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247 Cards in this Set
- Front
- Back
What is cryptorchidism?
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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 |
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What is hypospadias?
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congenital malformation of the urethral opening on the dorsal surface of the penis; failure to fuse
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What is epispadias?
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congenital malformation of the urethral opening on the ventral surface of the penis.
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What is the pathogenesis of hypospadias and epispadias?
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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.
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What is torsion of the testes?
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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)
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What is hydrocele?
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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.
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What is varicocele?
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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".
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What are common infections in younger men?
older men? |
younger men - STDs
older men - UTIs - urinary retention |
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What are common STDs?
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herpes virus, Treponema pallidum, Neisseria gonorrhea, Chlamydia tachomatis.
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Other infections?
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Ureoplasma urealiticum, E. coli, proteus, mumps
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Tumors of the testis...
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-are derived from the germ cell.
-90% cure rate -cryptorchidism is most important predisposing condition 30-40 yr olds |
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Where do tumors of the testis metastasize to?
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to periaortic arch, lymph nodes in the abdomen, then to upper abdomen, through the blood to liver, lungs, brain.
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Germ Cell Tumors
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-from germ cells
-neoplastic germ cell (CIS -carcinoma insitu) -5-20 yr latency next stage is either 1) seminoma or 2)neoplastic embryonic cell |
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4 fates of germ cell tumors:
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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) |
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What is a seminoma?
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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 |
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What is a neoplastic embryonic cell?
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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 |
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What is a teratoma?
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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 |
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What is an embryonal carcinoma?
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-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) |
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What is a teratocarcinoma?
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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) |
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What are the clinical symptoms of a testicular tumor?
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pain - not always
with or without enlargement of testis self exam crucial for early detection |
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What is benign prostate hyperplasia (BPH)?
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-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) |
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What is the pathogenesis of BPH?
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-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 |
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What drug is used to treat BPH?
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-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 |
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Prostate Cancer
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-most common cancer in males
-no adequate treatment for metastasis *does not develop in males castrated prior to puberty |
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What is the etiology of prostate cancer?
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hormones permit the growth of the malignancy but are not root cause
*increased consumption of fat is linked with development of prostate cancer |
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What is the pathology of prostat cancer?
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-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 |
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what are the clinical features?
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-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 |
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What are survival rates?
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-if tumor is limited to prostate, 5 yr survival is 75%
-with spread, it is 35-50%T |
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Treatement of prostate cancer:
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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 |
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Major diseases of the female reproductive system:
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-infections - inflammations
-hormonal disorders -benign and malignant tumors -disorders r/t pregnancy |
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What is pelvic inflammatory disease (PID)?
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-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 |
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Neoplasia in females:
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-common
-gynecologic malignant lesions for 15% of all malignant tumors -10% of all cancer deaths in women - significant source of morbidity and mortality |
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What is etiology carcinoma of the cervix?
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-risk factors - sexual activity, multiple sex partners, HPV infection, STDs
-originates in transition zone |
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What is the transition zone of the cervix?
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An area of high celllular proliferation between the squamous epithelium of the cervix and columnar epithelium of the endometrium
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What is the first step in the neoplastic process of carcinoma of the cervix?
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CIN - cervical intraepithelial neoplasia - dysplasia (abnormalities) of squamous cells --> progresses to invasive squamous cell cancer
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50% of all cervical lesions contain
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HPV - human papilloma virus
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Insitu refers to...
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CIS - carcinoma insitu means a malignancy has not pierced the basement memrane and invaded surrounding tissue.
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Clinical features of CIN
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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 |
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Squamous cell carcinomas are...
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highly proliferative.
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What are tumors of the uterus?
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endometrial carcinoma
lyeiomyoma others (very rare) |
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What is endometrial carcinoma?
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-2nd most common tumor of female genital tract
-adenocarcinoma - makes gland-like stuctures -postmenopausal women |
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What is the etiology and pathogenesis of endometrial carcinoma?
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-exogenous estrogen supplementation (but lowered risk if progesterone is supplemented also, for 2 weeks per cycle)
-family Hx |
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What is the pathology and clinical features of endometrial carcinoma?
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-adenocarcinoma
-grade 1(well-differentiated) to grade 3 (poorly differentiated) -staged I to IV (characterizes spread) -older women -vaginal bleeding -surgical resection |
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What is a leiomyoma?
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-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 |
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What is endometriosus?
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-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 |
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What is the long-term effect of endometriosus?
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-transforms tissue into fibrotic scars and can cause abdominal adhesions
-pelvic pain -occurs in 15-20% of all women of reproductive age |
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What is an ovarian neoplasm?
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-both benign and malignant
In the neoplasms that origiante from 3 types: surface epithelial cells sex cord cells germ cells |
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What are surface epithelial tumors?
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Ovarian neoplasms
type: surface epithelial tumor -serous -mucinous |
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What are sec cord cells?
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Ovarian neoplasms:
type sex cord cells -granulosa and thecal tumors |
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What are germ cell tumors?
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teratoma (benign)
teratocarcinoma and embryonal carcinoma |
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What is the etiology of surface epithelial tumors?
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-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 |
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What reduces the risk for surface epithelial tumors?
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-having children (no ovulation for 9 mos)
-use of oral contraceptives that suppress ovulation -family Hx - mutated genes BRCA1 BRCA2 (tumor suppressor genes) |
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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 |
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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 |
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What are clinical symptoms of surface epithelial tumors?
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-weakness, weight loss, cachexia from tumor cytokines (nausea, anorexia)
-mass lesion -metastasis to liver, lungs, GI tract |
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What does mass lesion effect mean?
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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
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What are germ cell tumors of the ovary?
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20% of all ovarian neoplasms
-teratomas -teratocarcinomas |
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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 |
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Germ cell tumors:
teratocarcinomas |
5% of ovarian neoplasms
-contain malignant embryonic and extra embryonic cells including placental elements *hCG and AFP a serum marker |
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Germ cell tumors:
embryonal carcinoma |
contain only 1 cell type --> decendants of spontaneously activated female germ cells
*hCG and AFP NEGATVIE ** VERY RARE |
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Pathology of pregnancy:
implantation |
Ectopic pregnancy - extrauterine implantation can occur anywhere in abd cavity - usual fallopian tube or ovary
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Causative factors of ectopic pregnancy
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-PID with salpingitis and endometriosus
IUD' smay increase risk |
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Symptoms of ectopic pregnancy
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severe abd pain about 6 weeks into pregnancy
+ pregnancy test complications: hemorrhae when rupture occurs -->rapid shock, acute abd -ultrasound, laproscopy is helpful |
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Pathology of pregnancy:
placentation |
abnormality with placenta late in development
-placenta accreta -placenta previa |
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Pathology of pregnancy:
placentation - placenta accreta |
deep penetration of placental tissue into the muscularis of the uterus, prevents normal shedding - serious condition
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Pathology of pregnancy:
placentation - placenta previa |
placement of placenta over the internal orifice of the cervix
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Major diseases of the breast
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tumors
hormonally induce diseases inflammatory diseases |
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Benign Breast Alterations
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fibrocystic change (middle-age women)
fibroadenomas (young women) |
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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 |
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Cysts associated with fribrocystic change:
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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 |
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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 |
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Malignant tumors of the Breast
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-2nd only to lung cancer deaths
-1/14 women develop (maybe 1/8) |
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Etiology and pathogenesis of breast cancer.
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-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 |
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Where does breast cancer usually develop?
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upper outer quadrant of the breast
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What slows breast cancer tumor growth?
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antiestrogen Tx - tamoxifin
(it blocks the estrogen receptor) |
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What is the pathology of breast cancer?
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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) |
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What are the clinical features of breast cancer?
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-mass lesion
-self-exam crucial (but recently reported as ineffectual?!!) -mammography |
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Why would a needle or incisional biopsy be performed after mammography?
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If mammography found a lump, to confirm/deny cancer.
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Treatments for breast cancer:
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surgical resection
chemotherapy radiation *sentinel node biopsy |
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Why would a sentinel node biopsy be perfomr during surgical resection for breast cancer?
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To look for route of possible metastasis in lmyphatics.
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If breast cancer cells found possess estrogen receptors, then...
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antiestrogen therapy is initiated - tamoxifen
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Why is tamoxifin not successful with AA women?
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The are usually estrogen receptor negative to they cannot respond to tamoxifen.
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What is survival rate for breast cancer?
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10 yr survival rate is 50%
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Mammography
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-women age 40-50 get baseline, then yearly
*not appropriate due to false negatives?!! |
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What are the developmental stages of the life cycle?
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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 |
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Normal stages of fetal development:
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germinal - conception to 2 weeks
embryonic - 2 to 8 weeks fetal - week 9 to birth |
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What happens during the germinal - conception to 2 weeks?
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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 |
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What happens to the ovum or zygote?
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hyperplasia (mitotic cell division)
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What happens to the morula?
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mass cells at 3 days in fallopian tube (traveling)
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What happens to the blastocyst?
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differentiated from the morula 4 days later (58 cells)
-trophoblast -embryoblast |
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What is the trophoblast?
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cells of the outer layer; secrete enzymes to digest endometrium (uterine wall) to implant, secrete hCG
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What is the embryoblast?
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cells of the inner layer which develop into embryo
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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 |
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What happens during the fetal period?
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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 |
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How is the placenta formed, what does it do?
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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 |
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What are the fetal membranes?
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chorion
amnion (secretes amniotic fluid) |
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What does the yolk sac do?
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produces RBCs (not nutrition)
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Characteristics of fetal circulation that change after birth:
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ductus venosus
foramen ovale ductus arteriosus umbilical cord *all disappear after birth |
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What are the maternal factors affecting biophysical fetal development?
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ILLNESS:
HTN disorders - prepregnancy or during Diabetes Mellitus - prepregnancy, gestational Cardiac Disease - prepregnancy Acute Fatty Liver of Pregnancy - during pregnancy STDs - prepregnancy, pregnancy |
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HTN during pregnancy:
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-10% of pregnancies
Sequelae -ecplampsia (convulsions) -CVAs -cardiopulmonary insufficiency -aspiration pneumonia -premature separation of placenta -infant growth retarded -maternal death -perinatal mortality |
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4 kinds of HTN assoc. w/ pregnancy:
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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 |
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DM during pregnancy:
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sequelae
infant mortality pre and post delivery maternal mortality spontaneous abortion congenital deformities *NO oral hypoglycemis during preg/nursing - only insulin |
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Cardiac disease during pregnancy:
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exacerbates any underlying condition
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What are fetal factors that effect fetal development?
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placental anomalies:
placenta previa - covers cervix (bleeding) abruptio placenta - separates ectopic pregnancy placental insufficiency multiple gestation |
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What are environmental factors during pregnancy?
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maternal nutrition:
overweight underweight adolescence PICA anemia teratogens |
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Adaptations of a neonate:
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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 |
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What are 3 health problems of a neonate?
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1. Low APGAR score
2. Birth Injuries: caput succadaneum cephalohematoma skull fractures clavicle fracture stretch of brachial plexus 3. Congenital Malformations |
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What are 3 health problems of a premature infant?
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1. birth before 37 weeks gestation
2. low birth weight 3. difficulties in extrauterine transition |
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What is RDS?
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Respiratory Distress Syndrome - hyaline membrane disease, lack of surfactant.
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What is IVH?
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Intraventricular Hemorrhage - hypoxic-ischemic episode leading to cerebral hyperperfusion and ruption of weak vessels in germinal matrix.
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What is NEC?
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Necrotizing Enterocolitis - acquired; risk factors - birth asphyxia, umbilical artery cath., patent ductus arteriosus, polycythemia, enteral feeding, indomethacin, Vit. E, xanthines
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Biophysical development of the infant:
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3x birth weight by age 1
dentition NM development Sensory development - visual (depth) and hearing |
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What are major factors affecting development and health of the infant?
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sleep (imbalance)
nutrition (and alterations in) immunity and immunizations |
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What are health problems in infants?
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SIDS
Accidents (leading COD) Otitis Media - because of short, straight, eustachian tube with underdeveloped cartilage |
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Biophysical development and Major Factors affecting early childhood:
|
increased nutrition
accidents control bodily functions hearing/vision problems secondary to other factors |
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Biophysical development and Major Factors affecting middle childhood:
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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 |
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Biophysical development and Major Factors affecting adolescence:
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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 |
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Biophysical development and Major Factors affecting adults:
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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 |
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Theories of aging:
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-programmed - genetic; absence of telomerase leads to shortened telomeres of chromosomes
-stochastic - accumulation of environmental hazards and random life events |
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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
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Eyeball and eyelid protrusion
Affects lid closure Delay or prevention complete closure Dry cornea If > 5mm protrusion, stretch optic nerve |
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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 |
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PSEUDOPTOSIS
|
Damage to sympathetic innervation from superior cervical ganglion to smooth muscle upper eyelid
|
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Weakness orbicularis oculi
|
damage or trauma to facial nerve CN VII
|
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ENTROPION
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Turning IN of eyelid
Causes: Scarring of palpebral conjunctiva Degeneration of fascial attachments to lower lid with aging Eyelids can irritate Surgical repair |
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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 |
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Blepharitis
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bilateral inflammation of eyelid margins
|
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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
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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 |
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CONJUCTIVA
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thin mucous membrane lines inner surface eyelids and anterior surface of eyeball
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CONJUNCTIVITIS
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(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 |
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Differential diagnostic cues for type of conjunctivitis:
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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 |
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INFECTIOUS CONJUNCTIVITIS
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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 |
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VIRAL CONJUNCTIVITIS
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Adenovirus
Unchlorinated pools, do not share eye make–up, towels, eye drops Herpes virus Enterovirus |
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CHLAMYDIA Trachomodis CONJUNCTIVITIS
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Spread by genital secretions:
Birth – babies Sex activities Swim in unchlorinated pools |
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Opthalmia neonatorium
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conjunctivitis:
< 1 month age vaginal delivery CHLAMYDIA Trachomodis, N. gonorrhea, Pseudomonas |
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ALLERGIC CONJUNCTIVITIS
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Hay fever – seasonal allergic rhinoconjunctivitis
IgE mediated hypersensitivity Bilateral |
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SCLERA
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Tough, opaque, white, fibrous outer layer
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CORNEA
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Clear with layers
No vessels Diffusion nutrients and O2 from sclera Innervated by sensory neurons CN V (trigeminal) |
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DISORDERS OF CORNEA AND SCLERA: TRAUMA
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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 |
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DISORDERS OF CORNEA AND SCLERA: Keratitis
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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 |
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DISORDERS OF CORNEA AND SCLERA: Ucerative Keratitis
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Epithelium, stroma, or both destroyed
Causes: Most common- Herpes Simplex 1 Other agents of conjunctivitis Trauma Extended wear contact lenses |
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DISORDERS OF CORNEA AND SCLERA: Nonulcerative Keratitis
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all layers epithelium inflamed, but remain intact
Causes: Syphilis TB Lupus Erythematosus |
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ABNORMAL CORNEAL DEPOSITS
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hypercalcemia
Cystinosis- hypercholesterolemia associated cystine crystals |
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ARCUS SENILIS
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Common degeneration
Gray, white infiltration from peripheral May be linked to lipids via hyperlipidemia No visual impairment No treatment |
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AQUEOUS HUMOR
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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 |
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GLAUCOMA
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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 |
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Closed angle (narrow angle) glaucoma
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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 |
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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 |
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CATARACTS
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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 |
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DISORDERS OF RETINA
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Painless because no sensory neurons
Does not cause redness eye Vision impairment across spectrum RETINITIS PIGMENTOSA BLOOD SUPPLY RETINOPATHIES RETINAL DETACHMENT MACULAR DEGENERATION |
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DISORDERS OF RETINA:
RETINITIS PIGMENTOSA |
Hereditary
Slow degeneration retinal receptor Rod destruction Range from night blindness to disrupted full time |
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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) |
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DISORDERS OF RETINA:
RETINAL DETACHMENT |
separation of the sensory retinal neurons/tissue from the pigment epithelium
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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 |
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Vision
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REFRACTION
ACCOMODATION - Lens flexibility HYPEROPIA - Farsightedness MYOPIA - Nearsightedness |
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PRESBYOPIA
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Changes in vision due to aging
Additional fibers added to outermost portion lens Thickens, less elastic Range accommodation decrease (can not make convex shape) |
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ASTIGMATISM
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Non uniform curvature of refractive medium
Horizontal vs. Vertical Lens, Retina, Cornea |
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EAR
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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 |
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DISORDERS EXTERNAL EAR
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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 |
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EUSTACIAN TUBE (auditory tube)
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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 |
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DISORDERS OF MIDDLE EAR and EUSTACIAN TUBE (auditory tube)
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1. ABNORMAL EUSTACIAN TUBE
2. BAROTRAUMA 3. OTITIS MEDIA (OM) |
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ABNORMAL EUSTACIAN TUBE
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Pathogenesis for ear infections
Abnormal patency- not close or close completely Obstruction: Functional- persistent collapse Mechanical – internal obstruction, external obstruction |
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BAROTRAUMA
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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 |
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OTITIS MEDIA (OM)
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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 |
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ACUTE OTITIS MEDIA (AOM)
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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 |
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Recurrent OM
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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 |
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OM with Effusion (OME)
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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 |
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DISORDERS OF INNER EAR
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TINNITUS
HEARING LOSS VESTIBULAR FUNCTION: NYSTAGMUS VERTIGO MOTION SICKNESS |
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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 |
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DISORDERS OF INNER EAR
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Presbycusis- aging
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VESTIBULAR FUNCTION
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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 |
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DISORDERS OF VESTIBULAR FUNCTION
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Peripheral- labyrinth
Central – vestibular connections |
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DISORDERS OF VESTIBULAR FUNCTION: NYSTAGMUS
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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 |
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DISORDERS OF VESTIBULAR FUNCTION: VERTIGO
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Illusion of movement;
Spinning, “to and fro”, fall Vertigo is NOT same as lightheadedness, faintness, syncope |
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Objective vertigo
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stationary person/environment in motion
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Subjective vertigo
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person in motion/environment is stationary
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DISORDERS OF VESTIBULAR FUNCTION: MOTION SICKNESS
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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 |
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What does exercise do?
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triggers physiological adaptation.
Acute adaptation and continues over time. |
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Long-term adaptations from exercise:
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increased BMR
stabilize posture increase #insulin receptors equalize calories in = calories out increase max VO2 capacity |
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Conditioned person:
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returns to normal within 60-90 sec of work.
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Unconditioned person:
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takes 5-10 minutes.
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ACTIVITY
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Process of energy expenditure in order to do something involved with daily living
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REST
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Inactivity with least amount of energy expended
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EXERCISE
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Activity that uses more energy for the purpose of physiological conditioning
Included in the “lifestyle improvement” strategy |
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BENEFITS OF EXERCISE
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Treat Disease
Prevent Disease Weight Management Overall conditioning Mental Well-being Increase reserve of fitness for periods of illness |
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TYPES OF EXERCISE
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Aerobic
Anaerobic Resistance (isometric) |
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Cardiovascular Response to Exercise
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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) |
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Pulmonary Response to exercise
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Open pulmonary capillary vessels in alveolar beds
CO2/O2 exchange Pulmonary ventilation Increase Respiratory rate Increase tidal volume to increase minute ventilation Chemical sensors |
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Neuromuscular Response to exercise
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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 |
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Metabolic Response to exercise
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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 |
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Thermal Response to exercise
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Direct blood flow to skin
Skin vessels dilate Sweat Plasma protein shift interstitial to vascular Osmotic P increase to maintain blood circulation |
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GI response to exercise
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Decrease in Motility, Secretions, absorption
May have cramping, urge to defecate, diarrhea |
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Hemostasis response to exercise
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EPI leads to increase fibrinolytic activity
*So, decrease coagulation |
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Immune response to exercise
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Not clear
Maybe moderate and regular exercise is beneficial, while higher intense may be harmful |
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ASSESSMENT ACTIVITY TOLERANCE
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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 |
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ACTIVITY INTOLERANCE
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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 |
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Mechanisms of Fatigue
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Can be normal and expected
Can be associated with disease or other abnormal states Mental or emotional stress Physical stressors |
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ACUTE PHYSICAL FATIGUE
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Rapid onset
Normal response to activity Relieved upon cessation of activity Protective mechanism Affected by degree of physical conditioning |
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CHRONIC FATIGUE
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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) |
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CHRONIC FATIGUE SYNDROME
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unknown etiology
complicated to diagnose cold-like symptoms Tx: individual relapses are unpredictable |
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ANTIGRAVITY EFFECTS OF BED REST
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Supine position leads to deconditioning
Loss of gravity on physiological conditioning |
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ALLOPATHIC MEDICINE
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all methods of proven value in the treatment of disease
Western medicine |
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TRADITIONAL MEDICINE
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complementary and alternative
used by 65-85% of world population historical |
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ALTERNATIVE MEDICINE
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modalities used in place of conventional (allopathic)
not widely taught in U.S. med schools limited availability in U.S. hospitals |
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COMPLEMENTARY MEDICINE
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use of "unconventional" modalities to complement the modalities of traditional medicine
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INTEGRATIVE MEDICINE
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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 |
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CAM
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Complementary and Alternative Medicine
general areas: chemical mind/body (behavioral) manual healing lifestyle changes |
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CHEMICAL
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Herbals
Supplements Megavitamins Off-Label use of Pharmaceuticals Homeopathy Aromatherapy |
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MIND BODY MODALITIES
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Aromatherapy
Biofeedback Dance therapy Guided imagery Hypnotherapy Meditation Tai Chi Yoga Prayer (spiritual) Visualization Energy medicine note: exercise is not considered CAM |
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ENERGY MEDICINE
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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 $$$$ |
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MANUAL THERAPY
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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 |
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LIFESTYLE CHANGES
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Specialized diets
Exercise |
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Herbal medicine
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pharmacologic use
European, Asian, Native American (North/South) |
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Diet, nutrition, and lifestyle changes
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supplements, vitamins, minerals, food
effects chronic disease and preventive |
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Mind/body or behavioral interventions
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biofeedback psychotherapy
relaxation prayer imagery mental healing art mediation dance hypnosis music therapy yoga |
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Alternative systems of medical practice
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traditional Oriental medicine
Ayurveda (Indian; diet, exercise, mediation) homeopathy naturopathic medicine environmental medicine community-based health care (e.g. shamanic) |
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Manual healing
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osteopathy physical therapy
massage therapy therapeutic touch chiropractic |
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Bioelectromagnetics
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living organisms interact with electromagnetic fields
used for wound healing, bone repair, immune system stimulation, pain |
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Pharmacologic and biologic treatments
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drugs and vaccines not accepted by mainstream medicine
off-label usually require a licensed provider e.g. chelation therapy |
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WHY SHOULD YOU LEARN ABOUT CAM?
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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" |
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WHICH CAM MODALITIES ARE MOST COMMON USED IN ACUTE CARE?
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massage
chiropractic herbs/supplements |
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THERAPEUTIC TOUCH
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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 |
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HEALING TOUCH (Therapeutic touch)
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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. |
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REIKI
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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 |
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HOW SHOULD YOU INCORPORATE CAM MODALITIES?
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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 |