Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/247

Click to flip

247 Cards in this Set

  • Front
  • Back
What is cryptorchidism?
Congenital abnormality; "hidden flower". Malpositioning of the testes outside of their normal scrotal location. It takes its blood supply from area near kidney. Adhesions within the fetal inguinal canal may be responsible. can be surgically repositioned.
-signs of atrophy, hypospermatogenesis not uncommon
-10x risk for malignancy
What is hypospadias?
congenital malformation of the urethral opening on the dorsal surface of the penis; failure to fuse
What is epispadias?
congenital malformation of the urethral opening on the ventral surface of the penis.
What is the pathogenesis of hypospadias and epispadias?
development of the penis occurs in the embryo at 7-8 weeks gestation, unknown genetic defect linked to the lack of production, or production of a defective enzyme 5 alpha reductase which prevents conversion of testosterone to dihydrotestosterone, the active homone.
What is torsion of the testes?
Usually seen in adolescents spontaneously or after exercise; results in loss of blood supply - may require surgery for relief. Results in RED infarction - blood can get in but cannot drain (low pressure venous return is blocked off)
What is hydrocele?
Accumulation of clear or straw colored fluid within the tunica vaginalis sac that encloses the testis - causes scrotal enlargement. May occur following infection. Use transillumination to differentiate between this and varicocele.
What is varicocele?
In young men 15-25 and up - common. Abnormal dilation of the venous plexus (drainage) of the testis - varicose veins of the testis and spermatic cord, caused by obstruction somewhere above the dilation - "bag of worms".
What are common infections in younger men?
older men?
younger men - STDs
older men - UTIs - urinary retention
What are common STDs?
herpes virus, Treponema pallidum, Neisseria gonorrhea, Chlamydia tachomatis.
Other infections?
Ureoplasma urealiticum, E. coli, proteus, mumps
Tumors of the testis...
-are derived from the germ cell.
-90% cure rate
-cryptorchidism is most important predisposing condition
30-40 yr olds
Where do tumors of the testis metastasize to?
to periaortic arch, lymph nodes in the abdomen, then to upper abdomen, through the blood to liver, lungs, brain.
Germ Cell Tumors
-from germ cells
-neoplastic germ cell (CIS -carcinoma insitu)
-5-20 yr latency

next stage is either 1) seminoma or 2)neoplastic embryonic cell
4 fates of germ cell tumors:
1. normal germ cell --> neoplastic germ cell (CIS) --> seminoma (malignant)
or
2. normal germ cell --> neoplastic germ cell (CIS) --> neoplastic embryonic cell --> tertaocarcinoma (malignant)
or
3. normal germ cell --> neoplastic germ cell (CIS) --> neoplastic embryonic cell --> embryonal carcinoma (malingnant)
or
4. normal germ cell --> neoplastic germ cell (CIS) --> neoplastic embryonic cell --> tertatoma (benign)
What is a seminoma?
tumor cells retain features of primitive promordial germ cells and lymphocytes and macrophages infiltrate the tumor - inflammation!
-present as firm, intratesticular mass, painless enlargement
-yellow and lobulated
-remain localized, 90% cure rate, good prognosis
What is a neoplastic embryonic cell?
Derived from neoplastic germ cell (CIS), they acquire characteristics of embryonic cells
-appear spontaneously in testis or ovary - can form any tissue type!
give rise to:
teratoma - benign
teratocarcinoma - malignant
embryonal carcinoma - malignant
What is a teratoma?
all neoplastic cells become fully differentiated into benign cells; localized to the testis
-form hair, teeth, etc.
-pure form in adult male very rare
-more common in children, but rare
-pure form fairly common in ovary
What is an embryonal carcinoma?
-appear grossly as vareigated and necrotic w/areas of hemorrhage
-more aggressive than seminomas - metastasize early
-60% of patients present with advanced disease
-peaks at age 30
-surgery and chemo: 5 yr survival rate of 85%
(Lance Armstrong)

derived from neoplastic embryonal cells; descended from spontaneously active male germ cells but totally undifferentiated
(the pure forms are rare and more aggressive)
What is a teratocarcinoma?
malignant lesion
-descended from spontaneously active male germ cells (neoplastic embryonic cells)
-hCG and AFP serum positive because they contain neoplastic placental hCG and neoplastic yolk sac cells (AFP)
What are the clinical symptoms of a testicular tumor?
pain - not always
with or without enlargement of testis
self exam crucial for early detection
What is benign prostate hyperplasia (BPH)?
-common, anytime after age 50
-#1 cause of prostate enlargement of men 50-60
-hyperplasia with resultant enlargement of the transitional zone of the prostate compresses the urethra and makes urination difficult
-S&S: urge to void, weak stream, increased frequency
*prone to UTI (urinary retention)
What is the pathogenesis of BPH?
-only within intact testis (not with castration)
-linked to testosterone
-dihydrotestosterone accumulates
-increased estrogen with age may contribute

*does not occur in males with genetic defect of lack of 5 alpha reductase deficiency
What drug is used to treat BPH?
-Proscar (finesteride) - to lower DHT levels so prostate shrinks
-TURP - transurethral resection of prostate performed through urethra; prostate is removed via electrocautery so patient can urinate
Prostate Cancer
-most common cancer in males
-no adequate treatment for metastasis


*does not develop in males castrated prior to puberty
What is the etiology of prostate cancer?
hormones permit the growth of the malignancy but are not root cause

*increased consumption of fat is linked with development of prostate cancer
What is the pathology of prostat cancer?
-poor blood supply and slow growing tumors mean chemo is not very effective
-malignant cells produce prostate specific antigen which can be detected in the serum

*** elevated serum alkaline phostphatase indicates bone metastases
what are the clinical features?
-older men
-grow in peripheral zone
-little urinary problems early
-asymptomatic
-digital rectal exam, baseline in males over 40
-PSA used to monitor but not 100% effective (prostatitis can also raise)
-grows slowly
What are survival rates?
-if tumor is limited to prostate, 5 yr survival is 75%
-with spread, it is 35-50%T
Treatement of prostate cancer:
surgery, radiotherapy, hormonal manipulations.
early stage: 90% of patients live 15 years
-advanced: 10-40% live 10 years - orchiectomy or hormone Tx to reduce testosterone
Major diseases of the female reproductive system:
-infections - inflammations
-hormonal disorders
-benign and malignant tumors
-disorders r/t pregnancy
What is pelvic inflammatory disease (PID)?
-a complicatio to genital inflammation, all female organs involved, fallopian tubes bear the brunt with scarring and blockage.
-severe and sudden lower abd pain, fever, nausea, discharge, bleeding -->peritonitis

-ascending - acquired sexually, complications of pregnancy, medical procedure

-descending - systemic or lymphatic
Neoplasia in females:
-common
-gynecologic malignant lesions for 15% of all malignant tumors
-10% of all cancer deaths in women - significant source of morbidity and mortality
What is etiology carcinoma of the cervix?
-risk factors - sexual activity, multiple sex partners, HPV infection, STDs
-originates in transition zone
What is the transition zone of the cervix?
An area of high celllular proliferation between the squamous epithelium of the cervix and columnar epithelium of the endometrium
What is the first step in the neoplastic process of carcinoma of the cervix?
CIN - cervical intraepithelial neoplasia - dysplasia (abnormalities) of squamous cells --> progresses to invasive squamous cell cancer
50% of all cervical lesions contain
HPV - human papilloma virus
Insitu refers to...
CIS - carcinoma insitu means a malignancy has not pierced the basement memrane and invaded surrounding tissue.
Clinical features of CIN
cervical intraepithelial neoplasia
-peaks at age 35
-no or very little symptoms

advanced cases:
-invasive carcinoma peaks at 50
-bloody discharge
-invade bladder, rectum, abd, thoracic

**PAP smear to detect
Squamous cell carcinomas are...
highly proliferative.
What are tumors of the uterus?
endometrial carcinoma
lyeiomyoma
others (very rare)
What is endometrial carcinoma?
-2nd most common tumor of female genital tract
-adenocarcinoma - makes gland-like stuctures
-postmenopausal women
What is the etiology and pathogenesis of endometrial carcinoma?
-exogenous estrogen supplementation (but lowered risk if progesterone is supplemented also, for 2 weeks per cycle)
-family Hx
What is the pathology and clinical features of endometrial carcinoma?
-adenocarcinoma
-grade 1(well-differentiated) to grade 3 (poorly differentiated)
-staged I to IV (characterizes spread)
-older women
-vaginal bleeding
-surgical resection
What is a leiomyoma?
-most common uterine tumor considered benign
-benign tumors originating from smooth muscles of the myometrium (fibroids)
-low potential for malignancy - leiomyosarcoma
-small tumors are resected
-lardge tumors - hysterectomy
What is endometriosus?
-foci of endometrial tissue that forms tumor-like nodules OUTSIDE THE UTERUS
-foci composed of uterine glands and stroma
-respond to estrogen and proliferation --> inflammatory response --> cycle, bleeding occurs
What is the long-term effect of endometriosus?
-transforms tissue into fibrotic scars and can cause abdominal adhesions
-pelvic pain
-occurs in 15-20% of all women of reproductive age
What is an ovarian neoplasm?
-both benign and malignant
In the neoplasms that origiante from 3 types:
surface epithelial cells
sex cord cells
germ cells
What are surface epithelial tumors?
Ovarian neoplasms
type: surface epithelial tumor
-serous
-mucinous
What are sec cord cells?
Ovarian neoplasms:
type sex cord cells
-granulosa and thecal tumors
What are germ cell tumors?
teratoma (benign)
teratocarcinoma and embryonal carcinoma
What is the etiology of surface epithelial tumors?
-unknown
-some relationship between development and ovulation --> on the surface of the ovary a cyst ruptures releasing an egg --> can undergo inflammation and unwanted cell proliferation
What reduces the risk for surface epithelial tumors?
-having children (no ovulation for 9 mos)
-use of oral contraceptives that suppress ovulation
-family Hx - mutated genes BRCA1 BRCA2 (tumor suppressor genes)
surface epithelial tumors:
serous tumors
-75% of serous tumors are benign and unilateral in origin
-serous cystadenomas - clear fluid filled - cystlike
-affect older women

25% malignant
-serous cystadenocarcinoma frequently seeds the other ovary and peritoneal cavity - poor outcome
surface epithelial tumors:
mucinous tumors
-less common than serous

85% are benign mucinous cystadenoma - thick yellow mucous, cystic in appearance and unilateral in origin; rare before puberty or after menopause but common in middle aged women

15% are mucinous cystadenocarcinomas - malignant form - seed the peritoneal cavity - can be hugh
What are clinical symptoms of surface epithelial tumors?
-weakness, weight loss, cachexia from tumor cytokines (nausea, anorexia)
-mass lesion
-metastasis to liver, lungs, GI tract
What does mass lesion effect mean?
abdominal cavity is seeded and all peritoneal surfaces are covered with diffus nodules; tumors can be huge and secrete massive amounts of mucin or serous fluid
What are germ cell tumors of the ovary?
20% of all ovarian neoplasms
-teratomas
-teratocarcinomas
Germ cell tumors:
teratomas
-benign lesions
95% of all germ cell tumors
-occur in women under 25
-same activation of germ cells as in the male
-fully differentiated cells give rise to a teratoma
-hair, skin, teeth, brain, etc.
-softball size
Germ cell tumors:
teratocarcinomas
5% of ovarian neoplasms
-contain malignant embryonic and extra embryonic cells including placental elements
*hCG and AFP a serum marker
Germ cell tumors:
embryonal carcinoma
contain only 1 cell type --> decendants of spontaneously activated female germ cells
*hCG and AFP NEGATVIE
** VERY RARE
Pathology of pregnancy:
implantation
Ectopic pregnancy - extrauterine implantation can occur anywhere in abd cavity - usual fallopian tube or ovary
Causative factors of ectopic pregnancy
-PID with salpingitis and endometriosus
IUD' smay increase risk
Symptoms of ectopic pregnancy
severe abd pain about 6 weeks into pregnancy
+ pregnancy test

complications:
hemorrhae when rupture occurs -->rapid shock, acute abd
-ultrasound, laproscopy is helpful
Pathology of pregnancy:
placentation
abnormality with placenta late in development
-placenta accreta
-placenta previa
Pathology of pregnancy:
placentation - placenta accreta
deep penetration of placental tissue into the muscularis of the uterus, prevents normal shedding - serious condition
Pathology of pregnancy:
placentation - placenta previa
placement of placenta over the internal orifice of the cervix
Major diseases of the breast
tumors
hormonally induce diseases
inflammatory diseases
Benign Breast Alterations
fibrocystic change (middle-age women)
fibroadenomas (young women)
Benign Breast Alterations:
Fibrocystic change
-most common disorder of the breast
-50% of all women of childbearing age, peaks at age 40
-rarely develops after menopause
-hormone imbalances - excess estrogen, lack of progesterone (oral contraceptive decrease risk)
-cysts form, multifocal, bilateral - lumpy breast
-solitary cyst looks like breast cancer, but is not
Cysts associated with fribrocystic change:
appears on mammograms
want to biopsy
dystrophic calcification - associated with unresolved healing from inflammation
--> worry about malignancy

*cysts can rupture and promote fibrosis - unwanted cell proliferation; may become nodular and tender; dull, heavy pain

**in the ABSENCE OF PROLIFERATION, it is not an elevated risk for cancer

***PAIN mean INFLAMMATION which means PROLIFERATION
Benign Breast Alterations:
Fibroadenoma
fibrous and glandular proliferation, well-outlined, solid, encapsulated, freely movable lump
-15-40 age most common
-surgical removal
-can recur

*assoc. w/slight increase in cancer risk if also fibrocystic change, proliferation, and family Hx
Malignant tumors of the Breast
-2nd only to lung cancer deaths
-1/14 women develop (maybe 1/8)
Etiology and pathogenesis of breast cancer.
-unknown
-genetic factors: women, Hx, other ca, mutated genes (BRCA1 & 2, p53, HER2/neu)
-racial: asians less, AA-more *all things being equal
-hormonal: estrogen exposure (early menarche & late menopause), obesity, oral contra., # preg.
proliferative breast disease
Where does breast cancer usually develop?
upper outer quadrant of the breast
What slows breast cancer tumor growth?
antiestrogen Tx - tamoxifin
(it blocks the estrogen receptor)
What is the pathology of breast cancer?
Adenocarcinoma
classifed primarily at ductal, lobular, infiltrating ductal, or infiltrating carcinoma - 90% of all breast cancers

-feel a dimple, retraction of adjacent skin and nipple
-metastasis through lymphatics - 80% to axillary nodes
-distant metastasis to blood, lungs, liver, bone, brain , adrenals (travel path of estrogen back to adrenals)
What are the clinical features of breast cancer?
-mass lesion
-self-exam crucial (but recently reported as ineffectual?!!)
-mammography
Why would a needle or incisional biopsy be performed after mammography?
If mammography found a lump, to confirm/deny cancer.
Treatments for breast cancer:
surgical resection
chemotherapy
radiation

*sentinel node biopsy
Why would a sentinel node biopsy be perfomr during surgical resection for breast cancer?
To look for route of possible metastasis in lmyphatics.
If breast cancer cells found possess estrogen receptors, then...
antiestrogen therapy is initiated - tamoxifen
Why is tamoxifin not successful with AA women?
The are usually estrogen receptor negative to they cannot respond to tamoxifen.
What is survival rate for breast cancer?
10 yr survival rate is 50%
Mammography
-women age 40-50 get baseline, then yearly

*not appropriate due to false negatives?!!
What are the developmental stages of the life cycle?
periods of growth
maintenance
degeneration

LIFE SPAN:
Fetal development:
germinal
embryonic
fetal

Neonate
Infant
Early Childhood
Middle Childhood
Adolescence
Young Adult
Adult
Middle Age
Older Adult
Very Elderly Adult
Normal stages of fetal development:
germinal - conception to 2 weeks
embryonic - 2 to 8 weeks
fetal - week 9 to birth
What happens during the germinal - conception to 2 weeks?
ovum or zygote
hyperplasia (mitotic cell division)
morula - mass cells at 3 days in fallopian tube
blastocyst - differentiated morula 4 days later (58 cells)
-trophoblast - cells of the outer layer; secrete enzymes to digest endometrium (uterine wall) to implant, secrete hCG
-embryoblast - cells of the inner layer which develop into embryo
What happens to the ovum or zygote?
hyperplasia (mitotic cell division)
What happens to the morula?
mass cells at 3 days in fallopian tube (traveling)
What happens to the blastocyst?
differentiated from the morula 4 days later (58 cells)
-trophoblast
-embryoblast
What is the trophoblast?
cells of the outer layer; secrete enzymes to digest endometrium (uterine wall) to implant, secrete hCG
What is the embryoblast?
cells of the inner layer which develop into embryo
What happens during the embryonic period?
weeks 2 through 8
complete implantation of blastocyst
hyplerplasia
placenta form and function
early structural development of organs
form recognizable as human

embryoblast - germ layers become fetal organs, heart first to establish circulation
What happens during the fetal period?
GROWTH
wks 9-12: hyperplasia
wks 13-24: hyperplasia and hypertrophy
wk2 25 to birth: hypertrophy

bones harden
muscles develop
sex features at 4th mo
reflexes and movements at 20 wks
How is the placenta formed, what does it do?
chorionic villi (blastocyst) and endometrium (uterine wall) fuse
-exchange O2, waste, nutrients by diffusion and active transport
-produce estrogen and progesterone
-acts as an infection barrier
What are the fetal membranes?
chorion
amnion (secretes amniotic fluid)
What does the yolk sac do?
produces RBCs (not nutrition)
Characteristics of fetal circulation that change after birth:
ductus venosus
foramen ovale
ductus arteriosus
umbilical cord
*all disappear after birth
What are the maternal factors affecting biophysical fetal development?
ILLNESS:
HTN disorders - prepregnancy or during
Diabetes Mellitus - prepregnancy, gestational
Cardiac Disease - prepregnancy
Acute Fatty Liver of Pregnancy - during pregnancy
STDs - prepregnancy, pregnancy
HTN during pregnancy:
-10% of pregnancies
Sequelae
-ecplampsia (convulsions)
-CVAs
-cardiopulmonary insufficiency
-aspiration pneumonia
-premature separation of placenta
-infant growth retarded
-maternal death
-perinatal mortality
4 kinds of HTN assoc. w/ pregnancy:
1. Late or transient HTN - ONLY during pregnancy , during labor, disappears within 10 post delivery
2. Chronic HTN - before week 20 until after delivery
3. Pregnancy-induced HTN (PIH) - preeclampsia
eeclampsia (seizures)
4. HELLP syndrome - variant of PIH, hemolysis, elevated liver enzymes, low platelets
DM during pregnancy:
sequelae
infant mortality pre and post delivery
maternal mortality
spontaneous abortion
congenital deformities

*NO oral hypoglycemis during preg/nursing - only insulin
Cardiac disease during pregnancy:
exacerbates any underlying condition
What are fetal factors that effect fetal development?
placental anomalies:
placenta previa - covers cervix (bleeding)
abruptio placenta - separates
ectopic pregnancy
placental insufficiency

multiple gestation
What are environmental factors during pregnancy?
maternal nutrition:
overweight
underweight
adolescence
PICA
anemia
teratogens
Adaptations of a neonate:
intrauterine pulmonary adaptation - surfactant
extrauterine pulmonary adaptation - trigger breathing reflexes, thermal, sensory, chemical (CO2 up, O2 down, pH down)
extruterine circulatory adaptation - closures
extrauterine thermoregulation adaptation - evap, convec, conduc, radiation (head), brown fat, they don't shiver
physiological hyperbilirubinemia - RBC breakdown - fat soluble heme - yellow
What are 3 health problems of a neonate?
1. Low APGAR score
2. Birth Injuries:
caput succadaneum
cephalohematoma
skull fractures
clavicle fracture
stretch of brachial plexus
3. Congenital Malformations
What are 3 health problems of a premature infant?
1. birth before 37 weeks gestation
2. low birth weight
3. difficulties in extrauterine transition
What is RDS?
Respiratory Distress Syndrome - hyaline membrane disease, lack of surfactant.
What is IVH?
Intraventricular Hemorrhage - hypoxic-ischemic episode leading to cerebral hyperperfusion and ruption of weak vessels in germinal matrix.
What is NEC?
Necrotizing Enterocolitis - acquired; risk factors - birth asphyxia, umbilical artery cath., patent ductus arteriosus, polycythemia, enteral feeding, indomethacin, Vit. E, xanthines
Biophysical development of the infant:
3x birth weight by age 1
dentition
NM development
Sensory development - visual (depth) and hearing
What are major factors affecting development and health of the infant?
sleep (imbalance)
nutrition (and alterations in)
immunity and immunizations
What are health problems in infants?
SIDS
Accidents (leading COD)
Otitis Media - because of short, straight, eustachian tube with underdeveloped cartilage
Biophysical development and Major Factors affecting early childhood:
increased nutrition
accidents
control bodily functions
hearing/vision problems secondary to other factors
Biophysical development and Major Factors affecting middle childhood:
epiphyseal disk vulnerability
myelination and fine tuned developement of nerves, CNS
less GI upset
immunity - better health (tonsils, adenoids issue)
urinary system
cardiovascular system

factors affecting:
physical fitness
nutrition
allergy
learning disabilities
ADD
Biophysical development and Major Factors affecting adolescence:
rapid physical growth - more lean mass, CNS - more myelination, resp. - vital capacity, CV - up BP, Skin - sebaceous glands overactive, BMR - up, thyroid-up, puberty
intellectual growth
emotional growth
social development

*Risk taking behaviors
eating disorders
acne
accidents, suicide
substance abuse
sexuality
Biophysical development and Major Factors affecting adults:
young - 20-30
adult - 30-45
middle - 45-65
older - 65-85
very elderly - over 85

Lifestyle is the major influence on health

*use muscles or lose
*lose CNS nuerons - but make up w/experience and problem solving skills
*GI less acid, less amylase

*purpose of fitness is to postpone the inevitable
Theories of aging:
-programmed - genetic; absence of telomerase leads to shortened telomeres of chromosomes

-stochastic - accumulation of environmental hazards and random life events
Factors making the older adult susceptible to disease:
general
height
weight
body composition
Factors making the older adult susceptible to disease:
CNS
decreased nerve impulse rate conduction leads to lower BMR, ischemia, decreased nerve fiber temperature; mood changes, degeneration of BBB, slower reflexes, lose memory, less dexterity, less agility
Factors making the older adult susceptible to disease:
CV
anatomic changes
physiologic changes - slower conduction, less contractile, less catecholamines
arterial changes
venule changes

DISEASES:
HTN
atherosclerosis
TIAs
Stroke
CHF
orthostatic HTN
aneurysm
Factors making the older adult susceptible to disease:
Respiratory
increased infection - pneumonia, pulmonary edema
Factors making the older adult susceptible to disease:
GU
kidney - lower mass, volume, filtering, nephons

DISEASES:
pyelonephritis secondary to less fluid intake, diarrhea, HTN, drugs
bladder changes
reproductive changes
Factors making the older adult susceptible to disease:
GI changes
Musculoskeletal changes
wasting muscles
arthritis
porosis
joint changes
functional changes
falling
fractures
Factors making the older adult susceptible to disease:
Skin
injury - skin tears
cancer
Factors making the older adult susceptible to disease:
Sensory
vision- cataracts, focus, glaucoma
hearing - high frequencies are lost, sclerosis or atrophy of tympanic membrane, hair cell loss
taste - salt and sugar increas
smell
tactile
EXOPHTALMOS
Space occupying lesion causes eyeball protrusion

Causes:
Orbital tissue swelling or trauma
Tumors
Forward eye displacement of pituitary or hypothalamic origin
e.g. Grave’s disease
PROPTOSIS
Eyeball and eyelid protrusion

Affects lid closure
Delay or prevention complete closure
Dry cornea

If > 5mm protrusion, stretch optic nerve
ENOPHTHALMOS
Deep, sunken eyes
Associated with:
Malnutrition, starvation, loss fatty tissue
ANOPTHALMOS
Development defects first month fetus
Absence one or both optic orbits
MICROPTHALMOS
Growth defects last 3 mos. Gestation
Abnormally small eyes
Eyelids
Palpebrae - folds of skin
Tarsus - plate of dense CT that gives shape and:
1. Contains sebaceous gland – Meibomian gland
2. Aids opening of eyelid margins
3. Allow airtight closure lids and prevent tear dry
How are eyelids raised?
Levator palpebrae superioris that is innervated by occculomotor cranial nerve (CN III)
How are eyelids closed?
Orbicularis oculi muscle innervated by facial nerve (CN VII)
PTOSIS
drooping eyelid; weak levator muscle (open) and unopposed orbicularis oculi (close)

Cause: damage to cranial nerves
PSEUDOPTOSIS
Damage to sympathetic innervation from superior cervical ganglion to smooth muscle upper eyelid
Weakness orbicularis oculi
damage or trauma to facial nerve CN VII
ENTROPION
Turning IN of eyelid
Causes: Scarring of palpebral conjunctiva
Degeneration of fascial attachments to lower lid with aging

Eyelids can irritate
Surgical repair
ECTROPION
Causes: Relaxation of orbicularis oculi muscle due to CN VII weakness or aging

Leads to: tearing and ocular irritation, inflammation of cornea
Surgical repair
Blepharitis
bilateral inflammation of eyelid margins
Anterior Blepharitis
eyelid skin, eyelashes, associated glands
a.) seborrheic b. – associated with seborrhea (dandruff scalp or brow)
b.) staphylococcal b. – S. aureus, S. epidermidis

(S/S) Of lids, margins: Irritation, burning, red, itching
Posterior Blepharitis
Inflammation of eyelids secondary to problems with meibomian glands
Bacteria – staph

S/S: Swollen and red lids
Meibomian glands and orifices: inflamed, dilated, abnormal secretions
Mild entropion (roll out)
Frothy tears, greasy coating
Stye (hordeolum)
Microbe infection of sebaceous glands of eyelid
Internal and external
S/S: pain, red, swell
Chalazion
Granulotomous inflammation of meibomian glands
After internal stye

S/S: small, nontender nodule on up or low lid
Where and what are lacrimal glands and tears?
Superior and lateral to eyeball

Tears from: the lacrimal gland
Tears collect in: puncta and tear sac
Tears empty into nasal cavity: nasolacrimal duct

Tears cover cornea and conjunctival epithelium
Lubricate, antibacterial

1.5% NaCl, 98% H2O, lysozymes, IgA, IgG, IgE
Tear film forms 3 layers:
Superficial lipid from meibomian gland
Aqueous from lacrimal
Mucinous on cornea and epithelial cells
CONJUCTIVA
thin mucous membrane lines inner surface eyelids and anterior surface of eyeball
Dry Eyes – Keratoconjuctivitis sicca (dry eye syndrome)
1. Lacrimal gland
age decrease secretion
congenital disorder
infection
irradiation
damage to parasympathetic innervation of gland

2. Sjorgren’s syndrome (autoimmune disorder)
Systemic: Lymphocytes and plasma cells get in lacrimal glands or parotid glands

S/S: dry eye
Gritty and dry
Burning, itching, no tears, red, pain, photosensitivity
Difficulty blinking
Corneal ulceration- lead to scar, blindness

Treat: artificial tear, ointments
Dacryocystitis
Infection of lacrimal sac:
One eye
Secondary to obstruction of nasolacrimal duct

S/S: tear discharge, pain, swell, tenderness

Infants: failure of nasolacrimal ducts to open before birth
CONJUCTIVA
thin mucous membrane lines inner surface eyelids and anterior surface of eyeball
CONJUNCTIVITIS
(RED EYE) (PINK EYE)

Red eye is sign of conjunctivitis, corneal irritation, acute glaucoma

Inflammation of conjunctiva
Uni or bilateral

Causes:
Bacteria (systemic or external)
Virus
Allergies
Chemicals
Physical irritants
Radiant energy

S/S: Range from mild hyperemia with tearing to severe necrotizing

Redness, ocular discomfort, gritty, burning, tearing
Differential diagnostic cues for type of conjunctivitis:
Pain severe- usually means cornea problem

Itchy could mean allergy
Discharge or exudates possible

Watery: allergy,
foreign body, viral

Mucopurulant: bacterial, fungal

*No change vision because not affect cornea
INFECTIOUS CONJUNCTIVITIS
Hyperacute:

Bacterial:
Neisseria gonorhoeae
Neisseria meningitidis
Yellow-green drainage
Severe, then sight is threatened

Acute:

Bacterial:
Streptococcus pneumoniae
S. aurea
Haemophilis influenzae
Burning, tearing, mucpurulant or purulent discharges

Chronic
Bacterial staph species
VIRAL CONJUNCTIVITIS
Adenovirus
Unchlorinated pools, do not share eye make–up, towels, eye drops
Herpes virus
Enterovirus
CHLAMYDIA Trachomodis CONJUNCTIVITIS
Spread by genital secretions:
Birth – babies
Sex activities
Swim in unchlorinated pools
Opthalmia neonatorium
conjunctivitis:
< 1 month age
vaginal delivery
CHLAMYDIA Trachomodis, N. gonorrhea, Pseudomonas
ALLERGIC CONJUNCTIVITIS
Hay fever – seasonal allergic rhinoconjunctivitis
IgE mediated hypersensitivity
Bilateral
SCLERA
Tough, opaque, white, fibrous outer layer
CORNEA
Clear with layers
No vessels
Diffusion nutrients and O2 from sclera
Innervated by sensory neurons CN V (trigeminal)
DISORDERS OF CORNEA AND SCLERA: TRAUMA
abrasions – depends on layer(s)
Can regenerate epithelial layer, can have scar
Stroma damage- slow to heal, danger infection, scar
Bowmans membrane- scar and opacification

VISION: Opacities – light reduction
Scar disturbs refraction
DISORDERS OF CORNEA AND SCLERA: Keratitis
Inflammation of cornea
Most common cause of blindness or impaired vision

Causes:
Infections
Trauma
Ischemia
Defects in tearing
Interruption in sensory innervation (e.g. surgery, antichol.)
Scar tissue: blindness or vision impairment
DISORDERS OF CORNEA AND SCLERA: Ucerative Keratitis
Epithelium, stroma, or both destroyed
Causes:
Most common- Herpes Simplex 1
Other agents of conjunctivitis
Trauma
Extended wear contact lenses
DISORDERS OF CORNEA AND SCLERA: Nonulcerative Keratitis
all layers epithelium inflamed, but remain intact
Causes:
Syphilis
TB
Lupus Erythematosus
ABNORMAL CORNEAL DEPOSITS
hypercalcemia
Cystinosis- hypercholesterolemia associated cystine crystals
ARCUS SENILIS
Common degeneration
Gray, white infiltration from peripheral
May be linked to lipids via hyperlipidemia
No visual impairment
No treatment
AQUEOUS HUMOR
Intraocular pressure greater than atmospheric
Nutrition source
Metabolism for lens and posterior cornea
Produced by ciliary epithelium
Flow – Between lens and posterior iris to back of cornea
GLAUCOMA
Imbalance between aqueous production and outflow such that increase intraocular pressure.
Usually from impedance of aqueous outflow from anterior chamber

Pressure induced changes in retina
Pressure induced changes in optic nerve
Pressure induced corneal edema and opacification
Temporary or permanent vision impairment

*named for location of impedance to aqueous circulation
Closed angle (narrow angle) glaucoma
Anterior chamber narrow
Outflow impaired when iris thickens as a result papillary dilation

Inherited
Sudden and intermittent increase pressure
Dark, emotional upset, extensive dilation pupil

S/S:
Ocular pain
Blurred vision
Iridescent vision
Red eye
Corneal edema
Can have headache

Sleep, or anything that causes pupil constrict can help
Surgery correction
Primary open angle (wide-angle) glaucoma


(not assoc. w/dilation)
Most common
Increase pressure in absence of obstruction at the iridocorneal angle
Abnormal trabecular meshwork that regulates flow aqueous humor into canal of Schlemm

Risk factors:
> 40 yrs
Diabetes Mellitus
Family history
Myopia

S/S- often asymptomatic
Chronic
ROUTINE screening for detection

Treatment is various pharmacological interventions
CATARACTS
Lens becomes opaque

Risk factors:
Age
Genetics
Environmental
Metabolic (e.g. CHO with diabetes)
Drug ADRs
Injury

TYPES:
Trauma - foreign body, blunt trauma
Congenital – from birth
Senile – most common kind
Gradual
Metabolic
Formation and dehydration of fibers in cortical zones of lens

S/S:
Blurred vision
Visual distortion – near and far

Correct by surgical replace lens
DISORDERS OF RETINA
Painless because no sensory neurons
Does not cause redness eye
Vision impairment across spectrum

RETINITIS PIGMENTOSA
BLOOD SUPPLY
RETINOPATHIES
RETINAL DETACHMENT
MACULAR DEGENERATION
DISORDERS OF RETINA:
RETINITIS PIGMENTOSA
Hereditary
Slow degeneration retinal receptor
Rod destruction
Range from night blindness to disrupted full time
DISORDERS OF RETINA:
RETINOPATHIES
Disorders of retinal vessels that lead to:
micoraneurysms
neovascularization
Hemorrhage
Formation of retinal opacities

Causes:
Diabetic retinopathy
Hypertensive retinopathy
Atherosclerosis retina vessels
Rentinopathy of Prematurity (prem. Infant)
DISORDERS OF RETINA:
RETINAL DETACHMENT
separation of the sensory retinal neurons/tissue from the pigment epithelium
DISORDERS OF RETINA:
MACULAR DEGENERATION
Leading cause blindness >75 yr
Destructive changes of the yellow pigmented area surrounding central fovea.
Results from vessel disorders
Loss of central vision
Bilateral
Progressive
Not sure exact cause
Vision
REFRACTION

ACCOMODATION - Lens flexibility

HYPEROPIA - Farsightedness

MYOPIA - Nearsightedness
PRESBYOPIA
Changes in vision due to aging
Additional fibers added to outermost portion lens
Thickens, less elastic
Range accommodation decrease (can not make convex shape)
ASTIGMATISM
Non uniform curvature of refractive medium
Horizontal vs. Vertical
Lens, Retina, Cornea
EAR
External ear – conduct sound waves to tympanic membrane
Middle ear- air filled, bony structures transmit sound vibration
Inner ear- fluid filled chamber, sensory hair cells
DISORDERS EXTERNAL EAR
Impact sound conduction

1. IMPACTED CERUMEN (ear wax)
reversible

2. OTITIS EXTERNA
Inflammation range from mild eczematoid dermitis to severe cellulites
Infection, trauma
Swimmer’s ear
Dermatoses

3. PRURITIS
External and internal ear canal
Cleaning that is too rough
EUSTACIAN TUBE (auditory tube)
Between nasopharynx and middle ear

Ventilation
Equalize air pressure of middle ear with ambient P
Protect middle ear from nasopharyngeal sound waves and secretion
Drain middle ear secretions into nasopharynx
DISORDERS OF MIDDLE EAR and EUSTACIAN TUBE (auditory tube)
1. ABNORMAL EUSTACIAN TUBE
2. BAROTRAUMA
3. OTITIS MEDIA (OM)
ABNORMAL EUSTACIAN TUBE
Pathogenesis for ear infections
Abnormal patency- not close or close completely
Obstruction:
Functional- persistent collapse
Mechanical – internal obstruction, external obstruction
BAROTRAUMA
Can not equalize pressure between middle ear and ambient

Usually from change in elevations
ACUTE Negative Middle Ear Pressure:
Increasing elevation is decreasing ambient P
Collapse of eustacian tube
Blockage of air flow into middle ear
Middle ear has low P
Hearing loss and discomfort

Reverse by: Swallow, yawn, chew gum,
Aggravated by congestion
OTITIS MEDIA (OM)
Infection with fluid increase

Associated with young children:
Eustacian tube short, wider, more horizontal
Does not drain well
Allows fluid flow into middle ear – infection spread
ACUTE OTITIS MEDIA (AOM)
alone or with systemic infection
Primarily bacterial
Some virus
Earache, fever, hearing loss, rhinorhea

Hearing loss due to fluid, can be reversed
Hearing loss due to tympanic or other damage can be permanent
Recurrent OM
3 new AOM episodes within 6 months or 4 episodes in 1 yr

each of above concurrent with URTI

Need to rule out:
Anatomical variations (e.g. adenoids)
Immune disorders

Consider prevention strategies
Vaccine for pneumococcal and influenza
OM with Effusion (OME)
Tympanic membrane OK
Fluids but NO infection
Serous, nonsupperative
3wks – 3mos to resolve (usually on own)

Difficult to differentiate from AOM in children

Treatment not specific- Antibiotics, corticosteroids.
Not decongestants
DISORDERS OF INNER EAR
TINNITUS
HEARING LOSS
VESTIBULAR FUNCTION:
NYSTAGMUS
VERTIGO
MOTION SICKNESS
DISORDERS OF INNER EAR:
TINNITUS
constant, intermittent
bilateral or unilateral
rings, hiss, roar, buzz, hum

Causes:
Drugs
Impacted cerumen

Objective- other people can hear the noise that triggers
Neuromuscular disorders
Vascular disorders

Subjective – no one else can hear a noise
Not sure of causes
Abnormal auditory receptor firing
Cochlear neurotransmitter dysfunction
Central processing

Tinnitus can be symptom of some other disease

Maybe associated with hearing disorder
DISORDERS OF INNER EAR
Presbycusis- aging
VESTIBULAR FUNCTION
Vestibular receptive organs inner ear
b. connect to CNS

The combination of “a” and “b” leads to reflex activity necessary for posture and movement with respect to gravity and movement

Balance

Tied to visual and proprioceptive (position) sensory systems
DISORDERS OF VESTIBULAR FUNCTION
Peripheral- labyrinth
Central – vestibular connections
DISORDERS OF VESTIBULAR FUNCTION: NYSTAGMUS
Vestibulo-ocular reflexes in response to head rotation;
Involuntary rhythmia and oscillatory eye movements that allow fixation of eye on stable object while the head moves
DISORDERS OF VESTIBULAR FUNCTION: VERTIGO
Illusion of movement;
Spinning, “to and fro”, fall

Vertigo is NOT same as lightheadedness, faintness, syncope
Objective vertigo
stationary person/environment in motion
Subjective vertigo
person in motion/environment is stationary
DISORDERS OF VESTIBULAR FUNCTION: MOTION SICKNESS
Form of normal physiological vertigo
Repeated rhythmic stimulus of vestibular system
Car, boat, plane, more

S/S:
Vertigo, malaise, Nausea, vomit
ANS: decrease BP, increase HR, sweat
Hyperventilation

Feel movement after stop the action
Prevent by visual focus on stable environment
What does exercise do?
triggers physiological adaptation.
Acute adaptation and continues over time.
Long-term adaptations from exercise:
increased BMR
stabilize posture
increase #insulin receptors
equalize calories in = calories out
increase max VO2 capacity
Conditioned person:
returns to normal within 60-90 sec of work.
Unconditioned person:
takes 5-10 minutes.
ACTIVITY
Process of energy expenditure in order to do something involved with daily living
REST
Inactivity with least amount of energy expended
EXERCISE
Activity that uses more energy for the purpose of physiological conditioning
Included in the “lifestyle improvement” strategy
BENEFITS OF EXERCISE
Treat Disease
Prevent Disease
Weight Management
Overall conditioning
Mental Well-being
Increase reserve of fitness for periods of illness
TYPES OF EXERCISE
Aerobic
Anaerobic
Resistance (isometric)
Cardiovascular Response to Exercise
Increase HR, SV leads to Increase CO
Increase Arterial BP
Increase Systolic BP
Minimal change diastolic BP due to vessel dilation

HOW?
SNS, Hormonal, Intrinsic (RA stretch receptors, Frank-Starling)
Pulmonary Response to exercise
Open pulmonary capillary vessels in alveolar beds
CO2/O2 exchange

Pulmonary ventilation
Increase Respiratory rate
Increase tidal volume to increase minute ventilation

Chemical sensors
Neuromuscular Response to exercise
Muscle strength
Flexibility
Endurance

Slow twitch
More energy efficient
Less overall force
Endurance
Large muscle groups

Fast twitch
High intensity
Anaerobic metabolism
Smaller muscle groups
Large forces

Increase blood flow
Vasodilation muscle
Vasoconstriction in organs not essential

Hypertrophy
Increase protein
Increase mitochondria
Increase O2 efficiency
Metabolic Response to exercise
Short term and intense for 1-2 min
ATP
Creatine P

Longer 3-40 min
Glycogen muscle
Creatine P

Intense > 40 min
Glycogen muscle
FA

Diet – 55% complex CHO, 30% fat, 15% protein
Water
Electrolytes
Thermal Response to exercise
Direct blood flow to skin
Skin vessels dilate
Sweat
Plasma protein shift interstitial to vascular
Osmotic P increase to maintain blood circulation
GI response to exercise
Decrease in Motility, Secretions, absorption
May have cramping, urge to defecate, diarrhea
Hemostasis response to exercise
EPI leads to increase fibrinolytic activity
*So, decrease coagulation
Immune response to exercise
Not clear
Maybe moderate and regular exercise is beneficial, while higher intense may be harmful
ASSESSMENT ACTIVITY TOLERANCE
1. Human Activity Profile
94 activity list
Person designates whether able to perform or has stopped performing

2. Fatigue Severity Scale
9 statements
Person rate each on a scale(1-7) of degree of agreement

3. Ergometers
Bicycle
Treadmill

Physiological response
HR (220- age = max)
85-90%
BP
MET (Metabolic Equivalents) 1= rest
Subjective assessment
Perceived exertion scale
ACTIVITY INTOLERANCE
Unable to complete necessary or desired daily activity due to insufficient physical or mental energy and endurance

Major factors why:
1. Overall physical condition
level of fatigue, pain, disease, deconditioning
2. Psychosocial
3. Lifestyle - obesity, smoking, lack of regular exercise
Mechanisms of Fatigue
Can be normal and expected
Can be associated with disease or other abnormal states
Mental or emotional stress
Physical stressors
ACUTE PHYSICAL FATIGUE
Rapid onset
Normal response to activity
Relieved upon cessation of activity
Protective mechanism

Affected by degree of physical conditioning
CHRONIC FATIGUE
Insidious onset
Perceived as relatively intense compared to activity
Long lasting (> 1 month)
Not protective in function

Limits amount of activity potential
May affect quality of life
May affect employment
The lifestyle changes may trigger depression
(note: some depressions, trigger fatigue S/S)
CHRONIC FATIGUE SYNDROME
unknown etiology
complicated to diagnose
cold-like symptoms

Tx: individual
relapses are unpredictable
ANTIGRAVITY EFFECTS OF BED REST
Supine position leads to deconditioning
Loss of gravity on physiological conditioning
ALLOPATHIC MEDICINE
all methods of proven value in the treatment of disease
Western medicine
TRADITIONAL MEDICINE
complementary and alternative
used by 65-85% of world population
historical
ALTERNATIVE MEDICINE
modalities used in place of conventional (allopathic)
not widely taught in U.S. med schools
limited availability in U.S. hospitals
COMPLEMENTARY MEDICINE
use of "unconventional" modalities to complement the modalities of traditional medicine
INTEGRATIVE MEDICINE
Andrew Weil term
hybrid of complementary and conventional modalities that are perceived to be synergistic

primarily herbal, manipulation, Ayurvedic combined with modalities such as antibiotics and surgery
CAM
Complementary and Alternative Medicine
general areas:
chemical
mind/body (behavioral)
manual healing
lifestyle changes
CHEMICAL
Herbals
Supplements
Megavitamins
Off-Label use of Pharmaceuticals
Homeopathy
Aromatherapy
MIND BODY MODALITIES
Aromatherapy
Biofeedback
Dance therapy
Guided imagery
Hypnotherapy
Meditation
Tai Chi
Yoga
Prayer (spiritual)
Visualization
Energy medicine

note: exercise is not considered CAM
ENERGY MEDICINE
Reiki
Qigong
Therapeutic touch (also called healing touch)
Acupuncture
Craniosacral therapy
Pranic Healing
Homeopathy
Shen
Magnet therapy
Polarity
Core energetics

Harmful if people do not get the medical help they need
$$$$
MANUAL THERAPY
Accupressure/Shiatsu
Applied Kinesiology
Chiropractic
Massage therapy
Deep Tissue Massage
Rolfing
Myofascial release
Neuromuscular massage
Osteopathy
Reflexology
Therapeutic touch (energy healing)
diagnostic or therapeutic
Reiki

Conventional Physical therapy
LIFESTYLE CHANGES
Specialized diets
Exercise
Herbal medicine
pharmacologic use
European, Asian, Native American (North/South)
Diet, nutrition, and lifestyle changes
supplements, vitamins, minerals, food
effects chronic disease and preventive
Mind/body or behavioral interventions
biofeedback psychotherapy
relaxation prayer
imagery
mental healing art
mediation dance
hypnosis music therapy
yoga
Alternative systems of medical practice
traditional Oriental medicine
Ayurveda (Indian; diet, exercise, mediation)
homeopathy
naturopathic medicine
environmental medicine
community-based health care (e.g. shamanic)
Manual healing
osteopathy physical therapy
massage therapy therapeutic touch
chiropractic
Bioelectromagnetics
living organisms interact with electromagnetic fields
used for wound healing, bone repair, immune system stimulation, pain
Pharmacologic and biologic treatments
drugs and vaccines not accepted by mainstream medicine

off-label
usually require a licensed provider
e.g. chelation therapy
WHY SHOULD YOU LEARN ABOUT CAM?
Your patients are paying others for CAM with or without your knowledge/endorsement
Many CAM practitioners are not certified, licensed
Your knowledge could provide patient safety
If you understand the CAM modality your patient receives, you may be more helpful to your patient when you determine it is not helping or even hurting them.
You will be more confident in your referrals
You may decide to incorporate CAM modalities into your practice
Fee for service
more competitive with non CAM practitioners
as an allopathic practitioner, give credibility to the unregulated "CAM world"
WHICH CAM MODALITIES ARE MOST COMMON USED IN ACUTE CARE?
massage
chiropractic
herbs/supplements
THERAPEUTIC TOUCH
Use of hands ON or NEAR the body
Practitioner has conscious intent to help or heal
Procedure basics:
Physical and psychological centering of oneself
assess subject's energy field differences
vibration, tingling, quieting, blocking, denseness, flowing, pain, pressure, pulsation, temperature
unruffling the field
modulation of energy to balance
HEALING TOUCH (Therapeutic touch)
Energy-based technique to balance and align the human energy field
Practitioner facilitates the patient's own self-healing process by energetically activating the body-mind-spirit connection
incorporates therapeutic touch
The practitioner may have some "intent" to assess and heal. This is not always clearly defined in textbook descriptions.
REIKI
Universal life-force (energy)
ancient hands on or distance healing
practitioner does not have to diagnose energy imbalances or have specific intent of realigning energy fields –therefore, easy to integrate while doing other tasks
Given enough time and experience, the practitioner has the option to diagnose energy imbalances or have specific intent of realigning energy fields.
recipient responsible for own (often without awareness) healing
the practitioner is conduit to universal life force energy and the recipient's body "takes" what is needed for healing.
May be performed with hands on or off the client
HOW SHOULD YOU INCORPORATE CAM MODALITIES?
Research the pro/cons for what interests you
Consider mind/body/spirit triad and select a modality from a component different than your current training.
Meet a practitioner in the area of your interest
Experience the modality yourself!
Take the best quality and highest level of training possible
Obtain credential or license