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Critical Care Mgmt > Final > Flashcards

Final Flashcards

0
Q

What is the primary function of ADH

A

to regulate fluid balance by regulating serum osmolality

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1
Q

Where does ADH come from?

A

Posterior pituitary

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2
Q

What happens to a pts serum osmolality if they become dehydrated?

A

It increases, above 300. Blood becomes thick/sludgey

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3
Q

What is a normal serum osmolality

A

275-295

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4
Q

What takes place when ADH is released?

A

water is reabsorbed into the renal tubules and urine becomes concentrated

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5
Q

What are three reasons ADH would be released in a normal person?

A

increased plasma osmolality
decreased fluid osmolality
hypotension

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6
Q

What are three reasons ADH would be INHIBITED?

A

decreased plasma osmolality
increased fluid volume
alcohol

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7
Q

What is the general idea of SIADH

A

overproduction of ADH - “cell swell”

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8
Q

A pt is admitted and the report you get includes a h/o malignant bronchogenic oat cell carcinoma. Which ADH impairment do you expect the pt to exhibit?

A

SIADH

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9
Q

What are causes of SIADH

A

severe head trauma, CNS tumors
meds (nicotine, tricyclic antidepressants, tegratol)
extended time on PEEP
oat cell carcinoma

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10
Q

What is the patho behind SIADH

A

the posterior pituitary releases ADH in spite of normal serum osmolality causing overhydration and low serum osmolality

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11
Q

What happens to serum osmolality & sodium with excessive ADH as in SIADH

A

they are both low.

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12
Q

What are some s/s of hyponatremia and when might you see them?

A

confusion, seizure, coma, death

SIADH as a result of overhydration

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13
Q

What findings do you expect to see from urine testing in a pt w SIADH

A

high osmolality, sodium, and specific gravity (> 1.030)

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14
Q

What are some clinical manifestations of SIADH

A

lethargy, anorexia, confusion, personality changes
really bad abdominal cramps
[seizure, coma, death from hyponatremia]
weight gain, N/V, decreased urine output

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15
Q

What finding would prompt you to advocate for your pt and request seizure precautions be initiated?

A

serum sodium levels less than 110

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16
Q

A 40y.o male pt p/w wt gain and confusion. The family reports that the he just isn’t acting like himself and can’t recall the last time he urinated. What do you suspect is going on?

A

SIADH

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17
Q

A student nurse is getting ready to hang normal saline for an SIADH pt at 100mL/hr for fluid resuscitation. What should the nurse do?

A

Stop the student nurse. pts w SIADH are to be on fluid RESTRICTION of 800-1000mL/day.

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18
Q

What replacement should the nurse anticipate for an SIADH pt and what does that entail?

A 
Sodium replacement w hypertonic solution (3%NSS)
2 RN signature admin
very slow infusion
freq v/s & BMP
q1hr neuro checks
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19
Q

What medication would the nurse anticipate administering for a pt p/w extreme lethargy, USG of 1.042, and a serum osmolality of 268

A

pt has SIADH

nurse would administer demeclocycline to increase renal water excretion

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20
Q

What would a pt p/w if they were experiencing overhydration as in SIADH?

A

Tachycardia
increased weight gain
crackles in lungs
not always Edemetous, swelling is intravascular

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21
Q

What should you do if you have a pt w SIADH who is AAO?

A

have them drink milk, tomato juice, or beef/chicken broth

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22
Q

A deficiency of production, excretion, or function of ADH is what condition?

A

Diabetes Insipidus

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23
Q

A pt c/o urinating non stop. After observation the nurse documents copious amounts of dull, tasteless urine. What is the pt experiencing?

A

Diabetes Inspidus

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24
Q

Tumors or Trauma that causes D.I is considered what type of cause?

A

secondary, Neurogenic/Central DI

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25
Q

What might be an indicator of Neurogenic/Central DI?

A

Rapid LOC and pt covered in urine

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26
Q

What is the patho of nephrogenic DI?

A

it has a slower progression

The hypothalamus is producing ADH but the kidneys can’t respond

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27
Q

What is the result of DI?

A

free water is excreted in the urine causing extracellular dehydr.
hypernatremia
decreased cerebral perfusion
can present like hypovolemic shock

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28
Q

What are the blood levels occurring with DI?

A

hypersolute/high osmolality

> 295

really high serum sodium…. >145

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29
Q

What are the urine levels with DI

A

hyposolute/dilute/low osmolality

< 300

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30
Q

A pt p/w serum osmolality of 341, serum sodium of 160, and urine osmolality of 262. Which endocrine issue might you expect?

A

DI

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31
Q

What is Desmopressin and what is it used for?

A

it is a synthetic form of vasopressin used for DI
There are NO vasoconstrictive properties
Intranasal is most effective

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32
Q

What is the sx of choice for DI?

A

Transphenoidalhypophysectomy

watch for increase ICP and glucose drainage!

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33
Q

What is an imp piece of pt edu with a transphenoidalphypophysectomy?

A

They’ll need hormone therapy for life

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34
Q

What is phenochromocytoma

A

tumor of the adrenal medulla r/t the anterior pituitary gland

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35
Q

What is the patho of phenochromocytoma

A

it produces an increased secretion of catacholamines

ie. epi, norepi, and dopa

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36
Q

how does phenochromocytoma manifest

A

with fight or flight response (SNS)

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37
Q

What are clin mans of phenochromocytoma

A 
classic triad:
tachycardia
severe HA
diaphoresis
also HTN & chest pain
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38
Q

What are possible complications of phenochromocytoma

A

severe hypertensive encephalopathy
DM
Cardiomyopathy
Death

39
Q

What is the gold standard test for phenochromocytoma

A

24hr urine to measure catacholamines + methanephrine

40
Q

What is the sx of choice for pheochromocytoma

A

adrenalectomy

41
Q

What is a critical consideration prior to an adrenalectomy

A

Goal BP is < 160/90

42
Q

What are possible meds for mgmt of pheochromocytoma

A

Alpha blockers(metyrosine) - dec HTN
BB - inderal
Nipride

43
Q

Considerations for Post Op adrenalectomy

A

really labile BP - treat HTN conservatively
fluids/blood
postural HTN - avoid rapid changes
elevate LE when sitting

44
Q

imp pt edu post adrenalectomy

A

life long steroids if it was B/L

45
Q

General info about pancreas

A

digestive & hormonal functions

endocrine & exocrine glands!

46
Q

What is the application of the word fulminant

A

incredibly rapid onset

associated w high mortality rate (10-15%)

47
Q

Common causes of pancreatitis

A

alcohol & Biliary disease (gallstones) make up 80% of cases

48
Q

Patho of pancreatitis

A

injury to asinar cells leads to inc infection and inc ischemia in pancreas causing leakage of enzymes into tissue

49
Q

Which enzyme is activated first in pancreatitis

A

Trypsin, which triggers the secretion of other enzymes

50
Q

Which enzyme is the most dangerous in pancreatitis

A

Elastase - it destroys the cells responsible for clotting

51
Q

what is autodigestion in relation to pancreatitis

A

breakdown of the pancreas d/t the release of enzymes

52
Q

How does pancreatitis initially manifest

A

as localized pancreatic inflammation!

53
Q

what is the acronym CARS

A

Compensatory anti-inflam response syndrome
Body’s attempt to pull back inflam to prevent it from becoming systemic
inc r/f infection, SIRS, MODS, etc

54
Q

What are the systemic comps of pancreatitis

A 
hypoxemia ( >60 on ABG)
hypovolemic shock 
- distributive d/t systemic inflam
-h.v d/t vomiting and/or GI bleed
increased intraabd pressure
pancreatic abscess
oliguria
dysrhythmias
55
Q

What are localized comps of pancreatitis

A 
incredibly severe pain
N/V
Abd distension
guarding
fever
56
Q

What is the definitive test for pancreatitis

A

elevated serum lipase

57
Q

What are other associated test results for pancreatitis other than elevated lipase

A 
elevated CONJUGATED bilirubin
hypocalcemia
elevated amylase
hyperglycemia toward the end
dec albumin & protein
58
Q

What might you find during a physical assessment of a pt w pancreatitis

A

Grey Turner’s Sign
- side/flank ecchymosis
Cullen’s Sign
- Ecchymosis @ the umbilicus

59
Q

What are the 2 most imp imaging studies for pancreatitis & what’s the difference

A

CECT is the gold standard

ERCP is used if A.P r/t gallstones so they can be removed during imaging study

60
Q

What is the ranson criteria

A

a predictability test to assess for increased chance of morbidity/mortality for pts dx’d w acute pancreatitis

61
Q

What are the stipulations for the ranson criteria

A

less than 3 = 1% mortality

more htan 7 = almost 100% mortality

62
Q

Hypocalcemia assessment findings

A

prolonged QT interval
tetany
+ chvostek’s sign - muscle twitching in face
+ Trousseau’s - tetany in arm r/t BP cuff inflation

63
Q

Hypokalemia assessment

A

dysrhythmias - inc r/f PVCs
muscle weakness
hypotension
decreased bowel sounds - ileus

64
Q

What electrolyte imbalance would produce really peaked T waves?

A

hyperkalemia

65
Q

What fluid replacement would be utilized for pancreatitis

A

isotonic crystalloids - NO Lactated Ringers if liver enzymes are elevated

66
Q

What is the suggested nutritional support for someone w pancreatitis

A

early enteral feeds once they’re not vomiting

67
Q

What is imp pain mgmt for pancreatitis

A

PCA or REGULARLY scheduled pain meds NOT just PRN

68
Q

Pharm mgmt for pancreatitis

A

prevent ulcers w histamine blockers/antacids

antibiotics

69
Q

What is the most common cause of hepatic failure

A

50% d/t meds

42% d/t tylenol alone

70
Q

What is the patho of hepatic failure

A

pts usually healthy before sudden onset of acute liver failure
FHF occurs over 1-3weeks
Hepatic encephalopathy within 8weeks

71
Q

What is the first sign of hepatic failure

A

jaundice or decreased MS

72
Q

What are results of Kupfer cell destruction in hepatic failure

A 
imp bilirubin conjugation = inc UNCONJUGATED bilirubin
Dec clotting factor production 
- inc INR ( >1.5)
- inc PT ( >14 can be up to 100)
hypoglycemia
metabolic acidosis & inc serum lactate
73
Q

What is a critical assessment/dx finding of hepatic failure

A

increased serum ammonia!!!!!!

causes change in MS

74
Q

What are other assessment findings of hepatic failure

A

resp alk or met acidosis
inc WBC
only thing dec is platelets and albumin

75
Q

What is the characteristic of urine in a pt p/w hepatic failure

A

orange, dark, incredibly concentrated

76
Q

Clin Mans of hepatic failure

A 
HA & personality changes
hyperventilation (early)
jaundice
palmar erythema
spider nevi bruises
asterixis/liver flaps
77
Q

Pharm mgmt of hepatic failure

A

neomycin
lactulose
vitamin k & FFP/platelets to treat bleeds

78
Q

How does lactulose assist with hepatic failure

A

creates acidic enviro which traps ammonia, and then the laxative effect excretes it

79
Q

What multi-system effects does hepatic failure create

A

brain - cerebral edema
lungs - resp failure
CV - hemodynamic instability

80
Q

What is the preferred tx for hepatic failure

A

ONLY tx is transplant

81
Q

What is the role of the OPO?

A

in charge of donations
bereavement care to families
DETERMINES MEDICAL SUITABILITY FOR DONATION!

82
Q

clinical determinants for brain death

A

2 physicians w separate assessments w SAME results
Apnea testing - NO respirations & ABG PaCO2 >60
Pupils non responsive, dolls eyes
EEG
Absence of gag reflex
GCS >3

83
Q

What is the definition of brain death?

A

complete irreversible cessation of brain functioning

84
Q

What is the criteria for live organ donation from non relative. aka benevolent donor

A

good overall health, no DM or CA, no heart or kidney disease

compatible blood type!

85
Q

What is the criteria for brain dead donor

A

complete irreversible cessation of brain function

86
Q

Organ donation after circulatory death (DCD)

A

complete irreversible cessation of heartbeats and respirations
no recovery from illness suspected
dependent on life sustaining measures

87
Q

Who determines medical suitability for organ donation?

A

the OPO NOT the physician or hospital

88
Q

What is the Major Histocompatability Complex

A

molecules on cell surface responsible for lymphocyte and antigen recognition.
determination of self vs non-self
initiates transplant rejection

89
Q

Nursing Mgmt goals for organ transplant pt

A

oxygenate organs
maintain hemodynamic stability
maintain fluid & electrolyte balance
maintain temp regulation

90
Q

Describe hyperacute transplant rejection

A

antibody acute rejection. not seen much anymore because we test for antibodies

91
Q

Describe acute transplant rejection

A

most common. weeks to months after transplant. Body needs time for the upregulation (helper t cells recognize there’s a foreign body takes time to build up troops.)
Everyone experiences some degree of this. effects reduces w immunosuppressant meds

92
Q

Describe chronic transplant rejection

A

both cell mediated and antibody (humeral) mediated.
always results in complete destruction of organ!
will eventually need another transplant

93
Q

what is the purpose of induction therapy

A

to create a tolerance for the transplant graft

94
Q

what is the goal of immunosuppressant therapy

A

to suppress the activity of helper T cells

95
Q

What do you monitor for rejection surveillance

A

elevated liver function tests, especially ASTs & ALTs
decreased bile output
fever

Critical Care Mgmt (2 decks)

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