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NP 612- Family Theory Adult > Unit 1- Abd/Renal/Skin > Flashcards

Unit 1- Abd/Renal/Skin Flashcards

1
Q

Acute diarrhea is how long

A

<1 week

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2
Q

Chronic diarrhea is how long

A

> 2 weeks

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3
Q

Epigastric discomfort, postprandial fullness, early satiety, anorexia, belching, bloating

A

Dyspepsia

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4
Q

Extreme pain, difficult to distinguish from angina pectoris

A

Heartburn

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5
Q

Black tarry stool, most common cause is upper GIB

A

Melena

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6
Q

Can use antihistamines, antidopaminergics, cholinergic, and SSRIs for symptomatic relief

A

N/V

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7
Q

Inflammation of stomach and intestine

  • acute from infectious process of food poisoning
  • chronic from food allergies, food intolerance, stress, lactase deficiency
A

Gastroenteritis

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8
Q

Management:
-fluids with sodium, diet with boiled starches, cereals and salt, possible hospitalization, anti motility drugs, antibiotics

A

Gastroenteritis

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9
Q

Appendicitis is dilation of appendix followed by obstruction and _____

A

Subsequent bacterial infection

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10
Q

Management of appendicitis

A

Surgery, correction of fluid/electrolyte imbalance, bedrest, NPO

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11
Q

Stomach or duodenal contents back flow into esophagus (lifelong condition, lifestyle modifications are key)

A

GERD

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12
Q

Penetrates muscular mucosa, larger than 5mm in diameter

A

PUD

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13
Q

Gluten sensitive autoimmune disorder that affects small intestinal villous epithelium

A

Celiac

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14
Q

Type types of Inflammatory Bowel Disease

A

Ulcerative colitis and Crohn’s disease

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15
Q

Risk factors are family history, diet high in fat, red meat, remind carbs, low plant fiber

A

Colorectal CA

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16
Q

Alcoholism is the cause of 70-80% of cases

A

Chronic pancreatitis

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17
Q

Usually indicative of renal pathology, most often glomerular origin

A

Proteinuria

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18
Q

 Acute onset of mild-severe colicky, epigastric or periumbilical pain
• Starts as vague pain but within 24 hours shifts to localized RLQ pain
• Worse with walking or coughing
• Can radiate to testicles or be associated with abdominal muscle spasm in both genders

A

Appendicitis

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19
Q

Diagnostic test for appendicitis: deep palpation over LLQ with sudden, unexpected release of pressure- positive sign is tenderness

A

Rovsing’s sign

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20
Q

Diagnostic test for appendicitis: lift right leg against gentle pressure applied by examiner or place patient in left lateral decubitus position and extend patient’s right leg at the hip- increase in pain is positive

A

Psoas sign

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21
Q

Diagnostic test for appendicitis: right hip and knee flexed, examiner rotates right leg internally- positive sign is pain over RLQ

A

Obturator sign

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22
Q

Diagnostic test for appendicitis: pressure applied halfway between umbilicus and anterior spine of ilium- pain with pressure is positive sign

A

McBurney’s sign

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23
Q
  • Management
    o Surgical- perforation occurs often, so refer to surgeon ASAP
    o Third gen cephalosporins for gram-neg aerobic and anaerobic organisms
A

Appendicitis

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24
Q

o Pouchlike protrusions of intestinal mucosa that occurs within descending and sigmoid segments of the colon
o Also occur in the small bowel

A

Diverticulitis

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25
Q

o Bleeding is the most common complication

A

Uninflamed diverticulitis

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26
Q

Subjective findings:
 LLQ pain, sometimes worse after eating
 Diarrhea and constipation alternating, distention/tenderness
 Bleeding
 Inflamed ______ can cause fever, chills, tachycardia
 Anorexia, n/v
 Fistula- depends on which organ is involved with it

A

Diverticula

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27
Q 
Objective findings:
	Tenderness of LLQ
	Can palpate a mass sometimes
	Rebound tenderness, guarding, rigidity
	Occult blood in stool
A

Diverticula

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28
Q

Diagnostic tests: Labs- leukocytosis, anemia, UA may show WBC and RBC is fistula forms with bladder, bacteremia with blood cultures if peritonitis
 Abd x-ray to look for free air, ileus, or obstruction
 Barium study
 Colonoscopy can rule out cancer
 CT scan with oral contrast is best to confirm diagnosis

A

Diverticulosis

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29
Q

Management:
o Increase fiber in diet for uninflamed diverticula
o Mild symptoms- rest/clear liquid diet
o If antibiotics are deemed necessary- amoxicillin and clavulanate potassium 875/125mg PO BID or Flagyl 500mg PO TID with Bactrim PO BID x7-10 days
o Then advance diet back slowly
o Acute illness- admit- IV abx, hydration, pain meds, bowel rest NG tube possibly

A

Diverticulitis

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30
Q

Usually the result of an impacted calculus within the cystic duct, causing inflammation proximal to the obstruction
- Epidemiology and Causes
o Stones contain cholesterol, bilirubin pigment, carbonate, bile acids, phospholipids, fatty acids, and proteins
o “Six Fs”- fat, female, forty, flatulent, fertile, and fat-intolerant

A

Cholecystitis

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31
Q

Subjective findings:
 Generalized GI complaints all the way to intractable pain
 Indigestion, n/v- especially after high-fat meal, 80% have the pain before too
 RUQ or epigastrium pain, can radiate to middle of back or right shoulder, increases with movement

A

Cholecystitis

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32
Q

Objective findings:
 Guarding
 Positive murphy’s sign
 Low grade fever
 Mild jaundice, increased bilis, diminished BS
 Can subside on its own in about 4 days, but if symptoms persist, perforation is likely and patient should have surgery

A

Cholecystitis

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33
Q

What sign? Right subcostal region is so tender that there is a painful splinting with deep inspiration or when palpation over RUQ causes transient inspiratory arrest

A

Murphy’s sign in cholecystitis

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34
Q

Diagnostic tests:
 WBC high, transaminases elevated, alk phos up, bili up, elevated amylase can indicate passage of stone through the common bile duct but can also indicate gallstone pancreatitis
 KUB can reveal gallstones, enlarged gallbladder or air in biliary system
 Gold standard- abd US
 CT scan to look for gangrene or perforation

A

Cholecystitis

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35
Q

Ursodiol breaks up what kind of gallstone?

A

Cholesterol

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36
Q

Management:
 Education on s/s
 Dissolution therapy/lithotripsy
 Hospitalization for moderate disease to monitor for perforation/gangrene
 IVF, GI rest, NGT, abx- 2nd or 3rd gen cephalosporin
 Surgical intervention- cholecystectomy

A

Cholecystitis

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37
Q

Functional GI d/o characterized by abdominal pain or discomfort and a change in bowel habits
- 2 features must be present:
o Abdominal pain or discomfort that is relieved by defecation
o Change in frequency in stool
o Change in appearance of stool
- Can be diarrhea or constipation

A

Irritable Bowel Syndrome

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38
Q

Alterations in colonic activity during periods of emotional stress
o Visceral hyposensitivity- perceived feelings of abdominal pain, lower tolerance
 No physical evidence of abnormal colonic smooth muscle activity necessarily….

A

Irritable Bowel Syndrome

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39
Q

Tests that rule in ______: elevated ESR, anemia, leukocytosis, blood/WBCs in stool, stool volume >300ml

A

Irritable Bowel Syndrome

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40
Q

Treatment:
oAntidiarrheals, laxatives short-term, antispasmodic agents- dicyclomine or hyoscyamine (anticholinergics?)
o Tricyclic antidepressants or SSRIs
o Educate that this disease is chronic and help with behavior modification and biofeedback

A

Irritable Bowel Syndrome

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41
Q

Only mucosal surface of the colon resulting in friability, erosions and bleeding- no small bowel

A

Ulcerative Colitis

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42
Q

Segmental or patchy transmural inflammation of bowel wall involving any portion of the GI tract from the mouth to the anus

A

Crohn’s Disease

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43
Q
  • Characterized by exacerbations and remissions that occur throughout the patient’s lifetime and result in disruption in their QOL
  • Epidemiology and Causes
    o Possibly genetic disposition
    o Also inflammatory- t cells increase production and secretion of cytokines and chemokines
A

Inflammatory Bowel Disease (UC and CD)

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44
Q

 Mucosa of colon and rectum
 Begins with neutrophil infiltration
 Cytokines released from macrophages and neutrophils during the inflammatory process are responsible for tissue damage
 Ulcers form in the eroded tissues and abscesses form in the crypts
 The abscesses become necrotic and ulcerate
 Muscularis mucosa becomes edematous and thickened, which narrows the lumen of the colon
 Causing bleeding, cramping pain and urge to defecate
 Causes diarrhea with blood and purulent mucus
fecal leukocytes are always present with active _____
 Increased risk of perforated colon

A

Ulcerative Colitis

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45
Q

 Begins in submucosa of the intestine and gradually spreads to involve the. Mucosa and serosa
 Any portion of the GI tract can be affected- mostly small bowel involvement though
 Proinflammatory cytokines, interleukins, and tissue necrosis factor produce areas of tissue damage
 Skip lesions are formed- some haustra segments are affected while others are not
 Ulcerations form longitudinal and transverse fissures, causing inflammatory Peyer’s patches and lymphoid tissue
• cobblestone appearance
 as the disease progresses, fibrosis thickens the bowel wall, narrowing the lumen
• serosal inflammation causes bowel loops to adhere to each other, contributing to inflammation, ulceration, and fibrosis, which can lead to obstruction, fistulas, and shortening of the bowel

A

Crohn’s Disease

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46
Q

All individuals with _____ are at greater risk of developing colon CA

A

Irritable Bowel Disease (UC and CD)

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47
Q

Subjective:
Multiple loose BM per day with cramps, blood and mucus in stool, and tenesmus (feeling of incomplete defecation)
• Moderate disease- more of this stuff plus systemic symptoms like fever, tachycardia, weight loss
• Severe disease- anemia, hypovolemia, and impaired nutrition

A

Ulcerative Colitis

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48
Q

Subjective:
Abdominal cramping/tenderness, fever, anorexia, weight loss, spasm, flatulence, RLQ pain or mass, blood in stool, steatorrhea
• More insidious and gradual onset

A

Crohn’s Disease

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49
Q

Objective
 LLQ tenderness or across entire abdomen, guarding, distention
 Digital rectal exam will reveal anal and perianal inflammation, tenderness, blood in stool

A

IDB- UC and CD

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50
Q

Diagnosis:
 Stool analysis/cultures
 Look for anemia and nutritional deficiencies, LFTs WBC, sed rate, PTT
 Sigmoidoscopy to diagnose acute ___
 Plain abd films
 ____ patients need colonoscopy but treat first to avoid perforation
 CT to identify bowel wall thickening or abscess formation

A

IDB- blanks are Ulcerative Colitis

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51
Q

Management:
 Nutrition counseling- avoid caffeine, raw fruits, veggies and other high fiber foods, maybe remove lactose from diet
• Bland diet high in protein and calories, low in fat to control diarrhea/flatulence
 Lomotil or immodium for diarrhea (not in acute phase)
 Steroid enemas/foams for rectosigmoid area QPM x14 days
 5-ASA, sulfasalazine, mesalamine, budesonide (oral cortico)
 Advanced disease- systemic cortico with sulfasalazine or other 5-ASA therapy
 Severe disease- surgical intervention- subtotal or total colectomy to prevent perforation
 Can use anti-tumor necrosis factor (TNF)- infliximab (Remicade) and adalimumab (Humira)
• Can also use monoclonal antibodies
 Patients that progress to fulminant disease are at risk for developing toxic megacolon- atonic and thin walled colon- fever, sepsis, lyte imbalance, hypoalbuminemia and dehydration
• If diagnosis is made- NPO, NGT, stop all antidiarrheal meds, correct lyte imbalances, TPN if necessary, broad spectrum abx for prophy, parenteral admin of glucocorticoids
• Loss of hepatic dullness on percussion may be the first sign of perforation- do daily KUB
 25% of US patients eventually require surgery
• Can do in stages- proctocolectomy with Brooke ileostomy

A

Ulcerative Colitis

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52
Q

Management:
 5-ASA meds have not been shown to have any benefit
 Def use sulfasalazine- 500mg BID to start- give folic acid with it since it interferes with folic acid absorption
• Metronidazole if intolerant of sulfasalazine
• Other meds- cipro, ampicillin, tetracycline
 Glucocorticoids when initial treatment fails for mod to severe disease
 Relapse is higher- most need long term steroids- oral prednisone daily maintanence of 5-10mg
 TNF blockers- remicade and humira, certolizumab- immunosuppression
 Surgical intervention is not usually indicated unless there are complications- obstruction, fistulas, abscess drainage or perforation- but 75% of patients will require surgery

A

Crohn’s disease

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53
Q

o Second leading cancer killer in US- 4.3% of population will develop this in lifetime
o Age is most important risk factor- increases with age
 Risk increases after 45
 Rare under 35 unless genetic risk factors
 Median age of diagnosis is 71
o Possibly higher with high fat, more red meat, more refined carb diets
 Excess fat interacts with colonic bacteria to form deconjugated bile acids, which can increase tumor producing activity
o Family history is huge- 25% of patients have family hx
o Hx of IBD and UC
o Hx of gynecological (breast, ovarian, endometrial) CA or Barrett’s esophagus have increased risk
o Overweight/obesity, low PA, smoking, heavy long-term alcohol use

A

Colorectal CA

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54
Q

o Most are adenocarcinomas- evolution from adenoma to carcinoma can take 10 years
o Polyps that increase in size can show villous changes with increasing dysplasia and 50% progress to CA

A

Colorectal CA

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55
Q

Diagnostic Tests:
 CBC for anemia, LFTs for mets to liver/bone
 Serum immune assay carcinoembryonic antigen (CEA) but its nots a great screening tool…can be used for monitoring response to therapy after diagnosis is made
 Colonoscopy is 100% accurate in diagnosis

A

Colorectal CA

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56
Q

Management:
o Stage disease first
o Surgical resection is the only cure- even with mets
o Chemo
o Liver resection for mets
o Close surveillance and follow up is necessary- CEA level every 3 months, CT of abd/pelvis every year, colonoscopy to monitor

A

Colorectal CA

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57
Q
  • Mass of dilated and tortuous veins that represent prolapsed submucosal tissue
  • Caused from straining during defecation, prolonged sitting, pregnancy, and anal infection
  • Some are asymptomatic and resolve on their own within 3 weeks
  • Sometimes can result in profuse bleeding and require emergency ligation
A

Hemorrhoids

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58
Q 
o	Subjective
	Abrupt onset of pain 
	Perianal lump
	Worse pain with defecation/straining
o	Objective
	Can be seen during Valsalva
	Thrombosed ones can be blue
	Internal- most often present with rectal bleeding- BRB
A

Hemorrhoids

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59
Q

Management
o Pain relief, sitz baths, stool softeners, increase fiber intake, witch hazel
o Internal can be treated depending on degree- can use sclerotherapy or infrared coagulation, rubber-band ligation
 More advanced are surgically removed

A

Hemorrhoids

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60
Q

 Sometimes asymptomatic- spread in crowded places- nursing homes, etc
 Contaminated food and water- transmitted be fecal-oral route
 Incubation period is 30 days, can be up to 6 weeks
 Low mortality rate, not chronic, no long-term damage usually

A

Hepatitis A

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61
Q

 High risk groups- gay men, IVDU, first-gen immigrants from Asia/Middle East, multiple sex partners, medical professionals (needle stick risk)
 Transmission from direct contact with blood and other body fluids (semen, cervical secretions, saliva, wound exudates)
 Virus can live on inanimate objects for up to 1 week- can be transmitted that way!
 Mortality rate is low but can be chronic or worse when combined with Hep D
• Increased risk of cirrhosis and hepatocellular cancer

A

Hepatitis B

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62
Q

 Transmitted via blood and blood products, body fluids
 Can be chronic
 Strongest risk factor is IVDU
 75% are asymptomatic, making diagnosis and treatment difficult
• Most do undetected until chronic liver disease is a problem
 Most develop chronic hepatitis
• Liver CA and cirrhosis

A

Hepatitis C

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63
Q

 Only at risk if you have Hep B, too
 IVDU biggest risk factor
 Transmission is parenteral
 Low incidence, low mortality rate

A

Hepatitis D

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64
Q

 Fecal-oral route, not easily transmitted
 Not really in US, usually from travel
 Usually self-limiting, low mortality rate

A

Hepatitis E

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65
Q

 Elevated AST and ALT for >6 months

A

Chronic hepatitis

66
Q

 Inflammation of the liver
 More serious cases lead to parenchymal inflammation and necrosis
 The body develops an immunological tolerance, which is why people are chronically asymptomatic…but can lead to liver CA
 Can rapidly mutate, causing inflammation and damage…leading to cirrhosis 20-30 years later

A

Hepatitis

67
Q

 Subjective
• Asymptomatic or jaundice, severe infection, death
• Prodromal phase- anorexia, n/v, malaise, URI, flu-like symptoms, myalgia, arthalgia, fatigue, d/c, fever, mild abdominal pain
• Icteric phase- jaundice and dark urine (5-10 days after initial symptoms)
• Convalescent phase- increased sense of well-being, symptoms dissipate

A

Hepatitis

68
Q

• Diagnostic, appears 1-10 weeks after exposure to the virus and remains positive throughout the acute phase of the illness

A

Hep B Surface Antigen

69
Q
  • Used as an index of viral replication/infectivity

* The higher the number, the more virus/infectivity

A

Hep B e antigen (envelope)

70
Q

IgM (4 weeks after exposure- gold standard) and IgG (2 weeks after IgM increases)

A

Hep A test

71
Q

 If IgM is elevated and IgG is not

A

Acute Hep A

72
Q

 If IgG is elevated and IgM is not

A

Previous exposure to Hep A

73
Q 
	Prevention of transmission and symptom relief
	Vaccines
	Hepatologist for chronic disease
	Abstinence from alcohol
	Liver transplant for advanced disease
A

Hepatitis

74
Q
  • backward flow of stomach or duodenal contents into the esophagus without associated retching or vomiting
    o chronic can result in gradual breakdown of mucosal barrier
A

GERD

75
Q

o Elevated pressure or gravity pushes gastric secretions into esophagus
 Causes inflammatory response
 Can be chronic
 Increased blood flow to the area, resulting in erosion
• Minor capillary bleeding
• Due to erosion, body replaces these areas with metaplastic columnar epithelium, containing goblet and columnar cells
o They are more resistant to acid but can be premalignant
o can also cause fibrosis and scarring, leading to esophageal strictures

A

GERD

76
Q

 Heartburn
 Regurg, water brash (reflex salivation), dysphagia, sour taste in the mouth in the AM, odynophagia, belching, coughing, Hoarseness, wheezing, substernal chest pain
 Chronic can present as dysphagia

A

GERD

77
Q

 Usually diagnose on history alone- can be hard to diagnose as symptoms are vague
 Can trial patient on 4-8 weeks PPI
 If unable to diagnose after this, can do EGD to directly visualize

A

GERD

78
Q

o Initial Treatment
 Education
 Lifestyle modification- weight loss, elevate HOB, avoid meals 2-3 hours before bed, avoid triggering foods (chocolate, caffeine, alcohol, spicy/acidic foods)
 8 week trial of PPI (usually once daily before first meal)
• Can increase to BID if need more
• If ineffective, refer to gastroenterologist

A

GERD

79
Q
  • Both gastric and duodenal ulcers
    o Larger than 5mm in diameter
    o Imbalance between protective factors of mucosa and aggressive factors like acid and pepsin
    o H pylori or NSAIDs
A

Peptic Ulcer Disease

80
Q

o Most are in duodenum and are usually within 3cm of pylorus
o Most have normal amounts of gastric acid
o Smoking increases risk, NSAIDs decrease prostaglandin synthesis, most is from h pylori

A

PUD

81
Q

o Subjective
 Burning or gnawing sensation or pain in apigastrium- relieved by food or antacids
 Can also be asymptomatic
 Nocturnal pain in 2/3 patients due to circadian stimulation of gastric acid

A

PUD

82
Q

Reduction of pain after eating

A

Duodenal ulcers

83
Q

More intense pain after eating (from secretion of acid during eating)

A

Gastric Ulcers

84
Q

 Diagnostic Tests
• Anemia if bleeding, lyte imbalance sometimes
• Leukocytosis= perforation
• Standard diagnostic is EGD- visualization and biopsy (sometimes these ulcers are cancerous)
-Urea breath test
-Fasting serum gastrin level

A

PUD

85
Q

H. pylori treatment triple therapy

A

Clarithromycin and either amoxicillin or metronidazole (preferred) with PPI x2 weeks

86
Q

Omeprazole 20mg PO QD 4 weeks for _____

A

Duodenal ulcers

87
Q

Omeprazole 20mg PO QD 8 weeks for _____

A

Gastric ulcers

88
Q

H. pylori quadruple therapy

A

Tetracycline QID, Flagyl TID, PPI, bismuth QID

89
Q

o Men more likely than women
o 65-75 years old
o AA more likely
o Underlying conditions- DM and primary HTN
 HTN present in 85% of patients with CKD

A

Chronic Kidney Disease

90
Q

Most common causes are diabetic nephropathy, hypertensive nephropathy, and glomerulonephritis

A

CKD

91
Q

o Subjective
 Symptoms don’t appear until GFR 10-15% of normal
 Anorexia, lassitude, fatigability, weakness
 Uremia
 Pruritis and dry skin, GI problems- anorexia, n/v, hiccoughing, neurological complaints- emotional lability, depression, insomnia, fatigue, confusion, HA, seizures, coma

A

CKD

92
Q

o Objective
 Pale turgor or hyperpigmentation, bruising, asterixis (hand flapping), peripheral neuropathy and altered mental status
 Peripheral edema, albuminemia, crackles in lungs, pericardial rub, HTN, tachycardia

A

CKD

93
Q

 Monitor CBC for anemia secondary to erythropoietin deficiency
 Electrolyte monitoring
 Renal US, doppler ultrasonography to assess renal artery stenosis, renal angiography gold standard for renal artery stenosis

A

CKD

94
Q

o Contamination from patient’s own GI tract
 E coli (most common) or staph saprophyticus
• Can also be proteus mirabilis, klebsiella, enterobacter, serratia, or pseudomonas, s. aureus
 Candida

A

Lower UTI

95
Q

o Subjective
 Urethritis, cystitis, dysuria, urinary frequency, urgency, nocturia, hematuria, low back/suprapubic pain, UI, cloudy fowl smelling urine
 Altered mental status in elderly

A

Lower UTI

96
Q

 Urine culture is gold standard

A

Lower UTI

97
Q

Type of UTI: can be resolved without addressing such factors/localized in the lower urinary tract

A

Uncomplicated

98
Q

Type of UTI: acute or chronic infection is accompanied by factors that predispose a patient to the infection or make treatments more difficult (indwelling catheter, underlying chronic disease, systemic symptoms, pregnancy)

A

Complicated

99
Q

Management:
3 day course of Bactrim or 10 days ampicillin
 Can also use nitrofurantoin (Macrobid) x7 days, especially for e coli or gram positive cocci
 Cipro and other flouroquinolones should be reserved as alternative class in cases when no other abx are appropriate

A

Uncomplicated UTI

100
Q

Needs 10-14 days of abx

A

Complicated UTI

101
Q
  • Infection of the kidney that is characterized by infection within the renal pelvis, tubules, or interstitial tissue- uni or bilateral
  • Acute or chronic (chronic can lead to atrophy/scarring of kidney which may lead to renal failure)
A

Upper UTI

102
Q

o Subjective
 Fever, costovertebral angle pain, n/v
• Can mimic pelvic inflammatory disease
 Can also be asymptomatic until they become septic
 Chronic- fatigue, nausea, weight loss, nocturia, polyuria, renal failure
o Objective
 Tenderness on abdominal palpation/percussion of affected flank
 Underlying HTN

A

Upper UTI

103
Q

 UA/culture (>100,000 CFU/ml)
 Blood cultures
 Cystoscopy with ureteral catheterization, renal US, IV pyelogram
 Dimercaptosuccinic acid (DMSA) scan most sensitive for pyelonephritis and renal scarring
 Renal biopsy may reveal abscess formation

A

Upper UTI

104
Q

o Aggressive therapy- oral abx for mild to moderate, IV for severe
o Hospitalize patients who are pregnant, vomiting, or dehydrated or have systemic illness (bacteremia or uroseptic)
o Treatment for 7-10 days for mild to mod, 14 days for severe, 21 days for slow responders

A

Upper UTI

105
Q
  • Involuntary loss of urine from the bladder
    o Common in women and older men from enlarged prostate
  • Epidemiology and Causes
    o Transient- sudden onset from delirium, infection, pharmacologic agents, underlying systemic illness (DM, fecal impaction, restricted mobility)
    o Persistent- stress, urge, overflow, functional
A

Urinary Incontinence

106
Q

From increased abdominal pressure
 From hypermobility of bladder neck, intrinsic sphincter deficiency, neurogenic sphincter deficiency, use of certain meds like sedatives, hypnotics, alpha blockers, antispasmodics that relax smooth muscle and increase urine flow
 Pelvic floor reeducation, biofeedback, electrical stimulation, weight loss, anti-incontinence devices/pessaries
 Meds- alpha-adrenergic agonists- improve muscle tone of urinary tract

A

Stress incontinence

107
Q

Detrusor instability- inability to delay voiding
 From UTI, vaginitis, bladder stones, bladder tumors, cortical, subcortical, and suprasacral CNS lesions, stroke, dementia, MS, PD, prostate issues, diuretics, etc
 Pelvic floor reeducation and biofeedback, scheduled voiding
 Anticholinergics, smooth muscle relaxants, tricyclic antidepressants (to improve neuromuscular function of the bladder/urethral sphincter)

A

Urge incontinence

108
Q

 Involuntary contractions of the detrusor muscle- similar to urge incontinence but includes urgency, frequency, and nocturia
 Antimuscarinic agents, botox injections in detrusor muscle

A

Overactive bladder

109
Q

 Normal functioning urinary system- causes are outside of urinary tract
• Delirium, fecal impaction, meds
 Remove barriers to effective toileting, scheduled toileting, PT/OT

A

Functional urinary incontinence

110
Q
  • Most deadly of all skin cancers
  • Arises from epidermal melanocytes found in skin
    o Melanocytes produce melanin, a brown-black pigment responsible for skin, hair and eye color
    o 90% of melanomas arise from the skin
A

Malignant Melanoma

111
Q
  • Usually curable if found early but if it extends beyond ____ in depth, the prognosis is extremely poor- 75% mortality rate
A

Malignant melanoma, 4mm in depth

112
Q

o Subjective
 Not usually any symptoms but can be itchy, ulcerated or bleeding moles
 Change in characteristics of a mole
o Objective
 Back and neck are most common- sun exposed areas usually, legs in women
 Asymmetric lesion with irregular border, notching and a diameter greater than 6mm
• Variegation in color- can have blue, red, tan, brown, black and white
 Must do skin biopsy to diagnose
 Thumb or great toe sometimes- Hutchinson’s sign- ominous physical finding (dark line on nail….)

A

Malignant Melanoma

113
Q

Management
 Mohs surgery (excision)
 Chemo- dacarbazine (DTIC), cisplatin, vincristine
• CNS - temozolomide
• Response to chemo is short lived…
• Can target chemo in the limb and avoid letting it reach the rest of the body
 Radiation- high dose interferon and interleukin-2, mAbs
 Biological therapy

A

Malignant Melanoma

114
Q

Originates in basal cells of the epidermis

o Slow-growing and locally invasive that rarely metastasizes

A

Basal Cell Carcinoma

115
Q

Originates from karatinocytes and is malignant

o Can invade dermis and can metastasize to distant site

A

Squamous Cell Carcinoma

116
Q 
o	Subjective
	Spot or bump that is getting larger
	Thick, rough patch that may bleed if scratched
	Asymptomatic or itchy
o	Objective
	Areas exposed to sun
A

Nonmelanomatous Skin CAs (BCC, SCC)

117
Q
  • Pearly with some crusting

- Central ulceration in later stages, may be same color as skin or variegated color- black, brown or blue

A

BCC

118
Q
  • Firm papule with scaly rough surface with irregular borders, may be friable with ulcerations later
A

SCC

119
Q

Superficial skin infections caused by 3 fungal species- Trichophyton, Epidermophyton, and Microsporum
o Transmission through direct contact

A

Tinea

120
Q

Tinea Capitis

A

Ringworm of scalp

121
Q

Tinea Corporous

A

Ringworm of the body

122
Q

Tinea Cruris

A

Ringworm of the groin/jock itch

123
Q

Tinea Pedia

A

Ringworm of the foot/athlete’s foot

124
Q

Tinea Manuum

A

Ringworm of the hands

125
Q

Tinha Unguium/onychomycosis

A

Fungal infection of the nail

126
Q
  • Toddler or school-aged
  • Painless bald spot
  • Kerion present- signs of discomfort or pain
A

Tinea Capitus

127
Q

• Erythematous round and elevated pruritic lesion that grows in size and starts to clear in the center

A

Tinea Corporis

128
Q

• Obese adult with pruritic rash on the grown that spreads to medial inner aspect of inner thigh

A

Tinea Cruris

129
Q
  • Male teenage athlete or adult- strong foot odor

* Macerated soft, whitened skin between the toes

A

Tinea Pedis

130
Q
  • More visible in summer, do not tan
  • Asymptomatic, gradual onset
  • Teen or young adult
  • Back, upper chest, arms, neck and face
A

Tinea Versicolor

131
Q

Management:
o 2-4 weeks of topical treatment with azole-class drugs like miconazole, clotrimazole, etc- page 176
 Continue 1 week after lesions have cleared
o Can use systemic formulations for more serious cases- these can cause SEs like hepatotoxicity, though

A

Tinea infections

132
Q

Management:
 Topical selenium sulfide (Selsun Blue) for 7 days- lather on and leave for 10 min
 Then once a month for maintenance
 Can use fluconazole for systemic treatment- risk of hepatoxicity

A

Tinea Versicolor

133
Q
  • Bacterial infection of skin involving both dermis and SQ tissue
  • Most cases caused by group A beta-hemolytic strep or s. aureus
  • Typically wide, diffuse area of erythematous skin that is warm and tender to palpation
  • Severe edema with systemic symptoms sometimes
  • Can sometimes result in loss of limb or death
    o SIRS
A

Cellulitis

134
Q

o Usually an insect bite or wound as portal of entry into the skin
o Any age

A

Cellulitis

135
Q

Management:
o Uncomplicated cases (no bites)- penicillin VK, dicloxacillin, clindamycin, cephalexin x5 days+
o Bites- Augmentin for 2 weeks- MD referral too
o Immunocompromised patients need to be treated more aggressively- hospitalization
 Cefuroxime (Ceftin) for H. influenzae

A

Cellulitis

136
Q

A small circumscribed, solid elevation of the skin less than 1cm in diameter (elevated nevis)

A

Papule

137
Q

A small bladder or sac as a small thin walled raised skin lesion, containing liquid (HSV, varicella)

A

Vesicle

138
Q

A thin walled blister of the skin or mucous membranes greater than 5mm in diameter containing serous or seropurulent fluid (blister/ second degree burns)

A

Bulla

139
Q

Circumscribed superficial elevation of the skin filled with pus (acne, impetigo)

A

Pustule

140
Q

A fatty lump of fat cells most often situated between the skin and underlying muscle layer. Move easily under skin- occur mostly in neck, shoulders, back, abdomen, arms, and thighs.

A

Lipoma

141
Q

Round or oval, regular borders, less than 5mm in diameter, color is evenly distributed

A

Nevi/Moles

142
Q

Soft brown or flesh colored papules. They occur on any skin surface but most often the neck, axilla, and intertriginous areas. Benign growths.

A

Skin tags

143
Q

A benign epithelial neoplasm of glandular tissue (adenocarcinoma)

A

Adenoma

144
Q
  • Most common skin conditions in primary care in adults and the elderly
  • Remissions and exacerbations- chronic
  • Seen in sebaceous glands like scalp, forehead, eyebrows, and area under nose and ears
A

Seborrheic Dermatitis

145
Q

Seborrheic dermatitis is also known as ____

A

Cradle cap

146
Q

o Genetic
o Could be a reaction of Malassezia furfur yeasts
o After second decade of life and in the elderly and immnocompromised
o Associated with AIDS/HIV
o Emotional stress is linked to acute flares

A

Seborrheic Dermatitis

147
Q

Management:
o Managing symptoms and reducing yeast count on the skin
o OTC antidandruff shampoo- keep on for 5-7 minutes
 Zinc pyrithione and selenium sulfide- keratolytic agents- fungicidal and cytostatic
 Sulfur and salicylic acid- keratolytic, antifungal, and antiseptic actions
 Coal tar shampoo- changes hair color sometimes when used
o Can prescribe 2.5% selenium sulfide for resistant SD
 Or ketoconazole shampoo or cream
o Topical steroid cream- 0.5% or 1.0% OTC
o Calcineurin inhibitors- tacrolimus topical
o Maintenance therapy 1-2 x per week after symptoms resolve

A

Seborrheic Dermatitis

148
Q

Group of skin disorders characterized by pruritis and inflammation where no cause is known

A

Atopic Dermatitis

149
Q

Atopic dermatitis is also known as _____

A

Eczema

150
Q

o Inherited, beings in infancy
o Cause is unknown
o Allergen-specific IgE disorder- atopic triad- asthma, allergic rhinitis, eczema
o Usually very itchy, more sensitive to itching
o Heat/tight clothing/stress/moisture/ irritants

A

Atopic Dermatitis

151
Q

o Subjective
 Low threshold for pruritis, “the itch that rashes”
• Itch before the rash, scratching makes it worse
• Cardinal sign is itching- must be present to make diagnosis
 Worse in fall and winter
o Objective
 Flexural eczema from 4-10 years
 Lesions are erythematous, papulovesicular, edematous, and weeping- then crusted, scaly, thickened, and lichenified

A

Atopic Dermatitis

152
Q

 Can do RAST (radioallergosorbent test) to identify antigen-specific mast cell activation/quantify levels of allergen-specific IgE
• False positive results are not uncommon
• Good for a lot of allergy testing
 Can also do allergen skin prick test- but done by an allergist

A

Atopic Dermatitis

153
Q
  • Management
    o Control s/s- no cure
    o Precipitating factors should be eliminated, wet lesions should be dried, dried lesions should be hydrated, inflammation should be treated with corticosteroids
    o Manage trigger factors
    o Nonpharmacologic Management
     Mild emollients- Cetaphil, instead of soap
     Soak baths and liberal application of moisturizers- soak and smear
     Pat dry, leave as much skin oil on
     Avoid acids in products
     Ointments are the best- containing petroleum jelly, then creams
     Humidifiers
    o Pharmacologic treatment
     Burrows solution, saline, silver nitrate to dry
     OTC corticosteroids or prescription steroid cream
     Oatmeal baths can be soothing
     Antihistamines are not affective- the pruritis is not caused by histamine only
     TCAs have been shown to be affective
     Monelukast (singulair)- leukotriene-receptor antagonist- inhibits eosinophil infiltration of the skin, which is a major histological characteristic of eczema
    • Not FDA approved for this, though
     Corticosteroids are effective- first-line- topical, not long term, especially sronger versions
    • Systemic rarely used but can help with acute exacerbation if needed- prednisone 40-60mg/day x7 days, does not require taper…
     Topical tacrolimus (protopic) BID is second line- immunomodulating calcineurin inhibitors
    • Can be used long term, reduces number of flares
    • This may cause malignancy, though- black box warning
     Can use cyclosporine, too- as affective as corticosteroids, fewer SEs- renal function must be monitored
    • Imuran
     Omalizumab- anti-IgE antibody- not FDA approved for this but good for severe cases
A

Atopic Dermatitis

154
Q

Weight, diet, social habits, lifestyle choices, stress

A

Modifiable risk factors

155
Q

Sex, age, genetic/family history

A

Nonmodifiable risk factors

156
Q

Significant healthcare problem with widespread effects. Defined as a pattern of coercive and controlling behavior exercised by one partner over the other. Can be economic control, social isolation, emotional abuse, sexual assault, and physical violence
Barriers to treatment- Power and control, Cycle of abuse
Barriers to identification- Patient barriers, Provider barriers
Clinical presentation- Physical complaints, Psychosocial barriers, Physical examination
Management- Clinical intervention: Universal screening, Framing the question, Patient denial of abuse, Patient disclosure of abuse,
Psychosocial intervention-Safety assessment and planning

A

Domestic Violence

157
Q

BP check, Bone mineral density, Mammography, Pap test, Cholesterol, Colorectal cancer, Diabetes, HIV, AAA, TB

A

Routine screenings

158
Q

Home safety, Personal preparedness, Biologic threats and epidemics, Sports and vehicular safety

A

Safety

159
Q
  • Severe cellulitis of sudden onset, spreads rapidly
  • Red or purple skin, severe pain, fever, vomiting
  • Most commonly affects limbs and perineum
  • Mostly bacterial infection, sometimes fungal
  • Surgery to remove infected tissue
A

Necrotizing Fasciitis

160
Q

Hallmark for this infection is progression with tissue destruction and the severity of symptoms. Progresses over hours- not days.
Caused by flesh eating bacteria- loss of limb is a potential complication.
Most cases caused by Group A strep pyogenes, staph aureus, clostridium perfinges, bacteroides fragilis, and aeromonas hydrophila.

A

Necrotizing Fasciitis

161
Q

Early stage- lesion appears bright red in color that profresses to purpuric changes (purple color) including gangrene,

Border will spread over a few hours

Symptoms that differ from cellulitis: severe pain at affected site-pain due to involvement of the fascia around the muscle

A

Necrotizing Fascitis

162
Q

Pressure around skin may reveal crepitus due to gas production. Gangrene can present in a few hours.
Hypotension, mental status changes

Violaceous bullae, hemorrhage, sloughing of skin, localized sensory loss.

A

Necrotizing Fasciitis

NP 612- Family Theory Adult (4 decks)

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