Unit 1- Abd/Renal/Skin Flashcards by Katherine Milley

Acute diarrhea is how long

<1 week

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Chronic diarrhea is how long

> 2 weeks

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

Dyspepsia

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Extreme pain, difficult to distinguish from angina pectoris

Heartburn

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Black tarry stool, most common cause is upper GIB

Melena

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

N/V

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Inflammation of stomach and intestine

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

Gastroenteritis

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

Gastroenteritis

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Appendicitis is dilation of appendix followed by obstruction and _____

Subsequent bacterial infection

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Management of appendicitis

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

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

GERD

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Penetrates muscular mucosa, larger than 5mm in diameter

PUD

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Gluten sensitive autoimmune disorder that affects small intestinal villous epithelium

Celiac

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Type types of Inflammatory Bowel Disease

Ulcerative colitis and Crohn’s disease

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

Colorectal CA

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Alcoholism is the cause of 70-80% of cases

Chronic pancreatitis

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Usually indicative of renal pathology, most often glomerular origin

Proteinuria

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 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

Appendicitis

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

Rovsing’s sign

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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

Psoas sign

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

Obturator sign

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

McBurney’s sign

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

Appendicitis

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

Diverticulitis

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o Bleeding is the most common complication

Uninflamed diverticulitis

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

Diverticula

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

Diverticula

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

Diverticulosis

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

Diverticulitis

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

Cholecystitis

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

Cholecystitis

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

Cholecystitis

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

Murphy's sign in cholecystitis

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

Cholecystitis

Ursodiol breaks up what kind of gallstone?

Cholesterol

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

Cholecystitis

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

Irritable Bowel Syndrome

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….

Irritable Bowel Syndrome

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

Irritable Bowel Syndrome

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

Irritable Bowel Syndrome

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

Ulcerative Colitis

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

Crohn's Disease

- 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

Inflammatory Bowel Disease (UC and CD)

 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

Ulcerative Colitis

 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

Crohn's Disease

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

Irritable Bowel Disease (UC and CD)

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

Ulcerative Colitis

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

Crohn's Disease

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

IDB- UC and CD

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

IDB- blanks are Ulcerative Colitis

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

Ulcerative Colitis

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

Crohn's disease

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

Colorectal CA

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

Colorectal CA

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

Colorectal CA

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

Colorectal CA

- 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

Hemorrhoids

``` 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 ```

Hemorrhoids

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

Hemorrhoids

 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

Hepatitis A

 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

Hepatitis B

 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

Hepatitis C

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

Hepatitis D

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

Hepatitis E

 Elevated AST and ALT for >6 months

Chronic hepatitis

 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

Hepatitis

 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

Hepatitis

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

Hep B Surface Antigen

* Used as an index of viral replication/infectivity | * The higher the number, the more virus/infectivity

Hep B e antigen (envelope)

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

Hep A test

 If IgM is elevated and IgG is not

Acute Hep A

 If IgG is elevated and IgM is not

Previous exposure to Hep A

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

Hepatitis

- 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

GERD

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

GERD

 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

GERD

 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

GERD

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

GERD

- 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

Peptic Ulcer Disease

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

PUD

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

PUD

Reduction of pain after eating

Duodenal ulcers

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

Gastric Ulcers

 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

PUD

H. pylori treatment triple therapy

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

Omeprazole 20mg PO QD 4 weeks for _____

Duodenal ulcers

Omeprazole 20mg PO QD 8 weeks for _____

Gastric ulcers

H. pylori quadruple therapy

Tetracycline QID, Flagyl TID, PPI, bismuth QID

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

Chronic Kidney Disease

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

CKD

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

CKD

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

CKD

 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

CKD

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

Lower UTI

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

Lower UTI

 Urine culture is gold standard

Lower UTI

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

Uncomplicated

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)

Complicated

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

Uncomplicated UTI

Needs 10-14 days of abx

Complicated UTI

- 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)

Upper UTI

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

Upper UTI

 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

Upper UTI

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

Upper UTI

- 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

Urinary Incontinence

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

Stress incontinence

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)

Urge incontinence

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

Overactive bladder

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

Functional urinary incontinence

- 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

Malignant Melanoma

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

Malignant melanoma, 4mm in depth

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….)

Malignant Melanoma

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

Malignant Melanoma

Originates in basal cells of the epidermis | o Slow-growing and locally invasive that rarely metastasizes

Basal Cell Carcinoma

Originates from karatinocytes and is malignant | o Can invade dermis and can metastasize to distant site

Squamous Cell Carcinoma

``` 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 ```

Nonmelanomatous Skin CAs (BCC, SCC)

- Pearly with some crusting | - Central ulceration in later stages, may be same color as skin or variegated color- black, brown or blue

BCC

- Firm papule with scaly rough surface with irregular borders, may be friable with ulcerations later

SCC

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

Tinea

Tinea Capitis

Ringworm of scalp

Tinea Corporous

Ringworm of the body

Tinea Cruris

Ringworm of the groin/jock itch

Tinea Pedia

Ringworm of the foot/athlete's foot

Tinea Manuum

Ringworm of the hands

Tinha Unguium/onychomycosis

Fungal infection of the nail

* Toddler or school-aged * Painless bald spot * Kerion present- signs of discomfort or pain

Tinea Capitus

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

Tinea Corporis

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

Tinea Cruris

* Male teenage athlete or adult- strong foot odor | * Macerated soft, whitened skin between the toes

Tinea Pedis

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

Tinea Versicolor

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

Tinea infections

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

Tinea Versicolor

- 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

Cellulitis

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

Cellulitis

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

Cellulitis

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

Papule

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

Vesicle

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

Bulla

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

Pustule

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.

Lipoma

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

Nevi/Moles

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

Skin tags

A benign epithelial neoplasm of glandular tissue (adenocarcinoma)

Adenoma

- 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

Seborrheic Dermatitis

Seborrheic dermatitis is also known as ____

Cradle cap

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

Seborrheic Dermatitis

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

Seborrheic Dermatitis

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

Atopic Dermatitis

Atopic dermatitis is also known as _____

Eczema

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

Atopic Dermatitis

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

Atopic Dermatitis

 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

Atopic Dermatitis

- 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

Atopic Dermatitis

Weight, diet, social habits, lifestyle choices, stress

Modifiable risk factors

Sex, age, genetic/family history

Nonmodifiable risk factors

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

Domestic Violence

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

Routine screenings

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

Safety

- 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

Necrotizing Fasciitis

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.

Necrotizing Fasciitis

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

Necrotizing Fascitis

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.

Necrotizing Fasciitis

Unit 1- Abd/Renal/Skin Flashcards

(162 cards)