Exam 2 (5/12 - week 6) Flashcards
(120 cards)
1
Q
Chronic Inflammation of GI tract
* Autoimmune disease
Pt’s may have constipation, diarrhea or both
Begins in teens or early adulthood, second peak in 60’s
2 classifications:
* Ulcerative Colitis (UC): Colon only
* Crohn’s Disease: Anywhere in GI tract (mouth to anus)
Dx based on symptoms
A
Inflammatory Bowel Disease
2
Q
What are lifestyle factors associated w/ IBD?
A
Diet, Smoking, Stress alter microbial flora (sedentary lifesyle)
High intake of refined sugar, fat, polyunsaturated fatty acids(Increase risk)
Anxiety, depression, PTSD, panic disorder (Psychological stressors)
NSAIDS, antibiodics, oral contraceptives (Increase risk)
Raw fruits, veg, omega 3-rich foods, diertary fiber (Decrease)
3
Q
You have a Pt w/ IBD, what foods should you educate them to avoid?
A
Gas producing foods:
* Broccoli
* Cabbage
* Cauliflower
4
Q
Who is most at risk for developing IBD?
A
White
Ashkenazic Jewish origin
5
Q
What is the greatest risk factor of IBD?
A
Genetics
6
Q
Form of IBD that occurs anywhere in the GI tract
* Mouth to anus
* Most often involves distal Ileum & proximal colon
Contain skip lesions
* Normal tissue inbetween areas of inflammation
Strictures at inflammation site can cause bowel obstruction
Leaks can allow bowel contents to enter peritoneal cavity & cause abcesses or peritonitis
Fistulas are common
Cobblestone apperance from deep ulceration
A
Crohn’s Disease
7
Q
Form of IBD that affects the colon & the rectum only
* Starts in rectum & spreads to cecum
Inflammation & ulceration occur in mucosal layer (Innermost layer of bowel wall)
Diarrhea & electrolyte loss are common d/t not being able to be absorbed through the inflammed tissue
Protein loss in stool
Pseudopolyps form tongue like projection into bowel
A
Ulcerative colitus (UC)
8
Q
What are S/s of UC?
A
Bloody diarrhea
Abd. pain
Mild: Fewer than 4 semi formed stools/day w/ little blood
Moderate: Up to 10 stools/day w/ increased bleeding , fever, malaise (discomfort), anemia, & anorexia
Severe: 10-20 stools/day containing bloody diarrhea w/ mucus along w/ fever, rapid weight loss, anemia, tachycardia, & dehydration
9
Q
What are S/s of Crohn’s Disease?
A
Abd. cramps
Diarrhea
Possible rectal bleeding
Weight loss from malabsorption
10
Q
What are some complications associated w/ IBD that effect the GI tract (local)?
A
Hemorrhage
Strictures (abnormal narrowing or constriction of a bodily passage)
Perforation (w/ possible peritonitis)
Abcess, Fistula
CDI (more severe & frequent)
Toxic megacolon (Common w/ UC)
* At risk for perforation
May need emergency colectomy
At risk for CRC (form of cancer)
* Get regular screening
11
Q
What are some complications associated w/ IBD that effect the body systems?
A
Multiple Sclerosis (MS)
Ankylosing Spondylitis (Chronic arthritis of the spine)
Malabsorption, liver disease, osteoporosis
* Routine liver function test
* Bone density scan basline & should be done every 2 years
12
Q
What are some Dx blood studies for IBD?
A
CBC (Anemia, Toxic megacolon, perforation)
* Show decreased electrolytes & increased WBC
WBC
Serum electrolyte levels (Diarrhea)
Albumin (Poor nutrition)
Erythrocyte sedimentation rate
C-reactive proteins
Occult blood test (Blood, pus, mucus, infection through stool)
13
Q
What are some Dx imaging tests for IBD?
A
CT/ MRI
Colonoscopy
Double contrast barium enema study
Transabdominal ultrasonography
Small bowel series
Capsule endoscopy (Crohns)
14
Q
What are some nursing interventions for IBD?
A
Rest bowel
Control inflammation
Correct malnutrition
* High calorie, high vitamin, high protein
Relieve symptoms
- Improve quaility of life
Goal: Tx from IBD (NPO)
15
Q
What medications could be given to a person Dx w/ IBD?
A
Aminosalicylates
* Treat inflammation in the gut
* Treats UC
Antimicrobials
* Kill or inhibit the growth of microorganisms (bacteria, fungi, viruses, & parasite)
* Ciproflxacin (Cipro), Metronidazole (Flagyl)
Corticosteroids
* Decrease inflammation
* Prednisone, hydrocortisone
* Treats Crohn’s & UC
Immunomodulators
* Supress immune response
Biological therapies
* Inhibit the ctyokine tumor necrosis (TNF)
* Treats Crohn’s & UC
16
Q
What are some Surgical interventions for UC?
A
Proctolectomy w/ ileal pouch/anal anastomosis (IPAA)
Proctolectomy w/ permanent ileostomy
Interventions are same for IBD
17
Q
What is a Surgical intervention for Crohn’s?
Usually done for complications (obstruction) or those who do not respond to therapy
A
Resecting diseased segments w/ reanastamosis
* Short Bowel Syndrome (SBS): Surgery or disease leave litte small intestine surface area to maintain normal nutrition & hydration
* Difficult to maintain nutrition & hydration
Strictureplasty: Opens narrowed areas
* Intestine stays intact
* Decrease risk for developing SBS
* Recurrences at site are uncommen
Interventions are same for IBD
18
Q
What are the 4 goals of diet management in IBD?
A
1) Provide adequate nutrition w/o worsening symptoms
2) Correct & prevent malnutrition
3) Replace fluid & electrolyte losses
4) Prevent weight loss
19
Q
What might cause some nutritional problems associated w/ IBD?
A
Decreased oral intake
* Try to decrease diarrhea (reduce appetite)
* Inflammatory medications reduce appetite
Blood loss
* Iron deficency anemia, zinc deficency (ostomies & diarrhea)
* Oral supplements, parenteral nutrition (AKA “PN” or “TPN”)
Impaired absorption
* Depends on location of inflammation
* Coalamine
* Bile acids
Drug Therapy
* Sulfasalazine or methotrexate
* Daily folic acid supplements to prevent deficiency
Corticosteroids
* Ca supplements to prevent osteoporosis
* K supplements
20
Q
What is the difference between objective & subjective data associated with IBD?
A
Objective Data: (Seen)
* General: Intermittent fever, emaciated appearance, fatigue
* Cardiovascular: Tachycardia, Hypotension
* GI: Abd. distention, hyperactive bowel sounds, abd. cramps
* Skin: Pale skin w/ poor skin turgor, dry MM, skin lesions, anorectal irritation, skin tags, cutaneous membranes
Subjective Data: (Told)
* Health Hx: Infection, autoimmune disease
* Medications: Antidiarrheal drugs
* Health perception/management: Family Hx of UC/crohn’s , fever, malaise
* Nutritional-metabolic: N/V/A, weight loss
* Elimination: D, blood, mucus, pus in stool
* Cognitive-perceptual: Lower abd. pain (worse before defecation), cramping, tenesmus
21
Q
What are clinical problems associated w/ IBD?
A
Impaired bowel elimination
Nutritionally compromised
Difficulty coping
Pain
22
Q
What are the overall goals included in a care plan for a Pt w/ IBD?
A
Fewer & less acute exacerbations
Maintain normal fluid & electrolyte imbalance
Pain / discomfort free
Adhere to medical regimens
Maintain nutrition balance
Improve quality of life
23
Q
What are some implementations for the acute phase of IBD?
A
Hemodynamic stability
Pain control
Fluid & electrolyte balance
I/O, Stool # and apperance
Fall risk w/ possible orthostatic hypotension
Personal hygeine & comfort
Post-op care
24
Q
You have a Pt Dx w/ IBD. What education would you provide this Pt?
A
Disease management
Rest & diet management
Perianal care
Drug action & side effects
Symptoms & when to seek help
Stress reduction
Short / Long term goals
25
You have a Pt w/ IBD. How would you know if the treatment is working *(evaluation)*?
Decreased # of diarrhea stools
Maintain weight
Pain free
Coping strategies
26
**Prevent or decrease inflammation of intestinal mucosa**
* *Oral form for mild to moderate disease*
* **IV for severe inflammation**
* *Tapered pre-op to prevent postop complications*
* Given for shortest possible time
* **Suppository, enema, foam forms for disease in left colon, sigmoid, rectum**
*Drug Ex:*
* **Methylprednisolone (Medrol)**
* **Dexamethasone (Decadron)**
* **Prednisone** (Orapred)
Corticosteroids
27
**Maintain remission after corticosteroid therapy**
* *For patients who do not respond to 5-ASA, corticosteroids, antibiotics or have side effects from corticosteroids*
* **When fistulas are part of the disease**
* Delayed onset – not useful for acute flare-ups
* **CBC monitoring: Suppress bone marrow; lead to infection and bleeding**
* No **methotrexate** with pregnancy
Immunomodulators
28
*Surgery or disease leave **litte small intestine surface area to maintain normal nutrition & hydration***
Causes:
* Damage to Intestinal mucosa
* Surgical removal of tto much small intestine (crohns, cancer)
* Congenital defects
*Common in Pt's w/ **Jejunoileal anastomosis** (Jejunum & Ileum removed)*
Short Bowel Syndrome (SBS)
29
**Abnormal tract between 2 hollow organs or a hollow organ & the skin**
* Named by tract they take from 1 body part to another
* Ex: **Entercutaneous fistula** *(Small intestine & skin)*, **Enterovaginal fistula** *(Small intestine & vagina- stool & gas excrected through vagina)*
Occur:
* **After surgery / trauma (most common)**
* **IBD, Cancer**, pancreatitis, diverticulitis
* *Perforation*
* *Radiation*
S/s:
* *Fever, Abd. pain*
* **Pus, drainage, or stool expelling through skin opening**
* **Fecaluria (Passing stool when urinating)**
* UTI, dysuria, hematuria
Fistula
30
How would you treat a Fistula?
**Identify fistula tract**
**Maintaining fluid & electrolyte balance**
* *Will see low potassium, magnesium, & phosphorus*
* Monitor vitals & for dehydration
Controlling infection
**Protecting surrounding skin**
* *Use barrier creams, powders & sealants*
Maintaining O/P
**Providing nutritional support**
* **Diet: High calorie, High protein**
* Vitimin & mineral support (copper, zinc, etc)
31
**Inflammation of glomeruli**
* Affects both kidneys
Conditions associated w/:
* Kidney infecion
* renal toxic drugs, immune system issues, systemic diseases
**Acute (sudden/reversible) or chronic (progresses slowly/irriversible)**
Dx studies & Hx:
* Sore throat
* Upper Resp. Infection
* DM Dx
Glomerulonephritis (GN)
32
**Most common form of acute Glomerulonephritis** worldwide
* Most common in ages 5-7 & adults older than 60
**Develop 1-6 weeks after infection of the tonsils, pharynx, or skin**
S/s:
* **Edema (d/t decreased glomerular filtration)**
* *HTN (d/t increased ECF volume)*
* **Olgiuria, Hematuria, & proteinuria**
* Abd. / Flank pain
Acute Poststreptococcal Glomerulonephritis
33
You have a pt w/ a suspeced Dx of Acute Poststreptococcal Glomerulonephritis. What test will often show the immune response to Streptococcus?
**Streptozyme tests**
*Measures 5 different streptococcal antibodies including antistreptolysin-O (ASO)*
34
What nursing interventions would be used to treat Acute Poststreptococcal Glomerulonephritis?
**Symptomatic relief (goal)**
Rest
Restrict Na & fluid intake, Diuretics to reduce edema
Antihypertensive drugs if severe, antibiodics
Restrict protein intake if evidence of increased nitrogeneous wastes
* Increased BUN
Early Dx: Sore throat, skin lesions
Good hygeine
35
Wha labs would be ordered for a Pt w/ Acute Poststreptococcal Glomerulonephritis??
**Dipstick UA & sediment microscopy**
* *Show significant RBCs w/ or w/o casts*
**BUN/Cr**
* *Increased BUN*
36
*Permanent & progressive renal fibrosis involving renal fibrosis involving the glomeruli*
* *Can progress to ESRD*
* **Most Glomerulonephritis & nephrotic symdrom can cause**
**S/s (develop slowly):**
* *Asymptomatic Renal issues (unaware of issues)*
* **Abnormal UA**, proteinuria, hematuria, uremia
* HTN
* **Increased Cr**, Increased WBC / RBCs, & casts
Dx tests:
* CT
* US
* **Renal biopsy (to determine cause)**
Chronic Poststreptococcal Glomerulonephritis
37
What nursing interventions would be used to treat Chronic Poststreptococcal Glomerulonephritis?
**Assessment of exposur to drugs**
* NSAIDS
**Monitor / prevent for infection**
* Hepatitis
**Evaluate for autoimmune diseases**
* Lupus
38
One of the most important nursing roles in relation to Acute Poststreptococcal Glomerulonephritis (APSGN) is to...
A) Encourage early Dx & Tx of sore throats & lesions
B) Encourage Pt to obtain antibiodic therapy for upper resp. tract infection
C) Teach Pt that long term prophylactic antibiodic therapy is needed to prevent recurrence
D) monitor for resp symptoms that indicate the disease affecting the alveolar basement membrane
A) Encourage early Dx & Tx of sore throats & lesions
39
**Increased glomerular permeability**
* Hypercoagulation
*Allows large molecules to pass through membrane to be excreted into urine*
* Can have DM or Lupus
S/s:
* **Severe proteinuria ( > 3.5g/24hr )**
* *FVE (HTN)*
* Hyperlipedema
* Hypoalbuminemia
* *Foamy urine*
* Massive generalized edema **(Anasarca)**
* *Ascites (Resp issues)*
* *Decreased immune response (Tx)*
Nephrotic Tissue
40
You have a Pt w/ Nephrotic Tissue. What nursing interventions would you perform?
**Cure / control symptoms**
*Immnuosuppresive therapy **(prednisone)***
**Heparin (Anticoagulants)**
*Thiazide, loop diuretics*, Ace inhibitors
**Dietary changes (Na restrictions)**
Lipid lowering agents (cholesterol)
**Daily weight, I/O**, *measuring abd gurth*
Labs
Fluid volume & nutritional interventions
41
**Rapid loss of kidney function** (within hours or days) w/ or w/o decreased urine O/P
* **Loss accompanied by progressive increases in blood urea nitrogen (BUN, Cr, & K)**
* Reversible w/ high mortality rate
* **Monitor Cr**
**Acute tubular necrosis is most common cause**
Severity can range from a small increase in Cr, or reduction in urine O/P to develop **azotemia ( accumlation of nitrogenous waste products (Urea nitrogen, Cr) in blood)**
S/s:
* **Increases BUN, Cr, & K**
* **Severe prolonged hypotension (maliignant HTN)**
* Hypovolemia
* Exposure to nephrotoxic agent
* **GFR 69 for 3 months**
Acute Kidney Injury (AKI)
42
**Decreased blood flow to kidneys**
* **Happens before it reaches kidneys**
* *Cardiovascular disease, hypovolemia, vasoconstriction*
**Leads to decreased GFR** & kidney filtration
Try to preserve blood flow to kidneys
* *Aldosteron, Norepinephrine, ADH*
**Prerenal** - AKI
43
**Problems causing direct damage to kidney tissue** resulting in impaired nephron function
Damage can cause:
* Prolonges ischemia
* Nephrotoxins
* **Hgb released from RBCs or myoglobin relased from nephrotic muscle cells**
Hgb & myoglobin block tubules & cause **renal vasoconstriction**
Parenchymal damage, acute tubular necrosis, malignant HTN
**Intrareal** - AKI
44
Mechanical obstruction in outflow of urine
* **Urine refluxes into the renal pelvis, impairing kidney functions**
* *Most common causes are BPH, prostate cancer, stones, trauma, & external tumors*
**Postrenal** - AKI
45
**Reduction in urine O/P to < 400 mL/day**
* *Occurs w/in 1-7days after injury*
* Lasts 10-14 days or longer
* *UA shows RBCs, WBCs, & casts*
**Often occurs w/ prerenal causes**
**Specific gravity may be fixed around 1.010 w/ urine osmolality**
* *Reflects tubular damage& loss of concintration ability by kidneys*
**Olguric Phase** - AKI
46
You have a Pt Dx w/ AKI. Your Pt is in the Olguric phase. What fluid volume symptoms would you expect to see?
Decreased urine O/P
**FVO: HF, pulmonary edema, pericardial & pleural effusion**
*Hypovolemia* (May exacerbate AKI)
*Random tip: The longer teh phase, the poorer the prognosis*
47
You have a Pt Dx w/ AKI. Your Pt is in the Olguric phase. What metabolic acidosis symptoms would you expect to see?
Severe decrease in bicarb production
**Severe acidosis:**
* Confusion, fatigue
* **Kussmal RR (rapid and deep breathing)**
* Coma, death
No excretion of H ions
48
You have a Pt Dx w/ AKI. Your Pt is in the Olguric phase. What symptoms would be associated w/ a Na imbalance?
Hyponatermia leads to **cerebral edema**
* D/t increased excretion of NA
49
You have a Pt Dx w/ AKI. Your Pt is in the Olguric phase. What symptoms would be associated w/ a K excess?
*Asymptomatic*
**EKG changes (Tall tented T wave**)
Impaired ability to excrete K
50
You have a Pt Dx w/ AKI. Your Pt is in the Olguric phase. What hematological problems would you expect to be done?
**Leukocytosis (Most common)**
*Infection (Urinary & Resp. most common)*
51
Describe the Diuretic phase of AKI?
**Daily urine O/p may reach 5L or more**
* Normal is around 1-3L
**Monitor for *hypovolemia (dehydration), hypotension*, hyponatremia, & hypokalemia,**
* *Hypovolemia & hypotension can occur from massive fluid loss*
**Pt's acid-base, electrolytes, BUN/Cr will stabilize**
52
Describe the recovery phase of AKI?
*Begins when GRF increases* allowing **BUN & Cr levels to decrease**
* Major improvments w/in first 1-2 weeks
**May take 12 months for kidneys to stabilize**
53
What Dx tests can be done for AKI?
**Thourough Hx & physical assessment**
BUN/Cr
**Kidney Ultrasound (Done first)**
**UA**
Renal scan, CT
**Renal biopsy (Best)**
Identify cause
54
What nursing interventions can be done for AKI?
Treat cause
**Low Vitals**
**Fluid restiction (600mL plus previous 24hr fluid)**
* Monitor closely in oliguric phase (I/O)
**Monitor for hyperkalemia**
Renal replacement therapy
**Dialysis**, labs
**Lung/heart sounds (PVC & Afib)**
Monitor Oral mucosa
Nutritional therapy:
* *Adequate protein (1kg/day)*
* *Adequate calorie intake (primary carbs & fats)*
* Enternal nutrition
* *Parenteral nutrition (PTN - last resort)*
* **Diet restrictions (K, Na, phosphate (P)**
*Loop diuretics:* **Furosimide (Lasix)**
*Osmatic diuretics:* **Mannitol**
55
What nursing interventions can be done for hyperkalemia?
Dietary restriction of K
**Hemodialysis (most effective)**
**Regular Insulin IV**
* K move into cells when given
* **IV glucose given to prevent hypoglycemia**
* *IV calcium gluconate to improve cardiac contractability*
**Calcium Gluconate IV:**
* Used in advance cardiac toxicity
**Na polyestyrene Sulfate (Kayexalate):**
* *K exchanged for Na*
* Procedes osmotic dirrhea
* **Do Not give to Pt w/ paralytic Ileum (Bowel necrosis could occur)**
**Patiromer (Veltassa):**
* CKD
* Delayed onset
* **Do Not give in emergent cases (Causes hyperkalemia)**
* **Do Not give to Pt w/ paralytic Ileum (Bowel necrosis could occur)**
*Sodium Bicarb IV*
56
T/F: Total Parenteral Nutrition (TPN) can go through an IV
**False:** TPN cannot go through an IV
Rationale: **TPN should be administered through a central line d/t sugar irritating the veins placing the Pt at risk for infection**
57
**Progressive, irriversible loss of kidney function**
**Often asymptomatic** resulting in *underdiagnosis & undertreating*
**Leading cause is DM (50%) & HTN (25%)**
*ESRD occurs when GFR is < 15mL/min*
* **< 60mL for 3 months**
**Monitor GFR**
Chronic Kidney Disease (CKD)/ ESRD
58
You have a Pt w/ Chronic Kidney Disease (CKD)/ ESRD. What S/s would you expect to see?
Result of retains substances
* **Urea, Cr**
* Hormones
* **Water (FVO)**
* **Electrolytes (K build up)**
**Uremia** (Kidney function decline = multiple body systems)
* **GFR < or equal to 15**
59
Describe the 5 stages of CKD:
**Stage 1: Kidney damage w/ normal or increased GFR**
* > or equal to 90
* Dx & Tx, slow progression
**Stage 2: Kidney damage w/ mild decreased GFR**
* 60-89
* Estimation of progression
**Stage 3a: Moderate decrease in GFR**
* 45-59
* Evaluation & Tx of complications
**Stage 3b: Moderate decrease in GFR**
* 30-44
* More agressive Tx
**Stage 4: Severe GFR**
* 15-29
* Prep for RRT (dialysis / transplant)
**Stage 5: Kidney failure**
* < 15 or dialysis
* RRT is uremia present & Pt consents to Tx)
60
What are some risk factors associated w/ CKD?
**Age > 60**
* Prevent insult or injury to kidneys
*CVD, DM (Glycemic control)*
**Ethnic/minority**
* *Black, Native Americans*
**Nephrotoxic drugs**
* Sodium bicarb
**Fam Hx**
* *Teach about risks & screenings*
**HTN**
* *Maintain BP w/ ACE inhibitors or ARBs*
61
What 3 Ethnic/minority groups are at risk for CKD?
**Blacks:**
* *D/t HTN*
* **Highest rates** - 4x whites
**Native Americans:**
* Have rate 2x as whites
* **6x higher if diabetic - High than any minority**
**Hispanics:**
* 1.5x higher tha non-hispanic whites
62
You have a Pt w/ Chronic Kidney Disease (CKD)/ ESRD. What Urinary S/s would you expect to see?
Usyally do not report any changes in urine O/P (Early S/s)
**Polyuria may be present if Dx w/ DM**
May have difficulty w/ **increased fluid retention & need diuretic therapy** (Late s/s)
May become **Anuric (no or little urine)** after dialysis
63
You have a Pt w/ Chronic Kidney Disease (CKD)/ ESRD. What electrolyte imbalances would you expect to see?
**Potassium (K):**
* **Hyperkalemia (most serious)**
* *Fatal dysrhythmias* **(K levels 7-8mEq/L)**
**Sodium (NA):**
* May be elevated, normal, or low
* **D/t impaired excretion, Na along w/ water excretion**
* **Dilutional hyponatremia (Edema, HTN, HF)**
**Magnesium (Mg):**
* Results in **absence of reflexes, decreased mental status, cardiac dysrhythmias, hypotension, resp failure**
64
You have a Pt w/ Chronic Kidney Disease (CKD)/ ESRD. What acid-base imbalance would you expect to see?
Metabolic Acidosis
* **Impared ability to excrete access acis***(Primary ammonia)*
* **Deffective reabsorption & regeneration of bicarb**
* Plasma Bicarb levels fall approx. **16-20mEq/L**
* **Treat w/ Bicarb**
65
You have a Pt w/ suspects Chronic Kidney Disease (CKD)/ ESRD. What Dx tests would you expect to do?
Hx & physical exam
Dipstick evaluaion or protein
UA, CT
**BUN/Cr, Hct, Hgb**
**Renal (US)**
**Renal biopsy (best way to Dx)**
**Albumin-to-Cr ration (First moring void)**
GFR trending
Lipid profile
66
You have a Pt w/ Chronic Kidney Disease (CKD)/ ESRD. What interventions would you expect to do?
Preserve existing kidney function
Reduce risk w/ CVD / Prevent complications
Provide pt comfort
**Correct FVO or FVD**
**RRT (Dialysis or transplant)**
**Nutritional therapies**
*Lower K*, Lipid lowering drugs
**Ca supplements, Phosphate (P) binders**
**Antihypertensive therapies, *ACE inhibitors*, ARBS**
Adjust drug dose
67
You have a Pt w/ Chronic Kidney Disease (CKD)/ ESRD. What 2 drugs could you expect to give if the patient is hyperkalemic?
**Sodium polystyrene sulfonate:**
* Given to lower K in **stage 4 CKD** (HD to remove leftovers)
* **Osmotic laxative acton & ensures K removed from bowel** *(Observe for Na & water retention)*
* Watch for EKG changes **(Peaked T wave, wide QRS)**
* **Educate pt to expect diarrhea**
**Patiromer (Veltassa):**
* **Binds K in GI tract**
* *Not used in emergent situation*
* Can cause *Hypomagnesemia*
68
You have a Pt w/ Chronic Kidney Disease (CKD)/ ESRD. What interventions could you expect to do if the patient is hypertensive?
Control HTN
Weight loss, Sedentary lifestyle change
**Diet recommendations (*DASH Diet*)**
* *Emphasizes foods like **fruits, vegetables, whole grains, & lean proteins**, & limits Na, saturated fat, & added sugars*
*Antihypertensive drugs (Can be on 2+)*
**ACE Inhibitors & ARBs w/ diabetic** & nondiabetic proteinuria
**Orthostatic vitals**
**Educate Pt on how to take BP on own**
69
You have a Pt w/ Chronic Kidney Disease (CKD)/ ESRD. What drug complcations could occur?
**Drug toxicity** d/t accumulation of meds
* Frequent dose changes
Digoxin toxicity
**Diabete agent like Metformin, glyburide**
* Hyper/hypoglycemia
**Antibiodics like vancomycin, & gentamicin**
Opioid drugs
70
You have a Pt w/ Chronic Kidney Disease (CKD)/ ESRD. What nutritional therapy would you expect to see?
**Normal protien diet for hemodialysis (HD) Pt's & Increased protien intake for Peritoneal Dialysis Pt's**
*Fluid restrictions (Depends on urinary O/p)*
Na restrictions (salt sub.)
**K restriction (2-3g/day)**
**Phosphate restrictions (1g/day)**
* **High protient foods to avoid: Meat & Dairy products**
* *Phosphate binder*
71
You have a Pt w/ Chronic Kidney Disease (CKD)/ ESRD, who is up for discharge. What Pt education should be provided?
*Na, K, Phosphate (P), & fluid restrictions*
**Alternate ways to reduce thirst (Sucking on ice, lemons, or hard candy)**
**S/s of electrolyte imbalance, especially hyperkalemia**
*Reason for prescribed drugs & side effects*
* *Ex: Phosphate binders take w/ meals, Ca supplements prescribed to treat hypocalcemia & should be taken on empty stomach*
**To repost weight gain > 4lb, increasing BP, SOB, edema, fatigue, weakness, confusion, or lethargy**
Need for support & encouragement, share concerns
Dialysis
72
*Movement of fluid molecules across a semipermeable membrane* & to **remove waste products in kidney failure**
**Used to correct fluid & electrolyte imbalances & to remove waste products in kidney failure**
Can be used to treat drug OD
2 types:
* Peritoneal dialysis (PD)
* Hemodialysis (HD)
**Begins when Pt's uremia can no longer be adequatley treated**
**Initiate whe GFR < 15mL/min**/1.73m^2
Dialysis
73
Why would a Pt Dx w/ ESRD be placed on dialysis
Lack of donated organs
Physcially/mentally for transplantation
Pt refused Tx
74
**Catheter surgically placed**
* Tip of catheter in peritoneal cavity
* **Initiaded immediately or delayed for 2 weeks after incertion**
* *Can shower & pat site dry once healed*
**Warm solution to body temp**
**Allows exchange of waste, fluids/electrolytes to occur in peritoneal cavity**
*Pt needs to be clean to avoid infection*
* Daily cath care varies
**Can be done at home or at a facilty**
*Less stressful on body, less dietary / fluid restrictions*
*Easier to learn, greater freedom, better BP control*
Not as effective as hemodialysis
Stort training program (3-7 days)
Peritoneal Dialysis
75
You have a Pt who is about to receive paritoneal dialysis. How would you as the nurse set up the procedure?
**Sterile tech**
**Dialysate 1-2L infused into peritoneal space (Fill) over 10-20 min period**
* When the solution is infused, cloes the clamp
**Fluid allowed to sit / dwell in peritoneal cavity for specific amount of time (per order)**
* AKA *equalibrium (Balance)*
* *Diffusion & osmosis occur between blood & peritoneal cavity*
**Fluid flows/drains from body into drainage bag**
* **Lasts about 15-30 min**
76
Describe the 2 peritoneal dialysis systems described below:
Automated peritoneal dialysis (APD)
Continuous ambulatory peritoneal dialysis (CAPD)
**Automated peritoneal dialysis (APD):**
* Cycler delivers dialysate
* Times & controls fill, dwell, & drain phase
**Continuous ambulatory peritoneal dialysis (CAPD):**
* Manual exchange during day (4x/day)
77
What are some complications to monitor for when doing peritoneal dialysis?
Exit site infection
**Peritonitis**
* **Pt complains of pain**
Hernias
Lower back problems
**Bleeding**
**Pulmonary complications**
**Protein loss**
78
List some advantages for peritoneal dialysis:
**Less complicated**, Simple
**Fewer dietary & fluid restrictions**
*Usable in Pt's w/ vascular access problems*
**Less cardiovascular stress**
**Preferable w/ DM**
*Home based*
Increased Pt participation
79
List some disadvantages for peritoneal dialysis:
**Bacterial / chemical peritonitis**
**Protein loss into dialysate**
*Exit site & tunneling infections*
*Self image issues*
**Hyperglycemia**
Requires completion of education program
**Catheter can move**
Best with partner
80
**Requires rapid blood flow & acess to large blood vessel**
* *Obtaining vascular access if most difficult problem*
**2 Types:**
* **Arteriovenous (AV) fistula / graft** *(Fell thril, listen bruit)*
* Temporary vascular access
**Uses dialyzer**
* *Plastic cartridge that contains thousands of parallel hollow tubes or fibers*
* Fiber are semipermeable membranes
*Majority are Community based centers*
* **Scheduled for 3-4hrs 3 days/week**
Can be:
* Short daily
* Long nocturnal
* Home
Hemodialysis (HD)
81
You have a Pt who is about to receive hemodialysis. How would you as the nurse set up the procedure?
**Before Tx:**
* **Weight (Compare to previous)**
* **Take vitals (*BP*, temp)**
* Look for s/s of periphreal edema
* *Listen to heart & lungs*
**Feel thrill, listen to bruit**
**During Tx:**
* Monitor vitals Q30-60min
**Post Tx:**
* **Weight**
* **Vitals, listen to heart & lungs**
* *Assess for bleeding*
* tolerration
82
What are some complications of hemodialysis to look out for?
**Hypotension**
*Mucle cramps*
Loss of blood
**Hepatitius C**
**infections disease, HIV **
**Clotting catheter**, Thrombus
Anurysm
*Ischemia of limb (cold, discolored)*
**Disequalibrium syndrome:**
* *Rapid decrease in fluid volumes & BUN levels during dialysis causing cerebral edema*
* **Monitor for headache, N/V, decreased LOC, seizure, & coma**
83
What are some advantages to having hemodialysis?
**Rapid fluid, Urea, & Cr removal**
**Effective K removal**
Less proiten loss
**Lower triglycerides**
Home hemodialysis possible
Can place temporata access
84
What are some disadvantages to having hemodialysis?
**Vascular access problems**
**Dietary / fluid restrictions**
Heparinization may be necessary
**Hypotension during Tx**
*Added blood loss contributing to anemia*
**Self image problems**
**Surgical placement**
Trained personnel Necessary
85
You have a Pt w/ a AV fistula or graft. What precautions might you take?
**Avoid BP, IV insertion, or venipuncture in an extremity**
* *Place sign in Pt's room & label the arm w/ a band that says "No BP, blood draws, or IV in this arm"*
Prevent infection & clotting of vascular access
86
**Uremic toxins & fluids are removed while acid-base status & electrolytes are adjusted slowly & continuously a hemmodynamically unstable Pt**
* Can be used w/ HD
The principle is to dialyze Pt's in a more physiologic way (over 24hrs)
**Contradicted if life-threatening manifestations of uremia (hyperkalemia, pericarditis) that need rapid Tx**
Vascular access obtained by double-lumen-catheter
*Blood pump propels blood through circut*
* **Highly permeable, hollow-fiber hemofilter removes plasma water & nonprotein solutes (Ultrafiltrate)**
Continuous Renal Replacement Therapy (CRRT)
87
How does Continuous Renal Replacement Therapy (CRRT) diifer from Hemodialysis (HD)?
**Blood pump runs a slower rate (150mL/hr)**
* *May improve hemodynamic stability*
Continuous instead of intermittent
* **Fluid volume removed over days (24hrs-2 weeks)**
**Solute removal occurs by convection (no dialysate needed)** in addition to osmosis & diffusion
Does not need monitoring by specialized nurse by **requires trained ICU nurse**
Does not require complicated HD equipment
88
**May result from impaired renal excretion, a shift of K from ICF to ECF, massive K intake**, or a combination of things
* **Most common cause is renal failure**
* **K >5 mEq/L**
**Factors that can cause K to move from ICF & ECF:**
* **Metabolic Acidosis**
* **Massive-cell destrucion (*Burn/trauma*, tumor lysis, *severe infection*)**
* Intense exercise
**Drugs that can cause an increase in K:**
* Digoxin- like drugs,*Adrenergic blockers (Propranolol)*
* **NSAIDS, K sparing diuretics**
* Angiotensis II receptor blockers (Losartan)
* **ACE inhibitor (Lisinopril)**
Hyperkalemia
89
What are S/s of Hyperkalemia?
**Abd. cramp**, V/D
**Confusion, Irritability**
Fatigue
Loss of muscle tone, muscle weakness
*Paresthesias (abnormal skin sensations)*, decreased refluxes
*Tetany (involuntary muscle contractions)*
**Irregular pulse:**
* Loss of P wave
* *Prolonged PR interval*
* *ST segment depression*
* **Widening QRS**
* **Peaked T waves**
* **V-fib**
* **Asystole (Ventricular standstill)**
90
How would you treat hyperkalemia?
Stop K intake
Increased K excretion
* Loop diuretics
* Dialysis
* Patiromer (veltassa)
* Sodium polystyrene sulfate (kayexalate)
**Kayexalate** is used to acutly bind K in the bowel
* Given PO or rectally
**Patiromer (veltassa)** exchanges Ca for K in lower GI tract
* Given PO
* May take 7hrs for initial effect & 2 days to see maximun results
**Force K in w/ regular insulin w/ dextrose IV**
**IV calcium chloride / calcium gluconate dont lower K, but can serve as antagonist to reverse toxic effect of cardic cell mebrane**
* *Protects from life-threatening dysrhythmias*
**Continue to monitor EKG changes**
91
**Can result from increased loss of K**
* *Increased shift of K from ECF to ICF, or decreased dietary K*
* **Most common causes are abnormal losses from kidneys or GI tract**
* **K < 3.5 mEq/L**
**GI tract losses:**
* **Diarrhea**
* Laxitive misuse
* *Vomiting*
* **Ileostomy drainage**
**Renal loses:**
* **Increased urinary O/P**
* *Using loop or other diuretics*
* *Low Mg levels (stimulates renin & aldosteron relase)*
Hypokalemia
92
What are S/s of Hypokalemia?
N/C, **Paralytic ileus (muscles in the intestines temporarily stop working properly)**
Fatgiue
**Hyperglycemia**
Soft / flabby muscles, muscle weakness
Leg cramps
*Paresthesia (abnormal sensation)*, *decreased reflexes*
**Shallow RR**
**Irregular / weak pulse**
* **Peaked P wave**
* **Prolonged QRS**
* ST segment depression
* **Flattened T wave**
* Presence of U wave
* *Ventricular dysrhythmias*
* **First & second degree heart block**
93
How would you treat Hypokalemia?
**Give PO potassium chloride (KCl) supplements & Increase dietary intake:**
* **Banana**, *Avacado*
* *Dried fruits*, cantaloupe, **grapefruit juice**
* **Butternut squash**
* *Cooked broccoli & spinich*
* Raw carrot, greens (No kale), canned mushrooms
* White & sweet potatoes
* **Milk (1 cup), yogurt, chocolate**
* *Peanut butter, nuts & seeds*
* **Lite salt, salt sub.**
**Give IV potassium choride (KCl):**
* Rate should not exceed 10 mEq/hr unless Pt is in critical setting w/ comntinoues EKG monitoring & central line access
* **Monitor for phlebitis & *inflitration* (*Necrosis & sloughing of surrounding skin*)**
94
What are some safety tips to remeber when administering IV Potassium chloride (KCl)?
**Always dilute**
Do not give in concentrated amounts
**Never give IV push or bolus**
* Do not add KCl to hanging IV bag to prevent giving bolus does
95
**Kidneys excrete too much phosphate (P)**
* **Common in Pts w/ AKI or CKD**
* **P > 4.5 mg/dl**
Other causes:
* **Phosphate-containing laxitives or enemas**
* Shift of phosphate from ICF & ECF
* *Sickel-cell*
S/s:
* **Asymptomatic**
* *Tetany (involuntary muscle contractions)*
* Muscle cramps
* *Paresthesia (abnormal sensation)*
* Hypotension
* **Dysrhythmias**
* **Seizures**
* Calcified bones
Tx:
* **Treat cause**
* **Phosphate restriction (avoid dairy)**
* *Calcium carbonate*
* *Hemodialysis*
Hyperphosphatemia
96
**Can result from decreased intestinal absprption, increased urinary excretions or ECF to ICF shifts**
* **< 3 mg/dl**
**Causes:**
* **Malabsorption**
* *Diarrhea*
* Phosphate binding antiacids lead to decreased absorption
Occurs in:
* **Resp. Alkalosis**
* DKA Tx
* **Re-feeding syndrome (Reinstitution of nutritionto severely malnourished Pt's)**
S/s:
* *CNS depression (Confusion, coma)*
* **Heart problems ( dysrhythmias, HF)**
* *Muscle weakness (resp. muscles included)*
* *Polyneuropathy*, **seizures**
* **Rhabdomyolysis (damage muscle tissue releases the protein myoglobin into the bloodstream)**
* Rickets, *osteomalacia (deficiency of vitamin D or calcium)*
Hypophosphatemia
97
**Usually occurs w/ increased Mg accompanied by renal insufficiency or failure**
* **> 2.1 mEq/L**
Excess Mg *inhibits acetylcholine release at myoneural junction*
Causes:
* **Adrenal insufficiency**
* **Antacids, laxatives**
* Hypothyroidism
S/s:
* **Facial flushing**
* Lethargy
* Urinary retention
* N/V
* *Decreased deep tendon reflexes*
* **Decreased HR & BP**
Tx:
* Mg restriction
* **Mg dietary restrictions (green veg, peanut butter, nuts, bananas, oranges,chocolate)**Increase fluids & diuretics
* *IV calcium gluconate*
Hypermagnesemia
98
**Occurs in Pt's w/ limited magnesium intake or increase in GI or renal losses**
* **< 1.3 mEq/L**
**Causes:**
* Acute pancreatitis
* *Chronic alcohol use*
* Diarrhea, **NG suctioning**
* **Hyperglycemia**
* Malabsorption syndrome
* **Prolongs fasting or starvation (Malnutrition)**
* Increased urine O/P
**S/s:**
* **Chvostek & Trousseau signs**
* Confusion, Vertigo
* *Hyperactive deep tendon reflexes*
* Muscle cramps
* **Increased pule & BP, dysrhythmias**
* Tremor, *seizures*
**Tx:**
* Treat underlying cause
* Increase intake
* **IV mag. sulfate**
Hypomagnesemia
99
What are some safety measures for IV mag. sulfate?
*Always give using infusion pump*
**Monitor vitals, LOC, & relfexes**
**Keep IV *calcium gluconate* on hand (Antidote)**
100
Define the following terms:
ACH-Acetylcholine
AChE-Acetylcholinesterase
Acetylcholine Receptor (AChR)
Acetylcholinesterase / cholinesterase inhibitors
**ACH-Acetylcholine:** Neurotransmitter
at neuromuscular junction
**AChE-Acetylcholinesterase:** Splits/deactivates Ach
**Acetylcholine Receptor (AChR):** Blocks receptor from taking
in Ach. Produced in Thymus
**Acetylcholinesterase / cholinesterase inhibitors:** Blocks
deactivation and increases ACh activity.
101
**Autoimmune disease**
* Fluctuating weakness
increases with muscle use
Precipitated by:
* Emotional Stress, Pregnancy
* **Illness/Surgery, Trauma**
* *Temperature extremes*
* **Hypokalemia**
* Medications
Myasthenia Gravis
102
What are S/s of Myasthenia Gravis?
**Droopy eyelids** (**Ptosis - early**)
**Blurry or double vision** (**Diplopia - early**)
Trouble chewing / swallowing (**dysphagia**)
Trouble speaking (**aphasia**)
Trouble breathing (**dyspnea**)
**Muscles stronge in morning but become exhaused w/ activity**
103
How can you Dx Myasthenia Gravis?
History and Physical examination
Chest Xray
Single fiber EMG
Tenislon test- IV injection of edrophonium chloride (anticholinesterase):
* MG-Improved muscle contractility
* Cholinergic crisis-No change or worsens symptoms
104
Over stimulation of receptors
**Secondary to overdose of anticholinesterase medications**
S/s:
* **Muscle Fasciculation (twitch)**
* Sweating
* *Excessive salivation*
* **Constricted pupils**
* *Hypotension*, blurred vision
* Pallor, abd cramps
*Edrophonium increases muscle weakness-* **Atropine**, *a cholinergic antagonist counteract the effects of edrophonium when used diagnostically*
Cholinergic Crisis
105
*Autoimmune process* that **occurs a few days or weeks following a viral or bacterial infection of the GI or Upper Respiratory Tract**.
* **Campylobacter bacteria- most common**
* Rare and effects approx. 1 in every 100,000 persons
Collection of clinical syndromes that manifest as *acute inflammatory
polyneuropathy*
Diagnostic:
* **EMG (confirms after 2 weeks)**
* *CSF*
* Increased protein
* Rules out other causes
Complications:
* **Cardiac**
* **Resp Failure**
* Resp infections
* UTIs
Guillain-Barre
106
What causes Guillain-Barre?
Immune response to
antigens plays a role in the
immune reaction directed at
the nerves
**Segmental loss of myelin
with edema and
inflammation of affected
*peripheral nerves*.**
**Nerve transmission is
stopped or slowed**
107
What Pharmacological management would you expect to see for a Pt Dx w/ Guillain-Barre?
Oxygen
Pain medication
Bronchodilators
*Vasopressors* (**dopamine & dobutamine**)
**Norepinephrine/Epinephrine**
**Plasmapheresis**
**Immunoglobulin g (IVIg)- Preferred treatment**
* *Only effective in the first 4 week*
108
**Chronic, progressive, degenerative disorder of central nervous system (CNS)**
Cause is unknown:
* Possible factors include *infection*, smoking,
*physical injury*, emotional stress, *excessive
fatigue*, *pregnancy*, poor state of health
* **Genetics**
**Attacks cause damage to myelin
sheaths** of neurons in brain and spinal cord
**Inflammation, myelin
loses ability to regenerate**. Glial scar tissue forms
* **Nerve impulse transmission is disrupted without myelin**
* *Results in permanent loss of nerve
function*
S/s:
* *Blurred / double vision* (**Diplopia**)
* Red-green color distortion
* Blindness in one eye
* *Involuntary, rapid eye movements* (**Nystagmus**)
* *Poor muscle control* (**Ataxia**)
* *Weak muscles used for speech* (**Dysarthia**)
* Dysphagia
* **Lhermitte's sign (electric shock felt in body)**
Drug therapy:
* **Interferon β-1a (SQ Rebif and Plegridy; IM Avonex)**
* **Interferon β-1b (SQ Betaseron and Extavia)**
* **Corticosteroids (ACTH, methylprednisolone, prednisone)**
Multiple Sclerosis (MS)
109
What are S/s of MS?
*Blurred / double vision* (**Diplopia**)
Red-green color distortion
**Lhermitte's sign (electric shock felt in body)**
*Involuntary, rapid eye movements* (**Nystagmus**)
*Poor muscle control* (**Ataxia**)
*Weak muscles used for speech* (**Dysarthia**)
Dysphagia
Emotional manifestations
Partial or complete paralysis
Numbness / tingling
110
MS is marks by what 3 processes?
Chronic inflammation
Demyelination
Gliosis in CNS
111
What ethnic group is the most effected by MS?
Northern European ancestry
112
What Dx test would you do for Multiple Sclerosis (MS)?
**MRI** of **brain & spinal cord may show presence of plaques, inflammation, atrophy, tissue breakdown & destruction**
**Cerebral spinal fluid (CSF) analysis**
* *↑ Immunoglobulin G*
* *Presence of oligoclonal banding*
* Evoked potential responses are often delayed in persons with MS
because of decreased nerve conduction from eye and ear to brain
**Evidence of at least 2 inflammatory
demyelinating lesions in at least 2 different**
locations within CNS
* *Damage or an attack occurring at different times (usually >1 month apart)*
113
**Chronic, progressive neurodegenerative disorder:**
* **Bradykinesia (Slow movement)**
* Rigidity
* **Tremor at rest**
* **Gait disturbance**
**Lack of Dopamine (DA)**
**Possibly a result of a complex interplay between environmental factors & genetics**
* Family history in 15% of cases
* **↑ Risk possible by well water, pesticides, herbicides, industrial chemicals, wood pulp mills, rural residence, head trauma**
S/s:
* *Mild tremor, slight limp, decreased arm swing, Pill rolling hand tremor, Diaphragm, tongue, lips, jaw may be involved (Early)*
* Shuffling, propulsive gait with arms flexed, loss of postural reflexes (Late)
* **Hypokinetic dysarthria (speech abnormalities)**
* **Cogwheel rigidity**
* **Akinesia (Involuntary movements)**
* **Postural Instability** (*Inability to stop themselves from going forward (Propulsion) or
backwards (retropulsion)*)
Parkinson's Disease
114
Describe the letter below associated w/ S/s of Parkinsons Disease:
T
R
A
P
**T - Tremor:** Shaking, usually one sided
**R - Rigidity:** Stiffness of lims, neck, or trunk
**A - Akinesia:** Loss or impairment in power of voluntary movemnet
**P - Posture:** Posture & balance
115
Cogwheel rigidity is associated w/ which disease?
A) Multiple Sclerosis (MS)
B) Myasthenia Gravis
C) Parkinson's disease
C) Parkinson's disease
**Cogwheel rigidity Characteristics:**
* Jerky quality
* Like intermittent catches in passive movement of a joint
* Sustained muscle contraction
116
You have a Pt Dx w/ parkinsons disease. What assessment tool can you uses to assess their postural reflexes and balance responses?
**Pull test**
* **0:** Recovers indepednently, may take 1-2 steps or ankle reaction
* **1:** three steps or more backwards but recovers independently
* **2:** Retroplusion, needs to be assisted to prevent fall
* **3:** Very unstable, tends to lose balance spontaneously
* **4:** Unable to stand w/o assistance (UPDRS method)
117
**The placement of electrodes in the:**
**1)Thalamus**
**2)Globus pallidus**
**3)Subthalamic nucleus**
**Connecting it to a generator placed in the upper chest**
**Most common surgical treatment**
Reversible and programmable
Increased neuronal activity produced by DA depletion
*Improves motor function*
*Reduces dyskinesia and medications*
Deep Brain Stimulator
118
Locate, target, destroy area of brain affected by Parkinsons Diseases (PD)
**Destroys tissue that produces abnormal chemical or electrical impulses leading to tremors or other symptoms**
Ablation Surgery
119
*Transplantation of fetal neural tissue into the basal ganglia*
* **Provides DA-producing cells in the brains of patients**
* Research and clinical trials are ongoing
Transplantation
120
What Nutritional Therapy would be implemented in a Pt Dx w/ parkinsons Diseases (PD)?
*Malnutrition and constipation* can be serious consequences
Patients with *dysphagia and bradykinesia* *need food that is easily chewed & swallowed* (**Modified diet**)
*Adequate fiber diet*
**Small frequent meals**
Provide ample time to avoid frustration
**Levodopa can be impaired by protein and vitamin B6 ingestion**
