Final Flashcards

(96 cards)

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
Tumors or Trauma that causes D.I is considered what type of cause?
secondary, Neurogenic/Central DI
25
What might be an indicator of Neurogenic/Central DI?
Rapid LOC and pt covered in urine
26
What is the patho of nephrogenic DI?
it has a slower progression | The hypothalamus is producing ADH but the kidneys can't respond
27
What is the result of DI?
free water is excreted in the urine causing extracellular dehydr. hypernatremia decreased cerebral perfusion can present like hypovolemic shock
28
What are the blood levels occurring with DI?
hypersolute/high osmolality > 295 really high serum sodium.... >145
29
What are the urine levels with DI
hyposolute/dilute/low osmolality < 300
30
A pt p/w serum osmolality of 341, serum sodium of 160, and urine osmolality of 262. Which endocrine issue might you expect?
DI
31
What is Desmopressin and what is it used for?
it is a synthetic form of vasopressin used for DI There are NO vasoconstrictive properties Intranasal is most effective
32
What is the sx of choice for DI?
Transphenoidalhypophysectomy watch for increase ICP and glucose drainage!
33
What is an imp piece of pt edu with a transphenoidalphypophysectomy?
They'll need hormone therapy for life
34
What is phenochromocytoma
tumor of the adrenal medulla r/t the anterior pituitary gland
35
What is the patho of phenochromocytoma
it produces an increased secretion of catacholamines | ie. epi, norepi, and dopa
36
how does phenochromocytoma manifest
with fight or flight response (SNS)
37
What are clin mans of phenochromocytoma
``` classic triad: tachycardia severe HA diaphoresis also HTN & chest pain ```
38
What are possible complications of phenochromocytoma
severe hypertensive encephalopathy DM Cardiomyopathy Death
39
What is the gold standard test for phenochromocytoma
24hr urine to measure catacholamines + methanephrine
40
What is the sx of choice for pheochromocytoma
adrenalectomy
41
What is a critical consideration prior to an adrenalectomy
Goal BP is < 160/90
42
What are possible meds for mgmt of pheochromocytoma
Alpha blockers(metyrosine) - dec HTN BB - inderal Nipride
43
Considerations for Post Op adrenalectomy
really labile BP - treat HTN conservatively fluids/blood postural HTN - avoid rapid changes elevate LE when sitting
44
imp pt edu post adrenalectomy
life long steroids if it was B/L
45
General info about pancreas
digestive & hormonal functions | endocrine & exocrine glands!
46
What is the application of the word fulminant
incredibly rapid onset | associated w high mortality rate (10-15%)
47
Common causes of pancreatitis
alcohol & Biliary disease (gallstones) make up 80% of cases
48
Patho of pancreatitis
injury to asinar cells leads to inc infection and inc ischemia in pancreas causing leakage of enzymes into tissue
49
Which enzyme is activated first in pancreatitis
Trypsin, which triggers the secretion of other enzymes
50
Which enzyme is the most dangerous in pancreatitis
Elastase - it destroys the cells responsible for clotting
51
what is autodigestion in relation to pancreatitis
breakdown of the pancreas d/t the release of enzymes
52
How does pancreatitis initially manifest
as localized pancreatic inflammation!
53
what is the acronym CARS
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
What are the systemic comps of pancreatitis
``` 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
What are localized comps of pancreatitis
``` incredibly severe pain N/V Abd distension guarding fever ```
56
What is the definitive test for pancreatitis
elevated serum lipase
57
What are other associated test results for pancreatitis other than elevated lipase
``` elevated CONJUGATED bilirubin hypocalcemia elevated amylase hyperglycemia toward the end dec albumin & protein ```
58
What might you find during a physical assessment of a pt w pancreatitis
Grey Turner's Sign - side/flank ecchymosis Cullen's Sign - Ecchymosis @ the umbilicus
59
What are the 2 most imp imaging studies for pancreatitis & what's the difference
CECT is the gold standard | ERCP is used if A.P r/t gallstones so they can be removed during imaging study
60
What is the ranson criteria
a predictability test to assess for increased chance of morbidity/mortality for pts dx'd w acute pancreatitis
61
What are the stipulations for the ranson criteria
less than 3 = 1% mortality | more htan 7 = almost 100% mortality
62
Hypocalcemia assessment findings
prolonged QT interval tetany + chvostek's sign - muscle twitching in face + Trousseau's - tetany in arm r/t BP cuff inflation
63
Hypokalemia assessment
dysrhythmias - inc r/f PVCs muscle weakness hypotension decreased bowel sounds - ileus
64
What electrolyte imbalance would produce really peaked T waves?
hyperkalemia
65
What fluid replacement would be utilized for pancreatitis
isotonic crystalloids - NO Lactated Ringers if liver enzymes are elevated
66
What is the suggested nutritional support for someone w pancreatitis
early enteral feeds once they're not vomiting
67
What is imp pain mgmt for pancreatitis
PCA or REGULARLY scheduled pain meds NOT just PRN
68
Pharm mgmt for pancreatitis
prevent ulcers w histamine blockers/antacids | antibiotics
69
What is the most common cause of hepatic failure
50% d/t meds | 42% d/t tylenol alone
70
What is the patho of hepatic failure
pts usually healthy before sudden onset of acute liver failure FHF occurs over 1-3weeks Hepatic encephalopathy within 8weeks
71
What is the first sign of hepatic failure
jaundice or decreased MS
72
What are results of Kupfer cell destruction in hepatic failure
``` 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
What is a critical assessment/dx finding of hepatic failure
increased serum ammonia!!!!!! | causes change in MS
74
What are other assessment findings of hepatic failure
resp alk or met acidosis inc WBC only thing dec is platelets and albumin
75
What is the characteristic of urine in a pt p/w hepatic failure
orange, dark, incredibly concentrated
76
Clin Mans of hepatic failure
``` HA & personality changes hyperventilation (early) jaundice palmar erythema spider nevi bruises asterixis/liver flaps ```
77
Pharm mgmt of hepatic failure
neomycin lactulose vitamin k & FFP/platelets to treat bleeds
78
How does lactulose assist with hepatic failure
creates acidic enviro which traps ammonia, and then the laxative effect excretes it
79
What multi-system effects does hepatic failure create
brain - cerebral edema lungs - resp failure CV - hemodynamic instability
80
What is the preferred tx for hepatic failure
ONLY tx is transplant
81
What is the role of the OPO?
in charge of donations bereavement care to families DETERMINES MEDICAL SUITABILITY FOR DONATION!
82
clinical determinants for brain death
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
What is the definition of brain death?
complete irreversible cessation of brain functioning
84
What is the criteria for live organ donation from non relative. aka benevolent donor
good overall health, no DM or CA, no heart or kidney disease | compatible blood type!
85
What is the criteria for brain dead donor
complete irreversible cessation of brain function
86
Organ donation after circulatory death (DCD)
complete irreversible cessation of heartbeats and respirations no recovery from illness suspected dependent on life sustaining measures
87
Who determines medical suitability for organ donation?
the OPO NOT the physician or hospital
88
What is the Major Histocompatability Complex
molecules on cell surface responsible for lymphocyte and antigen recognition. determination of self vs non-self initiates transplant rejection
89
Nursing Mgmt goals for organ transplant pt
oxygenate organs maintain hemodynamic stability maintain fluid & electrolyte balance maintain temp regulation
90
Describe hyperacute transplant rejection
antibody acute rejection. not seen much anymore because we test for antibodies
91
Describe acute transplant rejection
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
Describe chronic transplant rejection
both cell mediated and antibody (humeral) mediated. always results in complete destruction of organ! will eventually need another transplant
93
what is the purpose of induction therapy
to create a tolerance for the transplant graft
94
what is the goal of immunosuppressant therapy
to suppress the activity of helper T cells
95
What do you monitor for rejection surveillance
elevated liver function tests, especially ASTs & ALTs decreased bile output fever