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NUR 213 > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

7 major metabolic functions of the liver?

A

-Carbohydrate metabolism
-Fat metabolism
-Protein metabolism
-Steroid metbolism
-Detoxification/Filters
-Bile synthesis
-Storage
~Glucose/Vitamins A,D,E, K

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2
Q

_________ conversion of glucose into glycogen.

A

Glycogenesis

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3
Q

–Hepatitis A–
Transmission?
S&S?
At Risk?

A

t: contaminated water, food, fecal oral route, food contamination

s&s: mild, “flu” like sx, if are advanced in age or have chronic dx then s/s increase in severity, no jaundice (aniteric), acute onset

R: children, 3rd world countries, healthcare personnel, institutional settings

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4
Q

–Hepatitis B–
Transmission?
S&S?
At Risk?

A

t: occurs when infected blood or other body fluid enter body of person not immune to virus

s&s: jaundiced, insidious onset, sx may be more severe, or may be asymptomatic, can lead to chronic viral infection

r: young children & all age groups, institutional settings, healthcare personnel, adults that share things

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5
Q

What Labs will be elevated with Hep-B?

A

-ALT: indicates Liver damage
~Norm:8-20
-AST: Norm: 5-40
-ALP: Norm: 42-128

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6
Q

Hep-B has a complex

________ with 3________.

A

-Structure
-antigens
~Surface HBsAG
~Core HBsAG
~E antigen HBeAG

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7
Q

–Hepatitis C–
Transmission?
S&S?
At Risk?

A

t: percutaneously, blood to blood, illicit IV drug sharing, blood products & organ transplants prior to 1992

s&s: leads to chronic liver disease/cirrhosis, most are asymptomatic

r: HIV pts, hemophiliacs, sharing needles, body piercings, tattoos, perinatal transmission, healthcare workers

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8
Q

Which Phase of hepatitis is marked by:

a. Absence of jaundice
b. Lasts 5-7 days
c. N/V, malaise
d. Anorexia, fatigue
e. RUQ pain
f. Irritable
g. Requires rest

A

-Acute-Anicteric Phase

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9
Q

Which phase of hepatitis is marked by:

a. Jaundice present
b. Dark urine, clay stools
c. As jaundice worsens, child feels better
d. Lasts 4 weeks
e. Labs return to normal may take 1-3mos

A

-Acute- Icteric Phase

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10
Q

Icteric:__________

A

Jaundiced

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11
Q

What antieimetic can you give to a hepatitis pt?

A

Non hepatotoxic drugs like Dramaine

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12
Q

Nutrition for Acute Viral Hepatitis?

A
  1. Protein: maintain protein stores & prevent muscle wasting
  2. High CHO: ensure calorie intake & prevent protein depletion
  3. Low fat: Lessesns stomach distention
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13
Q

Drug therapy for Hep-C?

A
  1. Interferon
  2. Ribavirin: w/interferon
    ~SE: anemia, watch CBC. Flu like sx, itching, diarrhea, wt loss, anorexia, cough, insomnia, pruritus, rash, HA, fatigue
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14
Q

4 Types of Cirrhosis?

A
  1. Biliary Cirrhosis: gallbladder backs up & causes obstructions, diffuse fibrosis of the liver w/jaundice
  2. Cardiac Cirrhosis: heart failure & fluid buildup, portal HTN, from long standing R sided HF
  3. Postnecrotic Cirrhosis: caused by Hep C (10-20%), Hep B (10%), certain drugs & chemicals
  4. Laennec’s Cirrhosis: Alcohol induced
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15
Q

Esophageal and Gastric _______ are possible complications of what?

A
  • Varices

- Cirrhosis

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16
Q

With Esophageal and Gastric varices, why doesn’t the bleeding stop??

A

Production of bile is decreased which prevents absorption of fat soluble vitamins (specifically Vit. K), without K pt. lacks clotting factors

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17
Q

_______________: disorder of protein metabolism & excretion, liver can’t covert ammonia to urea, ammonia cross blood-brain barrier & cause neurologic toxic manifestations

A

-Hepatic encephalopathy

a. Affects function of the brain
b. Elevated ammonia levels
c. Flapping hands (asterixis), fector hepaticus (breath is odd, can’t break down all the food for digestion, glucose, etc)

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18
Q

4 Stages of Encephalopathy?

A

a. Prodromal: early stg, able to talk, possible agitation, subtle personality changes
b. Impending: disoriented x3, climbing out of bed, etc
c. Stuporous: drowsy, but able to arouse
d. Comatose: only respond to painful stimuli

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19
Q

Treatment of Encephalopathy:?

A

PO or enema lactulose, decreases protein b/c ammonia is formed when protein is broken down by intestinal flora

20
Q

Hepatorenal syndrome: ?

A
  1. When the volume or pressure of blood flow through the kidney drops, filtering of blood also drops or may not occur at all. Waste products stay in the blood & little or no urine is formed, even though kidney is working.
21
Q

4 CIWA stages?

Treatment?

A
  1. Minor withdrawal: 6-36 hrs
  2. Seizures: 6-48 hrs
  3. ETOH Hallucinations: 12-48 hrs
  4. Delirium Tremors (DTs): 48-96 hrs

Treat w/ Ativan, valium, Librium, thiamine, folic acid

22
Q

________: a disorder in which there are multiple defects in the coagulation cascade that causes inappropriate clotting within the vascular system throughout the body.

A

Disseminated Intravascular Coagulation (DIC)

In forming many clots, it depletes or consumes various factors needed for clot formation, eventually leading to bleeding & excessive clot formation

23
Q

What are the 3 most common cause of DIC?

A
  • Sepsis (Gram Neg)
  • Shock
  • Liver disease
24
Q

S&S of DIC depends on what 4 components?

A

i. Procoagulant Activation: recognition that clots are being formed at increased rate
ii. Fibrinolytic activation: evidence of increase rate of clot dissolution
iii. Consumption of inhibitory factors: evidence that coagulation cascade is overpowering the inhibitory factors
iv. End organ damage or failure: evidence that the coagulation problem is causing problem with organ system(s)

25
Q

Shock could also be called what???

A

Hypoperfusion

26
Q

_______ ________ occurs when either systolic or diastolic dysfunction of pumping action of the heart results in reduced CO

A

Cardiogenic shock

27
Q

Causes of Cardiogenic shock?

Early S&S?

A
  • MI 40% muscle mass loss often d/t MI, structural problems, dysrhythmias, primary ventricular ischemia
  • tachycardia, hypotension, anxiety, confusion, agitation, tachypnea, pulmonary congestion, pallor, cool/clammy skin, decreased cap refill time, Increased PAWP, decreased renal perfusion& UO
28
Q

Clinical S&S of hypovolemic shock?

A

anxiety, tachypnea, increase in CO, increase in HR, decrease stroke vol, decrease PAWP, decrease UO

29
Q

What is the 3:1 rule in treating hypovolemic shock??

A

3ml of isotonic crystalloid (LR or NS) for every 1ml of estimated blood/fluid loss

30
Q

In this type of shock the SNS vessels lose tone, the vessels completely relax & vasodilate everywhere causing BP, HR, CO to DROP. PNS kicks in and shuts down GI track, digestion, HR drops

A

-Neurogenic Shockc.

NO OTHER TYPE OF SHOCK HAS A LOW HEART RATE

31
Q

Clinical S&S of Neurogenic shock?

A

hypotension, BRADYCARDIA*, temperature dysregulation (cold/hot skin sensations do not reach hypothalamus), poikilothermia (pt. takes on the temp of the environment)

32
Q

Drugs for Neurogenic Shock?

A
  • atropine: to treat Bradycardia
  • solumedrol: used in spinal cord injuries to prevent secondary spinal cord damage caused by release of chemical mediators
33
Q

______ ________: acute, life-threatening hypersensitivity reaction. The body’s normal reaction to allergens have OVER REACTED

A

Anaphylactic Shock

34
Q

Clinical S&S of anaphylactic shock?

A

swelling of lips, tongue, angioedema (ACE inhibitors can also cause this), laryngeal/bronchial edema, wheezing, stridor (high pitch), flushing, pruritis, urticaria (hives), respiratory distress & circulatory failure, anxiety, confusion, dizziness, sense of impending doom, chest pain, incontinence, GI cramping, decreased LOC, SOB, metallic taste

35
Q

Treatment of anaphylactic shock?

A

a. Epinephrine, Benadryl
b. Maintain patent airways: nebulized bronchodilators, ET tube (can be difficult d/t edema) or cricothyroidtomy
c. Aggressive fluid replacement: to get pressure up
d. IV corticosteroids: if significant hypotension persists 1-2 hrs after aggressive therapy

36
Q

______ ______: presence of sepsis w/hypotension despite fluid resuscitation + Presence of tissue perfusion abnormalities. A systemic inflammatory response to document or suspected infection

A

-Septic Shock

Patho: endotoxin stimulates inflammatory response promoting vasodilation

 a. Vasodilation
 b. Maldistribution of blood flow
 c. Myocardial depression
37
Q

Clinical Manifestations of septic shock?

A

decreased EF, hyperventilation (resp alk → resp acidosis), hypoxemia, ARDS, resp failure, crackles, decreased UO, warm/flushed → cool/mottled (late s/s), alteration in LOC, agitation, GI bleeding, paralytic ileus.

38
Q

Name this stage of shock Progression???

  • Not usually clinically apparent – must know if your patient is at risk
  • MAY SEE: change in LOC, RR changes (up), O2 sat decreases, may need O2
A

Initial
-Metabolism changes from aerobic to anaerobic, lactic acid builds up & must be removed by blood & broken down by liver, this requires unavailable O2

39
Q

Name this stage of shock Progression???

Drop in BP d/t decrease CO & narrowing pulse pressure, increase HR/contractility, V/Q mismatch, increase RR, restless, change LOC, decrease GI motility, decreased renal blood flow, holding onto Na+ & H2O, decrease bowel sounds, nausea, cool/clammy (unless pt is septic)

A

Compensatory
-Selective Vasoconstriction (absolute hypovolemia/low vol): d/t alpha-adrenergic stimulation
Release of angiotensin I & II: vasoconstriction of arteries & veins
Release of aldosterone & antidiuretic: Hold onto H2O & Na, which increase blood vol, increasing CO & BP

40
Q

Name this stage of shock Progression???

Anasarca (diffuse, profound edema), pts skin will leak fluid, this decreases perfusion even more, LUNGS will be first hit & last to recover (fluid moves into alveoli), worsening V/Q mismatch, tachypnea, crackles, increased work of breathing, edema, decreased surfactant, Hypotension, weak peripheral pulses, ischemia distal extremities, hypo/hyperthermia, decreased response to stimuli, decrease UO, GI bleeding, jaundice, r/f DIC

A

Progressive
-SNS stimulation-> alpha & beta adrengeric stim. Alpha stimulation causes WIDESPREAD VASOCONSTRICTION- especially to Capillaries, Renal, Lungs
Results: Metabolic acidosis

41
Q

Name this stage of shock Progression???

Unresponsive, loss of reflexes, pupils nonreactive, profound hypotension, decreased CO, initially tachycardia worsens then bradycardia, dysryhthmias, resp failure, anuria, ischemic gut, decreased cerebral perfusion, no SNS response

A

Refractory

  - Vasomotor center cannot stimulate SNS resulting in respiratory &/or cardiac arrest, failure of one organ system affects others
42
Q

The cornerstone of therapy for SEPTIC, HYPOVOLEMIC, & ANAPHYLACTIC SHOCK is???

A

VOLUME EXPANSION (isotonic crystalloids NS or LR)

   -If the pt does not respond to 2-3 L of crystalloids then blood administration & central venous monitoring may be instituted
43
Q

____ + ____= Sepsis.

A

SIRS + Infection

44
Q

Must meet 2 or more criteria for SIRS… What are those criteria?

A 
1. Temp: >100.4F/38C  OR
   90
3. RR >20
4. WBC >12 or < 4 or >10% bands 
    (immature WBCs)
45
Q

_______ _______: Temporarily CO increases (around 10), SVR decreases, increased HR & systolic BP, warm skin/extremities (d/t vasodilation), normal cap refill, pt “looks better” but isn’t.

A
  • Hyperdynamic State

- Sepsis is the only type of shock that has a Hyperdynamic Phase.

46
Q

Pulmonary Artery Wedge Pressure (PAWP)
Left or Right of the Heart?
Normal?
Sick heart pawp and why?

A
  • Left
  • 6-14
  • 18; Big Floppy heart; Chambers are larger/ stretched out so they need more volume to help fill the added space and not stress the heart out further

NUR 213 (4 decks)

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