Module 8 Flashcards
what is urinary incontinence?
involuntary intermittent or perisistent loss of urine
urinary incontinence is a normal sign of aging T/F
false, urinary incontinence is abnormal in all ages
what are some risk factors of urinary incontinence?
impaired mobility, pelvic floor weakness, race, ethnicity, weight, frequent UTIs, BPH, medications
discuss the pathophysiology behind urinary incontinence
usually because of an underlying sphincter or bladder problem, could also be extrinsic (ie related to meds) that can be easily treated, could also be underlying neurological problem
what is stress incontinence?
leakage of urine due to increased intra-abdominal pressure, pressure in abdomen increases pressure on sphincter which causes urethral opening and leakage
can be classed into: anatomic (hypermobility of the bladder neck, bladder neck works but overly active ie-sphincter will close and open) or intrinsic (bladder neck is always open
what is urge incontinence
most common in older adults
uncontrollable sensation to void
can be caused by detrusor overactivity (detrusor muscle -musculature that stretches to contain urine; unknown causes) or poor bladder compliance (inability to store large amounts of urine, little amount causes increased pressure)
what is overflow incontinence
incomplete emptying of the bladder; urine builds because of incomplete emptying and leakage occurs
discuss management therapies for stress incontinence
behavioural therapies- timed/double voiding to ensure emptying of the bladder
smoking cessation- increases coughing and increases urgency
pelvic floor muscles- strengthen pelvic floor and urethra to prevent leaks during increased pressure
medical therapies - alpha adrenergic agonists (pseudoephedrine) increases urethral pressure
estrogen replacement for post menopausal related atrophic vaginitis
tricyclic antidepressants
caution meds in older adults for anticholinergic effects
discuss management therapies for urge incontinence
behavioural- timed/double voiding, smoking cessation, pelvic floor, weight reduction
bladder training - postpone urinating and waiting, use of kegels during urge to alleviate urge symptoms
medical therapies- antimuscarinic agents (oxybutynin)
discuss management therapies for overflow incontinence
timed/double voiding
may introduce intermittent catheterization (reserve for those who have poor emptying and are not surgical candidates)
medications can be used-those for BPH
complications of urinary incontienence
infections, sleep interruption, mental health, sexual dysfunction, poor social esteem
refer to specialist if incontinence type is unknown
What are the common causes of erectile dysfunction?
difficulty or inability to enjoy intercourse or disorder that interferes with sexual response, persistent inability to achieve and maintain an erection
younger populations with ED can lead to greater risk of CV events
higher incidence in those with neurological, endocrine, cancer, PTSD survivors
What are the clinical manifestations of erectile dysfunction?
broad history-may ilicit onset of concerns
discuss previous medical history that may contribute to ED
predisposing factors (relationships, trauma, upbringing)
precipitating factors (discordant relationships, depression/anxiety, medical conditions)
maintaining factors (performance, relationships, impaired self image, communication problems)
What are strategies to manage erectile dysfunction?
HCP discussing sexuality
determine cause of ED- organic, psychological, relational
counselling, anxiety reduction techniques
pharm: testosterone replacement, oral PDE5 (sildenafil, tadalafil) contraindicated in those taking nitrate medications)
tadalafil longer lasting than sildenafil (s/e: headache, flushing, nasal congestion, dyspepsia)
penile injections, pumps, penile prosthesis
Identify epidemiological factors of testicular cancer.
testicular cancer is uncommon, approx 1% of population
occurs in males aged 20-39, most common cancer in males aged 15-34
caucasian at greater risk
unknown reason for tumour cause; could be trauma, atrophy, increased estrogen exposure, family history, undescended testicle (increases risk)
What are some clinical manifestations that may indicate testicular cancer
abnormal mass felt by patient
may have edema, sensation of fullness or heaviness in scrotum
back, abdominal pain, nausea, anorexia, bowel or bladder symptoms may indicate metastatic disease
What are the diagnostics used to confirm testicular cancer/tumour
serum tumour markers (hCG, AFP, LDH) - all may be elevated in tumour
ultrasound used to determine size, locations of the mass
additional radiographs should be used if mets is suspected
What is useful to distinguish BPH from prostate cancer?
similar signs and symptoms (urinary hesitancy, nocturia, hematuria)
prostate cancer- symptoms increase in intensity in 1-2 months, may progress to back pain, impotence and bone pain (mets)
DRE and PSA may not be enough to indicate BPH or prostate cancer
biopsy is useful in determining malignancy
describe the difference between cholelithiasis and cholecystitis
formation of gallstones and then bladder inflammation
gallstones may be asymptomatic, doesn’t necessarily turn into cholecystits
what is the pathophysiology behind cholelithiasis and cholecystitis?
gallstones are bile crystals formed in the gallbladder, crystals vary in size-smaller ones often pass through bile duct and are excreted
larger stones can block bile duct
lack of bile= no fat breakdown, fats pass into larger intestine, changes osmality of large intestine
continued blockage causes inflammation
what are the clinical manifestations of chole?
epigastric, RUQ pain, nausea and vomiting (contractions from the gallbladder trying to pass stone)
pain worsens after eating esp fatty foods
fever, jaundice in cholecystitis
what are the physical findings in a patient with chole
tenderness and pain to RUQ during palpation
rigidity, muscle guarding due to pain
Murphy’s sign present (pushing on RUQ and pt unable to take a breath)
radiating pain may be present
how do you manage a patient with cholecysitis?
refer to ER
if asymptomatic-no need for referral
ultrasound is most sensitive diagnostic tool to confirm stones
liver enzymes, blood work (bili, AST, alk phos may be elevated)
What is acute pancreatitis? How is it different from chronic pancreatitis?
inflammation of the pancreas (mild to severe)
causes: most common from gallstones, trauma, alcohol, hyperlipidemia, infection
able to recover in acute pancreatitis, acute pancreatitis does not cause long term pancreatic insuffiencient
chronic is permament cell changes of the pancreas affecting endocrine function
what are some of the risk factors for gallstone formation?
occurs in middle aged population >40 years of age
ethnicity-indigenous at greater risk
females during pregnancy
family hx, obesity, medications (contraception), alcohol, diabetes
what are the clinical manifestations of pancreatitis?
abdominal, epigastric pain can refer to back or chest, rebound tenderness nausea/vomiting not relieved with food, actually worsens weight loss, steatorrhea
chronic pancreatitis- endocrine dysfunction, symptoms of diabetes
what are the primary causes of chronic pancreatitis?
alcohol (most common cause, 50-70%)
duct obstruction- tumours, trauma
metabolic causes- hypercalcemia, hyperlipidemia
genetic/environmental/medical conditions
a 37yr old presents with symptoms of pancreatitis, what other condition should be evaluated?
cystic fibrosis- can increase risk of pancreatic insufficiency
what are red flags that warrant immediate pancreatic cancer investigation?
>50 years of age new onset of DM changes in bowel habit no ETOH use weight loss insidious symptoms (fatigue, malaise, insomnia)
what levels of amylase and lipase would you expect to find in a pt with acute and chronic pancreatitis?
acute- increase in both amylase and lipase
chronic-no increase in amylase and lipase because cell levels are low due to cellular changes
discuss some management techniques in a pt with chronic pancreatitis
pain control-short term opiates
nutritional- lipase, enzyme supplements, vitamin supplements to aid in fat breakdown
surgery- stent, shock wave if stones present
what is the diagnostic criteria for chronic kidney disease?
loss of filtration of blood and increase of waste products in the bloodstream
CKD considered when kidney structure is impaired or abnormal for >3 months, GFR usually <60mmol
what are the largest risk factors for CKD?
HTN, DM, CKD
family hx of CKD
what are the recommended screening requirements for CKD
screening eGFR, creatinine, UACR
at risk populations: q1-2 years
DM q1 year
one incident of abnormality doesn’t mean abnormal kidney function
what factors can contribute to changes in eeGFR?
low body weight, diet, infections, medications, amputees, >75 years of age
discuss management strategies in a patient with CKD
avoiding factors that can cause AKI (med adjustments, avoiding nephrotoxic meds, avoid contrast dye)
BP monitoring (<140/90) -ACEi or ARB
q6 month b/w, increasing increments if changes in medical status
UACR q 6-12 months
potassium levesl <5.5
CVD risk assessments, statins if needed
DM monitorinng, avoid metformin or sulfpnylreas if GFR is unstable
weight/nutritio
smoking cessation
health maintenance, psychosocial heatlh
What medications are contraindicated in those with CKD? What are some common drugs that need to be adjusted in those with renal insufficiency?
nephrotoxic medications need to be avoided
NSAIDs, COX inhibitors, aminoglycosides
no IV contrast dyes
allopurinol wellbutrin lithium codein valcyclovir
What are some clinical presentations requiring surgical consultation for evaluation of abdominal pain?
appendicitis - pain in RLQ, abdominal rigidity, migrating pain from epigastrium, nausea/vomiting, fever
presence of mcburneys (pain to RLQ during palpation), rosvig (pain to LLQ during palpation), psoas (R leg raise illicits pain) obturator (rebound tenderness when knee flexed and raised)
perforated peptic ulcer - abrupt onset of sever pain, radiating abdominal pain from epigastrum, coffee ground emesis, hematemesis, melena stools, hematochezia
bowel obstruction - intermitted crampy abdominal pain, vomiting, fever, hyperactive bowel sounds, increased gas and flatulence
peritonitis - high fever, acute abdominal pain, tendeness, nausea, vomiting, diarrhea/constipation
aortic aneurysm- painful bulging mass to abdomen
what are risk factors that can cause GI bleeding?
NSAIDS, smoking, increased acid production, H pylori infection, trauma
how is upper and lower GI bleeding differentiated?
according to the anatomic source, upper-proximal to ligament of treitz (right before the start of the small intestine, includes the stomach)
how is upper GI bleeding classified and what are some of the conditions in each classification?
variceal and non-variceal classifications
variciel- esophagitis, varices
non variceal- PUD, gastric ulcers, erosions, use of NSAIDs
what are the clinical manifestations of upper and lower GI bleeds?
can be asymptomatic with vague symptoms
hematemesis (bloody vomitus), melena stools (black, foul smelling stool) - usually originates from an upper GI source
hematochezia (bright red stools) usually from lower GI source
what is the most common cause of lower GI bleed?
diverticulitis (inflammation of the diverticula) - trapped feces or particles causes inflammation, can lead to necrosis, inappropriate breakdown of foods
what are some diagnostic tools used for upper and lower GI bleed?
cbc diff
stool occult blood
electrolytes
LFTs, creatinine
may use imaginging -abdo CT scan, ultrasound
how would you manage a patient with a GI bleed?
- ensuring hemodynamic stability in case of severe blood loss ie) transfusions, fluid replacement
- reversing anticoagulants if the cause of bleeding
- pharmacological interventions (PPIs for upper GI bleed due to PUD)
- endoscopy to determine source of upper GI bleeding (most accurate diagnostic tool)
- LGIB- colonoscopy
what are common clinical manifestations that may indicate esophageal conditions?
heartburn (substernal burning, radiating to neck)- usually a sign of GERD
dysphagia (difficulty swallowing, feeling like it won’t go down)- mechanical/neurological disruptions, brainstem lesions, GERD, PUD
odynophagia (sharp pain with intake of food)- usually associated with esophageal esophagitis, infection in immunocompromised patients
what is peptic ulcer disease? who is at risk?
ulceration of gastric or duodenal mucousa; usually caused by H. Pylori or increased NSAID use
family hx, smoking, steroids, ETOH, biphosphonate therapy increases risk of PUD
what is the patho behind PUD?
acid and pepsin needed to break down food, alkaline used to protect the stomach lining
h.pylori (oral fecal route) causes inflammation and erodes stomach lining .
NSAIDS blocks prostagladins responsible for protecting the coating of the stomach
what is the clinical presentation of someone with PUD?
often asymptomatic
epigastric pain, dyspepsia common
sharp gnawing pain occurs 2-4 hours after eating a meal
pain is often alleviated right away with food/antacids
what tests are required to diagnose someone with PUD
cbc diff
stool cultures
H. pylori serology or breath test
endoscopy is the most accurate
what are some red flags that warrant immediate evalation in a person presenting with abdominal pain?
vomiting abdominal mass blood stools weight loss dysphagia >50 years of age
what is celiac disease and who is at risk?
immune response to gluten, intake causes inflammation and damage to small intestine leading to malabsorption
unclear who is at risk, genetic mutation (HLA DQ2)
symptoms occur for approx 10 years before idnentification, usually diagnosed in adulthood
what are clinical manifestations of celiac disease
malabsorption, weight loss, diarrhea, steatorrhea, weakness and flatulence
atypical symptom: dermatitis herpatiform- cutaneous variant of celiac disease, pruritic papulovesicles over trunk, scalp and neck
what serology test is used to diagnose celiac disease
IgA TGA antibody testing, 98% sensitive
what are some management strategies in someone with celiac disease?
remove all gluten from diet
assess diet and medications that may use gluten preservatives
usually symptoms resolve in 1-2 weeks of no gluten, excellent prognosis
what is IBS and who is at risk?
very common in primary care
functional GI disorder d/t no pathology or concerns with GI tract, no identifiable cause of IBS
more common in women than men, occurs later stages of life in 30-40s
what is the diagnostic criteria for IBS?
abdo pain/discomfort for at least 3x per week in the last 3 months + improvement with defecation, change in frequency of stool, change in appearance of stool
no underlying pathology for symptoms
what are some management strategies in someone with IBS?
dietary modifications, increase fibre, probiotoics. avoiding triggering foods
antispasmotics, antidiarrheals, psychotropic drugs if anxiety related
what symptoms are incompatible with a diagnosis of IBS and warrant immediate evaluation?
nocturnal symptoms bloody/greasy stool weight loss malnutrition GI bleeding recurrent vomiting anemia fever
what is the primary difference between IBS and IBD?
IBS-functioning GI disorder with no underlying pathology
IBD- inflammatory disorders with underlying pathology; divided into Chron’s and ulcerative colitis
what are the major risk factors of UC and CD?
genetics as significant cause of IBD- genetic mutations as a predictor of changes in the gut microbiome
CD has a poorer prognosis
tobacco smoking as the primary environmental cause of IBD
what part of the digestive tract does UC and CD affect? what are the clinical manifestations?
UC- rectum and colon
CD- any part of the digestive tract, most commonly found in the small intestine
similar clincal presentations, may be difficult to diagnose
abdominal pain-diffuse to LLQ or RLQ, cramping sensation
bloody stools (more often in UC)
vague symptoms in CD, fatigue, weight loss, anorexia
CD can lead to fissures, obstruction, fistulas
what is the diagnostic tool for CD or UC?
endoscopy is more accurate in determining UC or CD- cobblestone appearance of mucousa in CD
what pharmacological options are available for those with UC or CD?
mesalamine (helpful in UC)
corticosteroids
biologics
surgery (for CD)
what are the modes of transmission for Hep A, B and C
HAV: fecal oral route, contaminated water/foods, blood transfusions
HBV: bodily fluids ie) blood, seminal fluid, mother to fetus
HCV: blood and parenteral routes
what are the risk factors for Hep A B and C
HAV: more prevalent in areas with low socioeconomic status, poor sanitation and poor drinking water, common in Asia, Africa, South America
HBV: IVDU, tattoos, risky sexual behaviours, correctional factilities, HIV, HCV, HCPs
HCV: baby boomers, IVDU, HCPs, multiple sexual partners, tattoos
what are the clinical manifestations and incubation periods of HAV, HBV, HCV
HAV: acute infection, malaise, anorexia, jaundice, nausea, fever, symptoms appear after 4 weeks of virus acquisition
incubation period 2-6 weeks
no carrier state in HAV, body can rid virus itself
HBV: often asymptomatic, malaise, anorexia, jaundice, nausea, symptoms appear 6 weeks after exposure
incubation period 2-6 months
chronic carrier due to ongoing viral repetition
HCV: may be asymptomatic, anorexia, malaise, JAUNDICE IS RARE, chronic carrier, incubation period 2-22 weeks
what diagnostic tests are used to assess hepatitis?
cbc, diff, LFTs, antibodies, antigens
HCV RNA if positive HCV antibody
previous antibodies can be because of previous vaccination or infection
