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4th Semester Nursing > MedSurg2 - Exam 2 > Flashcards

MedSurg2 - Exam 2 Flashcards

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1
Q

Why is angiogenesis non-productive in cirrhosis?

A

Prevents effective, efficient flow of blood thru the liver

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2
Q

Why do you see anemia in liver patients?

A

Liver unable to store iron

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3
Q

What causes increase in ammonia in cirrhosis?

A

Breakdown of amino acids to ammonia, but liver can’t convert to urea
(GI bleeding exacerbates - breakdown of RBCs)
(Gut bacteria exacerbates - helps break down proteins)

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4
Q

Why use 1st gen beta blockers with liver prophylaxis?

A

Non-selective - vasodilation and effects on heart.

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5
Q

Why use vasoconstrictors for a GI bleed?

A

Constriction of blood vessels has been shown to decrease blood flow to organs

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6
Q

1 thing to do when a pt starts vomiting blood (or showing signs of GI bleed?)

A

1 sit upright. #2 suction (or have on standby).

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7
Q

Prioritization order of GI bleed (obvious)

A

Sit upright
Give blood
Stop the bleeding

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8
Q

Why would a GI bleed lead to increased ammonia levels?

A

B/c RBCs leftover in GI tract will be digested, broken down, protein —> ammonia.

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9
Q

Early manifestations of cirrhosis

A

GI probs (ANV, changes in bowels)
Abdominal discomfort
Hepatosplenomegaly
Weight loss

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10
Q

Late manifestations of cirrhosis

A 
Portal HTN
2nd & 3rd spacing
Jaundice
Hematologic, Endocrine & Hormonal disorders
Peripheral neuropathies
Hepatic encephalopathy (end stage)
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11
Q

What happens to PT/INR levels when liver isn’t functioning well?

A

They increase (check normal range - above 2ish, maybe?)

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12
Q

What happens to the CBC when liver function decreases?

A

RBCs, WBCs and Platelets decrease

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13
Q

What is an EGD (esophagogastroduodenoscopy) for?

A

Screens for esophageal varices

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14
Q

Insufficient packaging of what part of the RBC leads to hyperbilirubinemia and jaundice?

A

The “heme” portion, which is broken down into bilirubin.

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15
Q

Failing breakdown of RBCs (and hyperbilirubinemia) manifest in what physiological symptoms?

A

Jaundice
Anemia (iron from the RBCs can’t be stored).
Clay-colored stools
Increased ammonia levels

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16
Q

What happens to the biliary duct in cirrhosis and hyperbilirubinemia?

A

It gets clogged, so bilirubin can’t be excreted.

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17
Q

Why are GI bleeds more likely in cirrhosis and why are they so dangerous?

A

Varices in esophagus, stomach and spleen occur because of portal hypertension (backpressure from liver into veins) - these are likely to open/tear/rupture.
AND - there increased hydrostatic pressure in those vessels.

This is a risk because the liver isn’t producing as many clotting factors and the spleen is sequestering platelets.

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18
Q

Signs/symptoms of a GI bleed

A 
Low BP
Black, tarry stools or hemoccult
Change in LOC
Anemia
Cool skin
Emesis with frank blood or coffee ground texture
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19
Q

How to prevent GI bleeds in cirrhosis?

A

Avoid spicy, acidic, greasy or hard/crunchy foods
Avoid NSAIDs, ASA, ETOH
Treat URTIs quickly with cough suppressants (pressure/force from coughing can burst esophageal varices)

If severe, soft or puréed diet.

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20
Q

What meds are used to treat a patient with portal hypertension?

A

Propranolol (1st generation beta blocker - to vasodilate AND lower HR)
H2 receptor blocker and/or PPI (to decrease gastric acid d/t risk of bleeding varices)

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21
Q

Treatment for pts with bleeding varices (nursing and MD)

A
  • Airway management: (Sit upright, suction)
  • Give PRBCs and clotting factors
  • NGO tube for gastric lavage (need stuff out of the stomach) (NPO!)
  • Vasoconstrictive drugs (Octreotide, Vasopressin, Somatostatin)
  • Balloon Tamponade
  • Endoscopic Banding/ligation
  • Endoscopic scleropathy
  • TIPS (transjugular intrahepatic portosystem shunt)
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22
Q

What is a balloon tamponade?

A

Looks like an NG tube with inflatable balloons down it - function is to put pressure on bleeds in the esophagus or stomach

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23
Q

What is Endoscopic Banding/ligation? Pros and cons?

A

Surgical procedure to tie off the bulging/bleeding varice with the goal of causing ischemia/necrosis and scar tissue formation/healing.

Pros: Easy and common
Cons: need a puréed diet for healing. Can affect blood flow to other places.

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24
Q

What is Endoscopic scleropathy? What are its cons?

A

Injection of a solution into a varice to collapse/scar it.

Cons: Ulcers can form where the solution was injected.

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25
Q

What is TIPS (transjugular intrahepatic portasystemic shunt). What are the pros/cons?

A

Shunt that’s fed through the jugular to the liver and inserted into the portal vein.

Pros: eliminates portal hypertension that causes as a result of scarring and angiogenesis in the liver
Cons: no filtration occurs - liver filtration becomes 100% nonfunctional.

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26
Q

What is splenic sequestration and why does it happen?

A

Spleen traps RBCs and platelets (and WBCs) so serum levels are lowered. Results in Anemia, Thrombocytopenia and Neutropenia.

It happens because portal hypertension causes the spleen to enlarge and “increase” its function.

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27
Q

Can Portal hypertension cause systemic hypertension?

A

Yes, if severe enough.

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28
Q

What are caput medusae?

A

Varices on the surface of the abdomen around the umbilicus that occur as a result of portal hypertension.

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29
Q

What are the contributing factors to ascites in liver failure?

A
  1. Increase in hydrostatic pressure (d/t portal hypertension)
  2. Decrease in albumin synthesis (decreases oncotic pressure)
  3. Decrease in hormone metabolism (RAAS stays activated, body retains sodium and water).
    (4. Increase in lymph production and drainage into the abdominal cavity.)
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30
Q

Why is there a risk of hypokalemia in ascites (and liver failure)?

A

B/c hormone (aldosterone) metabolism decreases, RAAS stays active and the body retains sodium, releasing potassium in the urine.

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31
Q

How does bacterial peritonitis relate to ascites?

A

With bacterial peritonitis, there’s an increase in capillary permeability in the peritoneal cavity.

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32
Q

What are the treatments for ascites?

A
  1. Sodium restriction (b/c of effects of circulating aldosterone)
  2. Diuretic therapy (usually lasix + potassium-sparing)
    (Will often include a potassium supplement)
  3. IV albumin (to increase oncotic pressure)
  4. Paracentesis (to drain extra fluid)

Also, pt will likely need respiratory management (sit upright) and skin care (tight skin and/or peripheral edema can lead to breakdown).

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33
Q

What are some contributing factors to hepatic encephalopathy? 4 possible precipitating events?

A

Ammonia can’t be converted to urea by the liver any more.

  • protein in diet, muscle wasting AND digestion of RBCs from any GI bleed can contribute.
  • Gut bacteria also break down proteins and release ammonia
  • Muscles that usually help with ammonia to urea conversion are wasting.

Precipitating events:

  1. GI hemorrhage
  2. Constipation (increases bacterial digestion of protein)
  3. Infection (increases the metabolic rate, increasing production of ammonia)
  4. Hypovolemia (further decreases blood flow to both liver and kidneys, decreasing conversion and filtration)
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34
Q

Signs/symptoms of hepatic encephalopathy

A
  • Change in LOC (confusion, lethargy… eventually rage, somnolence, coma)
  • Change in coordination/motor response
  • Asterixis (late), tremor
  • slurred speech
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35
Q

What is Lactulose prescribed for? Titrate to ______

A

Reduce ammonia levels via 2 mechanisms:

  • trapping ammonia in the gut
  • prevents bacterial growth d/t lowered gut pH

Titrate to 2-4 soft stools per day

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36
Q

What are Neomycin or Metronidazole prescribed for in cirrhosis?

A

Hepatic encephalopathy: to reduce ammonia levels.

MOA: poor systemic absorption, so stay in the gut and kill the bacteria there. Prevents bacterial digestion of proteins/decreases ammonia production in the gut.

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37
Q

What is mannitol prescribed for in hepatic encephalopathy?

A

Reduces cerebral edema (by creating high osmolality of the blood), but does nothing to the ammonia levels.

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38
Q

When do you use a protein restriction with cirrhosis?

A

ONLY if pts have hepatic encephalopathy.

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39
Q

What are the mechanisms of cirrhosis that result in hematological changes? What are the physiological effects?

A
  • Less clotting factors produced
  • Less Vitamin K storage, iron storage
  • Splenomegaly: excessive removal of RBCs from circulation.

Coagulation disorders (bleeding, Purpura, petechia, bruising)
Thrombocytopenia
Anemia
Leukopenia.

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40
Q

What would you expect the physician would give if a pt with cirrhosis had a low Hgb/Hct level?

A

PRBCs

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41
Q

If PT/INR is too high in a pt with cirrhosis, what do you anticipate the physician would order?

A

Clotting factors

Maybe vitamin k

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42
Q

What hormonal changes happen with cirrhosis and why?

A

Liver can’t metabolize/deactivate hormones.

Aldosterone excess: fluid retention, sodium retention, hypokalemia

Estrogen excess in both sexes: ruddy complexion d/t vasodilation at subQ tissues, palmar erythema, spider angiomas.

Women experience changes to menstrual cycle and hair growth (testosterone not deactivated)
Men experience gynecomastia and testicular atrophy (estrogen not deactivated)

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43
Q

Why does Pruritis occur in cirrhosis?

A

Toxins accumulate and irritate the tissues (bilirubin, bile salts, histamine, endogenous opioids)

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44
Q

Malnutrition in cirrhosis occurs because of what factors?

A
  • Changes in the way the body metabolizes carbs, fats and proteins
  • ascites puts pressure on the GI tract
  • Loss of appetite
  • Abdominal fullness
  • Impaired digestion and nutrient absorption
  • Increased blood volume (remember fluid retention)= increased energy demand
  • catabolism and muscle wasting occur
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45
Q

What is the recommended treatment for malnutrition in cirrhosis patients?

A

Hi-calorie, High carb, LOW SALT, with NO protein restriction.

Protein supplements available for proteins metabolized by muscles

Supplements: B complex, folic acid, iron.

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46
Q

What is the mechanism of injury in acute pancreatitis?

A

Damage to acinar cells = leakage of digestive enzymes into tissue. Enzymes are activate prematurely and start digesting the pancreas.

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47
Q

What are the major risks with pancreatitis?

A

Bleeding risk (vascular damage d/t digestion of tissues)

Major fluid shift/3rd spacing (endothelial cell retraction d/t inflammatory response) can lead to hypovolemic shock, sepsis and organ failure.

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48
Q

What can cause acute pancreatitis?

A

Excessive alcohol consumption (increases permeability of pancreatic ducts)

Biliary tract disease (can become blocked so enzymes can’t get to the duodenum.

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49
Q

What is an ERCP (post endoscopic retrograde cholangiopancreatography) used for and what is the risk?

A

-Used to assess for pancreatitis or to assess/dislodge gallstones.

Risk: the injection of dye used to determine if blockages exist can worsen or cause pancreatitis.

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50
Q

What is the hallmark sign of pancreatitis?

A

Pain (LUQ) - very intense
Constant (not colicky) that worsens when eating
Does not go away with vomiting
May radiate to back or behind the left shoulder blade
May be relieved by fetal position d/t compression

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51
Q

What are all the signs/symptoms of Acute pancreatitis?

A

Pain
NVA
Fever (inflammatory response to digestion of tissues)
Jaundice (only if the bile duct is clogged/liver is also a problem)
Decreased bowel tones (SNS activation d/t pain, decreased perfusion to gut)
Decreased BP (if 3rd spacing)
Grey Turner’s sign
Cullen’s Sign
Trousseau’s sign
Dyspnea
Shock

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52
Q

What is Grey Turner’s sign?

A

Red/brown discoloration down flanks that indicates bleeding into the peritoneal cavity in Acute Pancreatitis.

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53
Q

What is Cullen’s Sign?

A

Red discoloration across the abdomen that indicates blood is leaking into the subcutaneous tissue.

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54
Q

What is Trousseau’s sign?

A

Contraction of muscles with 3m inflation of BP cuff: indicates hypocalcemia.

Likely to be positive in acute pancreatitis.

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55
Q

Why would Trousseaus’ sign be positive in pancreatitis?

A

Calcium in the blood binds with fatty acids that are released as pancreatic tissue dies.

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56
Q

What are the primary lab tests for Acute Pancreatitis? What other lab changes would you see?

A

Serum Amylase and Lipase levels increase (pancreas is trying to compensate for the enzymes not reaching the gut)

Increased Glucose (insulin function not working as well, stress response)
Decreased Calcium (fatty acids bind after death of pancreatic tissues)
LFTs and Bilirubin increase, but only if there’s a problem with the liver
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57
Q

What imaging test offers the clearest view of pancreatitis?

A

CT scans.

Also possible are abdominal US, X-rays, ERCP and MRCP - mri dye

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58
Q

A patient arrives with suspected acute pancreatitis in the ED - what are the order of operations?

A
  1. Give O2 (b/c there is a high risk of shock)
  2. IV fluid bolus
  3. Pain relief (perhaps opioid PCA) (HOLD if BP is super low)
  4. NPO with NG tube set on low/intermittent
  5. Insulin (sliding scale)
  6. Ranitidine or Omeprazole to decrease gastric acid.
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59
Q

How would you know if a pt with acute pancreatitis developed a pseudocyst or an abscess? What are the risks of each of these?

A

There would be continued pain despite treatment for both.

Pseudocyst would also have an increase in amylase levels.
Abscess would also have an increase in WBCs.

Both carry a risk for bacterial peritonitis.

60
Q

Why would a pleural effusion occur in acute pancreatitis?

A

Enzymes and exudate can migrate from the peritoneal cavity into the pleural cavity.

61
Q

Why would hypotension occur in pancreatitis?

A

Systemic inflammatory vasodilation and endothelial cell retraction can occur, leading to massive fluid shifts into the peritoneal space.

62
Q

Shock results from ______________. Cells receive inadequate ___________ and _______________ accumulates.

A

Inadequate tissue perfusion
…oxygen…
…metabolic waste….

63
Q

Clinical manifestations of shock occur because of ____________ and systemic effects of __________.

A

The body’s attempt to compensate

… tissue ischemia….

64
Q

What kinds of shock can result in SIRS (systemic inflammatory response syndrome)? (Why?)

A

All kinds of shock

Because the body launches a systemic inflammatory response d/t tissue damage from lack of oxygen.

65
Q

What is SIRS?

A

Systemic Inflammatory Response Syndrome

Inflammatory response system-wide
Fluid shifts out of vessels and into tissues
Further decreases perfusion and vascular volume

66
Q

What is MODS?

A

Two or more organ systems go into failure because of insufficient perfusion and ischemia.

67
Q

What are the three types of distributive shock?

A

Septic
Neurogenic
Anaphylactic

68
Q

Causes of RELATIVE hypovolemic shock

A 
2nd/3rd spacing
Internal bleeding
SIRS
Liver failure (ascites)
Pancreatitis
69
Q

Causes of ABSOLUTE hypovolemia

A 
vomiting
Hemorrhage
Diarrhea
Drains
Tons of urine output
Dehydration
70
Q

Treatment for hypovolemic shock

A

STOP fluid loss (know what fluid, where it went, how much)

Replace circulating volume

71
Q

Distributive shock - what is the problem here?

A

Lack of tone (vasodilation) prevents blood from getting back to heart.

72
Q

Hypovolemic shock - what is the problem here?

A

ALWAYS a lack of volume

73
Q

Are there any problems with the heart in distributive shock?

A

No - the heart pumps just fine

74
Q

Neurogenic shock - what is the problem here?

A

It’s a type of distributive shock - problem is lack of vessel tone

Some disruption of the SNS occurs (spinal cord injury, etc) and the SNS cannot activate

PNS runs without any opposition.
N

75
Q

Signs/symptoms of neurogenic shock

A

Warmth and flushing (massive vasodilation)
Hypotension
Bradycardia (PNS/vagal nerve)

(Note… over time, skin will eventually become cool and clammy d/t decreased cardiac output).

76
Q

Treatment for neurogenic shock

A

Vasopressors (ONLY for distributive shock) to vasoconstrict.
These include: epinephrine, norepinephrine and vasopressin.

Atropine (to increase HR)

77
Q

Septic shock results from________. What is the systemic response (4 things)?

A

An exaggerated immune response to an infection (ANY infection can eventually lead to this)

  • Massive cytokine release = system-wide vasodilation and endothelial cell retraction
  • Coagulation pathways activated = microemboli form (clotting in all the tiny blood vessels). This can lead to DIC.
  • Selective vasoconstriction occurs (compensatory) to shunt blood to heart and brain, and non-vital organs have decreased perfusion.
  • Hypermetabolic state results from increased HR, RR, stress and temp (fever), which increases O2 demand of tissues.
78
Q

Signs/Symptoms of septic shock

A 
Fever
Warm/Flushed (will eventually become cool/mottled)
Increased RR
Change in LOC (agitation, confusion)
Resp difficulty (fluid in alveoli)
Paralytic ileus or GI bleeding
Fluid loss (profound) from fever
79
Q

Treatment for Septic Shock

A

Vasopressors (to restore tone) - epinephrine, norepinephrine, vasopressin.
Fluids
Antibiotics (to treat cause)

80
Q

Cardiogenic shock results from _______. It’s then exacerbated by ________.

A

failure of the heart’s pump (systolic or diastolic)

the body’s attempt to compensate

  • (SNS activation increases O2 demand and ischemia)
  • (RAAS activation increases fluid retention and vasoconstriction, leading to increased preload, afterload and SVR, resulting in increased O2 demand and ischemia).
81
Q

Signs and symptoms of cardiogenic shock

A 
Chest pain
Lung congestion, crackles
Cool, clammy skin
Increased HR and RR
Decreased BP
Decreased cap refil
Change in LOC (anxiety, confusion, agitation)
82
Q

Treatment for cardiogenic shock

A

Diuretic (furosemide)
Vasodilator (nitroprusside)
Nitrate (to perfuse/dilate heart vessels)
An inotrope (usually dobutamine, could be digoxin)

83
Q

What would diagnostic tests show in a pt with cardiogenic shock?

A 
Increased cardiac biomarkers
Increased BNP
Increased Glucose
Increased BUN
Dysrhythmias (ECG)
Pulmonary infiltration (on chest x-ray)
84
Q

What are the stages of shock?

A

(1. Insult/precipitating event)
2. Compensatory phase (ideal to catch it here for best survival)
3. Progressive stage
4. Refractory stage (permanent organ damage likely, survival rare)
(5. Death)

85
Q

Compensatory mechanisms of shock? What triggers them?

A

Drop in BP triggers compensatory mechanisms.

SNS activation (except neurogenic)
-vasoconstriction to shunt to vital organs, increased HR, increased contractility

RAAS activation
-sodium and water retention, vasoconstriction

ADH released (from post pit)
-fluid retention
86
Q

What changes in LOC are you likely to see in the compensatory phase of shock?

A

Restlessness, confusion

87
Q

What effect does the body’s compensatory mechanisms have on cardiogenic shock?

A

They worsen it - increase O2 demand and work of the heart, further increasing ischemia in heart.

88
Q

How good is the body at activating compensatory mechanisms in septic shock?

A

It’s much harder in septic shock for the body to activate these.

89
Q

What happens in the progressive phase of shock?

Common signs/symptoms?

A

Compensatory mechanisms fail

  • can’t maintain CO and all organs (including brain and heart) become hypoxic.
  • massive peripheral vasoconstriction (cool, clammy)
  • fluid shifts d/t capillary permeability (inflammatory response): Ascites, Edema, Anasarca (general), in face and periphery.
  • DIC: Hemorrhage d/t all clotting factors/platelets being used up.

S/sx:

  • Chest pain
  • decreased LOC
  • profound metabolic acidosis (lactic acid production from anaerobic respiration)
  • hyperkalemia (increased potassium d/t H+/K+ pump at cell membrane).
  • massive peripheral vasoconstriction (shunting!)
  • inflammatory response and major/rapid fluid shifts (ascites, edema, anasarca, face/periphery).
  • DIC
90
Q

What is anasarca?

A

Generalized edema

91
Q

What happens in refractory stage of shock?

A
  • massive hypotension
  • hypoxemia
  • liver, lung, kidney failure
  • cardiac and cerebral ischemia
  • severe anaerobic metabolism (ph below 7)
92
Q

Treatment for shock (general)

A

-address underlying cause

AIRWAY
O2
Fluids (Circulation) - 2 large bore IV lines - warm if possible

CV stabilization
Pain and anxiety control

Blankets - prevent hypothermia
Fluid choice - usually NS, sometimes LR. Maybe FFP. Maybe FFP. Maybe colloids.

Assess efficacy of treatments

93
Q

What are the colloid fluid choices? What are the advantages/disadvantages?

A

Albumin, Dextran, Hetastarch

Advantage: stay in the intravascular space for longer.
Disadvantage: adverse effects (fluid shifts), expensive, poorer outcomes.

94
Q

Treating septic shock - what are the four D’s?

A

Drain
Debride
Device removal
Definitive control

95
Q

Septic Shock - what is the one hour bundle?

A
  1. Measure Lactate (repeat if over 2)
  2. Get blood culture
  3. Give ABX (10% risk of dying for every 1h delay)
  4. 30 ml/kg of crystalloid fluids
  5. Vasopressors to maintain map of over 65.
96
Q

When would you not use shock position?

A

In cardiogenic shock.

97
Q

What happens to PAWP in hypovolemic shock? What about cardiogenic shock?

A

PAWP is down in hypovolemic shock

Up in cardiogenic shock.

98
Q

What kind of VQ mismatch will happen in hypovolemic shock?

A

High (perfusion problem)

99
Q

Renal consequences of progressive stage hypovolemic shock?

A

Ischemia of the epithelium of the tubules
Pre-renal failure
Worsening acidosis

100
Q

CV consequences of hypovolemic shock (progressive stage)?

A

Decreased PAWP
Increased capillary permeability (edema)
Decreased coronary perfusion (pain)
Decreased peripheral perfusion (cool, clammy, etc)

101
Q

GI consequences of hypovolemic shock (progressive)?

A
  • Paralytic ileus
  • Mucosal ulceration (gastric acid will just sit) - might give H2RB’s, PPIs
  • Bacterial translocation (can get sepsis from bacteria in ulceration - give ABX if concerned)
102
Q

Is the acidosis from shock metabolic or respiratory?

A

Both.
Metabolic acidosis creates lactic acid
Impaired gas exchange means increased carbonic acid

Also, kidney and liver function is decreased so neither can process the acid levels

103
Q

Where is the dividing line for Tetraplegia/Paraplegia

A

Cervical / Thoracic transition.

104
Q

Injury at L1 means paralysis where?

A

Below the waist

105
Q

Injury at T6 means paralysis where?

A

Below the chest

106
Q

Spinal shock results in the loss of ______, _______ and _______ function below the level of injury (temporary).

A

Reflexive (no reflexes)
Sensorimotor (no sensation, no voluntary movement)
Autonomic (bowel, bladder, etc)

107
Q

What level(s) of injury is neurogenic shock most likely? Why?

A

Cervical and high thoracic - above T5/T6

Because SNS innervation of the organs and periphery starts at T5 and below (heart and lungs is T1-T4). So damage above T5 means heart/lungs don’t get SNS innervation.

108
Q

You determine neurologic level of injury by figuring out where ….

A

The lowest segment of the spinal cord with NOrMAL sensory AND motor function are.

109
Q

What will you find with C1-C3 injuries?

A

Long-term ventilator dependence
No cough
Can move head

110
Q

What will you find with C5-T1 injuries?

A

Diminished respirations
Weak Cough
May bend elbow

111
Q

What will you find with T1-T6 injuries?

A

Full use of fingers
Decreased respiratory function
Increased risk of atelectasis/pneumonia

112
Q

When is the Level of Injury most likely to change and why?

A

In the first 72 hours

Due to inflammation (maybe bleeding): secondary injury .

113
Q

What happens to phrenic nerve function with a C1-C3 injury?

A

Complete loss (no diaphragmatic control)

114
Q

What happens to phrenic nerve function with a C4-C5 injury?

A

Variable function (might have weak diaphragm or irreg resp rate

115
Q

What happens to respiratory with a low cervical or high thoracic injury?

A

Decreased vital capacity
Decreased Cough
Impaired voluntary resp muscle movements

116
Q

What kind of respiratory failure would a spinal cord injury lead to?

A

Hypercapnic respiratory failure

117
Q

What level of injury will result in decreased SNS reponse? What will this look like?

A

Anything above T6.

Bradycardia
Vasodilation
Hypotension

118
Q

How to be mindful of vagal stimulation risk in SCI injuries?

A

Use extra care for suctioning, turning, even with stress.
Be careful giving suppositories.

(Heart rate will drop)

119
Q

Why don’t you want to sit an SCI (esp Above T5/T6) patient up too quickly?

A

Orthostatic hypotension - hard to recover from

120
Q

What should we know about SCI patients and DVTs

A

Risk is really high. Lots of interventions (Ted hose, SCDs, elevating legs, ROM).

121
Q

Reflexic bowel: What is it and where is the injury?

A

Injury: above T12

Involuntary release of stool
Stool buildup - that pt can’t sense - triggers a reflex in the colon/rectum

122
Q

Areflexic bowel: what is it and what’s the level of injury?

A

Injury below T12

Constipation and fecal impaction
(pt has a hard time sensing and emptying stool).

123
Q

Spastic Bladder: What is it and level of injury?

Treatments?

A

Above T12

Combo platter of incontinence and urinary retention
This is because bladder will have contractions (involuntary) that aren’t coordinated with sphincter relaxation.

Tx: Foley/suprapubic catheter; Bethanechol (spasms)

124
Q

Flaccid Bladder what is it and level of injury?

Treatment?

A

Below T12

No contractions, no reflex signal to tell nerves to contract and empty bladder. Results in retention.

Teach routine self-catching.

125
Q

Why is temperature regulation a challenge for SCI patients? Particularly higher injuries)

A 
Lack vasoconstriction when cold
Can’t sweat to cool off
Lack piloerection (goosebumps)
126
Q

What sexual problems do men with SCIs have?

A

Erection difficulties
Ejaculation changes
Decrease in sperm motility

127
Q

What is Autonomic Dysreflexia?

  • What triggers it
  • What does the body do
  • what are the symptoms
A

Trigger: Strong sensory input (usually visceral - bowel or bladder)

SNS response at the spinal cord BELOW the level of injury.
Baroreceptors detect the HTN and body mounts PNS Response ABOVE the level of injury.

S/Sx: Super high BP
Severe Headache (vasodilation in brain)
Slow HR
Flushing, sweating ABOVE LOI (vasodilation)
Blurred vision, nasal congestion
Goosebumps BELOW LOI (SNS response)
128
Q

Treatment/Response for Autonomic Dysreflexia?

A

EMERGENCY

  1. Head of the bed to 45 degrees FAST (to create OH)
    (Loosen tight clothing)
  2. Check and empty bladder (scan, straight cath)
  3. Monitor the BP to see if it decreases (if so, was the bladder)
  4. If SBP is still over 150, give vasodilator or anti-HTN med
  5. Once SBP is below 150, THEN bowels can be addressed, but not before (b/c don’t want to stimulate vagus nerve and decrease HR even more).
129
Q

When would you give vasopressors to a pt with SCI?

A

If they were in neurogenic shock.(to increase vessel tone and BP)

130
Q

Definition of Sepsis

Not septic shock

A

Body’s response to infection injures its own tissues/organs.

Dx criteria:
2 or more SIR criteria and a source of infection (could be a potential source - doesn’t have to be a known source… ie, could have a urinary catheter)

131
Q

Definition of Septic Shock (not sepsis)

A

A subset of sepsis:
Body’s response to infection injuries its own tissues and organs

AND

There are various fatal abnormalities of blood circulation and cellular metabolism (like hypotension that’s refractory to fluid resuscitation)

132
Q

SIRS criteria (how many would you need to call the MD)?

A

Two!

Temp outside of normal range
RR over 20 
PaCO2 under 32 (compensation)
HR over 90
WBC outside of normal range
More than 10% immature bands

(Also, you might have elevated lactate or procalcitonin, but those aren’t specific to the diagnosis).

133
Q

What lactic acid level indicates stress but not tissue hypoxia?

What about lactic acidosis?

A

Stress: up to 2

Lactic acidosis: over 4.

134
Q

What sorts of things can contribute to secondary injury of the spinal cord?

A 
Bleeding
Clotting
Vasospasm
Inflammation (compresses)/edema
Free radicals and lipid peroxidation can damage neurons and blood vessels
135
Q

Can you use Glucocorticoids in SCIs?

A

MDs will, but they’re not recommended. Suppress the immune system and can cause greater risk of infection.

136
Q

What vitamins does the liver usually store?

A

DEAK

And B-12

137
Q

What are bile’s jobS?

How are these affected during cirrhosis?

A

Help digestion and absorption of fats.

Help eliminate waste products (bilirubin, cholesterol, metabolites of drugs)

Poor fat digestion/absorption, increased bilirubin, increased cholesterol, increased drugs in system.

138
Q

What will the effects of decreased fat metabolism in liver failure be?

A

Increased fatty acids
Increased triglycerides
Increased cholesterol

139
Q

What are the effects of decreased protein metabolism in the liver?

A

More ammonia (proteins still broken down, but it gets stuck in the ammonia phase)

Albumin isn’t well produced (protein)

Decreased energy (because AAs aren’t able to be adequately broken down)

140
Q

Effects of changed carbohydrate metabolism

A

Generally, in liver patients, blood sugars tend to be low because they can’t break down glycogen and make glucose…

BUT, after eating, blood sugar tends to be high.

141
Q

Effect of changes in fat/protein/carb metabolism?

A

Body thinks you’re starving, so it starts to break down muscles.

Malnourished, frail looking

Low energy

High lipids in lipid panel

142
Q

six clinical manifestations of compensated shock

A 
Increased HR (SNS)
Cool, pale skin (SNS)
Thirst (fluid shift)
Decreased urine output (ADH/aldosterone release)
Fluctuating BP
Decreased bowel sounds (SNS)
143
Q

In what stage of shock does metabolic acidosis occur?

A

Progressive

144
Q

What happens to glucose levels in the compensated stage of shock?

A

They’re elevated

145
Q

Decreased mean arterial pressure, jaundice, cold/clammy skin, agitation, tachypnea, increased serum creatinine. These indicate

A

Progressive stage of shock

146
Q

Severe hypoxia, lactic acidosis and bleeding indicate…

A

Refractory stage of shock

4th Semester Nursing (8 decks)

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