Wk 7: GI/ Hypersensitivity/ Urological/ Male Reporoductive/ Visual And & Sensory Flashcards
what is constipation
small, infrequent or difficult bowel movements
< 3 stools a week
dependent on patient, everyone has different patterns
causes of constipation
diet (low in fiber)
lack of exercise
slow peristalsis (elderly)
pathologic conditions (obstructions or diverticulitis)
what is impaction
unrelieved constipation
-firm/ immovable mass of stool obstructs lower GI tract
-continuous oozing or diarrhea
Sx: loss of appetite, abdominal distention, cramping or pain
-worse case, can lead to surgery
what is diarrhea
increase in frequency and fluidity of bowel movements
acute versus chronic diarrhea
Acute: infection, emotional stress, some medications, liquid stool around impaction
chronic: more than 4 weeks, chronic GI infection, alterations in motility, malabsorption, endocrine disorders
what is an example of episodic diarrhea?
food allergy or irritant
what are the four pathophysiologic mechanisms of diarrhea?
- osmotic diarrhea
- secretory diarrhea
- exudate diarrhea
- related to motility disturbances
osmotic diarrhea
-related to magnesium sulfate increase, ingesting causing a rush of sodium and water into the colon causing diarrhea
-can happen with tube feedings
secretory diarrhea
caused by bacteria or toxin
-can increase secretion and inhibits reabsorption in the gut
-usually involves vibrio cholerae and staphylococcus colitis bacteria
exudative diarrhea
active sites of inflammation in the bowel lumen that results in exudation of mucus/blood/proteins from the site. causes “open wounds”
-these substances pull water into the lumen, causing diarrhea
usually caused by crohns Dz and ulcerative colitis
diarrhea related to motility disturbances
result of decreased absorption in the small intestines, so large amounts of fluid are delivered to the colon
-caused decreased absorption of nutrients
-usually d/t dumping syndrome after a gastrostomy or IBS
Why is diarrhea a problem?
skin breakdown
flid and electrolyte imbalance
nutritional concerns
what are the different groups if antidiarrheals ?
adsorbants
anti-motility (anticholinergics and opiates)
probiotics
what route are most antidiarrheals given?
oral /PO
what is adsorbtion?
similar to absorption but involves the chemical binding of substances
when loperamide is given with atropine it causes what kind of side effects?
anticholinergic
-then there has to be a prescription, cannot be over the counter
-loperamide by itself can be given over the counter
lactobacillius organisms
natural bacteria that make up a majority of the normal flora of gut
-can go away when you take Abx
treatment of constipation is individualized, what do we consider before treating?
the patients age
severity of condition
contributing factors
what are the different groups of laxatives
bulk forming
emollient
hyperosmotic
saline
stimulant
hypersensitivity
nml immune response that is :
-inappropriately triggered
-excessive
-produces undesirable effects on the body
what are the basic triggers of hypersensitivity ?
- antigen-antibody reaction
- antigen-lymphocyte interaction
(antigen = foreign substance)
what are the four types of hypersensitivities ?
Types I, II, III = mediated by ANTIBODIES (produced by B cells, plasma)
Type IV = mediated by T cells
are types I, III, and III hypersensitivities immediate reactions or slow?
immediate
Type IV is slow
Type I hypersensitivity
IgE mediated reaction
developing an allergy
-immediate reaction (15-20 minutes)
-Rx can occur after being sensitized to an antigen
- antigens: common reactions to environment (pet dander, bees), food (nuts, seafood, eggs), medications (penicillin, contrast)
**inappropriate response to a protein)
etiology of type 1 hypersensitivity
1 parent allergic= 30% chance
2 parents allergic = 50 % chance
what are the main cells involved in type I hypersensitivity ?
B lymphocytes
IgE antibodies
Mast cells (granulocyte involved in immune responses)
Type I hypersensitivity: atopic reactions (local)
ex:allergic rhinitis, asthma, urticaria
usually d/t: pollen, dust, molds, animal dander
Type I hypersensitivity: anaphylaxis (systemic)
-systemic release of chemical mediators
-life threatening d/t: bronchial constriction, airway obstruction, vascular collapse
-most common triggers: medications, bees, food
Type II hypersensitivity: Cytotoxic reaction
-given wrong blood type
-antigens stimulate antibody production
antibodies recognize and attach to cell surface antigens
-direct destruction of targeted cells that contain the antigen (cell lysis and phagocytosis)
what immune cells are involved with Type II hypersensitivity
antibodies (IgG and IgM)
complement
WBC’s (phagocytes)
what are some examples of antigens associated with Type II hypersensitivity
blood
some of your body’s own cells (like with DM)
erythroblastosis fetalis (hemolytic anemia in fetus) rH
Type II hypersensitivity manifestations of a transfusion reaction
F, chills, flushing
increased HR, decreased BP
CP, back pain
restless, anxiety
HA
Type III hypersensitivity: immune complex reaction
-rheumatoid arthritis
-Antigen-antibody COMPLEXES forms and circulates around blood stream then deposits into tissues causing inflammation (compliment Cascade)
-can be localized or more systemic
Type III hypersensitivity: immune complex reaction etiology
autoimmune attack
low grade infection
inhaled antigens from molds or contaminated plants
Type III hypersensitivity: possible agents
bodys own tissue or DNA
inhaled antigens from mold or contaminated plants
bacteria or viruses
Type III hypersensitivity: key immune cells
antibodies (IgG and IgM) that clump with antigens
complement
neutrophils and mast cells
Type III clinical manifestations
depends on where the complexes are deposited in the tissue
-rheumatoid arthritis (primarily in joints)
-glomerulonephritis ( can lead to kidney failure)
-systemic lupus erythematosus
difference between type II and type III
type II: reactions occur on the cell surface and result in direct cell death or malfunction
type III: immune complexes are deposited into tissues and the resulting INFLAMMATION destroys the tissue
Type IV: delayed hypersensitivity
ex: poison IV, positive TB test, jellyfish sting, allergic reaction to jewelry, chrons Dz
-delayed response, NO antibody involvement
-T cells are involved along with cytokines, mast cells and macrophages
-takes times for T cells to migrate to site
Type IV pathogenesis
-small incomplete antigen called “hapten” penetrates the skin
-hapten combines with human protein to form complete antigen
- T cell becomes aware of antigen
-T cell attack the antigen three ways
1. direct attack
2. release of cytokines (inflammation)
3. macrophages (cell distruction)
Type IV manifestations
peak 48-72 hours
contact dermatitis (red, itching, edema, blisters)
tuberculin hypersensitivity (redness, induration, inflammation)
uncomplicated UTIs
lower urinary tract and bladder
more common in women
protein in urine is good for bacterial growth
why are UTI’s more common in women?
they have shorter urethras
incomplete emptying
irritation
urethritis
infection in the urethra
cystitis
infection in the bladder
S/Sx of uncomplicated UTI
sometimes asymptomatic
frequency, urgency, dysuria, hematuria, cloudy/foul urine, fever, chills, fatigue
how to diagnosis a UTI
H&P important
UA, urine culture, CBC
how to treat a UTI
Abx, increase fluid intake, avoid irritants, loose cotton clothes, frequent urination, probiotics
UTI protective factors
acidic urine
presence of urea
sex specific factors: men have prostatic secretions and women have urethral gland secretions
urine flow is unidirectional
one way valve at ureteral attachment to bladder
immune system
UTI risk factors
catheterizations
being a female
perineal irritation
age (older)
pregnancy
sexual activity
urinary obstruction or reflux
immobility (urinary stasis )
incontinence (urine or stool)
decreased cognition
bad personal hygiene
men more likely to have reoccurring UTIS b/c bacteria can hide deep in prostate
lower UTI clinical manifestations: urethritis versus cystitis
urethritis (urethra)
-dysuria, but mainly asymptomatic
cystitis (bladder)
-frequency, urgency, suprapubic discomfort, dysuria
Atypical Sx of a UTI in children
fever, irritability, poor feeding, vomiting, diarrhea, ill appearance
-are they old enough to verbalize
-if reoccurring UTIs happen, it is common to look into sexual abuse
atypical Sx of UTI in elderly
anxiety
CONFUSION
lethargy
anorexia
h/o falling
overactive bladder
muscle of bladder start to contract involuntarily even when urine is low, causing a sudden urge to urinate
-may experience urgency incontinence
-nocturia
-frequency 8+ times in 24 hrs
causes of an overactive bladder
neurological disorders
DM
UTIs
hormonal changes
tumors/stones
obstructions
urinary incontinence
any involuntary loss of urine
-not a normal symptom of aging but may be related to age related changing of the body
urgency incontinence
what is it?
causes?
involuntary leakage of urine immediately after a sudden sensation to urinate
Causes: overactive detrusor muscle that suddenly contracts (increases with age), bladder infection that irritates the lining of bladder, bladder outlet obstruction (enlarged prostate), CNS conditions, drugs
stress incontinence
what is it?
causes?
risk factors?
occurs when urine is involuntarily lost with increases in intra abdominal pressure
causes: loss of pelvic floor muscle, loss of fascial support of bladder and urethra
RF: age, obesity, childbearing related trauma, pelvic surgery
other types of incontinence
mixed (urgency and stress)
overflow (bladder too full)
functional (physical/environmental limitations)
transient (sudden and reversible)
cataracts
cloudy lens
gradual onset blurred vision
can lead to blindness if untreated
-cataracts blocks some light from passing through the lens ads scatters the light, preventing crisp focus on the retina
Risk factors for cataracts
older age
eye trauma
congenital risk
DM
corticosteroid use
smoking
EtOH use
manifestation of cataracts
painless
unilateral or bilateral vision changes (blurred, halo around lights, altered perception of color, glare issues at night, decreased accommodation)
what is the treatment for cateracts?
surgical
no pharm treatment
diabetic retinopathy
what are the two types?
40% DM pts over 40 y/o develop it
there are two types:
- non-proliferative:
capillary micro-aneurysms, retinal swelling, hard exudates
macular edema
capillaries rupture - proliferative:
more advanced retinopathy
new blood vessels are fragile and leaky
hypertensive retinopathy
etiology:
Trx:
etiology: HTN creates blockage in retinal blood vessels
-initially no vision changes
-constant severe HTN causes SUDDEN vision loss d/t swelling of optic disc and nerve
Trx: vision restored with treatment of HTN
retinal detachment
-tear or leak of retina, so vitreous humor (eye juice) flows behind the retina
-happens rapidly
-usually spontaneous
who is at risk for retinal detachment ?
people with myopia
age >40
trauma to head
eye tumors
complications / Hx cataract surgery
clinical manifestations of retinal detachment
SUDDEN onset
unilateral vision loss
painless
may see floaters
flash of lights
curtain effect on vision
macular degeneration (age related)
what are the two types ?
MOST common cause of irreversible vision loss in people over 60 y/o
- Dry (non-exudative): most common (90%)
yellow deposits in retinal pigment epithelium - wet (exudative): new blood vessel and hemorrhage in abnormal locations of the retina (only 10%)
who is at risk for macular degeneration
FHx, genetics, UV light, hyperopia (far sighted), smoking, light-colored eyes
dark green, leafy vegetables are protective
symptoms of macular degeneration
early on: none
later: blurred, darkened vision, blind spot (scotomas), distorted vision (metamorphopsia)
treatment of macular degeneration
vision does NOT improve
treatment is limited -> medications injected into the eye
glaucoma
what are the two types ?
- open angle
- closed angle
what is glaucoma?
an elevated intraocular pressure (IOP)
WITH
vision changes OR optic nerve damage
(need two )
-chronic condition, usually affects both eyes
risk factors for open angle glaucoma
elevated IOP
age (old)
race: african americans 3-4x higher
FHx
myopia
DM, HTN, migraines
what happens with open angle glaucoma?
abnormal trabecular meshwork causing:
-reduced drainage of aqueous humor (eye fluid) into canal of schlemm and an imbalance between inflow and outflow
-> resulting in increased IOP and vision problems
open angle glaucoma clinical manifestations
none usually
progressive loss of sight, vague eye pain, halos around lights, tunnel vision
what is closed angle glaucoma
abnormal angle between iris and later cornea
-outflow is blocked when pupil is dilated
closed angle glaucoma risk factors
Asian Americans
females
hyperopia
FHx
older age
which form of glaucoma is considered an emergency ?
closed angle glaucoma
-outcome is based on time from onset to treatment
what is something that can trigger and acute episode of closed angle glaucoma ?
anticholinergic drugs
clinical manifestations of acute closed angle glaucoma
typically unilateral, but other eye is at risk
SEVERE pain
N/V
blurry vision, halos
reddened eyes
dilated pupil (not reactive to light)
cloudy cornea
what are some considerations for pharm related to glaucoma?
need drugs that will DECREASE aqueous humor production or INCREASE aqueous humor drainage. or do both
-for acute angle crisis must treat with surgical intervention
-all topical agents, use nasolacrimal pressure with instillation, hold pressure for two minutes
miniere Dz
episodic/ transient of the middle ear
-unilateral or bilateral
-excessive endolymph and pressures in the membranes disrupt vestibular (balance) and hearing function
clinical manifestations of meniere Dz
recurring episodes of vertigo (with N/V) hearing loss, ringing in the ears, feeling of fullness
how to do you treat meniere Dz
treatment is symptomatic
risk factors for testicular cancer
FHx
caucasiam
cryptorchidism
HIV infection
(major CA in med 15-34, affects young men)
what is the main kind of testicular cancer ?
germ cell tumors (95%)
what are the two types of germ cell tumors?
how do you treat them?
- seminomas
arise form immature germ cells
slow growing, nonaggressive
easily cured with radiation - nonseminomas
arise from mature germ cells
more aggressive
usually treated with surgery
what are some early clinical manifestations of testicular cancer ?
enlargement of testicles
painless mass noted
if there is discomfort: ache in groin, sensation of heaviness in scrotum
caught early= VERY high survival rate
what are some late clinical manifestations of testicular cancer ?
possible frank pain
manifestations can be based on metastatic spread such as: cough, hemoptysis, leg swelling back pain, dizzy
how do you treat late stage testicular cancer
chemo
Benign prostatic hyperplasia (BPH)
nonmalignant enlargement of the prostate
-increase in epithelial cells
-increase in smooth muscle cells
blocking of urethra
what is the prostate ?
gland surrounding the urethra
produces seminal fluids
weighs between 4-20 grams
RF for BPH
age
FHx
race/ethnicity
what are the two theories of BPH etiology ?
- hormone imbalance
- DHT accumulation (testosterone and % alpha-reductase= DHT)
high levels of DHT activate _____ _____
growth factors
BPH Sx
similar to UTI
-frequency, urgency, delay in initiation, reduction in force, increased urination time, dribbling
-enlargement of prostate SIZE does not matter in relation to symptoms
complications related to BPH
obstruction
UTI
renal problems
bladder stones
treatment of BPH
mild Sx= watchful waiting
moderate Sx= drug therapy
severe Sx= invasive options
who has the highest rate of prostate cancer?
risk factors
african american men
>60y/0 (age)
family tendency
high fat diet
clinical manifestations of prostate cancer
prognosis?
early stage: asymptomatic
later signs: BPH type presentation, metastasis to bone or lungs
prognosis: stage dependent, early Dx.
how to test for prostate cancer
PSA screening or DRE (digital rectal exam)
survival benefit, but only 1 in 3 men with a positive PSA actually have cancer
gleason scrore
Erectile dysfunction (ED) or impotence
inability to achieve or sustain an erection sufficient for satisfactory sexual intercourse
-associated with chronic illness
primary Erectile dysfunction (ED)
rare
life long inability to have normal erection
severe psychiatric problems
early vascular trauma
secondary Erectile dysfunction (ED)
most common
ED in someone with a h/o normal erections
what are some causes of secondary ED
- organic cause: PVD, medications, endocrine problems, trauma, surgery
- psychogenic causes: depression, low desire, performance anxiety, strained relationship
physiology of a normal erection
sexual arousal
increases PNS and nitric oxide release
activation of cGMP
relaxation of arteries and smooth muscle
increased inflow and reduced outflow
engorgement and erection
priapism
erection is painful or lasts more than 4 hours
medical emergency
