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CH2 > Exam 3 (Mod 5&6) > Flashcards

Exam 3 (Mod 5&6) Flashcards

1
Q

Uncomplicated or Complicated UTI?

No anatomical or functional abnormality that increases risk for infection

A

Uncomplicated UTI

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2
Q

Uncomplicated or Complicated UTI?

Contributory factors of UTI include Pregnancy, male gender, obstruction, diabetes, neurogenic bladder, chronic kidney disease, decreased immunity.

A

Complicated UTI

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3
Q

Inflammatory condition of the bladder usually from infection

A

Cystitis

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4
Q

What type of cystitis?

Usually from E.coli, travels from the external urethra to the bladder. Infection can also occur in any area of the urinary tract and kidney.

A

Infectious cystitis

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5
Q

What type of cystitis?

Caused by some irritants such as drugs, chemicals, and local radiation therapy. Can also occur as a complication of other disorders such as: gynecologic cancers, pelvic inflammatory disorders, endometriosis, impaired immunity (systemic lupus erythematosus) and Crohn’s disease are examples.

A

Noninfectious cystitis

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6
Q

What type of cystitis?

Not related to infection. Rare, chronic inflammation of the entire lower urinary tract (bladder, urethra, adjacent pelvic muscle). Pain associated with bladder filling and voiding; frequency, urgency, and nocturia.

A

Interstitial cystitis

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7
Q

Etiology of Complicated UTIs/Cystitis

A

More than 80% of UTIs are caused by E. coli.

Candida is another infecting microbe (can occur during long-term antibiotic therapy).

Other microbial sources are mycobacteria, yeast, and parasites.

Catheters are the most common factor associated with new onset UTI and in long-term care settings.

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8
Q

Guidelines to prevent UTIs?

A

Sterile technique when inserting catheters. Clean technique when using intermittent catheters at home. Single-use catheter recommended for home settings.

Liberal fluid intake to flush out toxins.

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9
Q

Cystitis itself is not life-threatening; however, its associated complications are:

A

Pyelonephritis and severe kidney damage (rare, most at risk population includes anatomical abnormalities/complications).

Sepsis, bacteria from the urinary tract enters the bloodstream> bacteremia/urosepsis> potential septic shock.

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10
Q

Cystitis Laboratory & Diagnostic assessment

A

*Clean catch urine specimen (urinalysis, culture, and sensitivity) - usually need at least 10 mLs. UTI may be indicated with presence WBCs, RBCs, or casts (clumps of cells), combination of leukocyte esterase and nitrates.
*Serum WBC with differential: May be elevated. Left shift? # of immature WBCs (bands) is increasing and number of mature WBCs is decreasing.
*Why is it more common in urosepsis, as compared to cystitis? Local vs. systemic infection response.

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11
Q

What are some s/sx of UTI/Cystitis?

A

back pain, flank pain, frequency, dysuria, urgency, distention of abd, tenderness

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12
Q

What are some s/sx a UTI is getting worse?

A

fever, increased WBC/left shift, pain would radiate upward from urethra (systemic infections signs)

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13
Q

Cystoscopy is performed when pt has recurrent UTIs. Identifies structural abnormalities (calculi, diverticula, strictures, foreign bodies, etc). Needed to specifically identify interstitial cystitis. Why obtain culture first?

A

Because it could put the patient at risk for developing sepsis from a urinary source.

If a patient is suspected of developing SEPSIS (SIRS criteria), blood culture is required.

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14
Q

Two major goals of Cystitis drug therapy

A

Alleviate pain/discomfort & treat bacteriuria

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15
Q

What antibiotics are used to treat UNCOMPLICATED UTI?

A

-Nitrofurantoin
-Trimethoprim/sulfamethoxazole (Bactrim-watch for sulfa allergy)
-Fosfomycin is first line for patients with low resistance
-Cephalexin, ciprofloxacin, levofloxacin, and amoxicillin are also used.

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16
Q

What antibiotics are used to treat COMPLICATED UTI?

A

Fluconazole drug of choice for fungal infections (Candida).

May require longer therapy (7-21 days).

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17
Q

Other nonsurgical management of UTI/Cystitis

A

*Fluid intake: Maintain dilute urine (2–3 L of water)
*Comfort measures: Warm sitz baths, Analgesics: Phenazopyridine, Antispasmodics: Oxybutynin common.
*Avoid spices and acidic foods > can lead to bladder irritation
*Conflicting evidence related to cranberry juice

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18
Q

Conflicting evidence related to cranberry juice

A

*Benefits = may help decrease bacterial adhesion to epithelial cells
*Negative = may be an irritant and should be avoided in interstitial cystitis

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19
Q

If UTI/Cystitis is left untreated it can lead to

A

Pyelonephritis and severe kidney disease

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20
Q

What condition?

Inflammation of urethra

A

Urethritis

*Infectious: Highest incidence is adults aged 20-24. Most common cause is STI—treat with antibiotics
*Noninfectious: Postmenopausal women – uretero-genital tissue changes from low estrogen

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21
Q

Common STIs that cause infectious urethritis

A

Gonorrhea, chlamydia, trichomonas

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22
Q

Signs/sx of urethritis

A
  • Symptoms similar to cystitis, vaginitis, or heaviness in the genitals
  • Mucopurulent or purulent discharge, dysuria, and/or urethral pruritus.
  • Possible fever. Urgency and frequency. Urinalysis may show pyuria (WBCs in urine)
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23
Q

If urethritis is left untreated or patient does not complete abx therapy, the patient is at risk for

A

developing pelvic inflammatory disease

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24
Q

Interventions for Urethritis

A

-Test for STIs (both genders), pregnancy in women
-Pelvic exam: May reveal hormone-related tissue changes
-Antibiotic therapy for STI-related cases
-Noninfectious urethritis may resolve spontaneously; postmenopausal women may use local/topical estrogen cream.

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25
Q

What condition?

Presence of calculi (stones) in urinary tract. Commonly associated with dehydration.

A

Urolithiasis

Involves two conditions:
1. Supersaturation of the urine – element (e.g., calcium, uric acid) becomes crystallized.
2. Formation of a nidus (crystal deposit that becomes infectious) along the tract. High urine acidity or alkalinity, and drugs (corticosteroids), contribute to stone formation. Metabolic conditions that increase calcium absorption in the intestine (hyperparathyroidism, vitamin D intoxication)

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26
Q

Urolithiasis etiology

A

Metabolic risk factors (dehydration), hyperparathyroidism, urinary tract obstruction, inflammatory bowel diseases, and GI problems.

Patients who are obese, have diabetes or gout are at higher risk.

Certain vitamin supplementation may be connected with stone formation: Calcium, vitamin D, and vitamin C.

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27
Q

What is the pain described as w/ kidney stones?

A

EXCRUCIATING pain in the kidney region

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28
Q

Urolithiasis Assessment

A

*Major symptom is renal colic (sudden, unbearable pain in the kidney region). Often associated with: NV (usually 1st sign of kidney stone), pallor, & diaphoresis.

*Flank pain? Stone may be in the kidney or upper ureter. -Murphy’s punch-

*CVA(costovertebral angle) tenderness indicates implications of renal calculi. Radiating to lower abdomen/pelvic region = suggests stone is in ureters or bladder

*When is the pain most intense? When stone is moving OR the ureter is obstructed

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29
Q

When is the pain re: kidney stone most intense?

A

when stone is moving OR the ureter is obstructed

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30
Q

Kidney stones- What does frequency and dysuria indicate?

A

Stone has reached the bladder

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31
Q

Urinary tract obstruction is an emergency and must be treated to

A

preserve kidney function

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32
Q

Urolithiasis Interventions

A

*Promote hydration and natural passing of stones (<5mm). Strain urine.
*Opioid analgesics for severe pain.
*NSAIDs (ketorolac) in the acute phase (Nephrotoxic if used long term)
*Spasmolytic drugs (oxybutynin)
*Thiazide diuretic and allopurinol to aid in stone expulsion.
*Alpha-adrenergic blockers and calcium channel blockers to aid in relaxing smooth muscle.
*Lithotripsy: Temporary stent may also be placed for stone(s) >5mm
*Minimally invasive surgical procedures: Ureteroscopy with stenting, Percutaneous ureterolithotomy or nephrolithotomy.
*Open surgical procedures: Open ureterolithotomy (ureter), pyelolithotomy (kidney pelvis) or nephrolithotomy (kidney). Nephrostomy tube often left in place

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33
Q

Drug therapies to prevent obstruction depends on the type of stone.

Hypercalciuria?

Hyperuricemia?

A

Hypercalciuria- thiazide diuretics (promotes calcium reabsorption)

Hyperuricemia- fluid promotion, diet modifications to restrict purines and drugs to alkinize urine (potassium citrate, sodium citrate, and sodium bicarbonate)

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34
Q

Which stones require antibiotic therapy?

A

Struvite stones form as a result of UTI with urease-producing pathogens. As such, they are often referred to as infection stones.

Quinolones (risk for Achilles tendon rupture), ampicillin, or other broad-spectrums.

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35
Q

Why aren’t NSAIDS used in the long term?

A

Nephrotoxic if used long term

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36
Q

Approximately 60%-85% of bladder injuries result from blunt trauma, while 15%-40% are from penetrating injury. The most common mechanisms of blunt trauma are motor vehicle collision (87%), fall (7%), and assault (6%). In penetrating trauma, the most frequent culprit is gunshot wound (85%), followed by stabbing (15%).

Bladder trauma requires surgical repair.

Often patients will present w/

A

anuria or hematuria

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37
Q

What condition?

A bacterial infection that starts in the bladder and moves upward to infect the kidneys.

A

Pyelonephritis

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38
Q

Bacterial infection in kidney and renal pelvis (upper urinary tract).

Most common in women 20-30 years old.

Usually normal intestinal and fecal flora. Common causative bacteria is E.coli or enterococcus faecalis. Also common in the second trimester and beginning of the third trimester of pregnancy.

Acute or chronic Pyelonephritis?

A

Acute

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39
Q

Rarely characterized by infection alone. Structural deformities, urinary stasis, obstruction and or reflux. Incidence related to underlying condition that leads to inflammatory damage (congenital structural abnormalities, neurogenic bladder dysfunction).

Acute or chronic Pyelonephritis?

A

Chronic

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40
Q

Patients with Pyelonephritis are prone to

A

bacteriuria

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41
Q

Pyelonephritis Assessment

A

Recurrent UTIs, Diabetes, stone disease, GU defects, reduced immunity, kidney function.

Sx may be similar between acute and chronic presentation.

Presence of bacteriuria= changes in urine color/odor. Inspect flank, CVA tenderness.

Psychosocial assessment: acute confusion in elderly, anxiety, embarrassment, guilt.

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42
Q

BUN, Creatinine, and GFR trend indicate kidney function and/or deterioration. What does each mean?

A

BUN= influenced by dehydration
Creatinine= best for kidney function
GFR= best for nephron function

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43
Q

How to manage pain associated with Pyelonephritis?

A

Non-surgical: Antibiotics (usually IV), increased fluids (at least 2L/Day), pain management (Tylenol), catheter replacement for long-term indwelling catheters.

Surgical: Goal is to correct structural problems leading to reflux and remove source of infection: pyelolithotomy (kidney stone removal), urethroplasty (reconstruction of the ureter), nephrectomy (last resort).

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44
Q

Pyelonephritis- How to prevent CKD?

A

antibiotic compliance, BP control, encouraging fluid intake, dietary management: protein may be restricted.

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45
Q

What condition?

Condition of increased glomerular permeability. Allows larger molecules to pass through the membrane into urine and be excreted. Massive loss of protein into urine, edema formation, and decreased plasma albumin levels. Most common cause is altered immunity with inflammation.

A

Nephrotic Syndrome

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46
Q

What is the most common cause of Nephrotic syndrome?

A

Altered immunity with inflammation

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47
Q

What must be assessed frequently w/ Nephrotic syndrome?

A

assess for dehydration

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48
Q

What is the hallmark condition associated with nephrotic syndrome?

A

proteinuria

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49
Q

Which lab value findings are altered in pts with Nephrotic Syndrome?

A
  1. Severe proteinuria (more than 3.5 g in a 24-hour urine sample) (Protein in urine think Nephrotic syndrome or glomerulonephritis!)
  2. Serum albumin less that 3 g/Dl
  3. Elevated serum lipid levels
  4. Lipids in the urine
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50
Q

What medications are used to treat Nephrotic syndrome?

A

-ACE inhibitors decrease protein loss
-lipid lowering agents
-heparin decreases vascular defects and improves kidney function

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51
Q

Nephrotic Syndrome Sx

A

impaired kidney function with increased proteinuria, decreased serum albumin, hyperlipidemia, lipids present in the urine, hypertension, and facial edema

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52
Q

Problems of urine elimination with outflow obstruction: may begin with urethral strictures, may lead to permanent kidney damage if left untreated.

Name the two conditions.

A

Hydronephrosis and Hydroureter

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53
Q

What condition?

Enlargement in the renal pelvis and kidney tissue that leads to kidney enlargement.

A

Hydronephrosis

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54
Q

What condition?

Enlargement in the ureter and kidney tissue that leads to dilation above the obstruction. Causes kidney enlargement. GFR decreases or ceases due to pressure applied to the nephrons.

A

Hydroureter

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55
Q

S/sx of Hydronephrosis and Hydroureter

A

Pt may experience flank or abdominal pain, chills, fever, malaise.

Inspect flanks/abd, can complete bladder scanner

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56
Q

Nephrostomy drain for strictures:

A
  • Assess for bleeding or signs of infection at insertion site
  • Sterile technique with dressing changes
  • Never clamp the tube
  • Assess patency frequently
  • Never irrigate the tube
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57
Q

Kidney trauma may be caused by penetrating wounds, blunt injuries to the back/flank/abdomen, or certain urologic procedures.

How is is classified?

A

Classified into five grades depending on severity

One (low-grade= bruising) to five (most severe= shattering of kidney and tearing of blood supply)

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58
Q

When assessing kidney trauma it is important to

A

document the mechanism of injury to help determine severity

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59
Q

If the kidney trauma is a penetrating injury and graded 5, what is going to happen? Lots of bleeding. Important to restore circulating blood volume w/ crystalloid fluid, packed RBCs, & plasma. Why?

A

Can lead to low BP and then shock

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60
Q

It is important to teach pt how to assess for infection and complications post kidney trauma. It is important to contact a health provider if the following sx arise?

A

-Delayed bleeding and urine leakage most common
-Development of abscess
-New-onset HTN

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61
Q

What condition?

Rapid reduction in kidney function resulting in failure to maintain fluid and electrolyte balance and acid/base balance.

A

Acute Kidney Injury)

AKA Acute Renal Failure (ARF)

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62
Q

It is important to know what defines an Acute Kidney Injury (AKI)

A
  1. Increase in serum creatinine by 0.3 mg/dL or more within 48 hours
  2. Increase in serum creatinine by 1.5 times more than baseline in previous 7 days
  3. Urine output less than 0.5 mL/kg/hr for at least 6 hours
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63
Q

What are the three types of AKI?

A

pre-renal, Intra-renal, and post-renal

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64
Q

AKI Reduced perfusion to kidneys

A

Pre-renal

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65
Q

AKI Damage to kidney tissue

A

Intra-renal

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66
Q

AKI Obstruction of urine outflow

A

Post-renal

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67
Q

AKI Health Promotion & Maintenance

A

-Avoid dehydration by drinking 2 to 3 L of water daily
-Be aware of urine characteristic changes
-**Be aware of patient’s fluid status!
-Avoid nephrotoxic substances such as NSAIDs and antibiotics (specific class to avoid is aminoglycosides (tobramycin & gentamycin)

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68
Q

How much water should someone with AKI drink?

A

2-3 L daily

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69
Q

It is important to monitor electrolyte values for AKI. Hyperkalemia is the most serious electrolyte disorder in kidney disease because it can cause fatal dysrhythmias.

What do you do 1st if patient has hyper or hypokalemia?

A

Place the pt on a cardiac monitor.

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70
Q

Hyperkalemia cocktail includes:

A
  • Regular insulin IV (and glucose if needed)
  • Sodium bicarbonate: Treats metabolic acidosis which shifts K+ out of cells
  • Calcium gluconate IV: Treats muscle and cardiac effects
  • Kayexalate (Na+ polystyrene)
  • Dialysis (if hemodynamically unstable)
  • Dietary restriction: Limit sodium, protein, potassium. Salt substitutes are high in potassium
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71
Q

Notifiable STIs

Notifiable means they have to be reported to the state (FL).

A

Chlamydia, Gonorrhea, Syphilis, Chancroid, HIV infection,

Others per local legal requirements, e.g., genital herpes

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72
Q

Safer Sex Practices to reduce STIs

A

-Using a latex or polyurethane condom for genital and anal intercourse
-Using a condom or latex barrier (dental dam) over the genitals or anus during oral-genital or oral-anal sexual contact
-Wearing gloves for finger or hand contact with the vagina or rectum
-Practicing abstinence
-Practicing mutual monogamy
-Decreasing the number of sexual partners

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73
Q

What STI?

An infection caused by bacteria. Most often, it spreads through sexual contact. The disease starts as a sore that’s often painless and typically appears on the genitals, rectum or mouth. Spreads from person to person through direct contact with these sores.

A

Syphilis

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74
Q

What is the first sign of primary syphilis?

A

chancre- looks like an ulcer, can be anywhere (genitals or mouth)

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75
Q

What should ALWAYS be worn when treating patients with syphilis?

A

GLOVES

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76
Q

Secondary syphilis develops in 25% of untreated individuals within a few months.

Sx of secondary syphilis

A

*Rash on palms, soles, trunk, and mucous membranes
*Flu-like symptoms: Malaise, Low-grade fever, Headache, Muscle aches, Sore throat, Adenopathy, Joint pain

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77
Q

Tertiary syphilis occur 4 to 20 years after initial infection. It is uncommon due to antibiotics.

S/sx include:

A
  • Cardiovascular infection with T. pallidum.
  • Neurosyphilis, including progressive dementia and locomotor ataxia.
  • Gummatous syphilis lesions on the skin, bones, or internal organs.
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78
Q

What drug is used to treat syphilis?

A

Benzathine penicillin G

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79
Q

What STI?

*Chlamydia trachomatis- intracellular bacterium, causative agent of cervicitis, urethritis, proctitis
*Reportable to local health departments in all states
*Often asymptomatic
*High prevalence of rectal and pharyngeal infection in MSM

A

Chlamydia

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80
Q

What drug therapy is used to treat Chlamydia?

A

-1st-Line: Doxycycline (100mg, PO, BID, for 7 days)
-2nd-Line: azythromycin (1g orally, single dose), levofloxicin(500mg qd x 7days)
-Expedited Partner Therapy (EPT)

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81
Q

What is important to know about instructions for a patient taking doxycycline?

A

Photosensitivty –>Instruct pt to stay out of the sun, protect skin from the sun

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82
Q

Why was 1st line Chlamydia drug therapy switched from azithromycin to doxycycline?

A

due to antibiotic resistance

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Perfectly
83
Q

What STI?

*Sexually transmitted bacterial infection
*Can be asymptomatic
*First symptoms occur within a week after sexual contact with infected person
*Can cause PID, endometriosis, and salpingitis, and pelvic peritonitis in females
*Can cause epididymitis (which can lead to infertility) in males
*Typically goes hand in hand w/ Chlamydia

A

Gonorrhea

84
Q

What are the s/sx of Gonorrhea?

A

*Pharyngitis in both males and females
*Proctitis, epididymitis, purulent (yellow-green) penile discharge, prostatitis, and urethritis in men
*Endometritis, salpingitis, cervicitis, proctitis, and urethritis in women

85
Q

What drug therapy is used to treat Gonorrhea?

A

-Injected ceftriaxone 500mg-1000mg single dose. (Body weight dependent, 150kg +/-)
-Will give doxycycline as well (since they likely have Chlamydia too)

86
Q

An infection of a woman’s reproductive organs. It is a complication often caused by some STIs, like chlamydia and gonorrhea. Organisms move from endocervix upward through uterine cavity into fallopian tubes. Sepsis and death can occur if treatment is delayed or inadequate.

A

Pelvic Inflammatory Disease (PID)

87
Q

PID s/sx

A
  • Lower abdominal or pelvic pain
  • Irregular vaginal bleeding, dysuria, vaginal discharge, dyspareunia, malaise, fever, chills
  • Pelvic examination may show discharge, “friable” cervix
  • Patient may be anxious and fearful
88
Q

What is required if a patient w/ PID has a positive pregnancy test?

A

the patient will need further hospitalization & treatment

89
Q

How to manage infection and pain for PID

A
  • Antibiotic therapy
  • Mild analgesics
  • Apply heat to lower abdomen or back
  • Increase fluid intake
  • Eat nutritious foods
  • Rest in semi-Fowler position
  • Limit ambulation
  • May need surgery if no response to other treatment
90
Q

What can occur if treatment for PID is delayed?

A

infertility and sepsis

91
Q

What condition?

Inflammation in the oral cavity; painful & inflamed ulcerations

See lesions and cracking on assessment

A

Stomatitis

92
Q

What are the most common forms of primary stomatitis? secondary stomatitis?

A

Primary- canker sores, herpetic stomatitis (HSV)
Secondary- r/t to braces, mechanical issue

93
Q

What are the treatments for minimizing pain in a patient with stomatitis?

A

○ Viscous lidocaine
○ Diphenhydramine liquid
○ Aluminum hydroxide, magnesium hydroxide, and simethicone

94
Q

Stomatitis is extremely painful, so our biggest concern is

A

dysphagia- swallowing problems that can lead to aspiration and pneumonia

95
Q

What are the ways to minimize infection in a patient with stomatitis?

A

○ Perform proper oral hygiene
○ Meds include Nystatin suspension & chlorhexidine

96
Q

Secondary stomatitis due to candidiasis can develop if someone is taking

A

long-term antibiotics

97
Q

Esophageal trauma can occur from continuous vomiting, blunt injuries, chemical burns, and EGD. We treat w/

A

keeping the pt NPO to give the esophagus rest & prevent infection (sepsis)

98
Q

What condition?

Inflammation of the gastric mucosa. Often caused by long term NSAID use (NSAIDS damage the mucosal lining, causing ulcers in the stomach). Can also be caused by H. pylori.

A

Gastritis

99
Q

Gastritis is usually caused by?

A

long term NSAID use & H. pylori

100
Q

Health promotion and maintenance for a patient w/ gastritis

A

-Balanced diet
-Regular exercise
-Stress-reduction techniques
-Limit foods and spices that cause gastric distress
-Avoid alcohol & tobacco

101
Q

What is the gold standard diagnostic tool for gastritis?

A

EGD via endoscope

102
Q

Rapid onset of epigastric pain & dyspepsia. Usually related to exposure to irritants (NSAID use, overdose or accidental consumption of toxins) or radiation therapy. Accompanied by gastric bleeding, hematemesis, or melena.

Acute or chronic gastritis?

A

Acute gastritis

103
Q

Gastritis w/ few sx unless ulceration occurs. Accompanied by NV and upper abdominal discomfort.
● Risk for B12 vitamin deficiency

Acute or chronic gastritis?

A

Chronic gastritis

104
Q

Interventions for acute gastritis:

A

● Treated w/ supportive care
● Eliminate causative factors (w/ stress reductions, medications, diet, etc.)
● Complete labs- CBC and H&H to determine if blood transfusion is needed
● Drug therapy
○ H2 receptor antagonists- Famotidine and nizatidine
○ Mucosal barrier- Sucralfate
○ PPI (most commonly used)- Omeprazole and pantoprazole
○ Antacids

105
Q

Interventions for chronic gastritis:

A

● Treated based on causative agent (usually H. pylori)
● May require vitamin B12
● Likely complete H. pylori breath test to diagnose
● PPI triple therapy to treat H. pylori
● Pt education is needed r/t the increased risk of gastric cancers

106
Q

What do we need to educate our chronic gastritis on?

A

Pt education is needed r/t the increased risk of gastric cancers

107
Q

What is the drug therapy to treat H. pylori?

A

PPI-triple therapy:
Proton pump inhibitor + 2 antibiotics (metronidazole and tetracycline) or (clarithromycin and amoxicillin)

108
Q

Mechanical or Non-mechanical intestinal obstruction?

Physical blockage caused by adhesions, tumors, appendicitis complications, hernia, fecal impactions, strictures, intussusception, volvulus, fibrosis

A

Mechanical intestinal obstruction

109
Q

Mechanical or Non-mechanical intestinal obstruction?

No physical obstruction; r/t decrease in peristalsis
○ Handling of intestines during surgery
○ Paralytic ileus (neurological issue)
■ Diabetics are at higher risk due to meds they take
● Side effects include stopping the moving of food
● Important for them to take probiotics and eat foods high in fiber

A

Non-mechanical intestinal obstruction

110
Q

Early Signs of Bowel Obstruction

A

● Nausea
● Abd cramps
● High pitched bowel sounds
● Visible peristaltic waves

111
Q

Late Signs of Bowel Obstruction

A

● Severe distention
● No sounds distal to the bowel obstruction

112
Q

In regards to intestinal obstruction, if you do not hear bowel sounds what assessment needs to be completed?

A

Listen in all four quadrants for 5 minutes each to make sure they are really absent, then call the provider.

113
Q

Intestinal obstruction- If we have severe pain that stops and turns into tenderness, what does that mean?

A

We’ve perfed and need to contact the provider immediately.

114
Q

What are the PRIORITY collaborative problems due to obstruction?

A

● Acute pain
● Potential for injury (bacterial peritonitis, acute kidney injury, perforation, etc.)

Perforation is emergent. Fluid or air in the abdominal cavity is emergent and requires immediate notification of the provider! Nothing we can do as nurses

115
Q

Is perforation (fluid/air in the abd cavity) emergent?

A

Fluid or air in the abdominal cavity is emergent and requires immediate notification of the provider! Nothing we can do as nurses.

116
Q

Strangulation obstruction results in

A

major blood loss to the intestines –> leads to tissue death and ischemia

117
Q

Strangulation obstruction ALWAYS requires

A

surgical intervention

118
Q

Obstruction high in the small intestine (lack of absorbed gastric hydrochloride) =

A

metabolic alkalosis

119
Q

Obstruction low in the intestinal tract (lack of absorbed alkaline fluids) =

A

metabolic acidosis

120
Q

Intestinal obstruction interventions:

A

● Maintain NPO status
● Nasogastric tubes
● IV fluid replacement
○ Usually isotonic w/ K added
○ Long term = may require TPN
● Blood replacement
● Assess for signs of bowel function return
● Treat underlying source/condition
● Reduce opioid analgesics (these cause constipation)
● IV broad spectrum antibiotics (if strangulation is present)
● Meds that promote gastric motility (Metoclopramide (Reglan))

121
Q

Bowel or other abdominal structure protrudes through a weakened area of the abdominal muscle

A

Hernia

122
Q

Hernia- Absent bowel sounds indicate what medical emergency?

A

strangulation

123
Q

It is important to teach patients not to forcibly self-reduce their hernias. This may cause

A

strangulation

124
Q

What condition?

Potentially life threatening acute inflammation of the visceral/parietal peritoneum and endothelial lining of the abdominal cavity. Often caused by the contamination of the peritoneal cavity by bacteria or chemicals.

Increased capillary permeability r/t inflammatory process

Dominant cause of death from surgical infections

Causes:
● Most common cause- bacterial contamination of the peritoneal cavity by perforation –> Appendicitis, diverticulitis, peptic ulcer disease, penetrating wound, bowel obstruction, worsening GU infection
● Chemical- leakage of bile, pancreatic enzymes, gastric acid
● Less common causes –> Perforating tumors, contamination during surgery, complications r/t peritoneal dialysis

A

Peritonitis

125
Q

Most common cause of peritonitis?

A

bacterial contamination of the peritoneal cavity by perforation –> Appendicitis, diverticulitis, peptic ulcer disease, penetrating wound, bowel obstruction, worsening GU infection

126
Q

Cardinal signs of peritonitis

A

● Abdominal pain, tenderness, and distention
● Rigid abdomen (boardlike)
● May have rebound tenderness
● Pt movement may be guarded
● Fever (infection?)
● Bowel sounds often diminish with increased inflammation
● WBC count often elevated to 20,000

127
Q

Why do we monitor renal status (BUN & Creatinine) if we suspect Peritonitis?

A

Third spacing leading to hypovolemia. Decreased perfusion to our kidneys. Causing Acute Kidney Injury.

128
Q

What do we do for peritonitis?

A

■ Monitor for septic shock- monitor vital signs
■ Broad-spectrum antibiotics
■ IV fluids
■ NG tube for decompression if there is decreased or absent peristalsis
■ Manage respiratory distress due to increased abdominal pressure
■ Manage pain
■ Surgery- exploratory laparotomy

129
Q

What condition?

Inflammation of the vermiform appendix. Lumen is obstructed, leading to infection. Most common cause of RLQ pain.
● Greatest risks are peritonitis & septic shock
● Gangrene & sepsis may occur within 24-36 hours
● Risk for perforation

A

Appendicitis

130
Q

Appendicitis- when is the risk for perforation the greatest?

A

after 48 hours

131
Q

McBurney’s Point (RLQ) is located midway between the anterior iliac crest and the umbilicus in the right lower quadrant.

This is the classic area for localized tenderness during the later stages of appendicitis.

What should you do?

A

Call provider immediately. This is an emergency.

132
Q

Diagnostic results for appendicitis

A

● Possible elevation in WBC count (10,000-18,000). Greater than 20,000 may indicate perforation.
● Ultrasound may show enlarged appendix.

133
Q

Appendicitis interventions

A

– KEEP NPO & prep for surgery
– Post-op antibiotics
– Possible NG tube post-op
– Prevent respiratory concerns by getting the patient out of bed and using incentive spirometer

134
Q

What condition?

Inflammation of the mucous membranes in the stomach and intestinal tract.

■ Most cases are short-term, lasting around 3 days
■ Immunocompromised individuals are at an increased risk for complications

A

Gastroenteritis

135
Q

How to prevent outbreak of Gastroenteritis

A

○ Handwashing
○ Sanitize surfaces
○ Proper food storage and prep to prevent contamination

136
Q

What is the most common cause of gastroenteritis?

A

Norovirus- food borne illness

137
Q

What is the difference between gastroenteritis and appendicitis in terms of manifestations?

A

Nausea/vomiting followed by abdominal cramping (opposite from appendicitis)

138
Q

What do we do for gastroenteritis?

A

– Important to monitor for electrolyte imblanaces and cardiac dysrhythmias
– Replace fluids (oral or IV)
– Provide perineal care and avoid skin breakdown
– Avoid drugs that suppress motility (anti-diarrheals) We want the pt to get rid of causative agent
– Antibiotics for bacterial cases (Cipro and Zithromax (IV), Septra DS and Bactrim (PO))

139
Q

Gastroenteritis- What do you typically assess for dehydration?

A

Assessments typical of dehydration
○ Poor skin turgor, dry mucous membranes, hypotension and orthostatic BP changes, oliguria

140
Q

What condition?

Inflammation of a diverticulum that occurs when undigested food or bacteria become trapped in the diverticulum. Can occur in any part of the small or large intestine, usually in the sigmoid colon.

Most of the time can be taken care of outpatient.

A

Diverticulitis

141
Q

S/sx of Diverticulitis

A

May have no symptoms however sometimes have abdominal pain (specifically LLQ), fever, tachycardia,
nausea, and vomiting

Observe for distention and tenderness, guarding on palpation which would indicate peritonitis

142
Q

Diverticulitis- What is the criteria for hospitalization?

A

Temp > 101, persistent & severe abd pain for more than 3 days, presence of GI bleeding

143
Q

Interventions for Diverticulitis

A

– NPO for severe cases
– Low fiber
– NGT in severe cases
– Broad spectrum anti-microbial
– Analgesic
– IV fluids
– No laxatives or enemas
– Promote rest

144
Q

Most common surgery for Diverticulitis

A

colon resection w/ possible colostomy

145
Q

What are the dietary recommendations for diverticulosis vs. diverticulitis?

A

High fiber for diverticulosis
Low fiber for diverticulitis

Fiber increases inflammation

146
Q

What should Diverticulitis pts avoid in their diet?

A

nuts and seeds, popcorn

147
Q

What condition?

Widespread fibrotic (scarred) bands of connective tissue that change the normal makeup of the liver and affect cellular regulation. Inflammation from toxins or the disease process destroys hepatocytes and causes a smaller, hardened organ (nodular), impairing blood and lymph flow.

A

Cirrhosis

148
Q

Biggest complications r/t Cirrhosis

A

portal hypertension, ascites and esophageal varices, and hepatic encephalopathy

149
Q

Risk factors for Cirrhosis

A

■ Hepatitis C - leading cause of cirrhosis and liver cancer in the US
■ Hepatitis B and D - most common causes of cirrhosis worldwide
■ Non-Alcoholic Fatty Liver Disease is the cause of cirrhosis associated with obesity, diabetes, and metabolic syndrome. Diet and weight loss can lead to liver regeneration and better liver function.
■ Prolonged and excessive alcohol use can cause cirrhosis

150
Q

Labs for Cirrhosis

A

■ AST, ALT, LDH- all elevated because of hepatic inflammation**
■ Alkaline phosphatase- elevated**
■ Total serum bilirubin- increased**
■ Urobilinogen-bilirubin is present in the urine
■ Light or clay-colored stools- fecal urobilinogen
■ Albumin is decreased because the liver is not synthesizing it
– As this decreases fluid will third space which is ascites
■ PT/INR is increased because of the decreased production of prothrombin
■ Platelets are decreased leading to thrombocytopenia**
■ Hemoglobin and hematocrit may decrease causing anemia
■ Kidney function will begin to deteriorate leading to increasing creatinine
■ Ascites will cause dilutional hyponatremia
■ Ammonia levels begin to elevate in advanced liver disease

151
Q

Compensated Cirrhosis (advanced cirrhosis) may be asymptomatic and is commonly diagnosed in routine lab tests or pre surgical evaluations. What will we see?

A

thrombocytopenia

152
Q

Decompensated Cirrhosis (end stage liver failure) produces late signs that lead the patient to seek medical treatment. What sx will we see?

A

○ GI bleeding
○ Jaundice
○ Ascites
○ Spontaneous or easy bruising

153
Q

Physical assessment of Cirrhosis

A

– Fatigue, weight changes, abdominal pain, GI bleeding
– Respiratory: orthopnea or dyspnea
– Abdominal assessment: distended abdomen

154
Q

Cirrhosis- How do we monitor for fluid retention r/t ascites?

A

■ Abdominal girth
■ Daily weight - most reliable indicator

155
Q

Cirrhosis- What are our manifestations of alcohol withdrawal?

A

■ Tempers may begin 6-8 hrs after alcohol cessation
■ Neurological changes r/t delirium tremens - acute confusion, agitation, delusions, and hallucination
■ Tachycardia & HTN
■ May be a medical emergency in some cases

156
Q

What type of imaging is the best way to visualize and
assess for complications such as bleeding, esophageal varices, gastritis, changes in the gastric mucosa, etc.

A

EGD

157
Q

Cirrhosis- Caution with liver biopsies because

A

there is an increased risk for bleeding

158
Q

Cirrhosis- How do we manage fluid volume?

A

– Nutrition: low sodium diet, IV vitamin supplements like thiamine, folate, and multivitamins
– Diuretics to get the fluid off
– Paracentesis can drain the fluid
– Give them respiratory support
– Fluid and electrolyte balance

159
Q

Cirrhosis- How do we prevent or manage hemorrhage?

A

– Screen for esophageal varices on endoscopy
– Propranolol (decrease HR and hepatic venous pressure)
– If there is active bleeding, vasoactive drugs can vasoconstrict

160
Q

Esophageal Varices is enlarging of the veins in the esophagus that become weak and very fragile.

■ What is our priority assessment?
■ What will we see if they rupture?
■ What is the tube that we need to have bedside?

A
  • airway (can be compromised by esophageal varices)
  • uncontrollable breathing, coughing up blood
  • Sengstaken-Blakemore tube
161
Q

What is the earliest sign of Hepatic Encephalopathy?

A

change in LOC, confusion

162
Q

What is the goal of therapy for Hepatic Encephalopathy? What do we give?

A

The goal of therapy is decreasing the excessive ammonia which will improve the nervous system.

Lactulose to promote excretion in the stool and
Neomycin sulfate or rifaximin to decrease normal flora in the gut to aid in decreasing ammonia production

163
Q

When a pt has developed hepatic encephalopathy, the liver is no longer our priority. What is?

A

the nervous system

164
Q

All the vowels go with bowels

A

Hep A and E are oral-fecal transmission

165
Q

Hep B, C, and D

A

blood borne

166
Q

Hep C has the highest incidence. Is it curable?

A

No

167
Q

What type of Hepatitis?

*Enterovirus
- Commonly found in shellfish caught in contaminated water
- Fecal-to-oral and person-to-person contact
*Mild course similar to flu-like symptoms
Vaccine recommended especially if traveling to high risk areas.

A

A

168
Q

What type of Hepatitis?

  • Blood-borne pathogen
  • Unprotected sexual intercourse with infected partner
  • Sharing needles, syringes, drug-injection equipment
  • Sharing razors, toothbrushes with infected individual
  • Accidental needle sticks or injuries from sharps
  • Blood transfusions (before 1992)
  • Hemodialysis
  • Direct contact with blood or open sores of infected individual
  • Birth (mother to baby)
    Vaccine recommended especially if traveling to high risk areas.
A

Hepatitis B

169
Q

What type of Hepatitis?

  • MOST COMMON blood-born infection in U.S no vaccine is available
    *Blood-borne pathogen
  • Illicit IV drug needle sharing (highest incidence)
  • Blood, blood products, or organ transplants received before 1992
  • Baby boomers (those adults born between 1945 and 1965)
  • Needlestick injury with HCV-contaminated blood (health care workers at high risk)
  • Hemodialysis
  • People who are incarcerated (prisoners)
  • Sharing of drug paraphernalia

Causes chronic inflammation of the liver. Frequently leading to cirrhosis.
HDV
*Blood-borne pathogen that needs helper function of HBV
*Similar risk factors to HBV and HCV

A

Hepatitis C

170
Q

What type of Hepatitis?

  • Waterborne infection associated with epidemics in some countries
  • Fecal-to-oral transmission
  • Usually resolves on its own
A

Hepatitis E

171
Q

Physical assessment/signs and symptoms of Hepatitis

A

*Abdominal pain
*Changes in skin or sclera (icterus)
*Arthralgia (joint pain) or myalgia (muscle pain)
*Diarrhea/constipation
*Changes in color of urine or stool
*Fever
*Lethargy
*Malaise
*Nausea/vomiting
*Pruritus (itching)

172
Q

Which of the hepatitis have vaccines?

A

A & B

173
Q

True or False

You cannot have Hep-D without Hep-B.

A

True

174
Q

IgG means

A

GONE –> Previous Infection

175
Q

IgM means

A

Minute –> First sign of infection –> acute infection present

176
Q

Surface Antigen (sAg)=

A

current ACTIVE infection

177
Q

Surface Antibody (sAb)=

A

Antibodies Present –> Patient either had a vaccine or previous infection

178
Q

What are we worried about w/ Hepatitis?

A

– Weight loss
– Fatigue
– Immunocompromised
– infection risk

179
Q

Fatty liver (Steatosis) without inflammation & tissue damage is

A

NAFLD (Non-alcoholic fatty liver disease).

180
Q

Fatty liver (Steatosis), inflammation, and liver damage is

A

NASH (Non-alcoholic steatohepatitis).

181
Q

Fatty liver (Steatosis)- What are our interventions?

A

Interventions include weight loss, glucose control, and lipid lowering agents

182
Q

Liver transplant for pts w/ ESRD or acute liver failure. What is another reason (most common)?

A

Cirrhosis is the most common reason.

183
Q

What is the exclusion criteria for liver transplantation?

A

● Severe cardiac instability
● Severe respiratory distress
● Metastatic tumors
● Inability to follow instructions regarding drug therapy and self-management
● May also depend upon drug & alcohol use

184
Q

Transplant complications include

A

– Acute rejection (immune system attacks it)
– Infection (sepsis and MODS)
– Bleeding
– Breakdown/obstruction of the anastomosis which can lead to necrosis, abscess, peritonitis, or bacteremia

185
Q

What condition?

Inflammation of the gallbladder

■ A blockage from gallstones leads to bile building up and irritating the gallbladder which causes edema and distention which can lead to perforation, abscess, and peritonitis
■ Usually from a high-fat, cholesterol, and caloric diet

A

Cholecystitis

186
Q

What are the signs and symptoms of cholecystitis if fatty food is eaten?

A

Flatulence, Dyspepsia, Belching, N/V, and abdominal pain (Bloomberg’s sign/RUQ)

187
Q

What are the late signs of cholecystitis?

A

jaundice, icterus, fatty or clay-colored stools, dark-colored urine r/t biliary obstruction

188
Q

What is the gold standard diagnostic tool for cholecystitis?

A

ultrasound of the RUQ

189
Q

What will the labs look like for a pt w/ cholecystitis? If liver is involved? If pancreas is involved?

A

– If liver is involved- elevated AST, ALT, bilirubin and alkaline
phosphatase
– If pancreas is involved- elevated serum lipase and amylase
levels

190
Q

Nutrition Promotion for Cholecystitis

A

■ High-fiber, low-fat diet
■ Small frequent meals
■ Monitor albumin levels to monitor nutritional status
■ Eat lean meats

191
Q

How do we manage pain for Cholecystitis?

A

■ Opioids
■ Ketorolac IV for moderate pain
■ Possible antibiotics
■ Antiemetic

192
Q

Lithotripsy can be completed to break down stones, but only if the pt is

A

of normal weight, has good gallbladder function, and
cholesterol-based stones

193
Q

What type of surgical management for Cholecystitis?

-Performed far more than the traditional open approach.
-Complications are not common.
-Patient recovery is quicker.
-May usually resume normal activities in a week.
-Postoperative pain is less severe.

A

Laparoscopic

194
Q

What is the post-operative care for an open cholecystectomy?

A

– JP drain will be placed for 24 hrs
– Pain management
– Splint the incision when coughing and deep breathing
– Manage nausea and vomiting with antiemetics
– Encourage ambulation
– NPO until bowel function returns and then progress

195
Q

What condition?

Life-threatening inflammation of the pancreas

■ Attacks are common during the holidays and vacations when alcohol consumption is higher

A

Acute Pancreatitis

196
Q

Acute Pancreatitis- What do we ask for in terms of patient history?

A
  • Collect history after pain is controlled
  • Ask about alcohol usage
  • History of abdominal trauma or biliary tract disease
  • Recent abdominal surgeries
  • Medication history
  • Family history of pancreatic disease (including cancer)
197
Q

Acute Pancreatitis- What is the most common complaint?

A

Severe and constant abdominal pain, often mid-epigastric or LUQ (may radiate to back, left flank or left shoulder). Worse after consuming alcohol or high fat meal.

■ We can see jaundice and weight loss related to nausea and vomiting.

198
Q

Cullen Sign vs Grey Turner Sign

A

Cullen Sign= discoloration of umbilical region
vs Grey Turner Sign= discoloration of flank region

199
Q

What lab tests would you see ordered for a patient with acute pancreatitis?

A

■ Serum amylase and lipase will be increased up to 3x the normal levels
■ Serum bilirubin and alkaline phosphatase – may be increased with accompanied biliary dysfunction
■ ALT – increased in acute pancreatitis r/t biliary obstruction (3 fold increase=acute biliary pancreatitis)
■ WBC can be elevated
■ Erythrocyte sedimentation rate (ESR- inflammatory biomarker) – often elevated r/t inflammation
■ Glucose levels – often elevated
■ Other labs: CBC, BMP, albumin

200
Q

Diagnostic assessment for Acute Pancreatitis

A

■ Abdominal ultrasound - **most sensitive test to diagnose causes of pancreatitis
■ Contrast-enhanced CT – more reliable visualization of pancreas itself
■ Abdominal x-ray – may show gallstones and respiratory complications

201
Q

Why would a patient with acute pancreatitis be place on NPO?

A

to not stimulate pancreatic enzyme secretion

202
Q

Acute Pancreatitis- Biggest goal is to decrease GI tract activity, thus decreasing pancreatic stimulation

A

– NPO while acute
– IV isotonic fluid
– NG tube in more severe cases of biliary obstruction
– PPIs and H2 receptor agonists
– PCA morphine or hydromorphone
– Antibiotics if it is an infectious cause or sepsis progression

203
Q

Chronic Pancreatitis is progressive destructive disease of pancreas characterized by remissions and exacerbations
Inflammation and fibrosis of tissue contribute to pancreatic insufficiency.

What is the leading cause of Chronic Pancreatitis?

A

Alcohol abuse

204
Q

Most serious complication of pancreatitis. ALWAYS FATAL if untreated. Must be drained to prevent sepsis. NEEDS URGENT CARE.

■ They will have a high fever as high as 104.
■ We will do blood cultures and an abdominal CT/MRI.
■ Drain and antibiotic therapy. Antibiotics alone will not
resolve the abscess.

A

Pancreatic Abscess

205
Q

Pancreatic abscess (lesion) may wall off and encapsulated by fibrous tissue.

Complications (often rupture spontaneously): Hemorrhage, Infection, Bowel obstruction, Abscess, Fistula formation, Pancreatic ascites.
*May spontaneously resolve
*Surgical intervention after 6 weeks

A

Pseudocyst

CH2 (8 decks)

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