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final exam patho

endocrine, gi, ears/eyes

QuestionAnswer
amsler grid tests for macular problems
tonometry measures intraocular pressure
perimetry testing evaluates the field of vision
slit-lamp examination enables the user to examine the eye with high magnification
color vision testing tests the ability to differentiate colors
ultrasonography used to identify lesions in the globe or the orbit
fluorescein angiography dye is injected into retinal vessels
snellen chart visual acuity
refractive errors impairment due to shortened or elongated eyeball
myopia nearsightedness (distant vision is blurred)
hyperopia farsightedness (near vision is blurred)
presbyopia aging
astigmatism an irregularity in the curve of the cornea
amblyopia lazy eye
strabismus crossed eyes
color blindness cannot see certain colors
blindness vision that can't be corrected to better than 20/200; regular 20/20
blepharitis inflammation of eyelid (granulated eyelids)
appearance of blepharitis dry, gritty sensation in eye, photophobia present
stye (hordeolum) bacterial infection near root of eyelash that appears on the outside of the eye
most common cause of stye s. aureus
chalazion blockage of meibomian gland near margin of eyelid
keratitis inflammation of cornea, often caused by HSV that begins superficially, but may go deeper
acanthamoeba keratitis can occur if contact lenses are contaminated with ameba; usually localized infection that can lead to corneal scarring, uveitis, scleritis, and cataract
keratoconjunctivitis sicca dryness of conjunctiva; common in autoimmune disorders; associated with reduced tear production
dacryocystitis inflammation of lacrimal sac, fever is common, may occur in newborns; eye is red, watery with purulent exudate
scleritis inflammation of sclera; severe pain may radiate to eyebrow or temple; photophobia; associated with autoimmune disorders
photophobia sensitivity to light, especially in light
corneal abrasion damage of epithelial surface of cornea; most common type of eye injury, usually heals within 24 hrs
most @ risk for corneal abrasion contact lens wearers; may present with sense of foreign body in the eye, gritty eye, photophobia
what reveals corneal abrasion slit lamp examination
prevention of corneal abrasion antibiotic ointment
glaucoma group of ocular conditions characterized by optic nerve damage related to increased intraocular pressure (IOP); related to the impedance of aqueous fluid outflow from the eye
two types of glaucoma open-angle glaucoma and angle-closure glaucoma
open-angle glaucoma (POAG) asymptomatic, progressive damage to optic nerve and visual field; most common form
angle-closure glaucoma (PACG) inherited, acute; painful; halos, blurred vision, & ocular pain (vision loss)
glaucomas are not curable and have few early symptoms management is centered on systemic and topical ocular medications
diagnosis of glaucoma increase optic cup to optic disc ratio on fundoscopic exam
risk factors of glaucoma age >40, ethnicity, history of migraine headaches, cardiovascular disease
presentation of glaucoma history-age, use of lenses, fam history, anticholinergic medications; complaints-eye pain, redness, halos around lights, vision loss; fundoscopic exam necessary for central vision; signs-rapid in PACG, progressive in POAG
POAG patho not completely understood changes in ciliary muscle, trabecular meshwork, and canal of Schlemm preventing drainage of aqueous fluid from anterior chamber; as ocular fluid cant drain, pressure is placed on retina and junction of optic nerve
POAG patho not completely understood 2 optic cup enlarges under high IOP; high IOP not only factor resulting in optic nerve damage in glaucoma
PACG patho people born w narrow angle bw iris and cornea @ greater risk; certain drugs like sympathomimetics, anticholinergics, antidepressants may inc risk for AACG; more common in hyperopic individuals; sudden inc in IOP causes sudden loss of peripheral vision
acute angular-closure glaucoma (aacg) acute presentation, ocular emergency, immediate treatment needed
cataracts due to excessive growth of epithelial layer of lens; present with gradual vision loss and seeing halos at night; may have opacity covering
senile cataracts advancing age, smoking, obesity, diabetes, exposure to uv light
congenital cataracts develop in fetus due to infection, such as rubella, syphilis, cmv
retinal detachment retina pulls away from back of eye; patient reports photopsia; ophthalmoscopic examination, treatment depends on type and size of detachment
photopsia floaters in vision and shadows in peripheral field
age-related macular degeneration (amd) caused by genetic, environmental, and behavioral factors
macula area of retina that provides central vision begins to deteriorate leading to development of blind spot and painless loss of vision
two types of amd dry, wet;
dry (nonexudative) amd 90% of those w disease
wet (exudative) amd more severe
both dry and wet amd involve inability to remove cellular debris from retina drusen deposits form and appear as yellow-white accumulations in macular region
diagnosis of amd amsler grid to measure central vision; in macular degeneration central vision is compromised while peripheral vision remains intact
papilledema swelling of optic nerve caused by inc ICP; patient complains of headache, nausea, double vision; sign of life=threatening intracranial HTN; borders of optic disc are unclear and undefined; treatment involves managing cause of inc ICP
diabetic retinopathy high glucose levels, associated with diabetes mellitus, damage the vessels of retina
two forms of diabetic retinopathy nonproliferative and proliferative
nonproliferative diabetic retinopathy early in diabetes, fundoscopic exam reveals tiny aneurysms, microinfarcts, nerve damage "cotton wool spots"
proliferative diabetic retinopathy later in diabetic course; diabetes stimulates vasoactive growth factors, inc vessels in retina
presentation of diabetic retinopathy document glucose control, medications, prior ophthalmic exams; initially, may be asymptomatic; w disease progression, patient may complain of blurred vision, poor night vision
diagnosis of diabetic retinopathy involves slit lamp examination and fundoscopic exam; inc optic cup to optic disc ratio on fundoscopic exam
conjunctivitis inflammation of conjunctiva; major causes are microbial infection, allergy, irritating toxic stimuli
bacterial conjuctivitis acute or chronic; results in redness, burning, and discharge-pink eye
viral conjuctivitis acute or chronic; causes watery discharge
conjuctivitis is self-limiting severe cases require topical antibiotics, eye drops, or ointments
manifestations of conjunctivitis scratching/burning sensation, itching, photophobia, discharge/exudate; extreme pain (corneal disease)
allergic conjunctivitis confused w infective forms; inflammation caused by airborne antigens, condition may occur in individual w asthma or eczema
palpebral conjunctiva becomes inflamed and swollen w cobblestone appearance tearing and redness of eyes, accompanied by itching
anti-histamines, NSAIDS can be helpful for allergic conjunctivitis
inner ear structures labyrinth (bony and membranous), utricle, saccule, semicircular canals
fluids in inner ear perilymph and endolymph
functions of inner ear balance and hearing
oscillations in fluid due to physical movements in inner ear detected by CN VIII
balance depends on vision, inner ear, proprioception
hearing thru cochlea, organ of corti (spiral-shaped, receptor for hearing); contains perilymph and stereocilia which respond to vibrations of sound waves being transmitted; activation of stereocilia sends signals along CN VIII
audiometry most important hearing test
tympanogram measures middle ear response
genetic testing of ear connexin-26:marker for genetic deafness; mutation of protein (GJB2) that regulates endolymph in inner ear can cause hearing impairment
other diagnostics of ear mri and ct can detect ear abnormalities; audio brainstem response testing; otoacoustic emissions (OAEs) and audiometry testing
decibel unit to describe loudness of sound; o:threshold for sound
normal conversation in decibels 60 dB
whisper in decibels 0-20 dB
sounds greater than how many dB can cause hearing loss 85 dB
hearing loss is classified based on range of sounds that cannot be heard
mild hearing loss lower than 26-40 dB; difficulty following conversations
moderate hearing loss lower than 41-55 dB; hearing aid to hear normal conversation
severe hearing loss lower than 60-90 dB; can hear speaking, but can not make out words (unless watching lips and mouth); hearing aid needed
profound hearing loss lower than 90 dB; hearing aids, lip reading, sign language
hearing loss can be described as genetic, acquired, progressive, sudden, unilateral, bilateral, partial, complete, reversible, irreversible
conductive hearing loss (CHL) disorder of sound transmission from outer or middle ear to receptors of middle ear; common cause=impacted cerumen, otitis media
sensorineural hearing loss (SNHL) disorder of inner ear, auditory nerve, or auditory pathway in brain; central hearing impairment; commonly due to loss of stereocilia in organ of corti; can be caused by noise trauma, infections, genetic disorders
central hearing impairment damage to brain in which sounds are heard, cannot be understood
mixed hearing deficiency combination of chl and snhl
conditions of external ear cerumen impaction and foreign bodies
cerumen impaction can be removed by irrigation, suction, or instrumentation
foreign bodies can be difficult to remove but are treated in same way as impacted cerumen
otitis externa (swimmers ear) mild to severe inflammation of external ear; infectious agents/allergies (water in ear canal can predispose infection); movement of external ear may be painful; once infection resolved, swimming w ear plugs may be recommended
tympanic perforation caused by infection or trauma; causes whistling sounds upon sneezing and blowing nose, reduced hearing, purulent drainage, and pain; may heal spontaneously or require tympanoplasty
tympanoplasty surgical repair of tympanic membrane
tympanic membrane perforation complication of middle ear infection or trauma; symptoms of perforation (buzzing sound in ear, earache, and hearing loss); most small ruptures heal spontaneously (~4 weeks)
treatment tympanic membrane perforation ear drops should not be used, systemic antibiotics may be needed; cauterization of membrane edges and patching may be needed; surgical tympanoplasty can be done
otitis media infection of middle ear; can be related to URIs, most common in children (shorter, wider, and more horizontal eustachian tubes than in adults); pneumatic otoscope demonstrate dec movement of tympanic membrane
signs and symptoms include fever, earache children may present w nonspecific symptoms such as ear tugging, poor feeding, irritability; tympanic membrane rupture is possible; physical exam reveals reddened tympanic membrane
otosclerosis callus on stapes (stapes cannot transmit vibrations, progressive hearing loss, usually in one ear); audiogram shows conductive hearing loss; stapedial reflex; surgery only option for treatment
stapedial reflex special type of testing will show limited ossicle movement
vertigo misperception or illusion of motion of person or surroundings
nystagmus involuntary rhythmic movement of eyes
inner ear conditions affect balance and hearing
ménière disease disorder of inner ear causing vertigo, tinnitus, a feeling of fullness or pressure in ear, and fluctuating hearing loss; results from changes in pressure within the inner ear or mixing of inner ear fluids
ménière disease affects 40-50 years, unknown etiology; most patients successfully treated w diet and medication; some require antihistamines, tranquilizers, antiemetics, or surgery
tinnitus roaring, buzzing, or hissing sound in one or both ears that may be irreversible
tinnitus symptom underlying disorder of ear that is associated w hearing loss- red wine, caffeine, meniere's disease
vertigo sense of "room spinning", an exaggerated sense of movement, dizziness; nausea and vomiting may accompany; alterations in inner ear, meniere's disease; must distinguish from dizziness
ototoxicity results from medications that have adverse effects on the cochlea, vestibular appartus, or cranial nerve VIII; patients receiving potentially ototoxic medications should be counseled about this side effect
acoustic neuroma slow-growing, benign tumor of cranial nerve VIII (vestibular schwannomas); causes tinnitus and hearing loss; treated surgically
hearing loss in older adults presbycusis; begin @ around at 50 yrs; gradual loss of hair cells in cochlea; high-frequency sounds are lost first; hearing aids are often recommended
types of bone tissue cancellous (trabecular) and cortical (compact)
bone cells osteoblasts, osteocytes, osteoclasts
osteoblasts build bone matrix
osteocytes mature bone cells
osteoclasts dissolve and resorb bone
categories of bones long bones (femur), short bones (metacarpals), flat bones (sternum), irregular bones (vertebrae)
bone maintenance constant and simultaneous resorption (removal/destruction of tissue) and osteogenesis (bone formation)
bone maintenance affected by multiple issues calcium and vitamin d in the diet, physical activity, tobacco and alcohol, sex, size, age, race and family history; hormone levels-parathyroid, calcitonin, vit d, thyroid, testosterone; eating disorders and other conditions; certain meds
bone healing stages 1. early inflammatory/hematoma formation stage 2. granulation tissue formation; fibroblasts to injury growth of vascular tissue 3. repair stage 4. remodeling stage
early inflammatory/hematoma formation stage hematoma formation, granulation tissue, vascular tissue formation
repair stage laying down of new bone tissue (cartilaginous callus), angiogenesis continues
remodeling stage callus removed, bone strengthens returns to normal shape, size, structure, and strength
ball-and-socket joints hip and shoulder
hinge joints elbow and knee
saddle joints joint at the base of the thumb
pivot joints articulation bw radius and ulna
gilding joints joints of carpal bones in wrist
ligaments connect movable bones of joints
tendons connect muscles to bones
synovial fluid located in synovium of joint capsule lubricates and facilitates movement
bursa sac w synovial fluid that cushions movement of tendons, ligaments, and bones at a point of friction
fascia fibrous tissue that encases muscles
skeletal (striated) muscles involved in body movement, posture, and heat-production functions
skeletal muscle composed of skeletal muscle fibers; can undergo hypertrophy or atrophy
myofilaments actin and myosin
healing process of skeletal muscle regeneration heightened in response to injury, myocytes (muscle fibers), injury to surrounding nerves and blood vessels play a role in return to function, repaired muscle is not as strong as it was prior to injury
muscle tone (tonus) state of muscle readiness
flaccid muscle muscle that is limp and without tone
spastic muscle muscle w greater-than-normal tone
atonic muscle denervated muscle
hypertrophy inc in muscle size
atrophy dec in muscle size
diagnosis of musculoskeletal system x ray, computed tomography, mri, arthrography, bone densitometry, bone scan, arthroscopy, arthrocentesis, electromyography, biopsy, lab studies
major trauma following life-saving measures (ABCDE) airway w cervical spine protection, breathing and ventilation, circulation and hemorrhage control, disability and neurological evaluation, exposure and environmental control
closed (complete) fracture fracture in which bone fragments separate completely
open (compound) fracture fracture of bone that protrudes to the outside of the body
incomplete fracture fracture in which the bone fragments are still partially joined
compression fracture fracture that consists of crushing of cancellous bone
transverse fracture fracture where parts of bone are separated but close to each other
comminuted fracture fracture w more than one fracture line and more than two bone fragments, which may be shattered or crushed
stress fracture failure of one cortical surface of bone, often caused by repetitive activity
avulsion fracture separation of small fragment of bone at site of attachment of ligament or tendon
greenstick fracture incomplete break in bone w intact side of cortex flexed (one side is broken and other is bent); usually in children
impacted fracture one part of fracture is compressed into an adjacent part of fracture
fracture complete or partial break in continuity of bone; trauma, overuse, diseases that weaken bone
manifestations of fractures pain, lose of function, deformity, shortening, crepitus, swelling, and discoloration
priorities of fractures immobilization, assessment of neurovascular status, infection prevention, and maintenance of hemodynamic stability
long bone and pelvic fractures inc risk of fat embolism
fracture treatment reduction , immobilization, and regaining of normal function and strength thru rehabilitation
reduction restoration of fracture fragments to anatomic alignment and rotation; performed "open" (surgically) or "closed" (manipulation and manual traction)
open fractures management wound irrigation and debridement necessary
potential complications of fractures fat embolism syndrome (FES);delayed union, malunion, nonunion;venous thromboemboli;disseminated intravascular coagulation (DIC);avascular necrosis;reaction to internal/external fixation devices;complex regional pain syndome (CRPS);hetertropic ossification
treatments of fractures self-limiting; RICE therapy; realign bones; measures to prevent DVTs (compression stockings, meds to prevent clotting)
closed reduction realignment device worn outside
open reduction realignment surgical insertion of hardware
ORIF stands for open reduction and internal fixation
RICE therapy rest, ice, compression, elevation
neurological and vascular injury arterial injury is a concern in some fractures
to asses neurovascular status, check pulses and sensation distal to injury 5 P's- pain, pulse, pallor, paresthesia, paralysis (add temp too)
patient exhibits what during neurological and vascular injury pain, weakness, lack of sensation, decreased motor strength, absent or weak pulses
if neurological compression prolonged severe atrophy of muscle
compartment syndrome tissue pressure exceeds perfusion pressure in closed anatomical space; ischemia, necrosis, and functional impairment; weak distal pulses or pulselessness
patient complains of what during compartment syndrome pain out of proportion of degree of injury--> immediate surgical evaluation
rhabdomyolysis muscle breakdown; myoglobin accumulates in bloodstream; elevated CK levels; may occur in compartment syndrome
myoglobin in bloodstream kidneys must filter myoglobin, which is toxic to nephrons in large amounts; leads to acute reanal injury
triad of symptoms in rhabdomyolysis myalgia, weakness, and myoglobinuria
joint dislocations occur when articular surfaces of bones forming the joint are no longer in anatomic alignment; forced out of normal position due to injury, fall, accident; common in shoulders, elbows, fingers, ankles, knees, hips, jaw
joint dislocation manifestations pain and visible changes in alignment of joint, immobility of joint, swelling, muscle spasms
joint dislocations require immobilization followed by reduction (put back in place) and rehabilitation for several weeks
hip fracture (proximal femur) very high incidence among older adults and associated w high risk of mortality
surgical options for hip fracture replacement of femoral head w prosthesis (hemiarthroplasty) or open/closed reduction of fracture and internal fixation
priorities for hip fracture management of activity and mobility and prevention of postsurgical complications
total hip arthroplasty (tha) surgical replacement of hip joint w artificial prothesis; preoperative care prioritizes patient education about positioning and assessment for infection
postoperative priorities for THA positioning to prevent dislocation, promoting ambulation, monitoring for complications, monitoring wound drainage, preventing DVT and infection
contusion soft tissue injury produced by blunt force; bruise
strain injury to musculotendinous unit caused by overuse, overstretching, or excessive stress; pulled muscle
sprain injury to ligaments and supporting muscle fibers that surround a joint; rolled ankle
treatments for contusion, sprain, strains resting and elevating affected part, applying cold and using compression bandage (RICE)
important to monitor neurovascular status of injured extremity during injury color, sensation, pulse, temp, movement (6 Ps- pain, pallor, parasthesia, poikilothermia, paralysis, pulselessness)
bursitis inflamation of bursae of joints; pain, swelling, stiffness around joint; causes: repetitive movements, excessive pressure on joints, injury
tendonitis (ex lateral epicondylitis (tennis elbow)) inflammation of tendons, common in 30-50; pain @ or around joint, gradual or sudden severe pain @ affected part, stiffness or loss of motion in affected join, tenderness, mild swelling or thickening; causes similar to bursitis
carpal tunnel syndrome pain, tingling, numbness of hand, fingers, weakness in hands; occurs when median nerve @ wrist is compressed, pregnancy, trauma, occupation, diabetic neuropathy, hypothyroidism
ganglion collection of gelatinous material near tendon sheaths and joints that appear as round, firm, compressible, cystic swelling
bone health constant remodeling, dependent on calcium, hormones (vitamin d (calcium absorption), calcitonin, parathyroid hormone, testosterone and estrogen), mechanical stimulation
synarthrosis no mobility in joints
diarthrosis most movement; synovial joint
amphiarthrosis moderately movable joint
arthropathy joint disorder
arthritis inflammation of joint
bone remodeling destruction and reconstruction of bone
degeneration of bone involves osteoclasts and osteoblasts; stimulated by stresses upon bone
osteoporosis elevated osteoclast activity without adequate bone replacement
recommended calcium intake to maintain bone health 1,000-1,200 mg/day
osteoarthritis affects certain joints and not others cervical and lumbosacral spine, hip, knee, 1st metatarsal phalangeal joint; wrist, elbow, and ankle are often spared
chondrocytes produce cartilage cartilage loss w age, cartilage along w synovial fluid provide cushioning
articular cartilage deterioration excessive force causes cartilage to breakdown; subchondral bone deterioration
osteophytes form @ margin of cartilage loss, hallmark of osteoarthritis (OA)
osteoarthritis synovial membrane becomes inflamed; concentration of lubricin (glycoprotein that acts as lubricant) declines
osteoporosis "porous bone" low bone density, structural deterioration of bone, breaks in travecular matrix
osteopenia thinning of travecular matrix (before osteoporosis)
silent disease of osteoporosis may present w pathological fracture or height loss
primary osteoporosis prolonged negative calcium balance; poor dietary habits, lack of weight-bearing exercise, lack of daily exposure to sunlight
secondary osteoporosis disorders that affect bone tissue; hyperparathyroidism, corticosteroids
hormones play role in bone material density (BMD) estrogen slows osteoclast activity
female athlete triad w osteopenia amenorrhea, dec body weight, excessive exercise
risk factors for osteoporosis female, postmenopausal age, lack of estrogen, lack of testosterone, fam history, asian/caucasian women, thin/small-framed women, lack of Ca and vitamin d, lack of weight-bearing exercise, excess alcohol, excess caffeine, smoking
risk factors of osteoporosis 2 long term use of corticosteroids, excess carbonated soft drink consumption, gastric bariatric surgery, eating disorders, hyperthyroidism or excessive intake of thyroid medican, hyperparathyroidism, anticonvulsant medications
osteoporosis diagnosis dual energy x ray absorptiometry (DEXA); x-rays do not show osteoporosis until bone loss >40%; blood tests; urine; FRAX risk assessment
dual energy x ray absorptiometry (DEXA) measures BMD, compared w reference population of healthy adults (30); reported at T score
osteoporosis blood tests PTH, estradiol, osteocalcin (protein in bone, high level indicates bone breakdown)
osteoporosis urine telopeptides, bone breakdown product
FRAX risk assessment self-assessment tool to predict a person's risk of fracture; gives 10-year probability of a fracture in spine, hip, shoulder, wrist; age 40-90
osteoarthritis (OA) >40 yrs; associated w trauma to joints over course of life (slowly progressive, degenerative, inflammatory condition; changes in cartilage lead to inflammation and changes in joint surfaces); excess weight inc risk for OA in weight-bearing joints
risk factors osteoarthritis aging, obesity, history of participation in team sports, history of trauma or overuse of joint, heavy occupational work, misalignment of pelvis, hip, knee, ankle, or foot
presentation of OA deep, aching joint pain; pain relieved w rest; joint pain in cold weather; stiffness arising in morning; crepitus of joint during motion; joint swelling, deforming, tenderness; altered gait; limited/dec range of motion; fingers involved
heberden's nodes distal interphalangeal joint (DIP); swelling in OA
bouchard's nodes proximal interphalangeal joint (PIP); swelling in OA
OA diagnosis no specific lab test, serum markers (osteocalcin and hyaluronic acid), physical exam, xray confirms diagnosis (joint space narrowing/osteophytes)
degenerative disc disease (DDD) common cause of pain, motor weakness, and neuropathy; nervous system affected as vertebral disc distortions compromise spinal nerves; cervical/lumbar regions affected: L4, L5, S1
degenerative disc disease causes spinal impingement herniated disc, bulging disc, degenerated disc, osteophyte formation, slippage of disc and vertebrae
osteophyte formation for DDD bony formations can narrow the spinal canal, spinal stenosis
slippage of disc and vertebrae for DDD spondylolithesis: forward; retrolisthesis: backward
sings/symptoms of lumbar DDD pain in lower back that radiates down back of leg; pain in buttocks or thighs;pain that worsens when sitting, bending, lifting, or twisting;pain that is minimized when walking, changing positions, or lying down;numbness,tingling,weakness in legs;foot drop
sciatica pain in lower back that radiates down the back of leg
signs/symptoms of cervical DDD chronic neck pain that can radiate to shoulders and down the arms; numbness or tingling in arm or hand; weakness of arm or hand
physical exam of DDD muscle strength, deep tendon reflexes, sensory dermatomes (give info about which spinal nerve is affected)
diagnostics of DDD physical exam tests, xray, mri, emg
osteomyelitis infection of bone (s. aureus) acute or chronic; can result from extension of soft tissue infection, direct bone contamination, or hamatogenous (bloodborne) spread
osteomyelitis results in signs/symptoms of sepsis recurrent/persistent fever, pain, malaise, poor incisional healing, drainage @ wounds
antibiotic therapy depends on results of blood and would cultures surgical debridement may be indicated for DDD
bone normally resistant to infection
bacterial infections most common infection due to break in bone, infection from bloodstream
bacteria invades cortex via haversian and volkmann canals
risk for bone infections immunosuppression, comorbid diseases (diabetes mellitus), nutritional deficiency, prosthetic material
contiguous spread invasion of microorganism via puncture or wound; s. aureus
hematogenous spread spread via bloodstream, group a streptococci, or s. pneumoniae
cartilage covers the articular surfaces of bone avascular w limited ability to repair and heal
synovial fluid found in synovial joints, amount of fluid may in in disease states, joint effusion (edema of joint), limited blood supply: difficulty in delivering meds (use intra-articular injection)
stages of bone infection 1. inflammation 2. suppuration 3. sequestrum 4. involucrum 5. resolution or progression to complications
inflammation vascular congestion and inc pressure within interior bone
suppuration infectious material enters Haversian system and abscess formed
sequestrum inc pressure, vascular obstruction, and thrombi compromise blood supply, causing bone necrosis in approximately 7 days
involucrum new bone formation from surface of periosteum
resolution/progression to complications w antibiotics and surgical treatment early in disease process: osteomyelitis resolves; if no resolution: gangrene, necrotic tissue can develop
osteomyelitis infection of bone; normally bacterial (s. aureus); sickle-cell anemia: salmonellae
presentation of osteomyelitis assess for recent infections; chills, fever, malaise; localized tenderness, erythema, edema
3 categories of osteomyelitis hematogenous, contiguous, chronic
hematogenous osteomyelitis rapid onset of symptoms; most cases in children (inc vascularity in growing bone)
contiguous osteomyelitis trauma and surgery are common causes, as well as decubitus ulcers; individuals w DM, PVD are at inc risk
chronic osteomyelitis defined by length of time (longer than 6-8 weeks), lack of response to meds; necrotic bone (inc gangrene risk)
diagnosis of osteomyelitis CBC, ESR, C-RP; blood cultures (+ only 50% of patients); culture and aspiration may fail to identify pathogen; xray (normal at first, ct scan, mri)
treatment of osteomyelitis long-term antibiotics, debridement, surgical drainage of wounds
septic arthritis (infectious arthritis or pyogenic arthritis) direct invasion of joint space by pathogen; bacterial infections most common; present w inflammation and acute pain around joint, fever, and malaise may occur
diagnosis of septic arthritis defective diagnosis-detection of bacteria from blood or synovial fluid; joint aspiration required; culture of aspirated fluid
gout hyperuricemia triggers inflammation; affects specific joints (first metatarsal); primary and secondary forms
podagra acute inflammation of metatarsophalangeal joint of great toe
with gout, uric acid crystals may be deposited in subcutaneous tissue (tophi) patient presents w redness, warmth, swelling of joint; discomfort onsets during night or early morning
chronic gout involves several joints can be confused w OA and RA; hyperuricemia can lead to kidney stones
diagnosis of gout rule out other joint inflammatory conditions (24 hr urine uric acid); hyperuricemia may not be present and should not be used for as sole diagnostic criteria; aspiration of joint showing urate crystals is gold standard for diagnosis
risks for gout diet high in meat (purines:uric acid); high alcohol consumption, obesity (yo-yo dieting); fam history; chemotherapy resulting in cell destruction; meds
endocrine glands secrete chemical messengers (hormones) into bloodstream
hypothalamus sends signals to pituitary gland
anterior pituitary receives hormonal signals from hypothalamus
posterior pituitary releases hormones synthesized by hypothalamus
end organs targets for pituitary hormones, may or may not secrete additional hormones
hypothalamic-pituitary-hormonal axis link bw hypothalamus-pituitary-end organ
pituitary aka hypophysis
anterior pituitary aka adenohypophysis
anterior pituitary blood vessel connection w hypothalamus (hypothalamus-hypophyseal portal system); releases tropic hormones
posterior pituitary aka neurohypophysis
posterior pituitary neural connection w hypothalamus; hormones made by hypothalamus; stores and released by posterior pituitary
negative feedback mechanism end-product hormone negatively feeds back to prevent further stimulatory signals (ex: thyroid hormones suppress thyroid-stimulating hormone production)
positive feedback mechanism hormone response continues to inc to achieve desired response (ex: oxytocin is inc during labor to cause uterine contractions to birth baby)
upregulation inc receptor sensitivity and #
downregulation dec receptor sensitivity and #
3 major types of endocrine conditions hormone deficiency, hormone excess, hormone resistance
hormone deficiency gland destruction; autoimmune, infection, tumor
hormone excess tumor, autoimmune, genetic mutation
hormone resistance usually genetic (lack hormone receptor or ability to respond)
hypofunction inadequate amount of hormone
hyperfunction excessive amount of hormone
3 levels of endocrine dysfunction primary, secondary, tertiary
primary endocrine dysfunction endocrine gland itself
secondary endocrine dysfunction abnormal pituitary activity
tertiary endocrine dysfunction dysfunction of hypothalamic origin
causes of endocrine dysfunction autoimmune, neoplasia, endocrine-disrupting compounds (edcs)
autoimmune antibodies target endocrine gland, may cause hypofunction or hyperfunction
neoplasia hypofunction or hyperfunction of gland itself or any endocrine tissue that gland affects; some cancers: paraneoplastic disorder in which cancer cells secrete hormone-like substances
endocrine-disrupting compounds (edcs) chemical in environment that can alter endogenous hormone functions
assessment of endocrine disorderes current and past medical history; some endocrine disorders present w wide-ranging, multi-system signs and symptoms; endocrine dysfunction may affect mood and behavior, can be misinterpreted as psychological issues
diagnosis of endocrine disorders immunoassays or blood levels of hormones most importnant; urinary hormone levels assessed in some instances; urinary collection over 24 hrs; suppression/stimulation tests; ct scan/mri; ultrasound
hypothalamus is located in brain and serves as coordinating center of brain for endocrine, behavioral, and autonomic nervous system; link bw nervous system and endocrine systems; controls pituitary gland
hypothalamus hormones RIH, CRH/CRF, TRH, GHRH, GnRH, somatostatin, dopamine
releasing and inhibiting hormones (RIH) controls release of pituitary hormones
cortico-releasing hormone (CRH/CRF) stimulates secretion of adrenocorticotropic hormone (ACTH)
thyrotropin-releasing hormone (TRH) stimulates release of TSH
growth hormone-releasing hormone (GHRH) stimulates release of GH
gonadotropin-releasing hormone (GnRH) stimulates secretion of luteinizing horome (LH) and follicle-stimulating hormone (FSH)
somatostatin inhibits GH and TSH
dopamine inhibits secretion of prolactin
pituitary gland (master gland) controlled by hypothalamus (hypophyseal portal); divided into anterior and posterior lobes
anterior pituitary hormones GH, ACTH, TSH, FSH, LH, prolactin
growth hormone (GH) stimulates growth of bone and muscle, promotes protein synthesis and fat metabolism, dec carbohydrate metabolism
adrenocorticotropic hormone (ACTH) stimulates synthesis and secretion of adrenal cortical hormones
thyroid-stimulating hormone (TSH) stimulates synthesis and secretion of thyroid hormone
follicle-stimulating hormone (FSH) female: stimulates growth of ovarian follicle, ovulation; male: stimulates sperm production
luteinizing hormone (LH) female: stimulates development of corpus luteum, release of oocyte, production of estrogen and progesterone; male: stimulates secretion of testosterone, development of interstitial tissue of testes
prolactin prepares female breast for breast-feeding
posterior pituitary gland stimulated thru neural control
posterior pituitary hormones ADH, oxytocin
antidiuretic hormone (ADH)/vasopressin inc water absorption into bloodstream/antidiuretic function (inc blood osmolality)
oxytocin stimulates contraction of pregnant uterus, milk ejection from breasts after childbirth
hypopituitarism one or more of pituitary hormones; addison disease, di, dwarfism, panhypopituitarism
panhypopituitarism complete loss of all pituitary hormones, rare
causes of hypopituitarism pituitary tumor,brain surgery,radiation of brain tumor,congenital disorder(primary adenoma-->malignant/benign); trauma,ischemia,infarction cause sudden loss of pituitary function(sheehan's syndrome),tbi or brain herniation, hypothalamic dysfunction
sheehan's syndrome anterior pituitary damaged; develops after childbirth with severe hemorrhage
signs and symptoms of hypopituitarism depends on pituitary hormones suppressed, age of onset, if acute/rapid deterioration, neonate, adult
depends on pituitary hormones suppressed most serious concerns are adrenal insufficiency, hypothyroidism, and diabetes insipidus
age of onset children w hypopituitarism will have different complications than adults
neonate dwarfism, developmental delay, various visual and neurological symptoms, seizure disorder, congenital malformation
adult weakness, weight loss or gain, hypotension caused by adrenal insufficiency, sluggishness, depression, excessive urination and dehydration
diagnosis of hypopituitarism blood tests to assess hormone levels (pituitary, hypothalamic, and end-organ levels may be needed); corticotropin stimulation test:give acth; mri, ct scan
corticotropin stimulation test cortisol levels should rise; if cortisol levels rise w acth administration: pituitary problem; if cortisol levels do not rise w acth administration: adrenal gland problem
hyperpituitarism types: cushing syndrome, siadh, acromegaly/gigantism
pituitary adenoma most common cause of hyperpituitarism; may produce acth, tsh, or gh; prolactinoma most common form: secretes prl (high prl has antiestrogenic and antiandrogenic effects)
large tumors may cause headaches and visual disturbances bc of proximity to optic nerves
children hyperpituitarism acth-producing adenoma; corticotropinomas, common before puberty; cushing-like symptoms
gh-secretion adenoma children-gigantism; adults-acromegaly
diagnosis of hyperpituitarism serum hormone levels, urine hormone levels may also be assessed, dexamethasone suppression test to assess acth response
diabetes insipidus (DI) posterior pituitary hypopituitarism; lack of adh or response to adh; dilute, large volume urine (plasma concentration inc)
categories of diabetes insipidus central di and nephrogenic di
central DI lack adh from posterior pituitary
nephrogenic DI kidney fails to respond to ADH, distinguish by administering adh to see if kidneys can respond, if so central DI
signs/symptoms diabetes insipidus frequent urination, thirst, dehydration, disorientation, seizures; blood test will show high osmolarity and hypernatremia; urine osmolarity and specific gravity will be low
diabetes insipidus differs from diabetes mellitus no hyperglycemia in DI
syndrome of inappropriate adh (SIADH) excesive adh-causes: brain injury or neurosurgery; paraneoplastic disorder; causes fluid retention-concentrated urine, dilute plasma, hypervolemia
thryoid triiodothyronine (T3) and thyroxine (T4); iodine needed for synthesis
thryoxine regulates body metabolism
thyroid disorders more common in women
primary thyroid disorders most common
enlarged thyroid can indicate hypo- or hyperfunction
goiter enlargement of thyroid; may or may not present w thyroid dysfunction signs and symptoms; may develop w excess tsh, low iodine levels, goitrogens
goitrogens foods or other substances that promote thyroid gland enlargement
hashimoto's thyroiditis hypothyroidism autoimmune disorder, anti-thyroglobulin antibody and anti-thyroperoxidase antibody
causes of hyperthyroidism drugs, genetics, thyroiditis (postpartum period especially high incidence), congenital hypothyroidism: cretinism
systemic effects of hyperthyroidism hyperlipidemia, yellow-orange skin (elevated carotene levels), anemia, dec filtration by kidney, pendred's syndrome, myxedema, subclinical hypothyroidism (elderly)
pendred's syndrome defective iodine incorporation into thyroid hormone
myxedema adult severe hypothyroidism
signs/symptoms hypothyroidism cold intolerance, weight gain, lethargy, fatigue, memory deficits, poor attention span, muscle cramps, constipation, dec fertility, puffy face, hair loss, brittle nails
diagnosis of hypothyroidism primary: high tsh, low free T3, low free T4; secondary: low tsh, low free T3 and T4; hashimoto's thyroiditis antibodies: antithyroglobulin (anti-Tg), antithyroperoxidase (anti-tpo); ultrasound; thyroid test in women 35, and every 5 years after
hyperthyroidism elevated free T3 and free T4; graves disease
graves' disease most common cause of hyperthyroidism, autoimmune stimulation of thyroid gland
causes of hyperthyroidism subacute thyroiditis, thyroid adenoma, excessive TSH, subacute thyroiditis, toxic multinodular goiter, excessive iodine ingestion (jod-basedow syndrome), secondary to pregnancy, hcg is similar to TSH
Grave's disease thyroid-stimulating antibodies bind to thyrotropin receptors=gland enlargement and continual synthesis thyroid hormones
Grave's disease symptoms nervousness, insomnia, sensitivity to heat, weight loss, enlarged thyroid gland, atrial fibrillation, inc HR; inc sympathetic nervous system sensitivity; exophthalmos
exophthalmos wide-eyed stare, extraocular area filled w mucopolysaccharides; graves opthalmopathy: periorbital edema and bulging of eyes
hypothyroidism hypercholesterolemia, gains weight easily, dec fertility, delayed reflexes, sluggishness, feeling cold, constipation, lethargy, fatigue
hyperthyroidism anxiety, tremor, tachycardia, feeling warm, loss of weight, exophthalmos, atrial fibrillation, dec fertility
hyperthyroidism diagnosis primary, secondary, antibodies for graves' disease, ultrasound w color-doppler evaluation, radioactive iodine scanning and iodine uptake
primary hyperthyroidism diagnosis low tsh, high free t3 and t4
secondary hyperthyroidism diagnosis high tsh, high free t3 and t4
antibodies for graves' disease anti-thyroid peroxidase (anti-tpo), thyroid stimulating immunoglobulin
thyrotoxic crisis (thyroid storm) overwhelming release of thyroid hormones; stimulate metabolism (high fever, tachycardia, agitation, psychosis); often precipitated by surgery or trauma; medical emergency
thyroid nodules (most asymptomatic) hypo/hyperthyroidism=single nodule (inc malignancy risk), multiple nodules (benign); ultrasound and needle biopsy for diagnosis; technetium scan
technetium scan uses radioactive isotope, hot nodule (hyperfunctioning tumor), warm nodule (normal tissue), cold nodule (hypofunctional tissue, sometimes malignant)
malignant thyroid nodule <20 or >70; male; history of neck irradiation; firm, hard, or immobile nodule; presence of cervical lymphadenopathy
parathyroid gland four pea-sized glands on posterior thyroid; secrete pth (parathyroid hormone)
parathyroid hormone (PTH) released when blood calcium low; activate bone resoprtion, intestinal calcium absorption by kidneys
hypoparathyroidism rare, inadvertent damage w thyroid surgery, genetic disorders; presentation due to hypocalcemia (trousseau's sign, chvostek's sign, muscle cramps, tetany, convulsion)
hyperparathyroidism due to parathyroid adenoma (unorganized neoplasm)
primary hyperparathyroidism elevated PTH and calcium
secondary hyperparathyroidism elevated PTH, low to normal calcium; any disorder that causes hypocalcemia can induce secondary hyperparathyroidism
presentation of hyperparathyroidism due to excess calcium muscle weakness, poor concentration, neuropathies, kidney stones, osteopenia, pathological fractures
adrenal gland cortex and medulla
cortex contains glucocorticoids (cortisol), androgens, mineralocorticoids (aldosterone)
medulla contains neurotansmitters (epinephrine, norepinephrine)
adrenal insufficiency secondary (dec ACTH); primary (aka addison's disease)
Addison's disease autoimmune destruction adrenal cortex; antibodies to adrenal cortex and steroid enzymes
hypoadrenalism due to exogenous glucocorticoids; with prolonged glucocorticoid use, CRF-ACTH signals to adrenal cortex suppressed, adrenal gland down regulates receptors, steroid usage should not be abruptly stopped, individual may be unable to respond to stressor
to lessen adrenal atropy what is given to patient smallest dosage of steroid
diagnosis of hypoadrenalism rapid ACTH test; with ACTH administration, cortisol should rise w/in 30 mins; no cortisol rise: adrenal cortex insufficiency
symptoms of adrenal insufficiency weakness, hypotension, easy fatigue, emotional lability, anorexia, hypoglycemia, electrolyte imbalances (hyponatremia/hyperkalemia); tanned appearance due to melanocyte-stimulating hormone (MSH); acth and msh arise from same precursor molecule
symptoms of adrenal insufficiency w women loss of pubic and axillary hair; amenorrhea
hyperadrenalism/hypercortisolism Cushing's disease, cushing's syndrome; exogenous steroids most common cause of cushing's syndrome
cushing's disease elevated ACTH, tumor in pituitary
cushing's syndrome elevated cortisol, hyperfunction of adrenal cortex;
causes of hyperadrenalism pituitary adenoma (cushing's disease), cushing's syndrome=adrenal hyperplasia, adrenal neoplasm, carney complex (genetic disorder), mccune-albright syndrome (cushing's syndrome and precocious puberty), secretion of ACTH from tumors
symptoms of hyperadrenalism (cushing syndrome) weight gain; redistribution of body fat to face, trunk, and abdomen; puffy face (moon facies); extra subcutaneous fat in cervicothoracic area (buffalo hump); inc in waist-to-hip circumference ration; striae; easy bruising and poor wound healing
symptoms of hyperadrenalism for women hirsutism (sensitivity of the hair follicle to androgens.), male pattern hair growth, amenorrhea
effects of high cortisol levels block action of insulin (glucose intolerance and hyperglycemia); inhibit bone formation and accelerates bone reabsorption (osteopenia, osteoporosis); suppress immune response; hypertension
diagnosis of hyperadrenalism serum levels (inc wbcs, hyperglycemia, hypokalemia); salivary levels of cortisol (24 hr urine cortisol); dexamethasone suppression test; mri, ct scan
dexamethasone suppression test administer dexamethasone, serum cortisol should be suppressed, cushing's syndrome (no cortisol suppression w dexamethasone)
pheochromocytoma adrenal medulla tumor (secrete norepinephrine and epinephrine, excessive sympathetic stimulation); HTN, tremors, inc cardiac contractility, cardiac arrhythmias, tachycardia
diagnosis of pheochromocytoma 24 hr urine for catecholamine metabolites
pancreatic islets (islets of langerhans) pancreas lies transversely in upper abdomen
alpha cells--> glucagon--> when glucose levels are low-->inc blood glucose level
beta cells-->insulin--> transport blood glucose into body cell-->dec blood glucose level
delta cells-->somatostatin--> reduce food absorption from GI tract-->dec blood glucose level
acini tissue in pancreas secretes digestive juices
diabetes mellitus (DM) too much glucose (hyperglycemia)--> prediabetes, type 1 DM, type 2 DM, gestational DM
prediabetes blood glucose levels are elevated but NOT diabetes yet
type 1 DM destruction of pancreatic beta cells-->no insulin production
type 2 DM insulin resistance and impaired insulin secretion from beta cells
gestational DM secretion of placental hormone-->inc insulin resistance and glucose intolerance
risks for DM fam history/genetic factors, obesity/lack of physical exercise, ethnicity (afr amer, latino, native amer, asian amer, pacific islanders), age >45, HTN, high cholesterol levels, history of gestational MD
carbohydrate metabolism insulin-supported process of facilitated diffusion moves glucose from blood into cells, insulin produced by beta cells of islets of langerhans in pancreas; after eating: synchronous rise and fall of glucose and insulin
glucose used for energy, stored as glycogen, or converted to component of lipid molecules
glycogenesis glycogen formation, primarily in liver and muscle
glycogenolysis glycogen breakdown, occurs when blood glucose falls and body needs energy
gluconeogenesis amino acids and glycerol of lipids (fats) converted to glucose
fatty acids remains as lipids converted to acetoacetic acid, beta-hydroxybutyric acid, and acetone; known as ketones or ketoacids; fruity odor (breath, saliva, sweat); accumulation of ketones may lead to diabetic ketoacidosis (DKA)
normal blood glucose levels 70-100 mg/dL (fasting)
hypoglycemia <70 mg/dL; brain functioning affected
hyperglycemia >200 mg/dL
fasting blood glucose 100-125 mg/dL; impaired glucose tolerance (IGT) or prediabetes; greater than 126 mg/dL=diabetes
postprandial blood glucose glucose after eating; >200 mg/dL is diabetes
role of insulin facilitates glucose uptake by cells; stores extra glucose in muscle, adipose tissue, liver; glycogenosis in liver and muscle; fat sparer; anabolic hormome
hyperinsulinism inc insulin level to overcome insulin resistance
hyperinsulinism hypoglycemia low blood glucose levels from too much insulin
diabetes tests fasting and random BG tests; oral glucose test (OGTT), glycated hemoglobin (A1C), eAG, glucosuria, ketonuria, islet cell autoantibodies, c-peptide test
oral glucose tolerance test (ogtt) 75 g of glucose ingested, measure BG following
glycated hemoglobin (A1C) diagnose diabetes and assess BG levels over preceding 3 months, use may be limited due to variability in results; pair w fasting BG on same day (if values of both are in diabetic range, diagnosis of DM confirmed)
eAG average BG over last few months
glucosuria BG exceeds transport maximum for glucose of nephrons
ketonuria ketones are produced when glucose cannot be utilized, appear in urine when ketone formation elevated, more common in T1DM
islet cell autoantibodies (ICAs) present in T1DM
c-peptide test indicator endogenous insulin, c-peptide released when pancreas releases insulin, differentiate bw T1DM and T2DM
complications of DM hypo/hyperglycemia; acute: DKA (T1DM), HHS (T2DM); long-term systemic: blindness, kidney failure, neuropathy, cardiovascular disease, amputation
hypoglycemia (medical emergency!) bg <70mg/dL; excessive exogenous insulin, inadequate food intake, excessive physical activity, infection, illness, drug interaction
compensatory response to raise blood glucose epinephrine, glucagon, activation SNS
activation of SNS accounts for many signs and symptoms sweating, hunger, dizziness, headache, heart palpitations, confusion
need action plan to address hypoglycemia fast-acting carbs (15g), avoid fats (delay glucose absorption), transient response (provide meal or snack even if bg >70 mg/dL)
somogyi effect morning hyperglycemia present
somogyi effect due to insulin therapy (excessive dosage) or insulin peak during sleep causes hypoglycemia, compensatory mechanisms raise bg by morning, adjust insulin as needed
dawn phenomenon morning hyperglycemia present; nocturnal hypoglycemia doesnt occur; adjust meds, exercise, eating patterns
dawn phenomenon due to nocturnal elevations of growth hormone, dec cell utilization of glucose, raising bg levels
3 classic signs of dm polydipsia, polyuria, polyphagia
polydipsia high bg inc plasma osmolarity, fluid shifts from icf into ecf (cell dehydration), inc thirst
polyuria inc thirst and drinking (polydipsia), osmotic diuresis (glucose appears in urine (transport max of kidney exceeded)), water follows glucose, inc urine output
polyphagia if body cannpt use glucose: fat and muscle breakdown occur, weight loss w inc appetite, ketone levels may elevate
other signs of dm blurred vision, electrolyte imbalance, glycogenolysis and gluconeogenesis
blurred vision accumulation of glucose in aqueous fluid of eye, changes refractio of light
electrolyte imbalance fluid shifts: icf to ecf may cause dilutional hyponatremia; K+ moves out of cells (IC depletion of K+), false hyperkalemia (serum levels of K+ are elevated, but total body K+ not inc)
glycogenolysis and gluconeogenesis inc bg further, compounding problem; low bg is not problem, inability to use bg is the issue
diabetic ketoacidosis (DKA) requires immediate treatment develops in those w no insulin reserves (T1DM); high levels of ketone formation; 1/3 of children w T1DM first present w DKA
insulin lacking in presence of insulin, DKA does not occur, insulin prevents the lipolysis that leads to ketone formation, more common in T1DM than T2DM
without insulin (or glucose to use for fuel) ketone formation occurs ketones=strong acids, alter blood pH, metabolic acidosis
presentation of DKA nausea, vomiting, dehydration, tachycardia, hypotension, kussmaul's respirations, ketone body odor
diagnostic criteria DKA bg >250 mEq/L; pH <7.3; HCO3- <15 mEq/L; ketonuria; ketonemia
life threatening causes of DKA inadequate insulin, new onset of diabetes, stress of infection
cerebral edema is severe complication DKA 70% mortality rate if severe cerebral edema present, do not overhydrate, early signs=headache, confusion, lethargy; papilledema
hyperosmolar hyperglycemic syndrome (HHS) more common in T2DM than T1DM
ketones are not present, some insulin is present in Hyperosmolar Hyperglycemic Syndrome (HHS) bg>600 mg/dL, pH >7.3, HCO3- >18mEq/L, blood osmolarity >320 mOsm/L
hyperglycemia and inc plasma osmolarity in HHS hyperglycemia cant adequately facilitate glucose uptake, gluconeogenesis and glycogenolysis further inc bg; hyperosmolarity=osmotic diuresis and high bg, polyuria
hhs can develop insidiously over day to weeks
hhs presentation weakness, poor tissue turgor, tachycardia, rapid and thready pulse, confusion; 25% of patients present in coma
hhs causes infection (pneumonia, sepsis), noncompliance of DM management, substance abuse, and coexisting diseases
chronic complications of DM 1) diabetic foot ulcers/poor wound healings 2) infection 3) diabetic retinopathy-caused by damage to the blood vessels in the tissue at the back of the eyes, diabetic neuropathy and nephropathy, arteriosclerosis,
chronic complications of DM 2 peripheral angiopathy lack of circulation, autonomic neuropathy, immunosuppression
long-term complications in DM chronic hyperglycemia leads to damage of small and large arterial vessels; endothelial cells lining arterioles and arteries; poor wound healing (wbc functioning reduced); macrovascular angiopathy (cvd, pvd)
vascular damage (angiopathy) leads to downstream end-organ damage retina, glomeruli, neurons, autonomic neuropathy
DM and atherosclerosis acute cardiac events 2-4x more likely in DM patients; inc risk of atherosclerosis in both large and small arteries; vascular damage occurs due to several processes all resulting from hyperglycemia leading to oxidative stress
peripheral neuropathy distal, symmetric polyneuropathy; neural arteries damaged, begins in feet, progresses superiorly
sensorimotor nerves burning, tingling; pain sensation blunted (signs of injury or serious disease (MI) may be missed by patient (silent MI)
sensorimotor nerves 2 motor weakness (gait abnormality), mechanics of foot altered (charcot joint)
autonomic neuropathy affects cardiac system (tachycardia, hypotension),gi system (gastroparesis,gastric emptying abnormality,anorexia,nausea, bowel dysfunction);bladder problems(inc uti risk),erectile dysfunction,hypoglycemia(not apparent syptoms) dec sweating (hyperthermia/dry skin)
susceptibility to infection dec wbc function, inc colonization: s. aureus, candida (yeast)= high glucose changes pH of vagina, allowing candida to proliferate; chronic candida vaginitis may be presenting feature of diabetes
diabetic food complications most common cause of nontraumatic lower extremity amputation; peripheral neuropathy, poor circulation, suppressed immune response; inc infection susceptibility; can lead to gangrene/amputation or osteomyelitis (bone infection)
diabetic retinopathy and blindness leading cause of blindness in adults, retinal circulatory damage from high bg; proliferative retinopathy; regular fundoscopic exam and opthalmological examinations
retinal circulatory damage due to high bg signs: microaneurysms, macular edema, cotton wool spots (infarcted regions of retina)
proliferative retinopathy new vessel growth, vessels are fragile and may rupture leading to retinal detachment
diabetic nephropathy leads to renal failure; damage to glomerular capillary(microalbuminuria); glomeruluar basement membrane may eventually thicken due to glycosylation end-products; activation of RAAS w renal dysfunction compounds problem as bp elevates
gi system main functions ingestion, digestion, absorption, and elimination
upper gi tract mouth, esophagus, stomach, and small intestine
lower gi tract large intestine, rectum, anus
accessory organs of gi tract pancreas, gallbladder, spleen and liver
common disorders of gi tract gastroesophageal refulx disease (GERD), peptic ulcer disease (PUD), gastroenteritis
esophagus tube-like structure from mouth to stomach; has 4 sphincters=upper esophageal sphincter (UES), lower esophageal sphincter (LES), epiglottis-membrane protecting trachea, peristalsis-involuntary contraction and relaxation, wave like pushing food forward
stomach has fundus, body, pylorus; 2 sphincters=LES and pyloric
3 phases of digestion cephalic, gastric, intestinal
cephalic phase of digestion vagus nerve, Ach secretion
gastric phase of digestion gastric goblin cells secrete mucus, parietal cells secrete HCl and intrinsic factor (vitamin B12 absorption), chief cells secrete pepsinogen, G cells secrete gastrin
intestinal phase of digestion small intestine sends signals to slow stomach emptying
small intestine functions 1 absorption of nutrients/digestion; lined w villi/microvilli; enterogastric reflex-opens pyloric sphincter; duodenum-bile, pancreatic enzymes, and chyme come tg; secretin-ormone released by small intestine that stops gastric secretion;
small intestine functions 2 jejunum-absorb nutrients, glucose, iron, Ca, fat-soluble vitamins (ADEK); ileum-reabsorbs vitamin B12; enterophepatic circulation
enterophepatic circulation bile acids from ileum to liver, gastroileal reflex opens ileocecal valve to large intestine
assessment of gi tract swallowing, indigestion, eructation (belching), appetite, nausea/vomiting, appearance of emesis (vomit), meds (NSAIDS block protective mucus formation), unintentional weight loss or anorexia, last bowel movement, infections (candida albicans)
diagnosis of gi tract esophageal/gi pain may present similar to coronary event, upper endoscopy (most accurate), videocapsule endoscopy, barium xrays, H. pylori testing (peptic ulcer disease bacteria), cbc, cmp, kidney function, liver function, pancreas
dysphagia difficulty swallowing; begins w solid food, progresses to liquids
odynophagia painful swallowing
dysphagia is ususally neuromuscular dysfunction (cranial nerves)
structural abnormalities of esophagus esophageal structures, tumors/rings (schatzki ring), achalasia
achalasia esophageal motility problem
diagnosis of dysphagia barium swallow test; CXR rules out aspiration PNA,
dysphagia treatment thickened fluids/soft food, speech therapy and enteral feedings
esophagitis inflammation of esophagus
esophagitis irritation of mucosa of esophageal lining stomach acid, chemicals, vomiting; infection candida albicans, medications-NSAIDs bisphosphonates, H. pylori
who is at risk for esophagitis obese, pregnant, smokers, alcohol/coffee use
Mallory-weiss syndrome tear in lower esophagus
complaints of esophagitis burning sensation, dysphagia, odynophagia, nausea/vomiting
lifestyle changes for esophagitis stop smoking, weight loss, reduce alcohol/coffee intake, avoid NSAIDS
diagnosis of esophagitis endoscopy
gastroesophageal reflux disease (GERD) problem w tone of LES, regurgitation of stomach acid into esophagus
gastroparesis delayed stomach emptying also a problem
metaplasia of cells may occur w gerd esophageal epithelial cells transform to stomach-like columnar cells
barrett's esophagus precancerous change of cells at gastroesophageal junction and at high risk for developing cancer of esophagus
GERD signs/symptoms lying flat/bending over worsens symptoms, dysphagia, heartburn, epigastric pain, regurgitation, dyspepsia
dyspepsia acid indigestion
diagnosis of GERD endoscopy/manometry, barium studies and biopsy
upper gastrointestinal bleed (UGIB) bleeding in esophagus, stomach, or duodenum
causes of UGIB PUD, Esophageal varices, Esophageal cancer, Mallory-Weiss syndrome
acute UGIB rupture, tear or perforation leading to immediate blood loss; severe bleed=hypotension, hypovolemia, shock, tachycardia, tachypnea, pale/clammy skin; anxious, dizzy, weak, SOB, change in LOC
chronic UGIB small tear or opening causing gradual, small amount of blood loss; fatigue, lethargy, anemia, iron deficiency
UGIB signs/symptoms melena-visible blood in stool-black, tarry appearance; occult blood-presence of blood but not seen w naked eye; hematemesis-vomitus w bright red blood (active bleed); coffee ground emesis
coffee ground emesis indicates blood has mixed w acid of stomach (coagulated blood)
diagnosis of UGIB cbc=reduced Hb and Hct; iron defiiciency; fecal occult blood test (FOBT-3 tests on 3 diff days); endoscopy
esophageal varices engorged veins @distal end of esophagus: often due to portal vein HTN, veins may rupture-bleeding in esophagus, patient presents w signs of liver dysfunction, hematemesis, melena, hypotension, tachycardia, abdominal pain, confusion
diagnosis of esophageal varices ultrasound, mri, ct scan, endoscopy; ruptured varices are an emergency
squamous esophageal cancer cancer invades lining of esophagus
adenocarcinoma esophageal cancer glandular tissue near stomach
risks for esophageal cancer chronic alcohol use, smoking, barrett's esophagus (due to GERD)
signs/symtpoms of esophageal cancer dysphagia, weight loss, change in eating pattern, chronic cough, hoarse voice, hiccups, odynophagia
diagnosis of esophageal cancer endoscopy and tissue biopsy
hiatal hernia stomach pushes up thru opening in diaphragm, LES does not close properly leading to gastritis and GERD; can be asymptomatic
signs/symptoms of hiatal hernia dysphagia and epigastric discomfort
diagnosis of hiatal hernia endoscopy and upper GI barium xray
treatment of hiatal hernia weight loss, small meals, smoking cessation, HOB elevated when sleeping and not lie down after eating
pyloric stenosis constriction of pyloric sphincter= gastric propulsion of contents is compromised, can be congenital in babies; surgical repair needed
signs/symptoms of pyloric stenosis gastroparesis, abdominal pain, distention, nausea, vomiting, weight loss, dehydration; projectile vomiting-obstruction; firm abdomen over pylorus
acute gastritis inflammation of stomach lining; med like aspirin, nsaids, corticosteroids; infection, acute stress, bile reflux, alcohol abuse; complaints of heartburn, epigastric pain
diagnosis of acute gastritis endoscopy; must remove causative agents
chronic gastritis nonerosive gastritis; helicobacter pylori (h pylori); burning and gnawing epigastric pain, hematemesis, weight loss, precursor for development of stomach cancer
h pylori affects fundus and most common cause of chronic gastritis causes irritation and erosion of stomach mucosa, unlike acute gastritis, causes atrophy of glandular stomach lining (atrophic gastritis), dec intrinsic factor (b12 absorption), vicious cycle of bacterial replication and cellular tissue death occurs
diagnosis of chronic gastritis endoscopy, biopsy
peptic ulcer disease (PUD) inflammatory erosion of stomach or duodenum (more common in duodenum); hypersecretion of HCl, ineffective GI mucus production, and poor cellular repair
causes of peptic ulcer disease H. pylori, nsaids, stress, alcohol abuse, excessive caffeine, smoking; nsaids=counteract prostaglandin signal needed for gastric mucus production; dec mucus inc risk of ulcers
other causes of peptic ulcer disease genetic susceptibility, erosion-superficial layer of gastric mucosa affected, ulcer-extends beyond mucosa into muscularis layer
signs/symptoms of peptic ulcer disease epigastric, abdominal pain; episodes of pain occur bw meals, ab 2-3hrs after eating; pain is intense, burning and gnawing sensation; perforation of stomach or intenstine
diganosis of peptic ulcer disease serology=blood sample tested for presence of antibodiers to h. pylori; rapid urease test=endoscopic diagnostic test of choice for detection of h. pylori; endoscopy
zollinger-ellison syndrome gastrin-secreting tumor, excessive HCl leading to ulcer, severe epigastric pain, gi bleeding, vomiting
diagnosis of zollinger-ellison syndrome elevated gastrin in blood, ct/mri to visualize tumor
dumping syndrome rapid gastric emptying; common after bariatric surgery; hypotonic fluid enters intestines, causing fluid shift into intestines (hypovolemia, hypotension, tachycardia)
two phases of dumping syndrome early=30 mins after eating, cramping, nausesa, diarrhea, tachycardia, diaphoresis; late=2-3hrs after eating, epigastric fullness, palpitations, hypoglycemia
diagnosis of dumping syndrome endoscopy and upper gi series
diet management-frequent, small meals and fluids in bw meals dumping syndrome life changes
hernia intestinal protrusion thru abdominal wall
risk factors for hernia family history, obesity, ascites, pregnancy, heavy lifting, chronic cough or constipation
inguinal hernia most common
reducible hernia returned to normal position w manual pressure
incarceration hernia loop of intestine trapped bw muscle fibers
strangulation hernia blood supply to hernia compromised by pressure
gastroenteritis irritation of lining of stomach, small or large intestine by pathogen or toxin; transmitted person to person, water or foodborne; inc fluid shift into lumen of intestine, resulting in diarrhea; damage of villi by pathogen or toxins
infectious microorganisms for gastroenteritis norovirus, rotavirus, shigella, e. coli, giardia
gastroenteritis diarrhea osmotic dec absorption inc osmotic load in lumen, attracting water
gastroenteritis diarrhea inflammatory mucosal lining inflamed, unable to absorb fluid or nutrients
gastroenteritis diarrhea secretory organism stimulates intestinal secretions
gastroenteritis diarrhea motility intestinal neuromuscular disorders
symptoms of gastroenteritis diarrhea nausea, vomiting, diarrhea and abdominal cramps; borborygmi
borborygmi rushing of fluids and gurgling sounds
red flags of gastroenteritis diarrhea severe volume depletion, abnormal electrolytes, renal damage, blood stool, weight loss, severe abdominal pain, symptoms more than a week, >65 yrs, pregnant, hospitalization or antibiotic use in previous 6 months, cormorbidities
celiac disease (sprue) (gluten-sensitive enteropathy) hypersensitivity reaction to gluten (gluten-derived protein (gliadin), unknown cause/autoimmune disease
celiac disease gluten ingestion results in bloating and gas, steatorrhea may develop, malnutrition is concern
steatorrhea loss of fat in stools
diagnosis of celiac disease serology, celiac panel, positive antibody titer of IgA antitissue transglutaminase (IgA TTG), intestinal biopsy
short bowel syndrome any process that leaves <200cm of small intestine (normal is 600cm); several require removal of part of intestine (crohns disease, tumor, stricturesm ischemia)
pathology of short bowel syndrome depends on amount of tissue removed and health of remaining tissue; remaining intestine eventually adapts and inc absorptive capabilities
diagnosis of short bowel syndrome barium contrast xray, abdominal ct
small bowel obstruction (SBO) acute, chronic, partial, complete
acute sbo adhesions (post-surgical is major cause) or herniation
chronic sbo inflammatory disease or tumors
partial sbo dec the flow of intestinal contents
complete sbo prevents passage of all contents and fluid, considered surgical emergency
signs/symptoms of sbo presentation will depend on severity of obstruction; pain, nausea, vomiting, hyperactive bowel sounds; diarrhea may be present in partial obstruction
diagnosis of sbo abdominal xray
treatment of sbo nasogastric tube-decompression, surgery for complete obstructions
peritonitis inflammation of peritoneum, caused by bacterial infection or leakage of intestinal content into peritoneal cavity
classification based on perforation of organ primary (no perforation); secondary (perforation of organ, release of contents into cavity)
paralytic ileus dec motility of intestine w peritonitis, undigested content not moved further
other peritonitis complication abdominal abscess, cardiac arrhythmias and shock
classic triad of peritonitis abdominal pain (inflamed tissues), abdominal rigidity, rebound tenderness
signs/symptoms of peritonitis hypotension, tachycardia, tachypnea, clammy skin, dec or absent bowel sounds and oliguria; blood and fluid shift toward abdomen
diagnosis of peritonitis abdominal xray w air or fluid in abdominal cavity, cbc w elevated wbc/neutrophils, paracentesis-remove peritoneal fluid to analyze; ct scan or emergency surgical laparotomy
alterations in integrity of GI wall of large intestine inflammatory bowel disease (IBD)= crohns disease and ulcerative colitis; inflammatory conditions=appendicitis and diverticulitis
alterations in motility of large intestine irritable bowel syndrome (IBS), bowel obstruction or intestinal herniation
large intestine is how long 1.5 m long
large intestine functions absorb water and electrolytes; store feces until defecation
parts of large intestine cecum (blind pouch), appendix (at end of cecum), ascending colon, transverse colon, descending colon, sigmoid colon, rectum, anus
muscles of large intestine longitudinal (taenia coli) and circular (haustra)
movements of large intestine haustrations (shuffling effect) and propulsion (mass movements)
GI wall begins @ upper 1/3 of esophagus and has 5 layers 1. inner (mucosa) layer 2. middle (submucosa) layer 3. circular layer-peristalsis 4. longitudinal layer-facilitate peristaltic movement 5. outer layer
inner (mucosa) layer goblet cells-produce mucus to lubricate intestines and protect; columnar epithelial cells absorb fluid/electrolytes
middle (submucosa) layer connective tissue, blood vessels, nerves and cells that secrete digestive enzymes
outer layer peritoneal serosas is loosely attached to the entire outer wall of the intestine
large intestine absorption smooth surface for absorption of water and electrolytes (Na and Cl)=water follow by osmosis; no digestive enzymes=most absorption in small intestine, normal flora bacteria break down proteins, carbs, bile salts; bacteria=1/3 bulk of feces
defecation uses internal and external anal sphincter; reflex center; gas (flatus); and borborygmi
reflex center sacral portion of spinal cord
gas (flatus) swallowed air, bacterial fermentation
borborygmi rushing of fluids and gurgling sounds
intestinal motility dysfunction obstructive lesion, intestinal pseudo-obstruction, ibs, fecal incontinence, constipation, acute colonic pseudo-obstruction
acute colonic pseudo-obstruction same symptoms of nonpropulsion, but no obstruction (neuromuscular dysfunction), medications affect motility (opiates, benzos)
assessment of GI info about abdominal pain, nausea, excessive gas, rectal fullness, weight changes, bowel movements, diet, laxative, or enema usage, assess for bowel obstruction, pain location, pain type
colic pain occurs in waves
right lower quadrant tenderness appendicitis (inflammation of appendix)
left lower quadrant tenderness diverticulitits (inflammation of diverticulum; often a tear resulting in inflammation)
upper right quadrant tenderness murphy's sign, cholecystitis
acute abdomen peritonitis triad (fever, abdominal pain, increasing ascites (fluid buildup)
rectal examination pain elicited w appendicitis, hard stool w fecal impaction
female physical examination on GI pelvic exam to rule out gynecological issues, pregnancy test to rule out pregnancy
diagnosis of GI issue FOBT (fecal occult blood test), CBC, CMP, elevated serum amylase (pancreatitis), abdominal and chest xray, contrast barium images, ct scan, colonoscopy, pain (valuable diagnostic clue)
constipation common especially in elderly less than 3 stools per week, primary or secondary to other diseases, meds
severe constipation results in fecal impaction and obstipation
fecal impaction hard stool lodged in sigmoid colon and rectum, can develop liquid stools to pass around impaction
obstipation sensation to defecate w no passage of stool, liquid, or gas from colon
diagnosis of constipation barium contrast studies, endoscopy studies, colonic transmit studies in select individuals
inflammatory bowel disease (ibd) crohns disease and ulcerative colitis (uc), chronic/incurable; more prevalent in young adult, etiology unclear; may have autoimmune component, infectious agents, genetic component
crohn's disease chronic, transmural (entire gi wall) inflammatory process; can affect gi tract from mouth to anus (terminal ileum and ascending colon most common)
skip lesions of crohns disease areas of disease separated by healthy areas
cobblestone of crohns granulomas form in intestine
toxic megacolon (chrons) extreme dilation of disease colon; can cause complete obstruction or life-threatening perforation
remissions and exacerbations of crohns w episodes of diarrhea and abdominal pain
characteristics seen w crohns hyperactive bowel sounds, abdominal tenderness, weight loss, anorexia, nausea, vomiting, diarrhea, pallor, fever
malabsorption and nutritional deficiencies are common w crohns disease anemia from loss of blood in stool, dehydration, arthritis, uveitis, cheilitis, and dermatology issues may be present
uveitis eye inflammation
cheilitis lip inflammation
diagnosis of crohns disease colonoscopy (differentiaties bw crohns and UC), biopsy, crohns disease activity index (CDAI)
crohns disease activity index (CDAI) patient symptoms grading system and considered to be in one of 4 disease states= clinical remission, mild, moderate, severe
complications of crohns disease obstruction, chronic inflammation leading to stricture, microperforations, inc DVT and PE risk
ulcerative colitis (UC) involves large intestine, begins in rectum and moves upward; not transmural
ulcerative colitis (UC) inc risk for colon cancer peak age of onset=15-25 w another peak at 55-65
etiology of ulcerative colitis is unclear, autoimmune, infection and genetic component
pseudopolyps markers of severe inflammation in ulcerative colitis
toxic megacolon and severe uc lead to damage to nerves
uc has similar presentation of symptoms as crohns diarrhea, abdominal pain, and distention; fever, leukocytosis, uveitis, erythema nodosum (red bumps), arthritis
diagnosis of ulcerative colitis (UC) distinguished from crohns
ULCERATIVE COLITIS vs crohns affects large intestine, affects rectum upward toward colon, only affects upper layers of intestinal wall, pseudopolyps, no fistula or anal fissure, @ risk for colon cancer
fistula abnormal tunnel from colon to the surface of skin or to an internal organ like bladder, small intestine or vagina
ulcerative colitis vs CROHNS affects mouth to anus, affects gi tract w skip lesions, affects entire thickness of intestinal wall (transmural), cobblestone, anal fistula and anal fissure, does not predispose to cancer
large bowel obstruction (LBO) mechanical or nonmechanical; bowel becomes dilated proximal to obstruction, distention of abdomen induces peristalsis and perforation may occur
mechanical large bowel obstruction physical block (adhesion)
nonmechanical large bowel obstruction dysmotility, neurological
large bowel obstruction blocks moving of contents, partial or complete, acute or chronic, reversible or irreversible
peristalsis involuntary constriction of muscles of intestine
perforation hole that develops thru the wall of a body organ
if diagnosis/treatment for large bowel obstruction does not occur in first 24hrs high mortality rate
symptoms of large bowel obstruction abdominal pain, distention, tenderness, rigidity; partial obstruction, complete obstruction
partial obstruction high-pitched bowel sounds, gas or bowel movements possible, diarrhea
complete obstruction no bowel sounds, no feces in rectum, no bowel movement or gas production
diagnosis of large bowel obstruction abdominal xray, ct scan or mri; colonoscopy
appendicitis inflammation of appendix (blind-ended pouch off cecum); narrowing of appendix lumen can result from nearby blockages, development of medium for bacterial growth
common cause of appendicitis acute abdomen
appendix may rupture causing peritonitis abdominal pain originates umbilical region and move to rlq (mcburney's point); 1-3 days from onset of vague umbilical pain to the localized rlq pain
abdominal distention and rebound tenderness females: pelvic exam and pregnancy test
appendicitis signs positive psoas sign and obturator sign, legs may be drawn up in fetal position due to pain
psoas sign flex right leg against resistance or roll on left side and extend leg; pain in ruq
obturator sign flex knee and hip to 90 degrees, internally rotate thigh and extened calf outward; pain in rlq
appendicitis diagnosis physical examination, females: pregnancy test; ct scan (most accurate); elevated crp (inflammation) and wbc levels; urinalysis to rule out kidney stones and pyelonephritis; high 5-HIAA (serotonin breakdown product) may be present in urine
irritable bowel-syndrome (IBS) abdominal pain and altered bowel activity; abdominal discomfort and alterations of diarrhea and constipation
IBS has no specific pathology and unknown etiology should not be confused w inflammatory bowel disease; chronic abdominal pain lasting at least 6 months, w bouts of diarrhea and constipation
risk factors for IBS female, <40, stress; alarm symptoms require further testing weight loss, iron deficiency anemia
diagnosis of IBS patient symptoms, diagnostic tests to rule out other conditions
diverticulosis bowel wall has weakened areas; can collect intestinal contents and form a colonic obstruction; most common in sigmoid and descending colon
diverticula small outpouchings formed
diverticulitis diverticula inflammation
diverticular disease develops due to weakness of bowel wall, inc intraluminal pressure
risk factor for diverticular disease low fiber diet
signs/symptoms of diverticular disease depend on severity of inflammation and location in bowels, bowel habits may be altered; LLQ or RLQ depending on area affected; low grade fever, tachycardia, and anorexia; diverticulosis may be asymptomatic
diagnosis of diverticular disease abdominal xray, lower gi series, ct scan
volvulus twisting of large intestine; sigmoid volvulus most common; results in obstruction and ischemia
symptoms of volvulus bilious vomiting, abdominal pain (colicky and then steady), abdominal tenderness, anorexia, blood and mucus in stool and eventually shock
diagnosis volvulus abdominopelvic ct scan, abdominal xray
treatment for volvulus surgical
hemorrhoids are in varicose veins in perianal region
venous pooling in rectal blood vessels constipation and straining during defecation, high pressure w/in portal vein of liver, anal intercourse, pregnancy, prolonged sitting, aging, lack of fiber in diet
signs/symptoms of hemorrhoids hemorrhoids can bleed, hematochezia, prolapsed hemorrhoid,
hematochezia bleeding from hemorrhoids, small amounts, bright red
prolapsed hemorrhoid straining at defecation pushes an internal hemorrhoid thru anal meatus
diagnosis of hemorrhoid digital rectal exam, anoscopy
liver located in right upper quadrant (RUQ)
blood supply of liver hepatic artery (25%) and portal vein (75%)(venous drainage from GI tract)
hepatocytes functional cells of liver
kupffer cells macrophages of liver to help detoxify blood
bile made by liver and stored in gallbladder
hepatic duct empties into common bile duct empties into duodenum
enterohepatic recylcing bile salts reabsorbed from ileum recycled back to liver
bilirubin found in liver yellow-colored compounds, rbc breakdown
bilirubin metabolism 1 hemoglobin broken down to heme & globin; heme broken to down to iron & porphyrin; porphyrin converted to biliverdin; biliverdin converted to free or unconjugated bilirubin; unconjugated bilirubin travels to liver
bilirubin metabolism 2 in liver, unconjugated bilirubin converted to water-soluble form (conjugation); conjugated bilirubin excreted in bile, some conjugated bilirubin in colon converted to urobilinogen by bacteria, later excreted in urine (yellow color)
unconjugated bilirubin aka indirect bilirubin, not water soluble
conjugated bilirubin aka direct bilirubin, water soluble
functions of liver fat metabolism, protein metabolism, carbohydrate metabolism, hematologic role, endocrine role, detoxification,
other functions of liver storage of vitamins, iron, copper produces insulin-like growth factor 1; synthesizes thrombopoietin for platelet synthesis; produces angiotensinogen (RAAS), immune system
fat metabolism of liver bile from liver emulsifies fat, fats broken down in intestines, absorbed in portal vein and returned to liver, liver synchronizes cholesterol
protein metabolism of liver synthesizes albumin, performs deamination, removes nitrogen from proteins and converts to NH3; NH3 reabsorbed into blood and integrated into urea and excreted in urine
carbohydrate metabolism of liver glycogenesis, glycogenolysis, gluconeogenesis
glycogenesis produces and stores glycogen in liver
glycogenolysis breakdown of glycogen during stress or starvation
gluconeogenesis convert amino acids and glycerol into glucose
hematologic role synthesizes fibrinogen, coagulation factors
endocrine role of liver glucagon acts in liver to help w glycogenolysis and gluconeogenesis; stimulates lipolysis-converts fatty acids to ketones
detoxification of liver ingested substances and drugs; portal vein brings venous drainage from gi tract to liver; biotransformation and first pass effect-reduce bioavailability
liver dysfunction dec clotting factor synthesis, dec albumin, dec detoxification on activity, dec storage of nutrients, dec conjugation of bilirubin, dec deamination activity
jaundice yellowing of skin and sclera
hyperbilirubinemia high bilirubin levels in blood, leads to jaundice (icterus)
3 specific etiologies of liver dysfunction excessive rbc hemolysis, hepatocellular injury, bile duct obstruction
excessive rbc hemolysis prehepatic jaundice, elevated direct and indirect bilirubin
hepatocellular injury intrahepatic jaundice, elevated indirect bilirubin
bile duct obstruction posthepatic jaundice, elevated direct bilirubin
hepatocyte inflammation caused by virus, drugs, or toxic substances
hepatitis virus= a,b,c,d,e cmv and epstein-barr virus can also cause inflammation, viral hepatitis may become chronic; inc risk for hepatocellular cancer
toxic hepatitis liver affected by drugs (acetaminophen), enzymes (cytochrome P450 system)
nonalcoholic fatty liver disease (NAFLD) fatty buildup in liver, can lead to cirrhosis
severe hepatocellular injury may progress to hepatic failure lead to hepatic encephalopathy
other things that can affect hepatocyte inflammation/infection alcohol damage and nonalcoholic steatosis (NASH)
biliary obstruction blockage of any duct that carries bile from liver to intestines; hyperbilirubinemia
cholelithiasis gallstone
cholecystitis inflammation of gallbladder
cholestasis conjugated bilirubin backs up; builds up in blood
liver disease risk factors excessive alcohol abuse, certain medications, high cholesterol or triglycerides, chronic hbv or hcv, iron overload, malnutrition, metabolic syndrome/obesity, rapid weight loss, toxins/chemicals
signs of liver disease anorexia, ascites, dark urine, hepatomegaly, hyperbilirubinemia, jaundice, RUQ tenderness, splenomegaly, steatorrhea, pruritis, spider angioma, capsut medusa
steatorrhea fatty stool
pruritis sensation causes wanting to scratch
spider angioma dialtion of end vasculature found beneath skin surface
capsut medusa distended and engorged paraumbilical veins that radiate from umbilicus across abdomen to join systemic veins
diagnostic tests for liver disorders liver enzymes, direct (conjugated) and indirect (unconjugated)bilirubin levels, albumin level, prothrombin leve, hepatitis serology, ultrasound, ct scan, mri, liver biopsy (GOLD STANDARD)
liver enzyme tests alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatasre
hepatits a virus (HAV) (vaccine available) transmitted by the fecal-oral route=virus shed in feces; virus killed by thorough cooking; endemic in asia, africa, mexicp, and south america
hepatitis b virus (HBV) (vaccine available) transmitted by blood products, body fluids, or sexual contact; doesnt directly kill cell, but host's immune sytem destorys viral-infected cells; most dont recover completely and chronic hbv can lead to hepatocellular cancer
diagnosis of hbv IgM-type=anti-HBc antibodies//acute infection; IgG-type=anti-HBc antibodies//chronic infection; contacts can obtain HBIg for rapid, passive immunity
hepatitis c virus (HCV) (vaccine available) transmitted via blood and iv drug use, sex transmission not as likely; acute infection usually mild, most develop chronic hepatitis, long incubation period=2wks-8mths and patient is asymptomatic and can spread virus
diagnosis of hcv HCV-RNA assay and HCV genotyping
hepatitis d virus (requires helper function of hbv) transmission thru iv drug use or sex contact
hepatitis e virus (similar to hav) fecal-oral transmission
signs/symptoms of hepatitis fever, abdominal pain, flu-like symptoms, nausea/vomiting, fatigue, malaise, myalgias, arthralgias, mild headache, anorexia, loss of taste for food, smokers lose their taste for tobacco, hepatomegaly,jaundice,stool w pale appearance,dark urine,pruritis
nonalcoholic fatty liver disease (NAFLD) most common cause of chronic liver disease in us
etiology of NAFLD unclear, associated w metabolic syndrome, insulin resistance, ad obesity
NAFLD is when hepatocytes accumulate triglycerides (steatosis), accumulation of fat disrupts cell function, cells can rupture causing inflammatory response damaging to liver; most common cause of chronic liver disease in US
steatosis >5% liver contains fat
nonalcoholic steatohepatitis (NASH) extreme form of NAFLD in which scarring and inflammation of liver occurs; leads to hepatocellular carcinoma
signs/symptoms of NAFLD mild cases=none, abnormal liver enzyme levels may be present; NASH=obvious signs of liver impairment like edema, jaundice, fatigue-->can lead to hepatocellular carcinoma (HCC)
diagnosis of NAFLD no specific biomarkers or blood test; liver biopsy is key test (can have false negative if sample not taken from high fat content area); NAFLD fibrosis score
patient who is obses, metabolic syndrome w elevated liver enzymes should be evaluated for NAFLD
NAFLD fibrosis score age, hyperglycemia, body mass index (BMI), platelet count, albumin level, and ratio of AST to ALT
alcohol liver disease aka alcohol cirrhosis, develops over long period of time and is permanent
alcohol hepatitis acute disorder that develops reversible and transient symptoms, will resolve w cessation of alcohol ingestion, long-term effects often remain
men alcohol consumption 60-80g of alcohol/day for 10 yrs usually develop cirrhosis
women alcohol consumption 20-40g of alcohol/day for 10 yrs usually develop cirrhosis
ingestion of 160g of alcohol per day 25-fold inc risk of developing alcoholic liver disease
one beer 12 g
alcohol is potent toxin to hepatocytes hepatocytes can regenerate but are susceptible to repeated damage
steatosis initial cellular change
alcoholic liver disease can progress to cirrhosis
common for patients to not provide accurate history of alcohol intake
acute alcoholic hepatitis RUQ pain/tenderness, nausea, malaise, low grade fever, jaundice, dark urine, hepatomegaly
severe alcoholic hepatitis hepatic encephalopathy, coagulation dysfunction, spontaneous bruising and bleeding, jaundice, hematemesis
alcoholic liver disease hepatomegaly and splenomegaly, portal HTN w esophageal varices, ascites, spider angioma, proximal muscle wasting, gynecomastia in males, withdrawal symptoms=restless, mood, disturbance, delirium tremens, seizures
diagnosis of alcoholic liver disease AST and ALT elevation, hypertriglyceridemia and hypercholesterolemia, hyperbilirubinemia and hypoalbuminemia, coagulation disturbances, liver biopsy to confirm changes
cirrhosis silent and gradual; severe scarring of liver
liver is irreversibly damaged w collagen and connective tissue; portal HTN develops
causes of cirrhosis/liver failure hcv, alcoholic liver disease, NAFLD
liver failure complications portal hypertension, caput medusa, dec bile synthesis (dec fat digestion and steatorrhea), dec coagulation factors (bruising, bleeding)
portal hypertension esophageal varices, hematemesis, ascites
dec albumin synthesis edema; liver failure complication
lack of thrombopoietin low platelets; liver failure complication
dec conjugation of bilirubin jaundice; liver failure complication
loss of detoxification high level of drugs, ammonia levels inc leading to encephalopathy; liver failure complication
loss of deamination process high nitrogen in blood, lyses rbcs and platelets; anemia and thrombocytopenia; liver failure complication
dec fat-soluble vitamins absorbed hypocalcemia; liver failure complication
hepatic encephalopathy confusion, stupor, asterixis, cerebral edema and poor prognosis; liver failure complication
asterixis flapping tremor of wrists
hepatorenal syndrome renal failure asz well; liver failure complication
diagnosis of liver failure cbc, metabolic panel, liver panel
gallbladder function digestion and elimination; stores bile (synthesized in liver) which emulsifies fat; releases bile into cystic duct which empties into common bile duct; enterohepatic circulation
bile consists of bile acids, phospholipids and cholesterol;
released in response to signal from small intestine hormone cholecystokinin (CCK)
pancreas has endocrine and exocrine component
exocrine component of pancreas digestive secretions; lipase, amylase, peptidases; bicarbonate=neutralize acid in intestines
exocrine secretions ar secreted into pancreatic duct which drains into common bile duct
exocrine enzymes are triggered by hormone secretin produced in the intestines when we eat
gallbladder dysfunction motility disturbances and stasis of bile
choledocholithiasis stones in common bile duct-back up of bile
cholelithiasis stones in gallbladder itself
biliary sludge precursor to gallstones, combination of bile acids, bile pigments, and cholesterol
biliary stasis delayed emptying of the gallbladder, leads to stone formation
cholangitis gallstones enter the cystic duct, cause obstruction and ductal inflammation
gallstones can obstruct flow in the common bile duct, leading to backup of bile into liver leading to hepatic dysfunction; can move into the pancreas and cause pancreatitis
biliary colic pain associated w irritation of gallbladder, secondary to gallstones
biliary colic has steady and intense pain can last from 30 mins to several hrs; nausea, vomiting, and RUQ pain; murphy's sign
murphy's sign take a deep breath and pain with palpating RUQ- acute cholecystitis
pain from biliary colic often radiates to scapula and upper thoracic region
biliary colic leads to dilation of biliary tract, elevation of plasma liver enzymes, elevation of serum bilirubin
cholecystitis acute or chronic inflammation of gallbladder; due to gallstones (most common), cholecystectomy performed, gallstones are 2-3x more common in women
acalculous cholecystitis inflammation without stones
risks for cholecystitis female, >40yrs, obesity, high-calorie diet, oral conceptives
empyema infection of gallbladder leading to purulent effusion
cholecystitis is associated episodic colicky pain after eating and positive murphys sign
collins sign pain may refer to right scapular
symptoms w cholecystitis anorexia, nausea, vomiting, feeling of fullness
ruptured gallbladder medical emergency leading to peritonitis and sepsis
cancer of gallbladder >65; intense pain, weight loss, jaundice, anorexia, nausea
cancer of biliary tract (cholangiocarcinoma) is very rare
courvoisier sign w cancer of gallbladder palpable mass in RUQ
virchow's node w cancer of gallbladder enlargement of left sided supraclavicular lymph node
signs/symptoms occur late in cancer of gallbladder frequently metastasis occurs; high mortality rates//die w/in 1 yr
diagnosis of gallbladder cancer elevated wbc, esr, c-rp, liver function tests; serum amylase and lipase elevate w pancreatic inflammation; abdominal ultrasound/ct scan; cholecystogram; cholescintigraphy (HIDA scan); percutaneous transhepatic cholangiopancreatography (PTC); ERCP
cholecystogram swallow pill and have xrays
cholescintigraphy (HIDA scan) tracer travels into bile and track the tracer
percutaneous transhepatic cholangiopancreatography (PTC) dye injected directly into liver and take xrays
endoscopic retrograde cholangiopancreatography (ERCP) invasive procedure that use an endoscope w camera to inspect the anatomy of the biliary tract
pancreatic exocrine dysfunction digestive secretions
pancreatitis inflammation of pancrease, causes pancreatic insufficiency, malabsorption, and diabetes; acute vs chronic;
acute pancreatitis forms caused by alcohol, gallstones, high triglycerides, meds or surgery; potentially lethal
autodigestion by pancreas' own digestive enzymes
chronic pancreatitis repeated episodes of inflammation leading to fibrosis and atrophy
acute pancreatitis --> lethal dysfunctional pancreas undergoes inflammation and cell injury; leakage of pancreatic digestive enzymes into glandular parenchyma; hemorrhagic pancreatitis=retroperitoneal blood accumlation
acute pancreatitis risk factors biliary disease (cholelithiasis), excessive alcohol ingestion, hypertriglyceridemia, infections
severe abdominal pain w acute pancreatitis sudden in onset, gradually intensifies; located in epigastric region, pain can radiate to the back
symptoms of acute pancreatitis nausea, vomiting, diarrhea, anorexia, tachycardia, dec bowel sounds
signs of acute pancreatitis abdominal tenderness, guarding, distention, pale, diaphoretic, lethargic; cullen sign, grey turner sign; patients may be pale and diaphoretic; may exhibit jaundice
cullen sign discoloration around umbilicus due to hemorrhage around stomach
grey turner sign discoloration around flanks, retroperitoneal bleeding around flanks
ransom criteria on admission age>55, wbc>16,000; liver enzyme=lactic dehydrogenase>600 U/L; liver enzyme=aspartate aminotransferase >120 U/L; glucose>10mmol/L
ransom criteria w/in 48 hrs hematocrit dec<10%; BUN rise>0.9mmol/L; calcium <2mmol; PO2 <60mmHg; base deficit>4; fluid sequestration>6L
diagnosis of acute pancreatitis cbc, calcium, glucose, BUN, amylase and lipase (elevated lipase key sign of acute pancreatitis); abdominal US; ct scan; MRCP (magnetic resonance cholangiopancreatography)
complications of acute pancreatitis infected pancreatic necrosis; pseudocyst
pseudocyst occurs in 10-20% of acute cases of pancreatitis; collection of fluid rich pancreatic enzymes, blood and necrotic tissue
complications of acute pancratitis cardiovascular (hypotension); renal (kidney failure due to dec perfusion); respiratory (atelectasis, respiratory failure)
chronic pancreatitis chronic inflammation does not heal and leads to permanent damage; chronic, heavy alcohol use is primary risk factor
chronic pancreatitis commonly develops after several bouts of acute pancreatitis fibrosis and scarring; upper abdominal pain radiating to back or no pain at all; weight loss, anorexia, nausea, vomiting, diarrhea, steatorrhea, malabsorption; serum amylase and lipase-slightly elevated or may be normal
acute pancreatitis think acute, isolated episode, active inflammation, sudden and severe, short-term (days-weeks); elevated pancreatic enzymes; common causes=alcohol, gallstones
chronic pancreatitis think chronic, ongoing disease, chronic changes/damage; symptoms fluctuate, long term (months-years); normal pancreatic enzymes; common causes=recurrent acute episodes, alcohol, hereditary, diseass
pancreatic cancer risk factors cigarette smoking, obesity, diabetes mellitus, chronic pancreattitis, consumption of nitrites; exocrine or endocrine cell=exocrine ducts=ductal adenocarcinomas
pancreatic cancer tumor may compromise bile duct, leading to bile backup and jaundice (painless jaundice 1st common sign of cancer)
pancreatic cancer may present with vague back pain and worsens, especially in supine position weight loss, nausea, vomiting, anorexia, pruritis, darkening of urine, hyperbilirubinemia, steatorrhea
pancreatic cancer signs virchows sign and courvoisier's sign
courvoisiers sign jaundice and gallbladder that is enlarged but not painful
common w pancreatic cancer portal vein HTN, ascites, hepatomegaly, splenomegaly
new diagnosis of DM at later age and may present w DVT
diagnosis of pancreatic cancer ct scan of abdomen and tumor markers
chvostek's sign facial contraction when touch facial nerve
trousseau's sign spasm in upper arm bc of ischemia and pressure
function of t3,t4 control basal metabolic rate
function of calcitonin regulate levels of calcium & phosphate in blood
symptoms of addison's disease darkened pigmentation on skin (bronzing) across knuckles or around neck
prolactin-releasing hormone (hypothalamus) stimulates secretion of prolactin
4 main cells of stomach mucus cells, parietal cells, chief cells, G cells
mucus cells secrete alkaline mucus that protects epithelium against sheer stress and acid
parietal cells secrete hydrochloric acid
chief cells secrete pepsin (proteolytic enzyme)
G cells secrete gastrin
2 valves of small intestine are pyloric sphincter and ileocecal valve
contents move from small intestine to large intestine cecum-->ascending colon-->transverse colon-->descending colon-->sigmoid colon-->rectum-->anus
rovsing's sign (appendicitis) firmly press llq and pain in rlq
rebound tenderness pain when removed pressure from abdomen, not when applied
hemorrhoid dilated, swollen vessels in perianal region and can be either internal or external
risk factors for pancreatic cancer cigarette smoking, obesity, diabetes mellitus, chronic pancreatitis, consumption of nitrites
symptoms w pancreatic tumor on head of pancreas jaundice, itchy skin, dark pee, pale poop, loss of appetite, weight loss, tired/no energy
symptoms w late stage pancreatic cancer pain in back/abdomen, weight loss, anorexia, nausea, stool color change, abdominal bloating, dark urine, changes in breathing
Created by: cat9210
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