrolytes
Calcium/Phosphorus
Bicarbonate
CBC
Osmolality
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85
Q

diagnostics in renal patients

A 
KUB
IVP
Ultrasound
CT/MRI
Cystoscopy
Urethrogram
Renal Bx
Cystogram
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86
Q

Acute Renal Failure

A

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

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87
Q

AKI development

A

Usually develops over hours to days with progressive elevations of BUN, Cr & K+
60% of ICU pts with 70% -80% Mortality

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88
Q

AKI prerenal

A

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

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89
Q

infrarenal AKI

A

Direct damage to parenchyma resulting in impaired nephron fxn ( prolonged ischemia, nephrotoxins, myoglobin)
ATN (Acute Tubular Necrosis) 90% of all AKI

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90
Q

post renal AKI

A

Mechanical obstruction of urinary outflow (BPH, prostate CA, calculi, trauma) < 10% of AKI

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91
Q

initiating phase AKI

A

This begins at the time of the insult and continues until the signs and symptoms become apparent.
Lasting hours to days.

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92
Q

Oliguric Phase AKI

A

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

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93
Q

diuretic phase AKI

A

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

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94
Q

recovery phase AKI

A

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.

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95
Q

Acute renal failure diagnostics

A

H&P, UA, Chemistry, US, CT, MRI

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96
Q

care for ARF

A 
Adequate Perfusion
Diuretics
Fluids
K+
Nutrition – protein, potassium, sodium, calcium, phosphorous 
Dialysis
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97
Q

Rhabdomyolysis Patho

A

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.

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98
Q

causes of rhabdo

A

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

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99
Q

s/s of rhabdo

A

tea colored urine, Muscle Weakness, Gen. Fatigue

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100
Q

hallmark of rhabdo

A

increase in serum Creatine kinase

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101
Q

normal CK

A

45-260 units/L

102
Q

labs for rhabdo

A

CK, ABGs- possible acidosis, BUN/Cr, potassium/phos, calcium, clotting, too screen, U/A - positive protein, brown casts, uric acid

103
Q

early complications from rhabdo

A 
Hyperkalemia – can lead to arrythmias and death
Hypocalcemia 
Hepatic inflammation 
Cardiac arrhythmia 
Cardiac arrest
104
Q

late complications of rhabdo

A

multisystem organ failure
Acute renal failure
Disseminated intravascular coagulation

105
Q

nursing management for rhabdo

A

monitor!

106
Q

treatment for rhabdo

A 
Removal of Tight Clothing
Fasciotomy or Escharatomy
NS @ to 1000-1500ml/hr to maintain UOP @ 300ml/hr  
diuretic 
dialysis
107
Q

diffusion

A

greater to lesser

108
Q

osmosis

A

lesser to greater

109
Q

Continuous Renal Replacement Therapy (CRRT)

A

Used for hemodynamically unstable pts.

Artificial kidney support.

110
Q

Heparin Induced Thrombocytopenia (HIT)

A

immun reaction to heparin. lowers platelet count, and causes thromboses

111
Q

acute pyelonephritis

A

considered intrarenal - inflammation cause from bacteria

112
Q

acute pyelonephritis manifestations

A

flank pain, fatigue, chills, fever, dysuria

113
Q

urosepsis

A

systemic infection with a urinary source. seen a lot in geriatric population

114
Q

nephrotic syndrome marked by:

A

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
Q

what is nephrotic syndrome

A

immune response that leads to damage of the glomeruli and third spacing of fluids (fluid accumulates into the tissues rather than circulating)

116
Q

kidney’s glomeruli do what

A

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
Q

Anasarca

A

weeping of the skin- protein leaking from skin

118
Q

What’s Causing Nephrotic Syndrome?

A

infection, allergens, drugs

119
Q

Diagnosing Nephrotic Syndrome

A

blood and urine samples (Protein)

may order a 24-hour collection of urine

120
Q

Treatment and Care for nephrotic syndrome

A

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
Q

Nursing Care for nephrotic syndrome

A

Assessment of edema, I/O, Weigh dly, Measure abd. girth, hygiene, monitor dietary intake

122
Q

Renal trauma occurs most commonly from

A

blunt force. usually in men under 30

123
Q

diagnostics for renal trauma

A

U/A, US, cystogram, CT, MRI

124
Q

risk factors of renal cancer

A

2 X more often in men than women, cigarette smoking most common risk factor.

125
Q

s/s of renal cancer

A

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
Q

what usually occurs with renal cancer

A

Usually have mets before dx made.

127
Q

bladder cancer risk factors

A

Hematuria (painless), bladder irritability, dysuria, frequency, urgency

128
Q

Carcinomas

A

Cancers that begin in the skin or in the tissue that line or cover internal organs

129
Q

Sarcomas

A

Start in the connective tissue including bones, cartilage, tendons, and fibrous tissue

130
Q

Leukemia

A

Bone marrow makes too many white blood cells, and they do not form correctly, but continue to build up in the blood

131
Q

Lymphomas and Myelomas

A

cancer in the lymphatic system – system that filters bodily fluid and fights infection

132
Q

Brain and Spinal Cord Cancer

A

Most common start from glial cells

133
Q

Melanoma

A

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
Q

Liver Cancer

A 
common causes 
Cirrhosis (alcohol abuse)
Autoimmune disease
Hep B or C
Chronic inflammation
135
Q

Pancreatic Cancer common causes

A

Diabetics
Chronic pancreatitis
Smokers

136
Q

Clinical manifestations of pancreatic cancer:

A

Clinical manifestations
Dark urine & clay stools
Fatigue & weakness
Jaundice

137
Q

only tru way to diagnose cancer

A

biopsy

138
Q

grading system for cancer shows

A

how much the cells resemble the original tissue

139
Q

TNM staging system

A

T - tumor
N - nodes
M - metastasis
Once staging is complete is does NOT change

140
Q

treatment options for cancer

A

surgery, radiation, chemo, biotherapy, immunotherapy

141
Q

factors that affect the response to chemo

A

rate of tumor growth, genetics, hormones

142
Q

different chemos affect

A

different phases of cell growth

143
Q

immunotherapy

A

uses the body’s immune system but there us a chance for immune response side effects

144
Q

complications of central lines

A

extravasation, hypersensitivity, flare reaction

145
Q

flare reaction

A

distinguishable from extravasation by lack of pain or swelling, presence of good blood return

146
Q

sign of extravasation

A

Redness, swelling
Stinging, burning, pain at the site
Loss of blood return

147
Q

side effects of chemo

A

Blood-Related Side Effects
Nausea and Vomiting
Hair Loss
Mouth and Sore Throat

148
Q

nadir

A

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
Q

life span of a neutrophil

A

7-12 hours

150
Q

life span of platelets

A

7-8 days

151
Q

life span of erythrocytes

A

90-120 days

152
Q

mild neutropenic absolute neutrophil count

A

1000-1500

153
Q

moderate neutropenic absolute neutrophil count

A

500-1000

154
Q

severe neutropenic absolute neutrophil count

A

0-500

155
Q

how to calculate Absolute Neutrophil Count (ANC)

A

ANC = Total WBC × (% Segmented Neutrophils + % Bands)

156
Q

Leading cause of morbidity in chemo patients

A

infection leading to sepsis leading to septic shock

157
Q

often the only sign of infection

A

fever above 100.4

158
Q

infection prevention

A

good hand hygiene!!!

159
Q

what meds can we give a chemo patient for infection prevention

A

colony-stimulating factors - Neupogen andNeulasta

160
Q

Thrombocytopenia

A

Nadir 8-14 days after chemotherapy

risk for bleeding

161
Q

Thrombocytopenia – Assessment

A 
Petechiae, bruising and hemorrhage
GI bleeding
Neurological signs of bleeding
Hypotension 
Tachycardia
162
Q

Thrombocytopenia - Management

A

risk for bleeding to no blowing nose, use of electric razor, decrease activity, maintain SBP less than 140, prevent constipation, avoid NSAIDs

163
Q

anemia clinical manifestations

A

fatigue, tachycardia, dizziness, cold intolerance

164
Q

mouth and sore throat medication

A

MBX - magic mouthwash, nystatin, Stanford mouthwash

165
Q

UC/Crohns concept

A

concept of inflammation that causes manifestations of fluid and electrolytes

166
Q

both UC and Crohn’s are characterized by

A

chronic inflammation of the intestine w/ periods of remission & exacerbation

167
Q

UC

A

inflammation beginning in the rectum and spreading up the COLON (only) in a continuous pattern

168
Q

what occurs in UC

A

Ulcerations destroy the mucosal epithelium, causing bleeding and diarrhea
Fluid and electrolyte losses
Protein loss
Pseudo polyps

169
Q

Clinical manifestations of UC

A 
Major:
Bloody diarrhea 
Abdominal pain
Other:
fever
Tenesmus
rectal bleeding 
Rare malabsorption/ nutritional problems
170
Q

Tenesmus

A

painful spasm of the anal sphincter along with an urgent desire to defecate without the significant production of feces

171
Q

crohns

A

Can affect any part of the GI tract from the lips to the anus
Most often seen in the terminal ileum and colon

172
Q

Hallmark sign of crohns

A

skip lesions: Segments of normal bowel occurring between diseased portions causing classic cobblestone appearance

173
Q

Crohns manifestation

A

Major: Diarrhea
Major: Abdominal cramping
Fever
Weight loss- severe if small intestine involved
Common Malabsorption/ nutritional problems-if small intestine involved

174
Q

fistulas are seen more in

A

crohns - leaks out all the way to skin

175
Q

strictures and UC/crohns

A

occasional in UC and common in chrons

176
Q

Perforation and UC/Crohns

A

UC - Common d/t toxic mega colon

Crohns- Common d/t bowel wall destruction

177
Q

surgery and UC/Crohns

A

UC - Usually cured with colectomy

Crohns - Common reoccurrence at site of anastomosis

178
Q

cancer and UC/Crohns

A

UC - Significantly ↑ incidence after 10 years

Crohns - ↑ incidence w/ small intestine & colon but not as much colon CA as w/ UC

179
Q

what other reactions can occur with crohns

A 
Systemic Complications Triggered by circulating products of inflammation. Can cause: 
Arthritis
Eye inflammation 
Skin lesions
Liver failure
180
Q

management for UC/Crohns

A

drug therapy, surgery, nutrition

181
Q

nutrition with UC/Crohns

A 
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
Q

drugs for UC/Crohns

A

Aminosalicylates, Antimicrobials, Corticosteroids, Immunosuppressants, Biologic therapy, Antidepressants

183
Q

Aminosalicylates:

A

Sulfasalazine (Azulfidine)

184
Q

Antimicrobials

A

Flagyl, Cipro, Biaxin (more effective w/ Crohn’s)

185
Q

Corticosteroids:

A

Prednisone help to attain remission

186
Q

Immunosuppressants:

A

taken 3-6 mo (more effective for Crohn’s)

187
Q

Biologic therapy:

A

Remicade, given IV, to induce and maintain remission

Humira – monoclonal antibody blocks TNF-alpha

188
Q

IBD nursing diagnoses

A

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
Q

Solid organs

A

liver, spleen, kidneys and pancreas; bleed profusely

190
Q

Hollow organs

A

stomach, intestines, bladder, gallbladder; peritonitis/sepsis leakage after injury

191
Q

regions of the abdomen

A

Peritoneal
Retroperitoneal
Pelvis

192
Q

Two categories of trauma

A

blunt and penetrating

193
Q

________ are a frequent cause of trauma deaths

A

missed ABD injuries

194
Q

blunt trauma is associated with:

A

increase fatalities

195
Q

Blunt Abdominal Trauma

A

Leading cause of morbidity and mortality among all age trauma victims
Injury secondary to compressive, shearing, crushing, and deceleration forces

196
Q

most common cause of blunt abdominal trauma

A

MVCs

197
Q

Blunt Abdominal Trauma causes

A

serious damage to solid organs

198
Q

hollow organs can collapse

A

and absorb force

199
Q

why would you suspect visceral damage

A

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
Q

Cullen’s Sign

A

bruising around the umbilicus - Intra-peritoneal hemorrhage

201
Q

Grey Turner’s sign

A

flanks- Retro-peritoneal hemorrhage

202
Q

what type of organs are more prone to injury in Penetrating Abdominal Trauma

A

hollow organs - can lead to sepsis and infection

203
Q

what do you not want to do to during penetrating abdominal trauma?

A

do not remove the weapon! - the weapon may be holding the pt from bleeding

204
Q

Nursing Management ABD Trauma

A

indwelling urinary cath, oxygen, NG, 2 large bore IVs

205
Q

diagnostics for ABD trauma

A

Focused Abd Sonogram for Trauma (FAST) US or CT (sometimes both)
Surgery: Exploratory laparotomy
Unstable penetrating trauma, OR regardless of what FAST shows

206
Q

what is used with ABD trauma in rural areas when CT is not available

A

Diagnostic Peritoneal Lavage DPL - old technique

207
Q

Intra-abdominal pressure (IAP) in a normal adult

A

0-5

208
Q

Intra-abdominal Hypertension (IAH)

A

elevation in IAP ≥ 12 mmHg

209
Q

Causes of IAH

A

Surgical:
ruptured AAA, blunt/penetrating trauma, post op bleed
Medical:
pancreatitis, ileus, sepsis, burns, infection, fluid resuscitation
Recurrent: comes back

210
Q

Abdominal Compartment Syndrome

A

Defined as sustained IAP > 20 mmHg with new organ dysfunction or failure
Painful condition occurring when pressure within the abdomen builds to dangerous levels

211
Q

what happens during abdominal compartment syndrome

A

Pressure ↓ the blood flow, prevents nourishment and O2 from reaching nerves, cells and organs

212
Q

patients at risk for abdominal compartment syndrome

A

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

213
Q

What does ACS mean for your patient?

A 
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!!!

214
Q

Intra-abdominal Pressure indirect Monitoring

A
  • Urinary bladder pressure monitoring
  • NG tubes
  • Rectal tubes
215
Q

Gold standard for indirect intermittent pressures

A

Urinary bladder pressure monitoring

Utilizes a foley catheter for monitoring

216
Q

Nursing Interventions for Abdominal compartment syndrome

A

evacuate intraluminal contents (NG tube to suction), Monitor for daily BM/prevent constipation, Optimize fluid resuscitation, Optimize systemic and regional perfusion

217
Q

Acute Pancreatitis

A

An inflammatory disorder of the pancreas characterized by severe upper abdominal pain and increased serum concentration of pancreatic enzymes

218
Q

Most common prognostic systems Acute Pancreatitis

A

Ranson’s Criteria

219
Q

Ranson Criteria

A 
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
Q

Acute pancreatitis causes

A

Most Common (80% of cases):
Gallbladder Disease
Excessive ETOH

221
Q

clinical manifestations of Acute pancreatitis

A 
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
Q

labs for Acute pancreatitis

A 
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
Q

gold standard for diagnostics for acute pancreatitis

A

CT of abdomen
Gold standard for diagnosis, pancreatitis inflammation and necrosis
can also get ABD US, MRI, CXR

224
Q

pulmonary complications in acute pancreatitis

A

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
Q

complications seen from acute pancreatitis other than pulmonary

A 
Cardiovascular:
Hypotension and shock
Renal:
oliguria
Hematologic:
DIC
GI/Hepatic:
hepatic dysfunction 
bowel infarction
226
Q

Collaborative Management for Acute Pancreatitis

A

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
Q

Chronic Pancreatitis

A

Main features are abdominal pain, malabsorption, weight loss and diabetes

228
Q

Classic triad of chronic pancreatitis

A

calcification, steatorrhea, and diabetes

history of heavy ETOH use

229
Q

gold standard for dx for chronic pancreatitis

A

Surgical biopsy of pancreas

230
Q

Labs for chronic pancreatitis

A 
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
Q

causes of upper GI bleeds

A

55% peptic ulcer disease

others can be from Stomach cancer; Erosive gastritis…

232
Q

Variceal bleeding

A

Most often associated with ETOH use; large veins under increased pressure; rupture/hemorrhage

233
Q

What do I see during a GI bleed

A 
Severe ABD pain
Metabolic acidosis
Lactic acidosis
Anoxia
Hematemesis (Upper)
Hematochezia (lower)
Melena (Upper)
234
Q

Collaborative Care for GI bleed

A 
Correct the labs:
Hbg/hct (1/3 ratio), platelets
CMP: BUN/CR, LFTs, Electrolytes
Coags 
ABG (metabolic acidosis)
235
Q

Anticipate medications for GI bleed

A 
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
Q

acute liver failure causes

A 
Drugs are #1 cause
#1: Tylenol (acetaminophen), NSAIDs (all types), INH, mushrooms
#2: Hepatitis B &amp; C
237
Q

outcomes for acute liver failure

A

75 - 90% DIE!; 10-25% “SURVIVE”…W/ INTENSIVE CARE!

NEED A LIVER

238
Q

Collaborative CareAcute Liver Failure

A

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
Q

cirrhosis cause

A

alcohol - number 1 cause

240
Q

Liver DiseaseMnemonic: ABCDEFGHIJ

A

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
Q

TIPS

A

Trans jugular intrahepatic porto systemic shunt

Manage complications of portal HTN

242
Q

Bariatric Surgery

A 
to qualify: BMI>40 or >35 with comorbidities
5+ years
Understand risks/benefits
Tried and failed at weight loss
No serious endocrine disorders
243
Q

Restrictive bariatric Surgeries

A

gastric banding - ↓ stomach to 30 mL, feeling fuller faster

244
Q

malabsorption bariatric surgeries

A

Various lengths of the small intestine bypassed ↓ absorption of nutrients
Less food is absorbed – DOES alter digestion

245
Q

Roux-en-Y Gastric bypass

A 
Stomach size is ↓ w/ gastric pouch 
Most common bariatric procedure in US
Considered gold standard
Low complication rates
Excellent patient tolerance
246
Q

what can occur with Roux-en-Y Gastric bypass

A

DM II

247
Q

Preoperative Concerns with bariatric surgeries

A

Liquid Diet for up to 6 wks preop

Detailed health hx, address comorbidities; interdisciplinary team approach required

248
Q

post op complications in bariatric surgeries

A

Dehiscence or leaking
- First sign is tachycardia
Anemia: malabsorption of Iron and Vit B
Increased risk of Infection

249
Q

Long term bariatric surgery complications:

A

bowel obstruction, dumping syndrome, n/v/d, gallstones, hernias, hypoglycemia, malnutrition, stomach perforation, ulcers, death (rare)

250
Q

Post-operative bariatric Concerns

A

Assessment & intervention for complications
- Anastomosis leaks
- Thrombus formation
Airway management!!

251
Q

Nutritional Goals: after bariatric surgery

A 
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

Nursing school level 4 (6 decks)

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