Unit 1- Abd/Renal/Skin Flashcards
Acute diarrhea is how long
<1 week
Chronic diarrhea is how long
> 2 weeks
Epigastric discomfort, postprandial fullness, early satiety, anorexia, belching, bloating
Dyspepsia
Extreme pain, difficult to distinguish from angina pectoris
Heartburn
Black tarry stool, most common cause is upper GIB
Melena
Can use antihistamines, antidopaminergics, cholinergic, and SSRIs for symptomatic relief
N/V
Inflammation of stomach and intestine
- acute from infectious process of food poisoning
- chronic from food allergies, food intolerance, stress, lactase deficiency
Gastroenteritis
Management:
-fluids with sodium, diet with boiled starches, cereals and salt, possible hospitalization, anti motility drugs, antibiotics
Gastroenteritis
Appendicitis is dilation of appendix followed by obstruction and _____
Subsequent bacterial infection
Management of appendicitis
Surgery, correction of fluid/electrolyte imbalance, bedrest, NPO
Stomach or duodenal contents back flow into esophagus (lifelong condition, lifestyle modifications are key)
GERD
Penetrates muscular mucosa, larger than 5mm in diameter
PUD
Gluten sensitive autoimmune disorder that affects small intestinal villous epithelium
Celiac
Type types of Inflammatory Bowel Disease
Ulcerative colitis and Crohn’s disease
Risk factors are family history, diet high in fat, red meat, remind carbs, low plant fiber
Colorectal CA
Alcoholism is the cause of 70-80% of cases
Chronic pancreatitis
Usually indicative of renal pathology, most often glomerular origin
Proteinuria
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
Diagnostic test for appendicitis: deep palpation over LLQ with sudden, unexpected release of pressure- positive sign is tenderness
Rovsing’s sign
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
Diagnostic test for appendicitis: right hip and knee flexed, examiner rotates right leg internally- positive sign is pain over RLQ
Obturator sign
Diagnostic test for appendicitis: pressure applied halfway between umbilicus and anterior spine of ilium- pain with pressure is positive sign
McBurney’s sign
- Management
o Surgical- perforation occurs often, so refer to surgeon ASAP
o Third gen cephalosporins for gram-neg aerobic and anaerobic organisms
Appendicitis
o Pouchlike protrusions of intestinal mucosa that occurs within descending and sigmoid segments of the colon
o Also occur in the small bowel
Diverticulitis
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
