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202A > Test #3 > Flashcards

Test #3 Flashcards

1
Q

What are causes of hepatitis 6

A
  • Viral (most common)
  • Alcohol
  • Medications
  • Chemicals
  • Autoimmune diseases
  • Metabolic disorders
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2
Q

What is a good way to remember what causes hepatitis A

A

Remember I “ate” it, because it can be caused by fecal oral

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3
Q

What are the best ways to prevent hep A 2

A
  • Short-term Vaccine
  • Hand washing
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4
Q

What sucks about hep A

A

The greatest risk for transmission occurs before your symptoms even appear (so you can be out spreading it without even showing symptoms that you have it)

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5
Q

What is interesting about infants and hep A

A

They can be excreting hep A in their poop for months after (remember why we’re worried about daycare)

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6
Q

What antibodies indicate an acute hep A infection and what antibody indicates a previous infection or immunization

A

Acute = IgM

Past/current immunization = IgG

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7
Q

Is Hep A chronic?

A

No, it’s usually self resolving (so it will eventually go away)

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8
Q

How can we remember how hep B is transmitted

A

Think B for Blood and Bodily fluids

It can be transmitted through blood and other bodily fluids like semen

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9
Q

What are the different routes that hep B can be transmitted 3

A
  • Perinatally from mom to baby
  • Percutaneously (through IV drug use)
  • Small cuts on mucosal surfaces getting infected from something like semen, vaginal secretions or saliva)
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10
Q

Can hep B cause acute or chronic hepatitis

A

It can cause either

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11
Q

Do adults get chronic hepatitis after becoming infected with hep b? If not, what age group is more likely to develop chronic?

A

No - usually if you become affected as an adult with hep B it will not turn into chronic.

If a child under the age of 5 becomes infected with hep b, then they are more likely to develop chronic hepatitis later on in life

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12
Q

What hepatitis is more likely to cause Acute hepatitis, cirrhosis and liver cancer

A

Hep B

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13
Q

What is the best way to prevent hep B

A
  • No needle sharing
  • Practice safe sex
  • Get vaccinated (this is the vaccine we get for nursing school)
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14
Q

What is the at risk population for getting hep B

A

Men who have sex with men
Household contact of chronically infected
Patients on hemodialysis
Health care and public safety workers
IV drug users
Recipients of blood products

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15
Q

How can we remember hep C

A

Think C for Chronic

(can be acute, but most turn into chronic and people aren’t symptomatic until the disease has progressed)

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16
Q

How can we remember hep C? Why?

A

Think C for Chronic.

Most pts will usually develop chronic hepatitis from hep c (puts them at an increase risk of developing cirrhosis, liver failure)

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17
Q

How is hep c contracted? What are the big risk factors?

A

Contracted percutaneously

IV drug use
High-risk sexual behaviors
Occupational exposure
Perinatal exposure
Blood transfusions before 1992

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18
Q

What sucks about hep C

A

It usually takes 15-20 years before you have symptoms of liver damage (by then you may already have cirrhosis and liver failure)

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19
Q

What other virus do hep c pts commonly have? Why does this suck?

A

Usually have HIV, sucks because having both hep C and HIV puts them at an increased risk for progression of cirrhosis

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20
Q

What age group should be screened for hep C

A

1945-1965

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21
Q

What diagnosis test can determine if someone has hep C

A

Anti-HCV

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22
Q

If your viral load isn’t high for hep C, what does this mean

A

You’re in the chronic phase, not acute.

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23
Q

What is hep D also known as

A

The delta virus

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24
Q

Can a person be solely infected with hep D

A

No, they need to also have hep B in order for the hep D to replicate

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25
Q

How can we remember Hep E

A

Remember “Eat”, because it can be transmitted orally

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26
Q

Where is there Hep E

A

Developing countries where water is more contaminated

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27
Q

Since acute hepatitis is destroying destroying large amounts of hepatocytes (liver cells) what impact can this have? 6

A
  • Decreased bile production
  • Coagulation issues (poor clotting times)
  • Blood glucose issues (glucose isn’t being stored)
  • Protein metabolism issues
  • Liver stops making albumin
  • Processing of drugs, hormones, and metabolites can be impacted
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28
Q

After an acute infection, what can happen with the liver

A

One of two things:

  1. Liver cells can regenerate and resume normal functioning
  2. The acute hepatitis can be so severe and irreversible that pts can develop liver failure or die
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29
Q

What can chronic hepatitis do to the liver

A

It can cause continued destruction, which can lead to scar tissue developing, which can become fibrosis and compromise liver function. This can lead to cirrhosis and liver failure.

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30
Q

What are immune system manifestations in the early phase of hepatitis (basically where the immune system is freaking out because of the virus)

A
  • Rash
  • Angioedema
  • Arthritis
  • Fever
  • Malaise
  • Cryoglobulinemia (clotting of proteins)
  • Glomerulonephritis
  • Vasculitis
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31
Q

How long does the acute phase last? What are some symptoms? 5

A

Usually 1-6 months.

  • Icteric (jaundiced)
  • Pruritis (itching)
  • N/V
  • Right upper quadrant pain (where the liver is)
  • Smokers may develop a distaste for cigs
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32
Q

Simply, which hepatisis is acute and which may develop to chronic

A

A is acute, while B and C may become chronic

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33
Q

What are complications from hepatitis

A

Acute liver failure
Chronic hepatitis (Some HBV and majority of HCV infections)
Cirrhosis
Hepatic Encephalopathy (HE)
Ascites
Portal hypertension
Liver cancer

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34
Q

This might be skipping ahead…. But what are we really worried about with portal hypertension? Why?

A

Bleeding, because the pressure can become really high in the GI, and that pressure has to go somewhere, so it can lead to bleeding, like from varices

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35
Q

What are the symptoms of acute liver failure (ALF) 5

A
  • Encephalopathy
  • GI bleeding
  • Disseminated intravascular coagulation
  • Fever with leukocytosis
  • Renal manifestations like oliguria (why renal - tough to perfuse kidneys when liver is messed up)
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36
Q

What serious thing should you always be worried about with someone with liver disease

A

BLEEDING

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37
Q

What are symptoms of acute hepatitis (a lot)

A
  • Loss of appetite (anorexic)
  • Clay-colored stool (gray) (bile makes our poop dark colored)
  • Dark urine
  • Decreased sense of taste and smell
  • Diarrhea or constipation
  • Fatigue
  • Flu like symptoms
  • Hepatomegaly
  • Jaundice
  • Low grade fever
  • Lymphadenopathy (swollen lymph nodes in abdomen and groin)
  • Myalgias and/or arthralgias (muscle aches/joint aches)
  • N/V
  • Pruritus
  • Righter upper quadrant tenderness
  • Splenomegaly
  • Weight loss
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38
Q

What are signs of chronic hepatitis (a lot)

A
  • ALT/ASTs elevated
  • Ascites, edema in lower extremities
  • Asterixis (liver flap)
  • Increased bleeding
  • Fatigue
  • Hepatic encephalopathy (confusion, agitation)
  • Increased bilirubin
  • Jaundice
  • Myalgias and/or arthralgias
  • Palmar erythema
  • Spider angiomas
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39
Q

What platelet level are we SUPER concerned about

A

If they drop below 50 (normal range is 150,000-450,000)

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40
Q

What two risk factors make someone more at risk for HBV becoming chronic?

A
  • Acquiring the infection before age 5
  • Immunocompromised (say with HIV)
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41
Q

What is hepatic encephalopathy? What symptoms does it cause?

A

Potentially life-threatening neurologic, psychiatric, and motor issues caused by the liver-s inability to remove toxins (especially ammonia)

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42
Q

What are the risk factors for developing cirrhosis from hepatitis 4

A
  • Male gender
  • Alcohol use
  • Concomitant fatty liver disease
  • Excess iron deposition in liver
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43
Q

What treatment do we give for HE? What should we monitor with it?

A

Lactulose (to help remove the ammonia from the blood)

Monitor for electrolyte loss

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44
Q

The loss of what leads to ascites?

A

Albumin, which is a protein made by the liver (if your liver isn’t working, then your not able to make albumin)

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45
Q

What types of tests can we do to diagnosis hepatitis 7

A
  • Specific antigen and/or antibody for each type of viral hepatitis
  • Liver function tests
  • Viral genotype testing (don’t need to know the specific types)
  • Physical assessment findings
  • Liver biopsy
  • FibroScan
  • FibroSure (FibroTest) (blood test)
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46
Q

What is some interprofessional care to help pts with hepatitis 5

A
  • Adequate nutrition
  • Rest
  • Avoid alcohol and drugs metabolized by the liver
  • Might need to notify possible contacts
  • Supportive drug therapy like antihistamines (for the itching) and antiemetics
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47
Q

For a pt with hepatitis will their FLTs, bilirubin and ammonia levels be low or high? What are the normal levels?

A

They will be high

Normal:
ALT/AST 5-56
Bilirubin <1
Ammonia 15-45

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48
Q

Why type of med might someone with hepatitis receive to help boost their immune system?

A

Interferon (it’s a naturally occurring immune protein in the body, but it still might be given to someone with hepatitis to help fight off the virus)

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49
Q

Even though pts with hepatitis may not need to be put on a special diet, what kinds of “special diet” things may they have 4

A
  • May need to increase calories during the acute phase
  • Fat content may need to be decreased if bile production is decreased
  • May need b-complex and vitamin k (help with bleeding)
  • May need IV glucose
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50
Q

How can we protect people from hep A and hep B 2

A
  • Immunization (A vaccine doesn’t last very long - used for travel or to give to infants under 1 year of age)
  • Post-exposure prophylaxis
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51
Q

How can we protect people from hep C since there is not a vaccine or post-exposure prophylaxis 3

A
  • Practice safe sex
  • No needle sharing
  • Screen all people born between 1945-1965 (remember that C can turn chronic in your body and live in your body for years without you having any symptoms, so that’s why we screen these people)
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52
Q

What is cirrhosis

A

End-stage liver disease, where there is extensive degeneration and destruction of liver cells, where healthy tissue has now been replaced by fibrous and regenerative nodules

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53
Q

What are the 2 most common causes of cirrhosis

A
  • Hep C
  • Alcohol induced liver disease
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54
Q

What are other causes of cirrhosis 8

A

Nonalcoholic fatty liver disease (NAFLD) (anything that causes an increase in fat deposits in your liver not caused by alcohol)
- Viral hep B and C
- Biliary cirrhosis
- Cardiac cirrhosis (caused by right sided HF - things are getting backed up from the liver, remember the blood flow)
- Obesity
- Diabetes
- Extreme dieting
- Genetics
- Environmental factors

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55
Q

Good picture showing how esophageal varices happen

A
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56
Q

Do we often see early symptoms of cirrhosis? What might those be? 2

A

Not usually since there are only a few early symptoms that aren’t very unique -
Early symptoms:
- Fatigue
- Enlarged liver

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57
Q

What are late symptoms of cirrhosis 10

A
  • Jaundice
  • Peripheral edema
  • Ascites
  • Skin lesions
  • Decreased vitamin k absorption leading to bleeding risks
  • Splenomegaly
  • Varices (esophageal, gastric, hemorrhoids)
  • Endocrine problems (liver plays a role in metabolizing hormones, so it can lead to a buildup of hormones in the body, gynecomastia, amenorrhea, etc.)
  • Peripheral neuropathies
  • Hypoglycemia
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58
Q

What are the two types of skin lesions that we might see on someone with cirrhosis

A
  • Spider angiomas (small, dilated blood vessels with a bright red center point and spiderlike branches - usually on the nose, cheeks, upper trunk, neck and shoulders)
  • Palmar erythema (red area that blanches with pressure on the palms of hands)
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59
Q

Why does jaundice occur

A

Bile ducts get compressed and obstructed, which leads to a backup of bilirubin, and causes the jaundice symptoms. (basically an increase in bilirubin in the body)

(remember bilirubin is needed to make bile)

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60
Q

What is happening in splenomegaly

A

Backup of blood caused by the liver into the spleen which can lead to thrombocytopenia, leukopenia and anemia, because the spleen becomes hyperactive and starts removing a large amount of blood cells from circulation

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61
Q

Why do coagulation problems happen in cirrhosis

A

Because the liver is responsible for making prothrombin and other factors essential clotting factors and cirrhosis interferes with its ability to do so, thus increasing bleeding risks

(a high prothrombin time means that it’s taking too long for our blood to clot, which means the liver isn’t making enough prothrombin)

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62
Q

Basically the liver causes splenomegaly (where the spleen removes a large amount of cells leading to a decrease in RBCs, WBCs), and the liver isn’t able to make an adequate amount of clotting factors

A
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63
Q

What 3 mechanisms lead to ascites and why

A
  • Portal hypertension (excess proteins move into the lymph space from the blood vessels and water follows)
  • Hypoalbuminemia (liver isn’t able to make albumin so fluid isn’t staying in the blood vessels)
  • Hyperaldosteronism (liver cells aren’t able to metabolize aldosterone, so it builds up causing sodium retention) `
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64
Q

What is a normal range for albumin

A

3.5-5.5

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65
Q

The livers inability to remove what, causing a buildup of this substance, can lead to HE

A

Ammonia

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66
Q

Why is it bad to have a buildup of ammonia

A

Ammonia can cross the blood brain barrier and can cause neurologic toxic manifestations

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67
Q

What are signs of HE 8

A
  • Impaired consciousness
  • Inappropriate behavior
  • Sleep disturbances
  • Trouble concentrating
  • Asterixis (flapping tremors, usually arms and hands)
  • Apraxia (inability to construct simple figures when writing)
  • Trouble moving pen from left to right
  • Fetor hepaticus (musty, sweet odor breath - due to toxins building up)
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68
Q

What is it called when the kidneys are affected by issues with the liver

A

Hepatorenal syndrome

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69
Q

What are the symptoms of hepatorenal syndrome? Why is it happening? What can fix it?

A

Symptoms:
- Azotemia (elevated BUN & creatinine)
- Oliguria
- Intractable ascites

Caused by portal hypertension which leads to decreased renal blood flow (kidneys aren’t able to be perfused well enough)

Only treatment is a liver transplant

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70
Q

What lab levels might indicate cirrhosis

A
  • High alkaline phosphate, AST, ALT and glutamyl transpeptidase (GGT)
  • Low protein and albumin
  • Increased bilirubin and globulin
  • Prolonged PT time
  • Low cholesterol
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71
Q

What are normal alkaline phosphate
AST
ALT
GGT
Albumin
Protein
Bilirubin
PT time

A

alkaline phosphate (ALP) 40-120
AST 5-40
ALT 7-56
GGT 5-40
Albumin 3.5-5.5
Protein 6.2-8.2
Bilirubin 0.1-1.2
PT time 10-13 seconds

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72
Q

What is the gold standard for determining cirrhosis

A

Liver biopsy

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73
Q

What does it mean when we say a prolonged PT time

A

It takes longer to clot (that’s why liver issues pts have increased bleeding risks)

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74
Q

What is some conservative therapy for someone with cirrhosis

A
  • Rest
  • Administer B-complex vitamins
  • Avoid alcohol
  • Avoid aspirin, acetaminophen and NSAIDs (aspirin and NSAIDs increasing bleeding risk and acetaminophen is bad on the liver)
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75
Q

How can we treat ascites 5

A
  • Sodium restriction (2g/day)
  • Diuretics to remove fluid
  • Possible albumin infusion
  • Paracentesis
  • Transjugular intrahepatic portosystemic shunt (TIPS)
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76
Q

What is our tx for esophageal and gastric varices 6

A
  • Avoid alcohol, aspirin, NSAIDs
  • Nonselective beta blockers to decrease portal hypertension
  • Octreotide or vasopressin to cause vasoconstriction, decrease portal blood flow and decrease portal hypertension (no pharm on this test)
  • Endoscopic band ligation or schlerotherapy
  • Balloon tamponade (mechanically compresses varices)
  • TIPS
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77
Q

What is happening in TIPS

A

shunting blood away from the portal blood flow and into the systemic venous system to help reduce portal venous pressure and the pressure on those varices

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78
Q

What do we do if someone is having active bleeding 6

A
  • Fresh frozen plasma
  • Packed RBCs
  • Vitamin K
  • PPIs
  • Lactulose to help prevent HE
  • Antibiotics
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79
Q

What is interesting about protein for a pt with cirrhosis and no HE and a pt with cirrhosis and HE

A

Protein restriction may be needed for some pts right after a severe flare of symptoms (like HE), however, protein restriction is rarely needed in pts with cirrhosis and persistent HE, because malnutrition is a bigger issue than HE

(ammonia is a byproduct of the breakdown of protein into amino acids)

(so yes this breakdown of protein can cause HE, but often we’re more concerned about malnutrition)

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80
Q

What is some pt care for someone receiving a paracentesis 4

A
  • Have them go to the bathroom immediately before
  • Teach pt to remain immobile during procedure
  • Help the pt to a high-fowler position with feet on the floor
  • Weigh pt before and after
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81
Q

What should we do if a pt has a balloon tamponade 4

A
  • Verify balloon position with x-ray
  • Have scissors at the bedside to cut the tube and deflate the balloon if airway becomes obstructed
  • Pts can’t swallow with this so help by clearing the airway with suctioning
  • Have them in semi-fowler’s
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82
Q

What is our nursing care for someone with HE 4

A
  • Assess LOC every 2 hours
  • Prevent falls/injuries
  • Avoid constipation (this can make the ammonia buildup worse)
  • Assess for excessive diarrhea, fluid loss and electrolyte loss for pts taking lactulose
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83
Q

What is happening in acute pancreatitis

A

There’s acute inflammation of the pancreas and also spillage of pancreatic enzymes into the surrounding pancreatic tissue causing autodigestion and severe pain (remember pancreatic enzymes break things down, so you don’t want them out in the tissue breaking things down)

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84
Q

What are the causes of acute pancreatitis 8

A
  • Gallbladder disease (gallstones) (gallstones can block pancreatic ducts)
  • Chronic alcohol use
  • Trauma
  • Infections
  • Drugs reactions
  • Potop GI surgery
  • Hypertriglyceridemia (high fat diet)
  • Pancreatic cancer
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85
Q

What are the s/s of acute pancreatitis

A

Abdominal pain
- Sudden onset
- Left upper quadrant or mid-epigastric
- Radiates to back
- Deep, piercing, continuous, or steady
- Eating worsens pain
- Starts when recumbent
- Nausea/vomiting
- Pain not relieved with vomiting

Abdominal skin discoloration
- Grey Turner’s spots or sign (blue flank discoloration)
- Cullen’s sign (bluish discoloration around the belly button)

  • Decreased or absent bowel sounds
  • Abdominal tenderness with muscle guarding
  • Dyspnea (hurts to take a deep breath - can cause atelectasis)
  • Crackles in lungs
  • Low-grade fever
  • Hypotension, tachycardia = shock
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86
Q

What are 2 local complications of acute pancreatitis?

A
  • Pseudocyst
  • Pancreatic abscess
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87
Q

What is a pseudocyst? What are symptoms? How can we detect it? What are txs?

A
  • Accumulation of fluid, pancreatic enzymes, tissue debris, and inflammatory exudates surrounded by a wall next to the pancreas
  • S/S: abdominal pain, palpable epigastric mass, n/v, anorexia
  • Can be detected with imaging
  • Usually resolve spontaneously, but may perforate and cause peritonitis and need surgical tx

(body is trying to protect itself by walling off these enzymes and bad things - leading to a pseudocyst)

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88
Q

What is a pancreatic abscess? What are s/s?

A
  • Infected pseudocyst that may rupture or perforate
  • Abdominal pain, mass, high fever, leukocytosis
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89
Q

What are systemic complications of acute pancreatitis

A

Cardiovascular and pulmonary problems like:
- Pleural effusion
- Atelectasis
- Pneumonia
- ARDS
- Hypotension
- Thrombi, PE, DIC
- Hypocalcemia (tetany)

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90
Q

What lab values would we see for signs of acute pancreatitis

A
  • Elevated amylase
  • Elevated lipase
  • Elevated glucose
  • Elevated triglycerides
  • Elevated bilirubin
  • Decreased calcium
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91
Q

What are normal amylase and lipase labs

A

Amylase 30-110
Lipase 0-150

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92
Q

What type of diagnostic imaging might they do for acute pancreatitis

A
  • Ultrasound
  • X-ray
  • Contrast enhanced CT
  • Magnetic resonance cholangiopancreatography (MRCP)
  • Endoscopic retrograde cholangiopancreatography (ERCP) (fyi - ERCP can cause acute pancreatitis too)
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93
Q

What are our goals of care for someone with acute pancreatitis 6

A
  • Relief of pain
  • Prevention or alleviation of shock
  • Decreased pancreatic secretions
  • Correction of fluid/electrolyte imbalances
  • Prevention/treatment of infections
  • Removal of precipitating cause
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94
Q

What 4 things can we do to help manage acute pancreatitis

A
  • NPO with NG to suction (gut rest - want to stop the pancreas from working and releasing enzymes)
  • Albumin (if in shock)
  • IV calcium gluconate (if tetany present)
  • LR
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95
Q

Why would we want to put a pt on NPO if they have acute pancreatitis

A

We want to help reduce or suppress pancreatic enzymes, which can allow the pancreas to rest

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96
Q

What 2 things can help prevent infection

A
  • Enteral nutrition
  • Antibiotics
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97
Q

Why might a pt get a PPI

A

To help decrease stomach acid, which can trigger the pancreas

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98
Q

What two things might we give to help control pain

A
  • IV opioid analgesic
  • Antispasmodic (decreases vagal stimulation, motility, and pancreatic outflow)
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99
Q

What surgical things might they do for acute pancreatitis

A
  • If they have gallstones they might do an ERCP or laparoscopic cholecystectomy
  • Might do surgery if they’re not sure of diagnosis
  • If pts are not responding to conservative therapy
  • To drain necrotic fluid
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100
Q

What is some nutritional care for someone with acute pancreatitis 6

A
  • NPO status initially
  • Will try enteral before parenteral
  • Monitor triglycerides if IV lipids are given
  • Small frequent feedings of high-carb foods (carbs seem to be the less stimulating for the pancreas)
  • No alcohol
  • Supplemental fat-soluble vitamins
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101
Q

What are the 2 signs of hypocalcemia

A
  • Chvostek’s sign (contraction of the facial muscle w/light tap over the facial nerve)
  • Positive trousseau’s sign (carpal spasm caused by inflating a blood pressure cuff)
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102
Q

What 2 positions may help decrease a pts pain with acute pancreatitis

A
  • Flex the trunk and bring knees up to abdomen
  • Go into a side-lying position with the HOB elevated at 45 degrees
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103
Q

Basically what types of infections are we really worried about with someone with acute pancreatitis

A

RESPIRATORY

  • They may not be taking in deep breaths because of the pain (they’re not coughing and deep breathing)
  • The inflammation and gunk from the acute pancreatitis may travel up towards the lung
  • NG tube may introduce pathogens
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104
Q

Are crash diets good to do after acute pancreatitis

A

NO!

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105
Q

What pt/family teaching should you give to someone being discharged after having acute pancreatitis

A
  • Monitor for signs of infection, diabetes, steatorrhea (foul-smelling fatty stools)
    (these changes may indicate that the pancreas is still being destroyed by enzymes)

(hyperglycemia = excessive peeing, thirst and hunger)

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106
Q

What things might cause chronic pancreatitis 7

A
  • Alcohol
  • Gallstones
  • Repeated episodes of acute pancreatitis
  • Cystic fibrosis (clogging of the ducts)
  • Autoimmune pancreatitis
  • Tumor
  • Systemic diseases like lupus
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107
Q

What are the two major types of chronic pancreatitis

A
  1. Chronic obstructive pancreatitis
  2. Chronic nonobstructive pancreatitis (most commonly caused by alcohol abuse)
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108
Q

What are the s/s of chronic pancreatitis

A
  • Abdominal pain (same area as acute, it’s a heavy, gnawing feeling, can feel like burning and cramping, will be very frequent and almost constant)
  • Malabsorption with weight loss
  • Constipation
  • Mild jaundice with dark urine
  • Steatorrhea (fatty stools)
  • Diabetes
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109
Q

What are complications of chronic pancreatitis

A
  • Pseudocyst formation
  • Bile duct or duodenal obstruction
  • Pancreatic ascites
  • Pleural effusion
  • Splenic vein thrombosis
  • Pseudoaneurysms
  • Pancreatic cancer
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110
Q

What are some diagnostic studies to help determine if someone has chronic pancreatitis

A

(can be difficult to diagnosis)
- Amylase/lipase may or may not be elevated
- Bilirubin and alkaline phosphatase may be elevated
- Mild leukocytosis
- High sedimentation rate
- ERCP, CT, MRI, MRCP, ultrasound, EUS may be completed
- Stool samples are examined for fat
- Glucose intolerance/diabetes are assessed

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111
Q

What pt care and education might be do for someone with chronic pancreatitis

A
  • Analgesics for pain relief
  • Diet (small, frequent, low fat meals)
  • No smoking, alcohol or caffeine
  • Might need to replace pancreatic enzymes
  • Bile salts
  • Insulin may be needed
  • Acid-neutralizing and acid-inhibiting drugs
  • Antidepressants
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112
Q

Why don’t we want someone with acute or chronic pancreatitis to smoke

A

Smoking can accelerate the progression of chronic pancreatitis

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113
Q

What 3 enzymes are we trying to replace by giving pancreatic enzymes

A
  • Amylase
  • Lipase
  • Trypsin
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114
Q

How do we know if pancreatic enzymes are not working when given as a supplement

A

Steatorrhea will occur if they are not working (fat in stools because the enzymes aren’t breaking down the fat in the body)

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115
Q

Why might we give bile salts

A

To help with fat-soluble vitamin absorption and prevent further fat loss

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116
Q

Why antidepressants

A

Can help reduce neuropathic pain

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117
Q

What’s the process when the kidneys sense a drop in BP (picture)

A
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118
Q

How do the kidneys take part in RBC production

A

They create erythropoietin, which triggers the bone marrow to make more RBCs

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119
Q

What in the kidneys is responsible for filtration

A

The glomerulus

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120
Q

What is the glomerular filtration rate? What is the normal rate?

A

The amount of blood filtered each minute by the glomeruli, normal is 125mL/min

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121
Q

What is a normal amount of urine output per day

A

1500mL

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122
Q

How much urine can the bladder hold

A

600-1000mL

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123
Q

What does oliguria mean

A

Less than 400mLs of urine/day

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124
Q

What is anuria

A

No urine output

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125
Q

What is uremia

A

High levels of urea in urine

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126
Q

What is azotemia

A

High levels of nitrogen in the urine

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127
Q

Comparison table of AKI and CKD

A
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128
Q

What, overall, can cause AKI

A

Some “big event” - remember sisterwives

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129
Q

In general, what diseases can contribute to kidney disfunction and why? Which two are most common? 7

A
  • *Hypertension (squeezes off blood flow to the kidneys)
  • *Diabetes (damages blood vessels leading to poor blood flow)
  • Rhabdomyolysis (myoglobin gets lodged in the kidneys causing blockages and reduced blood flow)
  • Immune disorders- lupus, scleroderma (antibodies can cause blockages)
  • Peripheral vascular disease (lack of blood flow)
  • Cardiovascular disease (not enough cardiac output to perfuse the kidneys adequately)
  • Pregnancy (pre-eclampsia - high BP)

(hypertension and diabetes are the most common causes)

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130
Q

What sucks about AKI

A

Usually affects people with other life-threatening conditions and has a high mortality rate

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131
Q

What are the 3 different types of AKI

A
  1. Pre-renal
  2. Intrarenal
  3. Postrenal
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132
Q

What is happening in pre-renal injury

A

There is a reduced blood flow to the kidneys (so nothing is actually wrong with the kidneys, they’re just not getting any blood)

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133
Q

What can cause pre-renal injury and what are examples of each 4

A
  1. Decreased CO (like from HF, cardiogenic shock)
  2. Decreased peripheral vascular resistance (like from anaphylaxis)
  3. Decreased renovascular blood flow (could have an emboli blocking blood flow)
  4. Hypovolemia (like from burns, dehydration, GI losses, diuresis, hemorrhage, hypoalbuminemia)
134
Q

What does your body try to do in the case of pre-renal injury

A

It tries to compensate to preserve blood flow by increasing angiotensin 2, aldosterone, norepinephrine, and antidiuretic hormone try to preserve blood flow to essential organs (basically it tries to retain blood instead of turning it into urine)

135
Q

Pre-renal injury is reversible, but if the underlying issue isn’t resolved, what can happen?

A

The prolonged blood flow to the kidneys (ischemia) can cause intrarenal injury (damage to the kidney itself)

136
Q

What is happening in intrarenal kidney injury

A

There is direct damage to the kidneys themself

137
Q

What can cause intrarenal kidney injury 6

A
  1. *Acute tubular necrosis (most common cause)
  2. Nephrotoxins
  3. Prolonged ischemia (from pre-renal)
  4. Tubular obstruction like from uric acid casts
  5. Hemoglobin released from hemolyzed RBCs causing blockage
  6. Myoglobin causing blockage from rhabdo
138
Q

How can nephrotoxins damage the kidneys

A

By either crystallizing or causing damage to the epithelia cells of the tubules

139
Q

What are examples of nephrotoxins 3

A
  1. Aminoglycosides (drugs ending in “cin” like gentamycin)
  2. NSAIDs
  3. IV contrast (especially in older pts who might not have good kidney function due to aging)
140
Q

Is vancomycin an aminoglycoside

A

NO!

141
Q

What are the txs to reverse nephrotoxins or prevent toxicity from occurring 3

A
  • Administer Acetylcysteine 1200mg daily
  • Draw up trough levels to ensure therapeutic levels
  • Increase fluids to help flush the kidneys
142
Q

What is acute tubular necrosis

A

Damage or death of epithelial cells lining the renal tubules, which causes these damaged or death epithelial cells to collect and cause obstruction

143
Q

What can cause acute tubular necrosis 3

A
  • Ischemia
  • Toxins like contrast dye
  • Sepsis
144
Q

Is acute tubular necrosis reversible

A

Yes, if caught early enough

145
Q

Is

A
146
Q

How can we diagnosis acute tubular necrosis

A
  • UA will show muddy brown casts
147
Q

How can we treat acute tubular necrosis

A
  • Treat the underlying cause
  • Give IV fluids to help flush out the toxins causing the issue
148
Q

What is hepatorenal syndrome

A

Where cirrhosis causes portal hypertension, azotemia (elevated nitrogen waste because the liver is not removing this waste), prostaglandins causing vasodilation, which leads to hypoperfusion of the kidneys.

149
Q

How do the kidneys try to compensate during hepatorenal syndrome

A

They try to retain blood flow since they are not being perfused adequately, which activates the RAAS and causes retention of sodium, which leads to an increase in ascites

150
Q

What are common causes of hepatorenal syndrome 4

A
  1. GI bleed
  2. Excessive diuretics
  3. Large-volume paracentesis
  4. Infections
151
Q

What are 3 signs of hepatorenal syndrome

A
  1. Azotemia (increased nitrogenous waste)
  2. Ascites
  3. Oliguria
152
Q

Besides being on the ground for a prolonged amount of time, what can cause rhabdomyolysis 4

A

1 Crush injuries
2. Status epilepticus (from seizures with prolonged muscle contractions)
3. Too much exercise
4. Illegal drugs

153
Q

How can myoglobin cause AKI

A

It can get stuck in the kidneys

154
Q

What would urine look like for someone who has rhabdo

A

Dark tea/red urine due to the myoglobin in the urine

155
Q

What is the tx for rhabdo 4

A
  • Aggressive fluid replacement
  • Restore intervascular volume (because hypovolemia makes rhabdo worse) by giving mannitol
  • Give IV bicarb (because rhabdo causes metabolic acidosis
156
Q

What is post-renal kidney injury

A

Where there is a mechanical obstruction to the outflow of urine (something blocking the urinary tract)

157
Q

What can cause post-renal kidney injury 6 (probably only need to remember the most common cause)

A
  • *BPH (most common)
  • Prostate cancer
  • Calculi (stones)
  • Trauma
  • Extrarenal tumors
  • Bilateral ureteral obstruction
  • UTI causing a lot of urination
158
Q

How do we diagnosis post-renal kidney injury

A

Renal ultrasound

159
Q

What is it called when the urine backflows into the kidneys due to a post-renal injury

A

You have hydronephrosis

160
Q

What is hydronephrosis

A

Dilation and swelling of the kidney when urine can’t be drained caused by partial or complete blockage or reflux, where the renal pelvis swells with fluid

161
Q

Hydronephrosis may or may not cause s/s, if it does, what are they 5

A
  • Flank, abdominal or groin pain pain
  • Pain with urination
  • Increased urge to urinate, but unable to go
  • Nausea
  • Fever
162
Q

What classification system can we use to help classify the stages of AKIs? And what are the stages?

A

We can use the RIFLE classification
R = risk
I = Injury
F = failure
L = loss
E = end-stage renal disease

163
Q

What two things is the RIFLE system looking at to determine the classification

A

Changes in creatinine and GFR (ie creatinine level increased by 1.5 or GFR decreased by 25% = Risk category)

164
Q

What are the 4 stages of AKI? How can we remember them?

A
  1. Onset phase
  2. Oliguric phase
  3. Diuretic phase
  4. Recovery phase
    Think “oh oh darn renal”
165
Q

Picture of the 4 stages

A
166
Q

What is happening in the first phase, onset? What do we want to do?

A

The triggering event happens to cause the AKI.

We want to find and fix the problem to prevent long term affects

167
Q

What is interesting about the second phase, oliguric?

A

You will either be oliguric, where you will have urinary output of less than 400mL/day or you will be nonoliguric, where you will not have a decreased urine output.

168
Q

If you are oliguric, what will we see 7

A
  • 400mLs or less of urine per day
  • Decreased GFR
  • Increased BUN and creatinine
  • Azotemia can develop due to the buildup of nitrates
  • Urine will be concentrated and dark
  • Specific gravity will be concentrated (so low number)
  • UA may show casts, RBCs, WBCs
169
Q

How long can the oliguric phase last? What is not good about this phase?

A

It can last up to two weeks - very dangerous phase, because it can cause the most damage to your body if left untreated (causes waste buildup in the body, because the kidneys aren’t filtering)

170
Q

What is our tx for the oliguric phase? Why?

A

Dialysis, because we can’t give fluids or other things, because the kidneys are unable to process anything

171
Q

What changes in fluid volume may we see with the oliguric phase

A

Hyppervolemia bc we’re not getting rid of fluid

172
Q

What are 4 signs of hypervolemia

A
  1. Distended neck veins
  2. Bounding pulse
  3. Edema
  4. Hypertension
173
Q

What can this fluid overload in the oliguric phase lead to 3

A
  • HF
  • Pulmonary edema
  • Pericardial and pleural effusions
174
Q

Why does the oliguric phase lead to metabolic acidosis

A

Because the kidneys are unable to excrete hydrogen ions (acids) and sodium bicarb is trying to compensate, but it’s being all used up so it’s depleted

175
Q

As severe acidosis develops, what is a sign from respiratory trying to componsate for the increased acids

A

Kussmaul breathing (trying to breath off any excess CO2) - Deep, rapid breaths

176
Q

What would pH, CO2 and HCO3 look like for someone with metabolic acidosis in the oliguric phase

A

pH would be less than 7.35

CO2 would be normal

HCO3 would be below 22

177
Q

Why would someone develop hyperkalemia in the oliguric phase

A

Because the kidneys aren’t able to excrete the potassium

178
Q

AKI caused by what things, can increase the hyperkalemia risk? Why? 3

A
  • If the AKI is caused by a trauma, where the damaged tissue cells release more potassium into the extracellular fluid
  • If it is caused by bleeding or blood transfusions, which can cause cellular damage and lead to more potassium being released from these damaged cells
  • Metabolic acidosis, because excess hydrogen ions can go into cells and drive out potassium
179
Q

What 3 things on an EKG might show hyperkalemia

A
  • *Peaked T waves
  • Widening QRS
  • ST depression
180
Q

What are our txs for hyperkalemia and why? Which one is the only long term tx?

5

A
  • Insulin and glucose to push potassium into cells (glucose because we don’t want to drop their sugar) (D50)
  • Sodium polystyrene sulfonate (Kayexalate) (only long term tx)
  • Calcium gluconate (helps your body tolerate dysrhythmias more by raising the level of excitation)
  • Sodium bicarb to correct acidosis (also helps shift potassium back into cells)
  • Albuterol to drive potassium back into the cells
181
Q

What is important to remember about the txs for hyperkalemia

A

They’re all short term except for the kayexalate, because potassium will eventually shift back out of the cells

182
Q

How does Kayexalate work? When would you not want to give it?

A

Moves potassium into the bowel, so that it can be excreted in stool

Don’t want to give if someone’s bowel isn’t functioning

183
Q

Besides Kayexalate, what is the other way to excrete potassium

A

Dialysis

184
Q

What 2 drugs does Kayexalate decrease the absorption of

A

Lithium and thyroxine

185
Q

How can the oliguric phase effect the hematologic system

A

It can cause leukocytosis

186
Q

What are signs that waste is accumulating in the oliguric phase 4

A
  • Neuro status changes
  • Seizures, stupor, coma
  • Itching skin
  • Elevated BUN and creatinine
187
Q

What type of diet should someone be on when they’re in the oliguric phase

A

Low protein

188
Q

What is happening in the diuretic phase

A

This is when your kidneys start to work again by producing urine, but they are only able to excrete waste and unable to concentrate the urine (basically the kidneys are just dumping everything out, including electrolytes that they should be trying to hold onto)

189
Q

How much urine can the body dump out in the diuretic phase

A

Usually around 1-3 L, but it may even be as high as 5 L

190
Q

So if our body’s dumping out everything (including needed electrolytes) in the diuretic phase, what are we worried about

A
  • Hyponatremia
  • Hypokalemia
  • Hypovolemia
191
Q

Basically what is BUN and creatinine a measure of

A

How much waste the body can excrete (an elevated number indicates higher waste in the body, which indicates that the kidneys aren’t functioning as they should be)

192
Q

Towards the end of the diuretic phase, what will labs look like

A

They will start to normalize including acid base, electrolytes, waste product (BUN and creatinine)

193
Q

What will the specific gravity look like in the diuretic phase

A

Diluted

194
Q

What is the normal specific gravity

A

1.010-1.030

195
Q

What does a high and low urine specific gravity tell us

A

High = the urine is concentrated, so this can indicate hypovolemia
Low = urine is diluted, so we see low specific gravity (we would see low for diuretic)

196
Q

How long may the recovery period last

A

Can last for up to 12 months with major improvements occurring in the first couple of weeks

197
Q

What can permanent damage from AKI lead to

A

Chronic kidney disease (CKD)

198
Q

How will we know if someone is in the recovery phase

A
  • GFR will increase and normalize
  • Urine output will normalize around 1-2L/day
  • BUN and creatinine will normalize
  • Electrolytes will stable
199
Q

Picture of the s/s of AKI

A
200
Q

When doing diagnostic, what is contraindicated if you have AKI

A

Contrast dye

201
Q

What phase would we not want to give diuretics

A

The oliguric

202
Q

Basically are diuretics good to give for AKI

A

Not if the person already has AKI, can do more harm than good

203
Q

How do we calculate fluid restriction (probably don’t need to know is what she said - maybe just have a general idea of how to calculate to stay safe)

A

All up all of the previous losses in the last 24hrs (urine, diarrhea, emesis, blood) and add 600mL for insensible losses (respiration, diaphoresis), what that equals is your fluid restriction for the next day.
Ex - 300mL of urine + 600mL of insensible losses = 900mL fluid restriction

204
Q

What are some dietary restrictions we may have for our pts 3

A
  • Limit protein (protein becomes urea and we don’t want to give the kidneys extra work since they excrete this waste)
  • Increase fat to compensate for the low protein
  • Sodium restriction if holding a lot of fluid
  • Possible potassium restriction
205
Q

What foods are high in potassium (a lot)

A

Avoid foods high in potassium-Veggies-Avocado, acorn squash, butternut squash, pumpkin, kale, spinach, fennel, Brussel sprouts, broccoli, artichokes, arugula, sweet potato, yams, lima beans, white beans, white potato, carrots, beets, swiss chard,
Fruit-dried apricots, pomegranate, coconut water, watermelon, bananas
Meats-salmon, salami, ham, most luncheon meat, most pork, and red meats.
Grains- any enriched, whole grain products (breads pastas)
Dairy-milk, cheese, eggs, regular plain yogurt

206
Q

What are indications for renal replacement therapy (dialysis) for pts with AKI

A
  • Volume overload
  • Elevated serum potassium level
  • Metabolic acidosis
  • BUN level > 120 mg/dL (43mmol/L)
  • Significant change in mental status
  • Pericarditis, pericardial effusion, or cardiac tamponade
207
Q

What 2 types of dialysis are used for AKI and which is not used

A

Used:
- Intermittent hemodialysis
- Continuous renal replacement therapy (it’s like a 24hr thing)

Not used:
- Peritoneal dialysis (used for CKD)

208
Q

When would we use Continuous renal replacement therapy over intermittent hemodialysis

A

When the pt is hemodynamically unstable (like taking off a lot of fluid during hemodialysis may really mess them us)

209
Q

Give some more info about Continuous renal replacement therapy 5

A
  • Usually used in the ICU for critically ill pts
  • Not used when changes are needed urgently
  • Fluid is removed slowly over days instead of hours
  • Doesn’t require a hemodialysis nurse
  • Reduce tx interruptions by preventing clots and maintaining the line
210
Q

What is an important thing to remember about CRRT and medications

A

Different amounts of medication should be considered based on whether someone is having the therapy or not (it will be metabolized differently in the body depending on whether they’re receiving the CRRT at the time or they may be taking a break from it)

211
Q

What can we do to help prevent AKI 3

A
  • Monitor high risk populations (like geriatrics) for s/s
  • Control exposure to nephrotoxic drugs (ie if they’re on antibiotics, make sure they’re taking a lot of fluids to help flush them out)
  • Prevent prolonged episodes of hypotension and hypovolemia (prevent sepsis)
212
Q

Why are geriatrics more at risk for AKI (a lot)

A
  • Usually more dehydrated
  • Kidneys are less able to compensate for fluid volume changes
  • GFR decreases
  • Size and weight of kidneys decrease
  • Atherosclerosis accelerates decrease renal size with age
  • Might be taking many medications that can cause it if not well hydrated
  • Decrease thirst
  • Might not seek tx for infections
  • A lot of older men have BPH
  • Don’t handle contrast dye as well
  • Altered hormonal levels which decreases ability to concentrate urine and alters the excretion of water, sodium, potassium and acid
213
Q

What is glomerulonephritis

A

Inflammation of the glomeruli

214
Q

What often causes glomerulonephritis

A

Usually from strep A infections, especially when we see symptoms in children

215
Q

What three infections can be caused by strep A

A
  • Impetigo
  • Scarlet fever
  • Strep throat
216
Q

What would strep A cause glomerulonephritis

A

The body produces antibodies to the strep A, and these antibodies get lodged in the glomeruli, leading to inflammation

217
Q

What are s/s of glomerulonephritis (a lot, remember the key one)

A
  • Pink, smoky or rusty colored urine due to hematuria
  • *Pink/red Frothy, bubbly urine
  • RBCs casts
  • Proteinuria
  • Decrease in the urine pH
  • Hypertension
  • Edema (usually in the face, hands, feet and abdomen in children)
  • Oliguria
  • N/V
  • Increased potassium
  • Decreased GFR
  • Increased BUN and creatinine
218
Q

What is some good teaching for glomerulonephritis

A

You can have this time after time after having a strep A infection, so if you or your kid has strep A, make sure you come in and get tx otherwise you may develop this after each infection

219
Q

What is nephrotic syndrome

A

Body passing too much protein through the kidneys and into the urine, so excreting a large amount of protein

220
Q

What can cause nephrotic syndrome

A

Many different things like diabetes, lupus, allergic reactions, cancers, medications, etc

221
Q

Picture of nephrotic syndrome

A
222
Q

What are s/s of nephrotic syndrome and why? A LOT

A
  • Peripheral edema (low albumin levels cause water and sodium retention, which leads to edema)
  • Massive proteinuria (greater than 3g/day)
  • Hypertension
  • Hyperlipidemia (low protein causes the liver to create cholesterol and triglycerides to help compensate)
  • Hypoalbuminemia
  • Dark Foamy urine due to proteinuria
  • Loss of immunoglobulins (protein that helps fight infection)
  • Loss of anticoagulants (albumin helps prevent clots, so if we don’t have enough albumin we are at risk for blood clots)
  • Decreased appetite due to ascites pressing on abdomen
  • Low calcium and vitamin D levels
223
Q

What is a major cause of death due to nephrotic syndrome

A

Infection, because the body is excreting immunoglobulins

224
Q

What is our tx for nephrotic syndrome

A
  • Diuretics
  • Statins
  • Prednisone to decrease inflammation
  • Anticoagulants
225
Q

What are our nursing interventions for nephrotic syndrome

A
  • Looking for s/s of blood clots
  • Measuring abdominal girth or extremities
  • Low fat diet due to the hyperlipemia
  • Limit visitors to prevent infection
226
Q

What can cause kidney stones

A
  • Changes in diets
  • Genetic
  • Lifestyle choices
  • Dehydration
  • Metabolic
  • Excess body weight
  • Taking supplements
227
Q

At what size can most kidney stones pass

A

If they are less than 5mm

228
Q

Are kidney stones only lodged in the kidneys

A

No, they can be other places like the ureters, bladder, etc

229
Q

What are the 5 different types of kidney stones and what can cause them?

A
  • calcium oxalate (caused by too much calcium - hypercalcemia, hyperparathyroidism)
  • calcium phosphate (alkaline urine - most common type of stone)
  • cystine (too much amino acids)
  • struvite (formed from chronic UTIs)
  • uric acid (gout)
230
Q

What are the s/s of kidney stones 5

A
  • Renal colic - excruciating pain around flank, back or lower abdomen.
  • Uritic colic - pain going towards groin
  • N/V
  • Trouble sitting still
  • Possible signs of infection due to urinary retention
231
Q

What are 2 complications of kidney stones

A
  • Infections (like UTIs and pyelonephritis)
  • Hydronephrosis (causing a buildup of urine) (so urine is not flowing well with this blockage)
232
Q

What would we see in the UA for someone with kidney stones 2

A
  • Hematuria (caused from the stone scrapping the lining)
  • Crystalluria
233
Q

How can we tx kidney stones

A

We want to stop what is causing it, so we will look at a pts labs to see if something is off, like they may have high calcium, so that may be causing calcium oxalate stones, then we can work towards decreasing their calcium

234
Q

How can we manage kidney stones

A
  • Encourage fluid
  • Strain urine to catch stones so they can be analyzed to see what they’re made out of so we know what we need to correct
  • Monitor for s/s of UTIs
  • Flomax may help pass the stone
  • Keep pt mobile and not supine to help them move through
  • Lithotripsy (noninvasive shock waves can hit stones and help break them up)
  • Cystolitholapaxy (invasive go in and take out stone)
  • Possibly place a stent to help them pass
235
Q

What is the biggest thing to watch for with blunt renal trauma

A

These pts can bleed out very quickly if the kidneys have been through a trauma because they hold a large amount of the body’s blood

236
Q

Is CKD reversible?

A

No - it’s irreversible

237
Q

What is interesting about CKD and whether people know they have

A

A lot of people have CKD, but a lot of them don’t know they have it because it can be asymptomatic

238
Q

What is happening in CKD

A

More and more nephrons stop working so it’s unable to filter properly

239
Q

What is the criteria for being diagnosed with CKD

A

Have to have a low GFR at 60mL/min or less for longer than 3 months

240
Q

What are the 2 leading causes of CKD and why

A
  1. Diabetes - uncontrolled hyperglycemia causes glucose to stick to the artery walls, thus decreasing blood flow to the kidneys
  2. Hypertension - causes less blood to reach the kidneys

(both cause decreased perfusion to the kidneys)

241
Q

Picture of the stages of CKD

A
242
Q

Which stage is considered end-stage renal disease (ESRD) and what is the GFR

A

Stage 5, when GFR is less than 15

243
Q

At what stage is a pt most likely going to need dialysis or a kidney transplant

A

Stage 5

244
Q

What is uremia

A

Syndrome where kidney function declines to the point that the build up of waste (including uremia) pretty much cause damage to every body system

Typically occurs when GFR is less than or equal to 15

245
Q

How is the urinary system affected by CKD 3

A
  • Early stages: no change in urine output, may have polyuria as kidneys are unable to concentrate the urine, diabetes can make this worse
  • Middle stages: as CKD progresses, fluid retention is increased and there may be a need for a diuretic
  • Late stages: anuric (no urine phase),
246
Q

What are signs of increased urea nitrogen (BUN) levels in the body 5

A
  • n/v
  • lethargy
  • fatigue
  • impaired thought processes
  • headaches
247
Q

How does CKD affect carbohydrate metabolism

A

It can causes insulin in the body to desensitize itself to glucose, which causes the body to breakdown less glucose and leading to increased levels of glucose in the body, causing hyperglycemia, and that insulin is at an increased level (even though it’s not doing its job) because the kidneys aren’t able to excrete that extra insulin because they’re not working right

(basically not on dialysis you can have hyperglycemia and hyperinsulinemia, on dialysis you can have hypoglycemia and hyperinsulinemia if the amount of insulin you’re giving isn’t adjusted)

248
Q

What if your pt needs insulin and they are on dialysis

A

They may actually need less insulin when on dialysis, because the dialysis causes insulin to stay in the body longer, making it more effective, which means less insulin may be needed (should monitor glucose levels carefully)

249
Q

How can CKD impact triglycerides

A

The hyperinsulinemia may cause the liver to produce more triglycerides (which can lead to an increase in LDLs and a decrease in HDLs) which increases risk for CVD (most people who have CKD die from CVD) (LDL = bad, HDL = good)

250
Q

At what potassium level can fatal dysrhythmias occur

A

When potassium reaches 7-8

251
Q

Why does hyperkalemia happen in CKD

A

Because the kidneys are responsible for excreting 90% of the body’s potassium

And hydrogen ions are going into cells and pushing potassium out which leads to a buildup as well (metabolic acidosis)

252
Q

What can too much sodium while having CKD do? What can happen? 3

A

Cause dilutional hyponatremia (because sodium levels are being decreased by retaining too much fluid), which can lead to edema, hypertension and HF

253
Q

If the pt has dilutional hyponatremia should we have them eat more salt? What is the sodium restriction?

A

NO - this can actually make the probably worse by causing them to retain more sodium

Restrict to 2g/day

254
Q

How does CKD impact the body’s calcium levels

A

The kidneys are unable to make vitamin D, so the body can’t absorb calcium, leading to hypocalcemia

255
Q

How does CKD impact phosphate levels

A

The kidneys are responsible for excreting phosphate, so phosphate levels increase with CKD

256
Q

So what does the low calcium and high phosphate levels cause the body to do

A

The body wants calcium and phosphate to balance, so to help match the body tries to increase calcium by stimulating the parathyroid hormone to get more calcium from the bones, which leads to bone remodeling

257
Q

So what does the low calcium and high phosphate levels cause the body to do

A

The body wants calcium and phosphate to balance, so to help match the body tries to increase calcium by stimulating the parathyroid hormone to get more calcium from the bones, which leads to weak/brittle bones and hardening of arteries (leading to decreased perfusion to organs) (excess calcium coming out of the bones can cause plaques to form on blood vessels, causing them to harden)

258
Q

Simply, how does metabolic acidosis happen in CKD

A

Kidneys are unable to excrete hydrogen ions (leading to acidosis) and is not good at creating or absorbing bicarb, leading to metabolic acidosis

259
Q

How can CKD lead to anemia

A
  • Decreased production of erythropoietin
  • Decreased iron
  • Folic acid lost in dialysis
  • Decreased b12

(all lead to a decrease in RBC and hemoglobin production)

260
Q

What are s/s of anemia 4

A
  • Fatigue
  • SOB
  • Pale
  • Confused
261
Q

Does CKD cause bleeding issues? Why or why not?

A

Yes - because it causes dysfunction in platelet production leading to an increase risk of bleeding

262
Q

How does CKD impact the immune system

A

Causes a poor immune system so less able to fight off infection

263
Q

What about vaccinations and CKD

A

Since the immune system is decreased, having a vaccination, like to protect from the flu, won’t trigger a response that will make that vaccine effective (you want your body to make antibodies when it receives a vaccination, but it won’t with CKD, so vaccinations are pointless)

264
Q

Does dialysis help or weaken the immune system

A

It weakens the immune system

265
Q

Since CVD is the most common death caused by CKD, what factors increase the risk of death occurring related to the cardiovascular system (a lot)

A
  • Hypertension
  • Elevated lipid levels
  • Elevated calcium causing hardening in the arteries
  • RAAS system trying to fix perfusion, leading to increase hypertension
  • HF because the heart is working so hard
  • Dysrhythmias from electrolyte imbalances
  • Uremic pericarditis
  • Pericardial effusion
  • Cardiac tamponade
266
Q

Why would CKD cause dyspnea

A

Could be from fluid overload, pulmonary edema, uremic pleuritis or respiratory infection

267
Q

How can the GI tract be impacted by CKD (a lot)0

A

The excessive urea can cause:
- Stomatitis and ulcerations
- Uremic fetor (urinous odor of breath)
- Diabetic gastroparesis (delayed gastric emptying)
- GI bleeding cause by mucosal lining breakdown from urea
- Constipation caused by phosphate binders, iron salts, fluid restrictions or inactivity
- N/V
- Anorexia

268
Q

How does CKD affect the CNS 7

A

Causes CNS depression
- Lethargic
- Apathy
- Decreased ability to concentrate
- Altered mental status
- Seizures
- Coma
- Hypertensive encephalopathy

269
Q

How will CKD impact nerve conduction 3

A

Will cause it to slow down
- Restless leg syndrome
- Paresthesia
- Peripheral neuropathy (*can cause a burning sensation - different than diabetic, which is like numbness and tingling)

270
Q

How will CKD impact motor movements 3

A

Will cause:
- Foot drop
- Weakness and atrophy
- Loss of deep tendon reflexes

271
Q

If we see any the previous neuro symptoms, what are next steps

A

These pts need to go on dialysis because these symptoms are serious (dialysis can improve symptoms and stop the progression of these neuro symptoms)

272
Q

What are 3 complications caused by hypocalcemia and hyperphosphatemia

A
  • Osteomalcia - breakdown of bones and inability to create new bones effectively (soft bone syndrome)
  • Osteitis fibrosa - decalcification causes bone tissue to be replaced with fibrous tissue (also makes bones more breakable because they’re not as bendy)
  • Vascular and soft tissue becomes calcified (uremic red eye - calcium deposits on the eye, can interrupt the conduction of the heart)
273
Q

What does high levels or urea lead a person to have skin wise

A

Pruritus, really itchy skin that can lead to bleeding or infection risk due to the increase in scratching

274
Q

What is uremic frost

A

When urea crystalizes on the skin (usually BUN gets really high, usually above 200)

275
Q

Why would drug dosages need to be adjusted with CKD

A

As renal function declines with CKD, drugs can stay in the body longer, so dosages may need to be decreased

276
Q

How can we help control hypertension (which can accelerate CKD) 4

A
  • Weight loss
  • Lifestyle changes
  • DASH diet
  • Antihypertensives (ACE and ARBs) (careful with these because they can further decrease GFR and potassium)
277
Q

When it comes to calcium and phosphate, can we tell what’s going on by looking at labs

A

No - we’ll do a bone biopsy to find out what’s really going on

278
Q

What are our interventions for low calcium and high phosphate

A
  • Limit phosphate intake to less than 1g/day
  • Take phosphate binders with each meal (bind to phosphate so it can be excreted in the bowel)
279
Q

What is important to remember about phosphate binders

A

There are different types, like calcium based binders, iron based and non-calcium based binders

So if a pts calcium is high, we don’t want to give a calcium based binder, we will want to give a different one

280
Q

If phosphate levels are normal and calcium is still low what might we do

A
  • Give calcium or vitamin D supplements
281
Q

Should pts avoid magnesium with CKD

A

Yes, because the kidneys are no longer able to adequately excrete magnesium

282
Q

What 2 medications can we give for erythropoietin replacement

A
  1. Epoetin alfa (short acting)
  2. Darbepoetin alfa (long acting)
283
Q

When would we hold an erythropoietin replacement

A
  • If hemoglobin is above 13
  • If having uncontrolled hypertension (erythropoietin replacement can cause an increase in BP, because we’re creating more blood)
284
Q

What are the side effects of erythropoietin replacement

A
  • Thromboembolism
  • Hypertension
285
Q

When may someone need iron supplements

A

If ferritin falls below 100

286
Q

What are the side effects of iron supplements 3

A
  • Gastric irritation
  • Constipation
  • Dark color stool
287
Q

What is good teaching with iron supplements

A

Don’t take at the same time as calcium phosphate binders, because the calcium in the binder can bind with iron instead and decrease absorption of both

288
Q

If you have CKD, what do you want to avoid regarding blood? Why?

A

Avoid blood transfusions, because antibodies created during blood transfusions can make it harder to find a kidney donor. And blood transfusions can also cause iron overload.

289
Q

What should we limit our potassium to

A

2-3g/day

290
Q

What should phosphate be restricted to

A

1g/day

291
Q

Picture of foods high in phosphate

A
292
Q

Should CKD pts limit protein? What if they’re on dialysis?

A

Limit protein when not on dialysis

Increase protein when on dialysis

293
Q

What can help us remember what foods are high in phosphorus

A

Foods high in phosphorous are also high in protein (so if a food is high in protein, like diary or meat, then it’s probably also high in phosphorus)

294
Q

What is polycystic kidney disease (PKD)

A

A genetic disorder that causes fluid filled cysts to grow on or in your kidneys leading to CKD

295
Q

What are the 3 different types of PKD and what causes them?

A
  1. Infantile (appears in infancy and childhood) (autosomal dominant)
  2. Adult (autosomal recessive)
  3. Acquired (can be caused by CKD or long-term dialysis)
296
Q

Why are cysts bad in PKD

A

They put pressure on nearby tissue and vessels
- Pressure on the vessels decreases perfusion of kidneys and kidneys respond by activating the RAAS system and causing hypertension, this hypertension just causes less perfusion of the kidneys
- Cysts enlarge the kidneys and cause a decrease in function

297
Q

What are signs of PKD in adults

A
  • *Intense flank pain
  • Hematuria
  • Hypertension
  • Headaches
  • Palpable kidneys
  • UTIs
  • Kidneys stones
  • Inability to concentrate urine
298
Q

How do we diagnosis PKD 3

A
  • Genetic testing
  • Symptoms
  • Ultrasound or CT
299
Q

Since the size and amount of cysts increase with age, what if a pt only has 2 cysts but they have a family history of it

A

Then they can be diagnosed with PKD, they’re young, so we wouldn’t expect them to have a lot of cysts.

300
Q

Is there a tx? If not what do we do?

A

No cure - just work to manage symptoms
- Prevent infections of the urinary tract
- Nephrectomy may be done
- Dialysis and kidney transplant for end stage

301
Q

When would a pt have dialysis

A
  • GFR less than 15
  • Uremia can’t be managed with conservative measures
302
Q

How does peritoneal dialysis work

A

You inject a dialysis solution into the abdomen where it can come into contact with the peritoneal membrane for several hours, this membrane acts as a filter, allowing fluid and waste to pass through, which can then be drained out of the body

303
Q

Does peritoneal dialysis cause any pain?

A

Yes, at first, because your body doesn’t like the introduction of all of this fluid, but then after more and more txs it gets used to it.

304
Q

What are the 3 phases of peritoneal dialysis (PD)

A
  1. Inflow (fill phase) usually 2L of dialysate is infused.
  2. Dwell time: diffusion and osmosis takes place
  3. Drain: takes 15-30 min to drain out, usually need to massage the abdomen or change positions to make sure everything comes out
305
Q

Since dextrose is the most common osmotic agent used in PD solutions, what is a risk

A

Hypertriglyceridemia or hyperglycemia can occur due to potentially high rates of of the peritoneal membrane absorbing the glucose in the dextrose solution

306
Q

What are alternatives to dextrose solutions if increases in sugars are occurring? 2

A
  • Icodextrin
  • Amino acid solutions
307
Q

What are the 2 types of PD

A

Automated peritoneal dialysis: which has a machine insert and exchange the fluid while the pt sleeps

Continuous ambulatory peritoneal dialysis: done every few hours during the day, usually going through 4 cycles per day (manual - not a machine)

308
Q

What are the advantages of PD (a lot)

A
  • a flexible lifestyle and independence
  • few diet restrictions (bc you’re always having this exchange)
  • usually visit clinic just once a month
  • doesn’t use needles
  • gives better blood pressure control
  • is continuous therapy which is gentler and more like your natural kidneys
  • don’t have to travel to dialysis unit for treatment
  • easy to take your therapy with you when you travel
  • therapy occurs while you sleep (APD)
309
Q

What are disadvantages of PD (alot)

A
  • need to schedule exchanges into daily routine, 7 days a week
  • have a permanent, external catheter
  • risk of infection
  • may gain weight/have a larger waistline
  • larger people may need extra exchanges
  • need storage space in your home for supplies
  • need clean space in your bedroom for equipment (APD)
  • not appropriate for patients with respiratory disorders (ie COPD) (don’t want to add extra fluid into the body)
310
Q

What are complications of PD

A
  • Exit site infections (usually caused by staph because the cathether is right next to your skin flora)
  • Peritonitis (infection in the peritoneal)
  • Hernias (from the increased pressure - can decrease by decreasing the amount of volume put into the cavity)
  • Lower back problems from the increased fluid (can use orthopedic binder to help)
  • Bleeding (small amount is normal at first, women who are ovulating or mensurating may have blood in there)
  • Respiratory problems (atelectasis, pneumonia, and bronchitis can occur due to the upward displacement of the diaphragm, leading to the inability to expand lungs fully)
  • Protein (can be extra protein loss)
311
Q

What are s/s of peritonitis 8

A
  • Abdominal pain
  • Rebound tenderness
  • Cloudy peritoneal effluent
  • Increased WBCs
  • Diarrhea
  • Vomiting
  • Hypoactive bowels
  • Rigid abdomen
312
Q

What is one of the most difficult things about hemodialysis

A

Obtaining vascular access

313
Q

What is an AV fistula? Why do we connect an artery to a vein? 3

A

Fusing together an artery and a vein, so that arterial blood will flow in the vein

  • The vein will increase in size
  • Will have quicker blood flow in the vein needed for dialysis
  • Allows more repeated venipunctures
314
Q

What is the downside to fistuals

A

They can take 6 weeks to months to heal, so you can’t use right when you might need too (you’ll have to create a temporary access while it heals)

315
Q

When should a fistula be placed

A

At least 3 months before starting hemodialysis (so that it can heal)

316
Q

Since fistulas are harder to place in people with peripheral vascular disease (diabetics), prolonged IV drug use and obese women, what might be used instead

A

An AV graft

317
Q

What is the advantage of a graft

A

Only takes 2-4 weeks to heal (so not as long as the fistula)

318
Q

What are disadvantages of grafts

A
  • Because they’re artificial, they are more likely to become infected and have more clots
319
Q

When hemodialysis is urgently needed, what can we use

A

Temporary vascular access using a double lumen - one for blood removal and the other for blood return

320
Q

What are the disadvantages of temporary vascular accesses

A
  • High rates of infection, dislodgment and malfunction
  • Can’t discharge from the hospital with it
321
Q

How can we tell if a fistula is patent

A
  • We feel the “thrill”
  • We hear the bruit
322
Q

What don’t you want to do if someone has a fistula or graft

A
  • No BPs, IV insertions or venipunctures on the arm with the access (to help prevent clotting and infection)
323
Q

What is added to prevent clotting during hemodialysis

A

Heparin (blood wants to clot when out of the body)

324
Q

What are nursing responsibilities before hemodialysis

A
  • Assess fluid status
  • Condition of vascular access
  • Temperature
  • Calculate the difference between last post dialysis weight and present pre dialysis weight to determine ultrafiltration (how much fluid should be removed)
325
Q

What are nursing responsibilities during hemodialysis

A

Take vital signs every 30-60 minutes

326
Q

What are complications from hemodialysis 4

A
  • Hypotension (due to the rapid loss of fluid)
  • Muscle cramps (rapid changes in electrolytes)
  • Loss of blood
  • Hepatitis (can be caused by using a machine that someone with hepatitis was using)
327
Q

Is a kidney transplant more or less expensive than dialysis

A

A kidney transplant is actually less expensive than dialysis after the first year

328
Q

What are contraindications to kidney transplants 6

A
  • Disseminated malignancies
  • Refractory/untreated cardiac disease (this will just damage the new kidney)
  • Chronic respiratory failure (not a candidate for surgery)
  • Extensive vascular disease (just going to damage the new kidney)
  • Chronic infection (going to damage new kidney)
  • Unresolved psychosocial disorders (maybe the pt wouldn’t take care of their new kidney)
329
Q

What are some things that we should do at pre-op before a kidney transplant

A
  • Emotionally prepare the pt that this might not work
  • EKG: check for cardiac issues as these are the leading cause of mortality during kidney transplants
  • Chest x-ray
  • Labs
  • Restrict extremity where the fistula or graft is (don’t let anyone do pokes or BPs before, during or after surgery, incase that sight will be needed)
330
Q

What are some things that we should do post-op after a kidney transplant 5

A
  • Maintain fluid and electrolyte balance *first priority
  • Large volumes of urine may be produced right after surgery due to kidney’s new ability to filter BUN, abundance of fluids during operation, initial renal tubular dysfunction.
  • Avoid dehydration
  • Assess for hyponatremia and hypokalemia
  • Maintain catheter patency until we are sure kidney is optimally functioning
331
Q

What are the 3 types of transplant rejections

A
  1. Hyperacute (antibody mediated) occurs within minutes to hours.
  2. Acute rejection occurs within days to months
  3. Chronic rejection occurs over months or years and is irreversible

202A (5 decks)

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