Wk 7: GI/ Hypersensitivity/ Urological/ Male Reporoductive/ Visual And & Sensory Flashcards

1
Q

what is constipation

A

small, infrequent or difficult bowel movements
< 3 stools a week
dependent on patient, everyone has different patterns

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2
Q

causes of constipation

A

diet (low in fiber)
lack of exercise
slow peristalsis (elderly)
pathologic conditions (obstructions or diverticulitis)

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3
Q

what is impaction

A

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

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4
Q

what is diarrhea

A

increase in frequency and fluidity of bowel movements

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5
Q

acute versus chronic diarrhea

A

Acute: infection, emotional stress, some medications, liquid stool around impaction
chronic: more than 4 weeks, chronic GI infection, alterations in motility, malabsorption, endocrine disorders

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6
Q

what is an example of episodic diarrhea?

A

food allergy or irritant

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7
Q

what are the four pathophysiologic mechanisms of diarrhea?

A
  1. osmotic diarrhea
  2. secretory diarrhea
  3. exudate diarrhea
  4. related to motility disturbances
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8
Q

osmotic diarrhea

A

-related to magnesium sulfate increase, ingesting causing a rush of sodium and water into the colon causing diarrhea
-can happen with tube feedings

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9
Q

secretory diarrhea

A

caused by bacteria or toxin
-can increase secretion and inhibits reabsorption in the gut
-usually involves vibrio cholerae and staphylococcus colitis bacteria

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10
Q

exudative diarrhea

A

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

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11
Q

diarrhea related to motility disturbances

A

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

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12
Q

Why is diarrhea a problem?

A

skin breakdown
flid and electrolyte imbalance
nutritional concerns

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13
Q

what are the different groups if antidiarrheals ?

A

adsorbants
anti-motility (anticholinergics and opiates)
probiotics

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14
Q

what route are most antidiarrheals given?

A

oral /PO

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15
Q

what is adsorbtion?

A

similar to absorption but involves the chemical binding of substances

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16
Q

when loperamide is given with atropine it causes what kind of side effects?

A

anticholinergic

-then there has to be a prescription, cannot be over the counter
-loperamide by itself can be given over the counter

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17
Q

lactobacillius organisms

A

natural bacteria that make up a majority of the normal flora of gut

-can go away when you take Abx

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18
Q

treatment of constipation is individualized, what do we consider before treating?

A

the patients age
severity of condition
contributing factors

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19
Q

what are the different groups of laxatives

A

bulk forming
emollient
hyperosmotic
saline
stimulant

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20
Q

hypersensitivity

A

nml immune response that is :
-inappropriately triggered
-excessive
-produces undesirable effects on the body

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21
Q

what are the basic triggers of hypersensitivity ?

A
  1. antigen-antibody reaction
  2. antigen-lymphocyte interaction

(antigen = foreign substance)

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22
Q

what are the four types of hypersensitivities ?

A

Types I, II, III = mediated by ANTIBODIES (produced by B cells, plasma)
Type IV = mediated by T cells

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23
Q

are types I, III, and III hypersensitivities immediate reactions or slow?

A

immediate

Type IV is slow

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24
Q

Type I hypersensitivity
IgE mediated reaction

A

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)

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25
Q

etiology of type 1 hypersensitivity

A

1 parent allergic= 30% chance
2 parents allergic = 50 % chance

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26
Q

what are the main cells involved in type I hypersensitivity ?

A

B lymphocytes
IgE antibodies
Mast cells (granulocyte involved in immune responses)

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27
Q

Type I hypersensitivity: atopic reactions (local)

A

ex:allergic rhinitis, asthma, urticaria
usually d/t: pollen, dust, molds, animal dander

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28
Q

Type I hypersensitivity: anaphylaxis (systemic)

A

-systemic release of chemical mediators
-life threatening d/t: bronchial constriction, airway obstruction, vascular collapse
-most common triggers: medications, bees, food

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29
Q

Type II hypersensitivity: Cytotoxic reaction

A

-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)

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30
Q

what immune cells are involved with Type II hypersensitivity

A

antibodies (IgG and IgM)
complement
WBC’s (phagocytes)

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31
Q

what are some examples of antigens associated with Type II hypersensitivity

A

blood
some of your body’s own cells (like with DM)
erythroblastosis fetalis (hemolytic anemia in fetus) rH

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32
Q

Type II hypersensitivity manifestations of a transfusion reaction

A

F, chills, flushing
increased HR, decreased BP
CP, back pain
restless, anxiety
HA

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33
Q

Type III hypersensitivity: immune complex reaction

A

-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

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34
Q

Type III hypersensitivity: immune complex reaction etiology

A

autoimmune attack
low grade infection
inhaled antigens from molds or contaminated plants

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35
Q

Type III hypersensitivity: possible agents

A

bodys own tissue or DNA
inhaled antigens from mold or contaminated plants
bacteria or viruses

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36
Q

Type III hypersensitivity: key immune cells

A

antibodies (IgG and IgM) that clump with antigens
complement
neutrophils and mast cells

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37
Q

Type III clinical manifestations

A

depends on where the complexes are deposited in the tissue
-rheumatoid arthritis (primarily in joints)
-glomerulonephritis ( can lead to kidney failure)
-systemic lupus erythematosus

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38
Q

difference between type II and type III

A

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

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39
Q

Type IV: delayed hypersensitivity

A

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

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40
Q

Type IV pathogenesis

A

-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)

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41
Q

Type IV manifestations

A

peak 48-72 hours
contact dermatitis (red, itching, edema, blisters)
tuberculin hypersensitivity (redness, induration, inflammation)

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42
Q

uncomplicated UTIs

A

lower urinary tract and bladder
more common in women
protein in urine is good for bacterial growth

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43
Q

why are UTI’s more common in women?

A

they have shorter urethras
incomplete emptying
irritation

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44
Q

urethritis

A

infection in the urethra

45
Q

cystitis

A

infection in the bladder

46
Q

S/Sx of uncomplicated UTI

A

sometimes asymptomatic
frequency, urgency, dysuria, hematuria, cloudy/foul urine, fever, chills, fatigue

47
Q

how to diagnosis a UTI

A

H&P important
UA, urine culture, CBC

48
Q

how to treat a UTI

A

Abx, increase fluid intake, avoid irritants, loose cotton clothes, frequent urination, probiotics

49
Q

UTI protective factors

A

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

50
Q

UTI risk factors

A

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

51
Q

lower UTI clinical manifestations: urethritis versus cystitis

A

urethritis (urethra)
-dysuria, but mainly asymptomatic

cystitis (bladder)
-frequency, urgency, suprapubic discomfort, dysuria

52
Q

Atypical Sx of a UTI in children

A

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

53
Q

atypical Sx of UTI in elderly

A

anxiety
CONFUSION
lethargy
anorexia
h/o falling

54
Q

overactive bladder

A

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

55
Q

causes of an overactive bladder

A

neurological disorders
DM
UTIs
hormonal changes
tumors/stones
obstructions

56
Q

urinary incontinence

A

any involuntary loss of urine
-not a normal symptom of aging but may be related to age related changing of the body

57
Q

urgency incontinence
what is it?
causes?

A

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

58
Q

stress incontinence
what is it?
causes?
risk factors?

A

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

59
Q

other types of incontinence

A

mixed (urgency and stress)
overflow (bladder too full)
functional (physical/environmental limitations)
transient (sudden and reversible)

60
Q

cataracts

A

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

61
Q

Risk factors for cataracts

A

older age
eye trauma
congenital risk
DM
corticosteroid use
smoking
EtOH use

62
Q

manifestation of cataracts

A

painless
unilateral or bilateral vision changes (blurred, halo around lights, altered perception of color, glare issues at night, decreased accommodation)

63
Q

what is the treatment for cateracts?

A

surgical
no pharm treatment

64
Q

diabetic retinopathy
what are the two types?

A

40% DM pts over 40 y/o develop it

there are two types:

  1. non-proliferative:
    capillary micro-aneurysms, retinal swelling, hard exudates
    macular edema
    capillaries rupture
  2. proliferative:
    more advanced retinopathy
    new blood vessels are fragile and leaky
65
Q

hypertensive retinopathy
etiology:
Trx:

A

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

66
Q

retinal detachment

A

-tear or leak of retina, so vitreous humor (eye juice) flows behind the retina
-happens rapidly
-usually spontaneous

67
Q

who is at risk for retinal detachment ?

A

people with myopia
age >40
trauma to head
eye tumors
complications / Hx cataract surgery

68
Q

clinical manifestations of retinal detachment

A

SUDDEN onset
unilateral vision loss
painless
may see floaters
flash of lights
curtain effect on vision

69
Q

macular degeneration (age related)
what are the two types ?

A

MOST common cause of irreversible vision loss in people over 60 y/o

  1. Dry (non-exudative): most common (90%)
    yellow deposits in retinal pigment epithelium
  2. wet (exudative): new blood vessel and hemorrhage in abnormal locations of the retina (only 10%)
70
Q

who is at risk for macular degeneration

A

FHx, genetics, UV light, hyperopia (far sighted), smoking, light-colored eyes

dark green, leafy vegetables are protective

71
Q

symptoms of macular degeneration

A

early on: none
later: blurred, darkened vision, blind spot (scotomas), distorted vision (metamorphopsia)

72
Q

treatment of macular degeneration

A

vision does NOT improve
treatment is limited -> medications injected into the eye

73
Q

glaucoma
what are the two types ?

A
  1. open angle
  2. closed angle
74
Q

what is glaucoma?

A

an elevated intraocular pressure (IOP)
WITH
vision changes OR optic nerve damage
(need two )

-chronic condition, usually affects both eyes

75
Q

risk factors for open angle glaucoma

A

elevated IOP
age (old)
race: african americans 3-4x higher
FHx
myopia
DM, HTN, migraines

76
Q

what happens with open angle glaucoma?

A

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

77
Q

open angle glaucoma clinical manifestations

A

none usually
progressive loss of sight, vague eye pain, halos around lights, tunnel vision

78
Q

what is closed angle glaucoma

A

abnormal angle between iris and later cornea
-outflow is blocked when pupil is dilated

79
Q

closed angle glaucoma risk factors

A

Asian Americans
females
hyperopia
FHx
older age

80
Q

which form of glaucoma is considered an emergency ?

A

closed angle glaucoma
-outcome is based on time from onset to treatment

81
Q

what is something that can trigger and acute episode of closed angle glaucoma ?

A

anticholinergic drugs

82
Q

clinical manifestations of acute closed angle glaucoma

A

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

83
Q

what are some considerations for pharm related to glaucoma?

A

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

84
Q

miniere Dz

A

episodic/ transient of the middle ear
-unilateral or bilateral
-excessive endolymph and pressures in the membranes disrupt vestibular (balance) and hearing function

85
Q

clinical manifestations of meniere Dz

A

recurring episodes of vertigo (with N/V) hearing loss, ringing in the ears, feeling of fullness

86
Q

how to do you treat meniere Dz

A

treatment is symptomatic

87
Q

risk factors for testicular cancer

A

FHx
caucasiam
cryptorchidism
HIV infection

(major CA in med 15-34, affects young men)

88
Q

what is the main kind of testicular cancer ?

A

germ cell tumors (95%)

89
Q

what are the two types of germ cell tumors?
how do you treat them?

A
  1. seminomas
    arise form immature germ cells
    slow growing, nonaggressive
    easily cured with radiation
  2. nonseminomas
    arise from mature germ cells
    more aggressive
    usually treated with surgery
90
Q

what are some early clinical manifestations of testicular cancer ?

A

enlargement of testicles
painless mass noted
if there is discomfort: ache in groin, sensation of heaviness in scrotum

caught early= VERY high survival rate

91
Q

what are some late clinical manifestations of testicular cancer ?

A

possible frank pain
manifestations can be based on metastatic spread such as: cough, hemoptysis, leg swelling back pain, dizzy

92
Q

how do you treat late stage testicular cancer

A

chemo

93
Q

Benign prostatic hyperplasia (BPH)

A

nonmalignant enlargement of the prostate
-increase in epithelial cells
-increase in smooth muscle cells
blocking of urethra

94
Q

what is the prostate ?

A

gland surrounding the urethra
produces seminal fluids
weighs between 4-20 grams

95
Q

RF for BPH

A

age
FHx
race/ethnicity

96
Q

what are the two theories of BPH etiology ?

A
  1. hormone imbalance
  2. DHT accumulation (testosterone and % alpha-reductase= DHT)
97
Q

high levels of DHT activate _____ _____

A

growth factors

98
Q

BPH Sx

A

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

99
Q

complications related to BPH

A

obstruction
UTI
renal problems
bladder stones

100
Q

treatment of BPH

A

mild Sx= watchful waiting
moderate Sx= drug therapy
severe Sx= invasive options

101
Q

who has the highest rate of prostate cancer?
risk factors

A

african american men
>60y/0 (age)
family tendency
high fat diet

102
Q

clinical manifestations of prostate cancer

prognosis?

A

early stage: asymptomatic
later signs: BPH type presentation, metastasis to bone or lungs
prognosis: stage dependent, early Dx.

103
Q

how to test for prostate cancer

A

PSA screening or DRE (digital rectal exam)
survival benefit, but only 1 in 3 men with a positive PSA actually have cancer
gleason scrore

104
Q

Erectile dysfunction (ED) or impotence

A

inability to achieve or sustain an erection sufficient for satisfactory sexual intercourse
-associated with chronic illness

105
Q

primary Erectile dysfunction (ED)

A

rare
life long inability to have normal erection
severe psychiatric problems
early vascular trauma

106
Q

secondary Erectile dysfunction (ED)

A

most common
ED in someone with a h/o normal erections

107
Q

what are some causes of secondary ED

A
  1. organic cause: PVD, medications, endocrine problems, trauma, surgery
  2. psychogenic causes: depression, low desire, performance anxiety, strained relationship
108
Q

physiology of a normal erection

A

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

109
Q

priapism

A

erection is painful or lasts more than 4 hours
medical emergency