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Patho > Exam 5 > Flashcards

Exam 5 Flashcards

1
Q

What is the function of the mouth

A

-digestion starts

-breaks up food

-language

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2
Q

What is the function of the salivary glands

A

-saliva moistens and lubricates food

-amylase digests polysaccharides

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3
Q

What is the function of the pharynx

A

swallows

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4
Q

What is the function of the esophagus

A

transports food

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5
Q

What is the function of the stomach

A

-stores and churns food

-pepsin digests protein

-HCl activates enzymes, breaks up food, kills germs

-mucus protects stomach wall

-limited absorption

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6
Q

What is the function of the liver

A

-breaks down and builds up biological molecules

-stores vitamins and iron

-destroys old blood cells

-destroys poisons

-bile aids digestion

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7
Q

What is the function of the gallbladder

A

-hormones regulate BG levels

-bicarbonates neutralize stomach acid

-trypsin and chymotrypsin digest proteins

-amylase digests polysaccharides

-lipase digests lipids

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8
Q

What is the function of the small intestine

A

-completes digestion

-mucus protects

gut wall

-absorbs nutrients, most water

-peptidase digests proteins

-sucrases digest sugars

-amylase digests polysaccharides

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9
Q

What is the function of the large intestine

A

-reabsorbs some water and ions

-forms and stores feces

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10
Q

What is the function of the rectum

A

stores and expels feces

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11
Q

What is the function of the anus

A

opening for elimination of feces

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12
Q

Dysphagia

A

difficulty swallowing

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13
Q

Dysphagia etiology

A

-neuromuscular dysfunction

-structural dysfunction

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14
Q

dysphagia complications

A

-malnutrition

-aspiration

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15
Q

Dysphagia S&S

A

-pain/cough with swallowing

-choking/aspiration

-malnutrition

-weight loss

-regurgitation

-pooling of food

-drooling

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16
Q

Dysphagia treatment

A

-thickener

-aspiration precautions

-keep head up

-surgical correction

-dont use straw, increases risk for aspiration

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17
Q

esophageal pain types

A

-pyrosis (heartburn)

-pain in middle of chest (mimics angina pectoris, may radiate)

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18
Q

esophageal pain pathophysiology of pyrosis

A

reflux gastric contents into esophagus

-feeling of heartburn

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19
Q

esophageal pain pathophysiology chest pain

A

-esophageal distention

-powerful esophageal muscle contraction

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20
Q

esophageal pain S&S

A

-chest pain

-SOB

-retrosternal burning

-water brash (regurgitation sour or tasteless saliva into mouth)

-nausea

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21
Q

esophageal pain treatment

A

-prevention

-causative agent specific

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22
Q

diarrhea

A

increase in frequency and fluidity of bowel movements

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23
Q

what are some causes of acute diarrhea

A

-infection

-stress

-food allergy

-leakage stool around an impaction

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24
Q

chronic diarrhea

A

-greater than 4 weeks

-malabsorption

-chronic infection

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25
Q

diarrhea pathophysiology

A

-motility disturbance: decrease contact time of chyme with small intestine

-exudative: inflammatory process of mucous, blood, protein

-toxins stimulate intestinal fluid secretion impairing absorption

-increased amount poorly absorbed solutes

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26
Q

constipation

A

-small, infrequent or difficult bowel movements

-fewer than 3 stools per week

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27
Q

constipation etiology

A

-low fiber diet

-slow peristalsis

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28
Q

constipation risk factors

A

slow peristalsis in elderly, post op, narcotic users

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29
Q

constipation complications

A

lead to impaction

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30
Q

gastroesophageal reflux disease (GERD)

A

-backward flow of gastric contents into esophagus

-may or may not produce symptoms

-#1 cause esophageal pain

-leads to metaplasia

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31
Q

gastroesophageal reflux disease (GERD) pathophysiology

A

-incomplete closure lower esophageal sphincter

-increased abdominal pressure

-drugs

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32
Q

GERD incomplete closure lower esophageal sphincter may be affected by

A

-fatty foods

-caffeine

-ETOH (alcohol)

-smoking

-sleep position

-obesity

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33
Q

GERD increased abdominal pressure is affected by

A

-pregnancy

-hiatal hernias

-tight clothing

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34
Q

drugs causing GERD

A

-beta agonist

-CCB

-nitrates, anticholinergics

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35
Q

GERD S&S

A

-heartburn (dyspepsia)

-regurgitation

-dysphagia

-chronic cough, asthma, aspiration pneumonia

-chest pain after meal

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36
Q

GERD complications

A

-bleeding

-esophageal strictures (ulcers)

-barrett esophagus (from metaplastic mucosa)

-cough, asthma, laryngitis

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37
Q

GERD treatment

A

-increase function of lower esophageal sphincter: HOB elevated

-surgical repair

-H2 blockers, PPI

-avoid alcohol, fatty foods, eating before bed, quit smoking, small meals. increase fluid

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38
Q

Hiatal hernia

A

-cause not understood

-associates with conditions of increased intra abdominal pressure: ascites, pregnancy, obesity, chronic straining/coughing

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39
Q

Hiatal hernia pathophysiology

A

defect in diaphragm allowing portion of stomach to pass into thorax

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40
Q

Hiatal hernia S&S

A

-ulcerations

-predisposed to GERD: heartburn, chest pain, dysphagia

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41
Q

Hiatal hernia complications

A

incarcerated hernia- strangulated: rare and life threatening, portion of stomach caught above diaphragm and occluded

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42
Q

Hiatal hernia treatment

A

-alleviate symptoms, avoid food late at night, elevate head (same as GERD)

-surgery for incarceration and intractable reflux

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43
Q

Gastritis

A

inflammation stomach lining

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44
Q

What can cause Acute gastritis

A

-overuse alcohol

-aspirin

-NSAIDS

-tobacco

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45
Q

Chronic gastritis

A

precursor to cancer

-helicobacter pylori

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46
Q

Acute gastritis pathophysiology

A

self limiting

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47
Q

Chronic gastritis pathophysiology

A

Helicobacter pylori promotes inflammation in gastric mucosa, interferes with prostaglandins which normally provide protection

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48
Q

Gastritis S&S

A

-anorexia

-nausea

-vomiting

-hematemesis (vomit blood)

-dyspepsia (burps burn)

-postprandial discomfort (after eating)

-chronic gastritis: pernicious anemia

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49
Q

Gastritis complication

A

acid makes hole in stomach if untreated

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50
Q

Gastritis treatment

A

-remove causative agent

-small meals, lower gastric pH, avoid irritants

-antibiotic to get rid of helicobacter pylori

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51
Q

Gastroenteritis

A

(food poisoning)

-irritation stomach and small intestine lining from pathogen or toxin

-norovirus is common cause

-usually self limiting

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52
Q

Acute gastroenteritis pathophysiology

A

-direct pathogen or toxin invasion in GI tract causing inflammation

-ingested bacteria

-imbalance normal flora: predisposes travelers gastroenteritis

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53
Q

Chronic gastroenteritis pathophysiology

A

-result to another GI disorder such as ulcerative colitis or Crohn’s

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54
Q

Gastroenteritis S&S

A

-fluid and electrolyte imbalance signs (dry)

-abdominal discomfort

-pain

-nausea, vomiting, diarrhea

-12-72 hr course

-elevated temp and malaise

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55
Q

Gastroenteritis complications

A

dehydration and electrolyte imbalance

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56
Q

Gastroenteritis treatment

A

fluid replacement and electrolyte replacement

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57
Q

Peptic ulcer disease (PUD)

A

-from acid and pepsin

-injuries in esophagus, stomach, duodenum, jejunum

-slight to mucosal injury ulcerations in severity

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58
Q

Peptic ulcer disease (PUD) etiology

A

-H pylori

-aspirin/NSAIDS

-caffeine

-diet/stress

-smoking

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59
Q

Peptic ulcer disease (PUD) stomach pathophysiology

A

-hypersecretion HCL acid

-breaks in lining may be exacerbated by meds

-10 min pain onset

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60
Q

Peptic ulcer disease (PUD) duodenum pathophysiology

A

-excessive secretion acid

-couple hours till pain onset

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61
Q

Peptic ulcer disease (PUD) S&S

A

-epigastric pain

-nausea

-abdominal upset

-chest pain

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62
Q

Peptic ulcer disease (PUD) complications

A

GI bleeding from it eroding to blood vessel

-upper stomach: dark tarry stool

-lower stomach: bright red stool

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63
Q

Peptic ulcer disease (PUD) treatment

A

-PPI (protonic pump inhibitor)

-eradication H pylori

-coating agents

-smoking cessation

-avoid aspirin/NSAIDS

-avoid stress and dietary irritants

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64
Q

Ulcerative colitis (UC)

A

-inflammatory disease of mucosa of rectum and colon

-affects epithelial layer

-remission/exacerbations

-mostly lg intestine

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65
Q

ulcerative colitis (UC) etiology

A

poorly understood

-genetic: Jewish

-environmental

-immunological

-stress doesnt cause but increases severity of attack

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66
Q

ulcerative colitis (UC) pathophysiology

A

-immunological changes in cytotoxic T cells

-leukocytes invade and crypt abscesses develop

-abscesses drain, become necrotic and ulcerate

-sloughing: bloody, mucous filled stools

-increased risk colorectal cancer

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67
Q

Ulcerative colitis (US) S&S

A

-abdominal pain

-blood, mucous filled diarrhea (brighter red)

-rectal bleeding

-weight loss

-anorexia

-anemia

-dehydration

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68
Q

Ulcerative colitis (UC) treatment

A

-steroids: short term

-immunosuppressive therapy

-antibiotics

-colectomy and ileectomy

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69
Q

Crohns diseases

A

-inflammation extends through all layers intestinal wall

-commonly effects terminal ileum

-mostly sm intestine

-diagnosed by age 20

-cause unknown

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70
Q

Crohns disease risk factors

A

-genetics

-ethnicity: Caucasians

-Jewish

-smoking

-urban dwellers

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71
Q

Crohns disease pathophysiology

A

-lymph nodes in GI tract enlarge blocking flow

-inflammation leads to deep linear ulcer and crypt abscess

-thickened with fibrous scarring

-bowel becomes incapable of absorbing intestinal contents (cant absorb food)

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72
Q

Crohns disease S&S

A

-constant abdominal pain in RLQ during flareups!

-diarrhea

-abscesses

-weight loss

-nutrient deficiencies

-fluid imbalance

-fever

-distention

-arthritis

-uveitis: eyes

-cheilitis: lips

-dermatological lesions: erythema nodosum

(more systemic than ulcerative colitis)

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73
Q

Crohns disease complications

A

-Perianal fissures

-Fistulas

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74
Q

Crohns disease treatment

A

-antitumor necrosis factor

-corticosteroids

-antidiarrheals

-opoids

-stress reduction

-vitamin supplements

-limit fruits, veggies, high fiber, dairy, spicy fatty foods, carbonates and caffeinated drinks

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75
Q

Enterocolitis/Pseudomembranous colitis

A

-c diff diarrhea

-inflammation and necrosis large intestine

-“antibiotic associated colitis”

-can be from surgery/cancer as well

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76
Q

Enterocolitis/Pseudomembranous colitis pathophysiology

A

-antibiotic exposure: kills microflora then C diff toxins infect

-bacterial toxins

-colon develops “pseudo membrane” with leukocytes, mucous, fibrin, inflammatory cells

-mucosal necrosis

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77
Q

Enterocolitis/Pseudomembranous colitis S&S

A

-diarrhea (often bloody)

-abdominal pain

-increased HR first sign

-major cause of fever among hospitalized patients receiving antibiotics!

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78
Q

Enterocolitis/Pseudomembranous colitis complications

A

perforation

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79
Q

Enterocolitis/Pseudomembranous colitis treatment

A

-stop antibiotic

-oral flagyl or vancomycin

-supportive care

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80
Q

appendicitis

A

-inflammation of vermiform appendix

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81
Q

appendicitis risk factors

A

-peak age 10-19yrs

-more common in men

-low fiber diet

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82
Q

appendicitis pathophysiology

A

-caused by obstruction

-inflammation can lead to necrosis of appendix and lack of perfusion

-infection

-perforation

-peritonitis (inflammation peritoneum from bacteria or irritating substances)

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83
Q

appendicitis S&S

A

-generalized periumbilical for 1-3 days

-pain localizes to RLQ (McBurneys point!)

-rebound tenderness!

-nausea

-diarrhea

-anorexia

-fever: increased WBC!

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84
Q

appendicitis treatment

A

-removal

-open surgery of ruptured or perforated

-laparoscopic is preferred removal

-antibiotic therapy

-fluid replacement

-fever still persists for 1-2 days after surgery

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85
Q

irritable bowel syndrome (IBS) risk factors

A

-more common females

-onset before age 35

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86
Q

irritable bowel syndrome (IBS) pathophysiology

A

-poorly understood

-disorder of motility

-increased wave activity in colin

-heightened sensory response to distention and stimulation

-greater visceral pain sensitivity

-no test to determine

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87
Q

irritable bowel syndrome (IBS) S&S

A

-alternating diarrhea/constipation

-abdominal pain

-different variations

-mucous in stool

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88
Q

irritable bowel syndrome (IBS) treatment

A

-anti diarrheal agents

-anti spasmodic agents

-increase fiber

-hydration

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89
Q

colon polyps

A

-protrusion into lumen of GI tract (unknown cause)

-benign or not yet malignant lesion

-found in colonoscopy

-chunk of tissue

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90
Q

colon polyps treatment

A

removal upon identification

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91
Q

colon cancer risk factors

A

-over age 40

-high fat, low fiber diet

-obesity and insulin resistance

-inactivity

-african american

-tobacco

-heredity!

-ulcerative colitis, chrons disease, polyps (remove to prevent cancer)

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92
Q

Colon Cancer Pathophysiology

A

unknown

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93
Q

colon cancer S&S for right side of colon

A

-obstruction

-abdominal cramping/fullness

-ribbon or pencil like stools

-blood or mucous in stool

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94
Q

Colon cancer S&S for rectum

A

-change in bowel habits

-rectal fullness (late)

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95
Q

Colon cancer treatment

A

-surgical removal so need colostomy from portion of colon being removed

-chemo

-radiation

-prevention: screening age 50

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96
Q

warning signs GI tract cancer

A

-black tarry or bloody stool

-pencil shaped stool

-change in bowel habits

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97
Q

bowel obstruction internal etiology

A

tumors, fecal impactions, inflammation, strictures

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98
Q

bowel obstruction external etiology

A

-adhesions, hernias

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99
Q

bowel obstruction non mechanical etiology

A

loss or decreased peristalsis

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100
Q

bowel obstruction pathophysiology

A

-intestinal contents accumulate above obstruction causing failure to absorb contents and abdominal distention

-loss fluid from vascular space

-fluid/electrolyte and acid/base imbalance

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101
Q

bowel obstruction complications

A

-hypovolemic shock then death

-necrosis and perforation if blood flows cut off

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102
Q

bowel obstruction S&S

A

-N/V

-hiccups

-no gas and obstipation

-pain

-distention: rounded and tight!

-high pitched bowel sounds or absent bowel sounds!

-dehydration

-hypotension

-shock

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103
Q

bowel obstruction treatment

A

-NG tubes

-fluid and electrolyte replacement

-pain management

-surgical correction

-dont give narcotics

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104
Q

peritonitis etiology

A

-contamination peritoneal cavity

-perforation visceral organs

-ascending infections

-hematopoietic/lymphatic spread

-leakage during surgery

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105
Q

Peritonitis Pathophysiology

A

inflammation of peritoneum causes vasodilation/capillary permeability and fluid shifts to peritoneal cavity

-fluid/electrolyte and pH imbalances

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106
Q

peritonitis complications

A

hypovolemic or septic shock, multiple system organ failure and death

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107
Q

peritonitis S&S

A

-rigid board like abdomen from fluid or blood!

-shoulder and thorax pain!

-rebound tenderness!

-no gas or BM!

-N/V

-high fever

-decreased bowel sounds

-increased HR and WBS

-hiccups

-signs of shock

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108
Q

peritonitis treatment

A

-remove cause with surgery

-antibiotics

-fluids

-increase BP meds

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109
Q

role of bile

A

-aid in digestion of lipids

-transport waste products: bilirubin, cholesterol, IgA, toxins

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110
Q

bile is formed in the

A

liver

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111
Q

bile is stored in the

A

gallbladder and bile ducts

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112
Q

Cholelithiasis etiology

A

-gallstones composed of mainly cholesterol

-many asymptomatic

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113
Q

Cholelithiasis risk factors

A

forty, fat, fair, female

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114
Q

Cholelithiasis pathophysiology

A

-supersaturation of bile with cholesterol

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115
Q

Cholelithiasis S&S

A

-persistent RUQ abdominal pain (biliary colic) from obstruction of cystic duct by gallstone

-sometimes radiates to back

-N/V

-often precipitates by fatty meal followed by abdominal pain

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116
Q

Cholelithiasis diagnosis

A

ultrasound

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117
Q

Cholelithiasis treatment

A

-Surgery: cholecystectomy

-Lithotripsy: mechanical breakdown of stones

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118
Q

Cholecystitis

A

inflammation of gallbladder wall following stimulating event

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119
Q

Cholecystitis pathophysiology

A

-obstruction of cystic duct which passes into bile duct from gallbladder

-stasis of bile

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120
Q

Cholecystitis complications

A

if left untreated the gangrene of gallbladder wall may rupture

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121
Q

Cholecystitis S&S

A

-acute severe right upper abdominal pain

-fever

-nausea, vomiting, eructation (burping)

-heartburn

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122
Q

Cholecystitis treatment

A

-pre treatment with antibiotics

-percutaneous catheter or endoscopic drainage with stent placement

-open or laparoscopic surgery

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123
Q

Chronic Cholecystitis

A

-chronic inflammation of gallbladder

-diabetes and obesity are predisposing factors

-sporadic symptoms

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124
Q

acute pancreatitis predisposing factors

A

-biliary tract disease

-elevated triglycerides

-alcohol abuse

-infectious origin

-hypercalcemia

insecticides

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125
Q

acute pancreatitis pathophysiology

A

obstruction pancreatic duct by stone or other cause

-outflow of pancreas gets blocks and enzymes stay and break down pancreas

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126
Q

acute pancreatitis S&S

A

-increasing pain in LUQ

-radiates to back

-guarded position

-cullens sign: blueish coloration around umbilicus

-grey turner sign: red/brown discoloration at flank

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127
Q

acute pancreatitis diagnosis

A

serum lipase and amylase

-ultrasound

128
Q

acute pancreatitis treatment

A

-NPO: nasogastric suctioning, TPN

-IV fluids

-pain management

129
Q

chronic pancreatitis etiology

A

vast majority of cases are related to alcohol abuse. African americans are most likely race. It is due to chronic inflammatory lesions within the pancreas and destruction of endocrine and exocrine parenchyma.

130
Q

Chronic pancreatitis clinical manifestations

A

Malabsorption of fats and fat soluble vitamins

131
Q

What is treatment for chronic pancreatitis

A

Endocrine and exocrine insufficiency management: oral hypoglycemics, insulin, low fat diet, and pancreatic enzyme replacement

132
Q

What are risk factors for pancreatic cancer

A

smoking, alcohol abuse, diabetes, high fat diet, excessive salt intake, nitrates, and older age

133
Q

What are clinical manifestations for pancreatic cancer

A

It has an insidious onset, with dull epigastric or back pain. Jaundice, weight loss/anorexia, and nausea/vomiting

134
Q

How is pancreatic cancer treated

A

Has a 99% mortality rate. Pain control, supportive care, and chemo/radiation

135
Q

Describe the livers dual blood supply

A

25% comes from hepatic artery while 75% comes from the portal vein that drains capillary bed of alimentary canal and pancreas. This blood drains into the hepatic vein then onto the inferior vena cava

136
Q

Name 7 manifestations of liver disease attributable to hepatocellular failure

A

Jaundice, decreased clotting factors, hypoalbuminemia, glucose imbalance, decreased absorption of vitamins D and K, feminization, and hepatic encephalopathy

137
Q

Name 5 manifestations of liver disease attributed to portal hypertension (disruption of blood flow)

A

This is GI congestion leading to: esophageal varices, gastric varices, hemorrhoids, splenomegaly, and ascites

138
Q

What is the etiology of jaundice

A

Yellow/green staining of tissues by bilirubin due to impaired bilirubin metabolism. One of the most characteristic signs of liver dysfunction

139
Q

Describe pathogenesis of jaundice throughout pre-hepatic, hepatic, and post-hepatic

A

Pre-hepatic:
hemolysis and ineffective erythropoiesis
Hepatic:
Impaired liver function
post-hepatic:
defective transport of bile salts and obstruction

140
Q

Describe the etiology and pathogenesis of portal hypertension

A

elevated pressure in the portal system leads to sluggish or obstructed flow through the portal vein/system. Venous drainage of much of the GI tract is congested. Usually the result of alcoholic or post hepatic cirrhosis (in western society)

141
Q

Describe the clinical manifestations of portal hypertension

A

caput medusae (superficial periumbilical varices) as well as esophageal, gastric, and rectal varices

142
Q

What is the etiology/pathogenesis of gastroesophageal varices

A

Collateral venous pathway that occurs due to portal hypertension. As portal pressure elevates, becomes vulnerable to rupture. Main cause of death in chronic cirrhosis

143
Q

What are clinical manifestations of gastroesophageal varices

A

Hematemesis, melena, rapid intestinal transit and vigorous bleading

144
Q

How do we treat gastroesophageal varices

A

fluid resuscitation (normal saline). Medications to lower portal pressure or reduce flow to susceptible organs: vasopressin, nitroglycerin, and somatostatin.

145
Q

Describe hepatic encephalopathy etiology/pathogenesis

A

exact cause unclear. Hepatic failure or severe chronic liver disease. Associated with elevated ammonia levels. Asterixis (classic physical finding) is a “liver flap” spastic jerking of hands when in forced extended position

146
Q

Describe clinical manifestations of hepatic encephalopathy from Grade 1-Grade 4

A

Grade 1: mild confusion, no flap. Grade 2: drowsy, confused, flap present Grade 3: stuporous, marked confusion, flap present Grade 4: coma, no flap

147
Q

How do we treat hepatic enecphalopathy

A

identify precipitating factors: GI bleeding. Reduce dietary protein intake. Diuretics to enhance elimination of nitrogenous wastes. Osmotic cathartic (lactulose) and antibiotics to reduce normal flora to reduce protein breakdown

148
Q

Describe ascites etiology and pathogenesis

A

Accumulation of fluid in peritoneal cavity
Advanced liver disease:
Portal hypertension
Hypoalbuminemia
Intraabdominal accumulation of sodium, water, and protein
Also caused by:
Malignancy
Infection
Pancreatitis
Nephrosis
Cardiac failure

149
Q

List clinical manifestations of ascites

A

Abdominal distention

Difficulty breathing

Abdominal or umbilical herniation

150
Q

What is the treatment for ascites

A

Reduce dietary sodium
Diuretics
Bedrest
Therapeutic paracentesis

151
Q

What is the etiology for cirrhosis

A

Irreversible end stage of multiple liver diseases
Severe acute hepatitis
Chronic hepatitis
Alcoholism
Toxic hepatitis
Hepatitis C
Nonalcoholic fatty liver disease – related to DM, obesity, hypertriglycemia

152
Q

What is the pathogenesis of cirrhosis

A

Fibrosis and wide spread scarring secondary to inflammation
Results in permanent alteration of hepatic blood flow
Decreased liver function results

153
Q

What are clinical manifestations of cirrhosis

A

Jaundice
Portal hypertension
Esophageal varices
Ascites
Hepatic encephalopathy

154
Q

What is the treatment for cirrhosis

A

Nutritional supplements
Antacids
Diuretics

155
Q

What is an alcoholic fatty liver and describe some treatments

A

Abnormal deposits of fat in liver cells
More fat than liver can metabolize
Most from ETOH (5 beers or glasses of wine per day) but also:
Diabetes
Obesity
TPN
Drugs
Normally asymptomatic
Treatment:
Stop alcohol intake
Nutritional support
If left untreated may go on to progressive liver fibrosis and cirrhosis

156
Q

What is alcoholic hepatitis and give some treatments

A

Active inflammation Associated with “binges” Ranges from mild to very severe
Liver shows signs of hepatocyte necrosis
Treatment:
Stop alcohol intake
Nutritional support
Steroids
Complicated by DTs

157
Q

Describe the etiology of hepatitis A (enteric)

A

Transmission
Fecal-oral
Sexual (oral-anal contact)
Common in areas of overcrowding
Day care centers
Institutional settings

158
Q

What is the pathogenesis of hepatitis A virus (enteric)

A

Despite the cause, changes to the liver are usually similar in each type of viral hepatitis
Liver call destruction
Self-destruction of cells
Tissue death
Anorexia
Jaundice
Hepatomegaly

159
Q

What is treatment for hepatitis A virus

A

Vaccination
Added to routine childhood vaccines in 2006
May be vaccinated after exposure
Prevention
Handwashing
Prognosis good

160
Q

Give the etiology for hepatitis B

A

Transmission by parenteral contact with
blood
blood products
contaminated needles
sexual contact
perinatal

161
Q

Give treatment for hepatitis B (serum)

A

Supportive
Hepatitis B immune globulin
May be given within 7 days of exposure
Recommended as part of childhood vaccination regimen
Recommended for high-risk individuals:
Multiple sex partners
Male homosexuals
Illicit drug users
Hemodialysis patients
Health care workers
Prognosis worsens with age and debility

162
Q

Give clinical manifestations of hepatitis B (serum)

A

More insidious onset
Similar to Hepatitis A but may involve:
Urticaria & other rashes
Arthralgia
Angioedema
Glomerulonephritis

163
Q

Give the etiology for hepatitis C virus

A

Important occupational risk for health care workers
Transmission similar to Hepatitis B
IV drug use
Blood transfusions prior to availability of screening test
Intranasal cocaine use

164
Q

Give treatment for hepatitis C virus

A

Interferon alfa
Developing drug therapies
Supportive
Rest
Nutritional support
Prognosis moderate

165
Q

Give etiology for hepatitis D virus

A

Requires an infection with Hepatitis B to survive
Transmission by parenteral routes
Exposure to blood and blood products
IV drug users
Hemophiliacs

166
Q

What is the treatment for hepatitis D

A

No specific treatment for Hepatitis D
Prognosis fair, worsens with chronic disease
Prevention
Safe sexual practice
Screening of blood products
Avoidance of IV drug use
Vaccination with Hepatitis B vaccine

167
Q

Give etiology for hepatitis E virus

A

Transmission fecal-oral (especially contaminated water)
Most common cause of acute hepatitis in developing countries
Cases in the US typically follow travel
India
Africa
Asia
Central America

168
Q

Give treatment for hepatitis E virus

A

Supportive
No vaccine
Prevention
Avoid undercooked foods
Careful handwashing
Drink safe water and beverages
Canned
Bottled
Purified

169
Q

Renal disorder is associated with pain in what area of the back?

A

costovertebral angle

170
Q

An infection of the renal pelvis and interstitium is known as:

A

pyeolonephritis (caused by streptococcus)

171
Q

A classic manifestation of chronic pyelonephritis is:

A

atrophic kidneys with diffuse scarring

172
Q

The most common physiologic abnormality found in patients with a renal stone is:

A

hypercalcemia

173
Q

glomerulonephritis results from:

A

antigen-antibody complexes

174
Q

Autosomal Dominant Polycystic Kidney Disease (ADPKD):

A

> presents with pain being the most frequent client complaint

> results from formation of cysts that involve the entire nephron

> results in urinary tract infections, often due to Enterobacter organisms

175
Q

What are some predisposing factors associated with pyelonephritis?

A

urinary obstruction, pregnancy, diabetes, catheterization, neurogenic bladder

176
Q

Complete urinary obstruction causes:

A

> increased urinary stasis (inactivity)

> increased urinary frequency

> decreased glomerular filtration rate

> increased predisposition to infection

177
Q

Clinical manifestations of glomerulonephritis include:

A

proteinurea, periorbital edema, coffee-colored urine

178
Q

What clinical findings suggest a diagnosis of nephritic syndrome?

A

hypercoagulability, hypoalbuminemia, hyperproteinemia, hyperlipidemia, edema

179
Q

Kidneys are responsible for:

A

maintaining fluid and electrolyte homeostasis

180
Q

What are the functions of the renal system?

A

> maintain fluid, electrolyte, and acid-base balance

> detoxifying the blood and eliminating wastes

> regulating blood pressure

> production of erythropoietin (red blood cell growth catalyst)

> activation of Vitamin D to facilitate absorption of calcium

181
Q

How many liters of blood are filtered by the kidney per hour? What percentage is returned to the body?

A

7 L; 99 percent

182
Q

Why is renin released?

A

to cause vasoconstriction to increase BP

183
Q

Functions of the renal system

A

Maintain fluid, electrolyte, and acid-base balance

Detoxifying the blood and eliminating wastes

Regulating blood pressure (increase in volume = increase in pressure)

Production of erythropoietin (renal failure will be enemic)

Activation of Vitamin D to facilitate absorption of calcium (chronic renal failure have bone disorders)

184
Q

If kidneys are failing which metabolic dysfunction will you have?

A

Metabolic acidosis

185
Q

What are the parts of the urinary system?

A

kidneys, ureters, bladder, urethra

186
Q

What are the three principle areas of renal parenchyma?

A

> pelvis: large collecting area for urine

> medulla: pyramids

> cortex: glomeruli, nephron tubules

187
Q

What is the nephron?

A

functional unit of the kidney

188
Q

How much urine filters through the kidneys per hour?

A

7 liter per hour

189
Q

What are the three major functions of the nephron?

A

> filtration of water soluble substances from the blood

> reabsorption of filtered nutrients, water, and electrolyes

> secretion of waste products

190
Q

What are the functions of the glomerulus?

A

> site of fluid filtration from blood to the nephron

> more permeable than other capillaries in the body

> prevents passage of blood cells and proteins

191
Q

What is the glomelular filtration rate (GFR)?

A

> 125 mL/min

> each glomeruli can regulate its own GFR (effective as long as SBP is 90-180)

> one of the most important factors of blood volume

192
Q

best way to measure GFR

A

> creatinine clearance is a good measure of GFR

kidneys dont reabsorb it, how much runs through per minute gives gfr

193
Q

Describe the proximal convoluted tubule?

A

> reabsorbs about 2/3 of the filtered water and electrolytes

> reabsorbs all of the glucose, amino acids, and vitamins

194
Q

if there is sugar in blood stream?

A

lots of sugar in your blood and kidney gets rid of it

> 200

195
Q

Describe the Loop of Henle.

A

> overall process includes pushing fluid into interstitial space to further concentrate filtrate

196
Q

Descending loop of henle

A

transports water

delivers concentrated filtrate to ascending loop

197
Q

Ascending loop of henle

A

> ascending loop: actively transports Na+, Cl-, K+; increased interstitial osmolarity

198
Q

Describe the distal convoluted tube.

A

> “fine tune” of sodium and water reabsorption: ADH (antidiuretic hormone- vasopressin), aldosterone

> site from which filtrate enters the collecting tubule

199
Q

What does ADH do in the distal convoluted tube?

A

monitors the osmolality (thickness) of your blood and causes you to retain water to thin out your blood

200
Q

What does aldosterone in the distal convoluted tube do?

A

makes you hold onto sodium and water

201
Q

best way to measure urine output

A

catheter

202
Q

Describe the collecting tubule.

A

> distal tubules empty into the single larger collecting tubule

> merges into larger collecting ducts

> more than 99% of the original filtrate is reabsorbed by the time it reaches the renal pelvis

> creates 30-60 mL of urine/hour

203
Q

Describe BUN. (meaning, normal value, what it measures, what it can also reflect)

A

Blood urea nitrogen - byproduct of protein metabolism that can be affected by diet, GI bleed causing blood cells to be digested

> normal value: 10-29 mg/dl

> indirect measure of overall hydration

> can also reflect diet, GI bleeding, tissue breakdown

204
Q

Describe creatinine.

A

> reflects GFR

> most commonly used “quick” method to estimate renal function

byproduct of muscle metabolism and ONLY excreted by kidneys

205
Q

What are normal values for creatinine?

A

> female: 0.5-1.1 mg/dL

> male: 0.6-1.2 mg/dL - higher muscle mall

206
Q

Describe urinalysis.

A

Normal urine is clear, pale yellow to amber, slightly acidic, may contain a few cells

207
Q

What causes glycosuria?

A

exceeding the threshold for glucose reabsorption

208
Q

What is the main driving force for glomerular filtration?

A

hydrostatic pressure in the glomerular capillaries

209
Q

What would increase GFR?

A

fluid volume excess

hydro-static pressure in glomerular capillaries is main force driving force for glomerular filtration

210
Q

Serum creatinine may be increased by:

A

muscle breakdown

211
Q

What is the etiology of cystic kidney disease? (cause, two types)

A

> genetically transmitted

> autosomal recessive (evident in childhood) or autosomal dominant (occur later in life) polycystic kidney disease

> involves one or both kidneys – cyst may be found in other organs

> Develops more quickly in men

212
Q

ARPKD etiology - cause

A

> identified in neonatal period

> kidneys retain shape but are enlarged

> dilated collecting ducts

> abnormal portal (liver) ducts

213
Q

ARPKD clinical manifestations that can lead

A

> respiratory distress

> palpable - feelable- kidneys

> systemic hypertension even as a baby

pulmonary hypoplasia - not enough cells of pulmonary system

214
Q

ARPKD diagnosis

A

> recessive pattern of inheritance in the family

> liver biopsy

> CT, MRI, ultrasound will be similar to ADPKD

215
Q

ADPKD etiology

A

> most common

> no gender/ race risk factor

> usually diagnosed at 40-59 yrs old

> kidneys cannot concentrate urine

> cysts multiply and expand: kidney size increases, decline in GFR, decreased renal perfusion, local ischemia (cyst can rupture, cause kidney ischemia)

> involvement of other organs, most commonly the liver

216
Q

ADPKD clinical manifestations

A

inability to concentrate urine, hypertension, proteinuria, hematuria (blood in urine), pain (from cyst rupturing or kidney stones), kidney stones, UTI, cyst infections

217
Q

ADPKD diagnosis

A

> genetic history

> ultrasound

218
Q

ADPKD treatment

A

> supportive: control BP, manage other conditions

> dialysis

> kidney transplant

219
Q

Renal Cell Carcinoma

A

> 2-3% of all malignancies in the US

> 85% all renal cancers

> 39000 new cases annually

> 13000 deaths annualy

> 2x more common in men

> 20% higher incidence in African Americans

> mean 5 year survival for advanced RCC is <10%

220
Q

RCC etiology

A

> risk increased 3-4x when a 1st degree relative has the disease

> primary risk factors: cigarette smoking, obesity, hypertension (quit smoking and lose weight RF goes dow)

221
Q

RCC clinical manifestations - S/S

A

> often asymptomatic until late - hard to catch early because kidneys have large reserve to function even if large portion is damanged

> costovertebral angle tenderness - bottom of ribs meet spine on the back - land mark for kidneys - very painful

> hematuria

> palpable abdominal mass

> bone pain, SOB, chest pain, from metastatic - spreading disease late

222
Q

RCC treatment

A

> surgical removal

> metastasis usually unresponsive to chemotherapy (metastasis occurs in 1/3 cases

223
Q

What are the four RCC stages?

A

I: tumor w/in capsule

II: tumor invades perirenal fat

III: tumor extends into renal vein or regional lymphatics

IV: metastasis (other kidney, bone, liver, lungs, heart)

224
Q

What prevents against kidney infection?

A

normal host defenses:

> acidic pH and urea in urine

> prostatic secretions in men

> urethral secretions in womean

> microurition - unidirectional flow - voiding/peeing in one direction to flush out

> epithelial cells trap bacteria and provide additional protective barrier

225
Q

How does decreased estrogen increase risk for infection?

A

larger urethra with thinner membranes

226
Q

What are the risk factors for renal system infection?

A

> increasing age

> vesicoureteral reflus of urine

> congenital abnormalities

> female gender

> pregnancy

> neurogenic bladder (bladder can’t empty due to a neurological condition)

> urinary obstruction

> obesity

> diabetes

> uncircumcised male children

> instrumentation (catheters)

227
Q

Risk factors of acute pyelonephritis

A

> pregnancy is a major risk factor

> highest incidence in young women, infants, and the elderly

> usually unilateral

> right kidney involved >50 percent of the time

228
Q

What usually causes acute pyelonephritis?

A

Ecoli

229
Q

Pathogenesis of acute pyelonephritis

A

> usually an “ascending” infection

> can arrive via bloodstream

> bacteria binds to epithelial cells

> inflammatory response/damage to parenchymal tissue

230
Q

What is acute pyelonephritis?

A

common bacterial infection of the renal pelvis and kidney

231
Q

What are the clinical manifestions of acute pyelonephritis?

A

> sudden onset

> fever/chills

> nausea, vomiting, anorexia

> CVA tenderness

> dysuria (painful urination), urgency, frequency

> complications: septic shock, ARDS (adult respiratory distress syndrome)

> chronic kidney disease due to scarring

232
Q

What is the treatment for acute pyelonephritis?

A

> diagnosis made via urinalysis (bacteria, RBCs, WBCs)

> antibiotic therapy for 7-10 days usually outpatient

> may be hospitalized for more severe cases (urine culture, IV antibiotics, IV fluids)

233
Q

What is chronic pyelonephritis?

A

continuing pyogenic infection of the kidney that occurs almost exclusively in patients with major anatomic abnormalities

234
Q

What is the etiology of chronic pyelonephritis?

A

> small atrophied kidneys with diffuse scarring

> risk factors: vesicoureteral reflux, urinary obstruction, neurogenic bladder

235
Q

Pathogenesis of chronic pyelonephritis

A

> chronic or recurrent infections

> chronic interstitial inflammation

> reduction in the number of functional nephrons

end stage renal failure is worst thing that can happen

236
Q

clinical manifestations of chronic pyelonephritis

A

> minimal symptoms

> flank pain less intense than in acute pyelonephritis

> incidental diagnosis at times (hypertension, UTI, elevated creatinine levels)

237
Q

treatment of chronic pyelonephritis

A

> correction of underlying problem

> antibiotic therapy (prolonged)

> support existing renal function

238
Q

Renal obstruction does what?

A

> interferes with the flow of urine

> can occur at any point within the system

> causes urinary stasis

> predisposes to UTIs

> can lead to post renal acute renal failure and acute tubular necrosis

239
Q

renal obstruction etiology

A

> congenital: anatomical malformation

> acquired: calculi (low urine output, abnormal pH, medications), tumors

240
Q

renal obstruction pathogenisis

A

> changes secondary to obstruction depend on location and size of obstruction

> hydrostatic pressure increases proximal to the obstruction

> dilation follows with reduction in GFR

> eventually portions of the kidney become ischemic

241
Q

Obstruction of renal S/S

A

Depends on location and degree of obstruction:

Bilateral

Weight gain

Nausea

Anorexia

Malaise

Headaches

Increased abdominal girth

Edema

242
Q

What is hydroureter?

A

complete obstruction of ureter leads to:

Hydronephrosis

Decreased GFR

Ischemic kidney damage

243
Q

urinary tract obstructions of the pelvis, ureter-intrinsic, ureter-extrinsic, bladder, urethra, prostate

A

> pelvis: calculi, tumors, ureteropelvic stricture

> ureter-intrinsic: calculi, tumors, clots, sloughed papillae, inflammation

> ureter-extrinsic: pregnancy, tumors, retroperitoneal fibrosis

> bladder: calculi, tumors, functional (neurogenic)

> urethra: posterior valve stricture, tumors (rarely)

> prostate: hyperplasia, carcinoma, prostatitis

244
Q

Urintary tract obstruction clinical manifestations

A

> depends on location and degree of obstruction

> bilateral: weight gain, nausea, anorexia, malaise, headaches, increased abdominal girth, edema

> hydroureter: complete obstruction of ureter

> hydronephrosis

> decreased GFR

> ischemic kidney damage

245
Q

Urinary tract obstruction treatment

A

> depends on cause

> location of obstruction

> size

> lithotripsy (shock waves)

246
Q

What is the two-word technical term for kidney stones?

A

renal calculi

or named for where they are

247
Q

What causes the pain?

A

movement with peristalsis

248
Q

What adverse effects could arise if a renal calculi completely blocks a ureter?

A

hydronephrosis, where the urine backs up into the kidney

249
Q

Why is it important to increase fluid intake to 8-10 glasses?

A

to flush out stones

250
Q

What is a primary glomerular disorder?

A

primary glomerulopathies: only the kidney is involved

251
Q

What is a secondary glomerulopathy?

A

injury due to drug exposure, infection, systemic, or vascular pathology

252
Q

Glomerular disorders are responsible for?

A

end stage renal disease; glomerular disorders account for 90%

253
Q

What may glomerular damage result in?

A

hematuria, proteinuria, abnormal casts (composed of WBCs, RBCs, or kidney cells), decreased GFR, edema, hypertension

254
Q

What are glomerulopathies?

A

things that are wrong with the glomerulus

255
Q

How are glomerulopathies typically classified?

A

by the degree of proteinuria

256
Q

What is nephritic syndrome (inflammation)?

A

hematuria, mild to moderate proteinuria main thing to know

, decreased GFR, hypertension, edema of hands and face, elevated creatinine, and may lead to renal failure

257
Q

What is nephrotic syndrome?

A

protein loss through hyperexcretion

258
Q

Acute glomerulonephritis (inflammation and glomerular damage) etiology

A

> more common in men

> a leading cause of ESRD (end stage renal disease)

> wide variety of triggers (bacterial, viral, parasitic, systemic disease

259
Q

acute glomerulonephritis clinical manifestations

A

> dark urine

> proteinuria

> edema

> hypertension

> oliguria: <400 mL in 24 hours (not enough)

> increased BUN/creatinine

260
Q

acute glomerulonephritis diagnosis

A

> patient history

> clinical manifestations

> BUN and creatinine levels

> urinalysis

261
Q

acute glomerulonephritis treatments

A

> supportive care

> may include temporary dialysis

262
Q

nephrotic syndrome (too much protein excretion) etiology

A

> greater than 3-3.5 grams of protein loss per day

> common systemic disease cause: diabetes mellitus

> genetically linked in children

263
Q

nephrotic syndrome clinical manifestations

A

> hypoalbuminemia

> hyperlipidemia (increased lipid production)

> edema

> hypercoagulability (proteinuria causes decrease in proteins that maintain blood levels, so the body releases clotting factors to compensate)

264
Q

nephrotic syndrome treatment

A

> diuretics

> lipid lowering meds

> immunosuppressive therapy

> hypertensive therapy

treat problem thats causing glomerus to be too permeable

265
Q

chronic glomerulonephritic

A

> pathologic process same as acute

> progresses into chronic end stage renal disease (ESRD)

> nephrons atrophy, become scarred and non-functioning

266
Q

The condition characterized by oliguria and hematuria is:

A

acute glomerulonephritis

267
Q

Nephrotic syndrome does not usually cause:

A

hematuria

268
Q

It is true that polycystic kidney disease is _________ transmitted

A

genetically

269
Q

Acute kidney injury was formerly known as what?

A

acute renal failure

270
Q

AKI (acute kidney injury)

A

> potentially reversible

> characterized by abrupt deterioration of renal function

> increase in serum creatinine 0.5 mg/dL

> mortality rates very high in critically ill patients

271
Q

What is oliguria?

A

uop of less than 400 mL/24 hours

272
Q

What is anuria?

A

uop of less than 100 mL/24 hours

273
Q

AKI risk increases with what comorbitities?

A

diabetes, heart failure, liver failure, hypertension, atherosclerosis, advanced age (GFR at 80 is half of what it was at 30)

274
Q

What are the 3 broad categories of acute renal failure?

A

pre-renal - (perfusion problem)

post-renal

intra-renal

275
Q

What is meant by pre-renal kidney injury?

A

> decreased perfusion to the kidney

> could be due to drug use (ACEI, ARB, NSAIDS - vasodilating drugs)

> decrease in blood volume (dehydration, vomiting, hemorrhage, diuretics, burns, large volumes of fluid in interstitial space or peritoneal space)

276
Q

pre-renal injury pathogenesis

A

> decreased perfusion = decreased GFR

> autoregulatory mechanisms protect the renal parenchyma to a point

> correction of underlying problem will prevent tissue damage if done quickly

> if uncorrected: hypoperfusion=ischemia of renal parenchyma=acute tubular necrosis

277
Q

What does post-renal kidney injury mean?

A

> obstruction of normal urine outlfow

> S&S of fluid overload present

> most common causes: BPH (enlarged prostate), kinked or obstructed catheters, tumors, strictures, calculi

278
Q

In post-renal kidney injury, what happens to the unaffected kidney?

A

it increases production to compensate

279
Q

Which kidney injury is easiest to treat?

A

post-renal kidney injury

280
Q

What is intra-renal kidney injury?

A

> caused by dysfunction of the nephrons (vascular, interstitial, glumerular, tubular)

inside the kidneys

281
Q

What is ATN? What causes it? What does it cause?

A

Acute Tubular Necrosis

> drug induced

> ischemia, contrast media, nephrotoxins, sepsis

282
Q

What are the phases of ATN?

A

> prodromal phase: insult has occurred, duration will vary

> oliguric phase: up to 8 weeks, diuresis occurs but tubular function remains impaired (50-400 mL/day), uremic syndrome (decreasesd GFR = oliguria)

> postoliguric phase: 1 week- 1 year, normal creatinine is marker for full recovery

283
Q

What is the treatment for AKI?

A

> identify risk factors

> treat hypoperfusion promptly

> nephrology consult

> nutrition

284
Q

Describe chronic kidney disease

A

progressive and irrevocable loss of functioning nephrons

285
Q

In chronic kidney disease, how many nephrons may be lost before symptoms manifest?

A

75%

286
Q

What is the final outcome of chronic kidney disease?

A

ESRD imporant

biggest risk factors are DM and HTN

287
Q

What are risk factors for CKD?

A

diabetes and hypertension

288
Q

Stages of CKD

A

> decreased renal reserve: <75%

> renal insufficiency: 75-90%

> ESRD: >90% loss

289
Q

Complications of CKD

A

> cardiovascular disease (hypertension and heart failure)

> uremic syndrome (inability to eliminate waste)

> metabolic acidosis

> electrolyte imbalances

> renal osteodystrophy (high phosphate, low calcium), fractures

> malnutrition

> anemia

> pain

> depression

290
Q

CKD treatment

A

treat symptoms (sodium bicarbonate for metabolic acidosis, vitamin D for deficiency, etc)

> hemodialysis

> peritoneal dialysis

> kidney transplant

291
Q

Describe micturition (urniation)

A

> often taken for granted but requires CNS, ANS, and PNS

> continent ability means control of voiding patterns

292
Q

What is normal bladder capacity?

A

300-500 mL

293
Q

What is normal post-void residual volume?

A

50-100 mL

294
Q

When does the urge to void usually happen?

A

150-250 mL

295
Q

What is the process of catheterization?

A

one provider has to watch and do a check-off while the other provider performs the procedure

296
Q

What is a CAUTI?

A

Catheter-Associated Urinary Tract Infection

> most common nosocomial infection today

> sentinel event/never event

> evidence based bundles of care: aseptic technique, discontinue ASAP, catheter care, must justify insertion and continued use

297
Q

What is cystitis?

A

bladder infection

298
Q

etiology of cystitis

A

> bacteria normally cleared by flushing of urine

> more common in females due to shorter urethra

> risk factors: obstruction, instrumentation, pregnancy, obesity, catheterization

299
Q

Cystitis risk factors

A

Obstruction

Instrumentation

Pregnancy

Obesity

Catheterization

300
Q

cystitis pathogenesis

A

> inflammatory response secondary to bacterial invasion

> E. coli responsible for most infections

> typically travel “up”: sexual activity, poor hygiene, contraceptive use (diaphragm)

301
Q

clinical manifestations of cystitis?

A

frequency, urgency, dysuria, pain, hematuria, cloudy urine, odor

302
Q

cystitis treatments

A

> prevention

> antibiotic therapy

303
Q

Micturition requires what NS

A

Central nervous system

Autonomic nervous system

Peripheral nervous system

304
Q

Normal bladder capacity? When do you need to pee?

A

300-500 mL

pee at 150-250 mL

post residual 50-100 mL

305
Q

What is incontinence?

A

involuntary urine loss

> 2x more common in women

> prevalence increases w/age

> by age 50, 30% females have it

> In 2000, $20 billion spent on incontinence

306
Q

Risk factors for incontinence

A

> pregnancy, vaginal delivery

> impaired cognition

> immobility

> diabetes

> spinal cord injuries

> UTI

> pelvic muscle weakness

307
Q

pathogenesis of incontinence

A

normal functioning requires: CNS, bladder/urethral function, cognition

308
Q

What is a neurogenic bladder?

A

a disruption in the nervous control of micturition (stroke, parkinsonism, spinal cord injuries/defects)

309
Q

What are the types of incontinence?

A

> urge - over active bladder

> stress

> mixed

> overflow

> functional

310
Q

Incontinence treatment

A

> review of contributing factors

> behavioral (pelvic floor muscle training)

> pharmacologic

> surgical (bladder sling, artificial urinary sphincter)

311
Q

Describe urge incontinence

A

> most common in older men

> urgency/leakage of urine

> overactive detrusor muscle that contracts

> causes: aging, bladder infections, tumors/radiation, calculi, idiopathic

312
Q

Describe stress incontinence

A

> most prevalent

> small amounts of urine lost with increased abdominal pressure (sneezing, laughing, coughing, heavy lifting)

> weakened pelvic floor

> childbearing

313
Q

Describe mixed incontinence

A

> combo of stress and urge

> common in older women

> greater volume of urine leakage can disrupt ADLs

314
Q

Describe overflow incontinence

A

> bladder becomes overfull

> causes: obstruction, bladder weakness

315
Q

Describe functional incontinence

A

> physical or environmental limitations that prevent access “in time” Lack of facilities

Cognitive deficits

Physical limitations

Health care workers play a critical role in manipulating the environment!!

316
Q

Treatment of incontinence

A

Review of contributing factors

Behavioral

Pelvic floor muscle training

Pharmacologic

Surgical

Bladder sling

Artificial urinary sphincter

317
Q
A

Patho (10 decks)

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