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