PHASS PAMS-608A Study Guide (2013-14 Sailer)
- University of St. Francis
- Physician Assistant Studies
- Physician Assistant Studies Pams 608a
- PHASS PAMS-608A Study Guide (2013-14 Sailer)
Created: 2014-04-17Size: 4114 Views: 42
Last Modified: 2014-06-16
Last Modified: 2014-06-16
3 ways cells respond to injury:
mild, short lived change, ride it out
2. cellular adaptation
3. necrosis or apoptosis
severe or prolonged-cell death
2 causes of reversible cell injury:
1. hydropic swelling
caused by lack of ATP
2. intracellular accumulations
cause of Hydropic swelling and its characteristics
Malfunction of Na/K pump-no ATP-Na stays in cell-water follows via osmosis
1. large pale cytoplasm
2. dilated ER
3. Swollen mitochondria
suffix for organ enlargement
What are Intracellular accumulations & where do they happen?
accumulations of materials that cells cannot immediately use or dispose of
in cytoplasm (lysosomes) or nucleus
3 categories of intracellular accumulations
1. normal body substances in abnormally large amounts
2. abnormal endogenous products
3. exogenous products
ex. of accumulation of normal components and causes
fatty liver: accumulation of triglycerides
2. diabetes mellitus
3. disruption of hepatic metabolism of lipids (alcoholism)
ex. of endogenous accumulation
genetic disorders of metabolism
1. normal enzyme replaced with abnormal (substance formed can't be removed/replaced)
2. enzyme missing (intermediate accumulates)
Exs. of pigment accumulation (endogenous & exogenous)
1. Icterus (juandice) bilirubin
2. lipofuscin (indigestible residues during normal turnover of cellular structures-as age, build up in: liver, heart and nerves (heart and nerves non-mitotic so non reversible)
carbon (black lungs)
lead (blue lines on skin)
tattoos (macrophages can't move)
Cellular adaptations can change cell in terms of __ __ __
are reversible T or F?
size, number (if mitotic), type of cell (but stay in same group)
T (may take awhile)
5 types of cellular adaptation:
(2&3 often happen together)
What are the molecular mechanisms of cellular adaptation
1. housekeeping genes: all cells have similar housekeepers->change size and number
2. differentiation genes: cells have diff. differentiation genes depending on function. > change cell types
what is atrophy?
decrease cell size.
2. denervation (paralysis)
3. loss of endocrine stimulation (menapause)
4. inadequate nutrition
5. ischemia (no O2)
What is Hypertrophy?
2 most common tissues types it occurs in?
increase in cell size & functional mass
1. normal physiology:exercise
a. adaptive: thickening to maintain function. ex: male that can't pee
b. compensatory: after removal of portion. ex: kidney *hypertrophy + hyperplasia) or heart
skeletal m. & cardiac m (non mitotic can't increase in #)
What is hyperplasia?
increase in # of cells in tissues capable of mitosis
1. physiologic stimuli:
a. hormonal: prego-bigger boobs/uterus
b. compensatory: organ regeneration: liver
2.non-physiologic stimuli: excess hormonal or GFS: warts
3. normal response of connective tissue during wound healing
What is metaplasia?
replace 1 cell type with another
reprogramming of stem cells (never outside primary cell group)
due to chronic irritation and inflammation
ex: cervix-squamous to cuboidal (pap smear)
ex: smokers: damage pseudo stratified cilia, replace with stratified squamous
can be precursor to cancer
What is dysplasia?
frequent in what tissues?
disorderly cell growth
chronic irritation & inflammation
frequent in metaplastic squamous epithelium of respiratory tract & cervix
can be precursor for cancer
ex: reflux gastritus-acid in esophagus
cervix: pap smears
reversible if remove insult
What causes Necrosis?
always pathologic T or F?
ischemia or toxic injury
1. cell rupture
2. spill contents
4. unregulated enzymatic digestion of cell components: lysosomes
What are steps of necrosis?
1. Ischemic cellular injury ( no O2,nutrients-->stops ATP-->Na/K pump stops-->hydropic swelling-->surface develops blebs)
2. loss of plasma membrane integrity
3. influx of Ca, mitochondrial dysfunction
4. degradation of plasma membrane & nucleus
5. dumps contents-
6. immune system comes for clean up duty-causes inflammation
Most common type of necrosis:
ex: hit by lightening
what is Liquefactive necrosis:
quick dissolution of dead cells, absess in area takes place. most common in brain: ex: Terry Shivo anorexic heart attack
What is fat necrosis?
Ex: of Caseous necrosis
death of adipose tissue
release activated enzymes into cells
lung tissue damaged by tuberculosis
What is gangrene?
characteristics of dry gangrene:
considerable mass of necrotic tissue
char'cts: becomes dry & shrinks
color change: dark brown or black
line of demarcation
lack of arterial flow in
characteristics of moist gangrene
diff /b/ moist and dry
skin moist, black, under tension
blebs on surface:liquefaction
foul odor(inaerobic bact.)
no line of demarcation
ex: viagra penis
moist: interference w/ venous return (too much juice)
dry: lack of arterial flow in (no juice)
what causes gas gangrene?
infection by clostridium bact. (in soil)
common in trauma & compound fractures
bacterial toxins dissolve membranes
hydrogen sulfide gas produced
amputate that shit!
What is Apoptosis?
exs nonpatho & patho:
cell suicide (the good kind)
response to injury-triggers intracellular signaling cascades
no cellular rupture-phagocytosis-a tidy mess-no inflammation
Non pathologic ex: web-free hands
ex pathologic: coronary artery diseas
characteristics of signaling cascade in apoptosis:
1. endogenous enzymes activate
2. cells/organelles shrink
3. DNA disruption-cleavage /b/ nucleosomes
4. nucleus & cell fragment into membrane covered apoptotic bodies
5. change to membrane signal phagocytes (chagnes phospholipid cell from inner to outer leaflet as flag)
exs: of apoptosis
or inability thereof
1. sun burns trigger it
2. parkinsons may be excessive apop
3. tumors lack ability for apoptosis-why it goes to cancer
causes of cellular injury & death:
1. lack of O2/nutrients
2. infection & immune response (collateral damage)
4.physical mechanical factors
Etiology of cellular injury:
Most commonly caused by what?
Hypoxia: lack of O2-->inability to produce ATP oxidative phosphorylation
1. Ischemia: interruption of blood flow to an area-most common cause of hypoxia and faster injury than hypoxia along bc deprive o2 & nutrients/accum. wastes
Other causes of Hypoxia:
1. inadequate O2 in air
2. respiratory disease
5. inability of cells to use O2
chain of events in hypoxia that causes cellular power failure:
1. oxidative metabolism (1 glucose= 36 ATP) ceases
2. kicks over to fermentation (anaerobic met.) 1 glucose=2 ATP
3. build up of lactic acid=pH falls
4. <pH alters chromatin structure & cytoskeleton
5. Na/K and Ca pumps stop
excess or deficiencies
total deficit (starvation) or single item
body requires 60+ organic/inorganic substances (minerals, vits., fatty acids, a.a.)
Infectious & Immunologic injury:
due to ___
why so dangerous?
biologic agents (viruses, parasites, bact.)
danger! able to replicate!
air, water, pollutants, gases, insecticides, trace metals,
alcohol , recreational, therapeutic
Physical & Mechanical Injury:
1. mechanical force: body impact w/ object
2. Temp extremes
a. elevated: coagulation of blood/tiss. proteins 43-46 C is heat stroke >=cooking a person
b. depressed: increase blood viscosity + induced vasoconstriction
c. freezing: ice crystals + vasoconstriction (explode)
3. electrical injuries:
disruption of neural + cardiac impulses
hyperthermic tissue destruction (4th degree burn)
exs of Physical & Mechanical injuries cont.
1. radiation injury: gamma - radio waves
a. ionizing: above uv
hits target molecules or creates free radicals (changes structure of other molecules)
Uv Radiation: creates ROS to damage skin & T-T dimers
b. non-ionizing: below uv
vibration and rotation of atoms & molecules
creates heat/visible light
2 layers of Integumentary System:
1. epidermis: superficial
2. dermis: deeper dense connective tissue./ vascularized
supports epi with nutrients
the major kinds:
2. body T regulation
3. cutaneous sensation
4. metabolic functions
5. blood reservoir
kinds of protection:
1. chemical barriers
2. physical/mechanical barriers
3. biological barriers
1. acid mantle: inhibits bacterial growth. low pH due to sebum
2. human defensin: antibacterial peptide punches holes in bacterial cells
3. cathelicidins: come from damaged skin cells, prevent against streptococci
4. melanin:pigment-sun screen from UV damage
1-3=secretions from skin
4=by product physically injected from one cll type to another
1. skin is continuous layer:antibacterial cell structure
2. hard,keratinized cells
3. waterproofing glycolipids (not 100% i.e. pruned fingers)
4. some substances penetrate skin: lipid solids ex: plant resins (poison ivy), organic solvents (paint thinner), DMSO, heavy metals (lead)
Langerhans' cells: immunological dendritic cells
2. macrophages: in dermis
3. DNA: radiation absorbed by DNA minimizes damage to underlying structures
Body Temperature Regulation:
low T: sweat continuously low
high T: sweat glands stimulated
evaporation: cools body surface
constriction/dilation of dermal blood vessels
Cutaneous sensory reception
1. meissner's corpuscles
2. merkel discs
3. pacinian receptros
4. hair follicle receptors
5. bare nerve endings
all these are examples of ___
1. close to dermis/epi border-awareness of slight touch
2. dermis/epi border-awareness slight touch
3. deeper/stronger contact awareness
4. threat response-can feel stimuli before hits skin
5. pain stimulated by chemicals released when skin is damaged
--exteroceptors:pick up info from external enrivo-->CNS
1. conversion of cholesterol--> Vit. D
no Vit D=rickets
~disarm chemicals (disarm cancer causing agents as penetrate skin)
~convert harmless chemicals into carcinogens
~activate steroids: hydrocortisone-cortisone
5% of blood in body.
sweat-components of urine leak out of skin
-anchors skin to underlying muscle, allows skin to slide over muscle
-acts as a shock absorber & insulator
-NOT APART OF SKIN
superficial fascia on outside of skeletal m.-not part of skin
allows skin mobility
deep subcutaneous tissue
How many layers in thin skin?exs of extra thin skin:
exs of normal thin:
normal thin: everything else
how many layers in thick skin?
where is thick skin found?
moderate thick skin?
palms of hands/soles of feet
moderate thin: shoulders/ neck
cellular morphology of epithelium?
4 types of cell types?
structure of epidermis reflects life stages of what cell type?
~stratified squamous keratinized epithelium
~1.keratinocyte (bulk of cells-make up layers of epidermis)
3. langerhans' cell
4. merkel's cell
- Stratum corneum - dry cell membranes dead filled with keratin waterproof.
- Stratum lucidum - thick skin only. Clear.
- Stratum granulosum - cells flatten and die no division.
- Stratum spinosum - less dividing, many langerhans
- Stratum germinativum/basale -Rapid division
`single layer of columnar of cuboidal cells
`anchored to dermis via abundant desmosomes
`mitosis occurs to produce new cells
`composed of spiny/prickle shaped cells
`cells flatten toward surface (cuboidal-->squamous)
`many desmosomes connected to intermediate filaments in cytoplasm (intermediate filaments become keratin later)
Stratum Germinativum and Spinosum=mitotic layers
plenty of O2/nutrients to support cells
where other skin cell types hang out bc of nutrients
`3-5 layers of flattened cells
`cytoplasm contains keratohyalin granules
+ intermediate filaments= keratin waterproof hard protein
`also contain lamellated granules=waterproof glycolipid
`cells of epidermis die here
(black layer in pics)
`only in thick skin!`clear translucent layer
`cytoplasm contains keratohyalin which is distributed on intermediate filaments (keratin still wet b/c in thick skin h2o can't evaporate totally at this pt.)
`3-5 layers deep-very thin
`dead,scaly, horny cells
`cytoplasm gone-replaced by soft-keratin (has less sulphur than hard keratin)
`cells constantly lost from surface
(other epidermal cell types)
2. langerhans' cells:
3. merkel cells:
all in malphhigian layer!
1. synthesize melanin: put into keratinocytes-sunblock for nucleus
2. part of immune system: eat pathogens, presents antigen to rest of I.S.
3. part of merkel discs-touch receptors
The neuroglial cells in the PNS include satellite cells and Schwann cells. What do they do?
Satellite cells-surround soma w/i ganglia. Fxn is unknown
Schwann cells (neurolemmocytes_ surround larger nerve fibers. Form myelin sheaths in PNS.
One fiber/Schwann cell
important part of the immune response; provide defense against disease by attacking foreign bodies and abnormal cells
Characteristics of Dermis
`strong flexible connective tissue
`cells-similar to areolar tissue
`="hide" leather on animals
`determines development of epidermis
`2 layers: papillary & reticular
Papillary layer of dermis
only places don't have ridges?
dermal ridges and papillae
made of areolar connective tissue
has capillary loops (bring nutrients to epi layers), nerve endings, Meissner's corpuscles in papillae
papillae determine epidermal ridges which determine sweat glands-fingerprints-sweat left behind
~forehead, ear, paraneum, scrotum
Reticular layer of dermis
main fibrous bed=80% of dermis
dense irregular connective tissue
`less dense areas, run in patterns in body-where surgeons cut-less blood
`skin marking, dermal folds near joints, dermis tightly anchored to underlying body part ex: lines on hand
`rapid growth of dermis
what is scar tissue?
dermis exposed through the epidermis
Skin color depends on three factors:
1. carotene: into stratum corneum and adipose tissue in derm/hypoderm
2. blood: reddish glow
`elastic keratinized threads developing from epidermis (like stratum corneum)
`hard keratin: higher sulfur
`composed of shaft + root
`root encircled by hair follicle
`over body except: palms, soles, urogenital
Hair's 3 concentric layers of keratinized cells:
1. medulla: central core (large cells w/ air gaps. blondes/fine body hairs lack this layer)
2. cortex: surrounds medulla (like stratum granulosum, thin flat cells stacked tightly)
3. cuticle; outermost hair layer: single layer like roof shingles overlapping. cells interlock with cuticle of hair follicle
melanocytes in base of shaft
characteristics of hair follicle:
folds of epidermis into dermis
hair bulb: expanded deep end
papilla: indent at basal end of hair bulb, contains capillary bed and hair follicle receptor
layers of hair follicle
(outside of hair shaft)
`connective tissue root sheath: outer layer-derived from dermis
`glassy membrane: separates outer from inner sheath
`epithelial root sheath: derived from epidermis-inner and outer components
`hair matrix: above papilli (active growth)
`arrector pili: smooth m.
`follicle + m. + glands= pilosebaceous unit
pale fine hair
puberty causes production of terminal hairs in axillary and pubic regions (face,torso,legs of males)
what affects hair growth?
androgens, nutrition, disease
parts of nail:
1. free edge
4. nail bed
6. nail folds
7. cuticle (eponychium)
1. extends beyond distal end of phalange
2. main part
3. portion embedded in skin ends in nail matrix
4. epidermis underlying body of nail
5. white crescent at base
6. skin on proximal and lateral borders
7. extension of proximal nail fold
8. area under free edge
sweat (sudoriferous) glands
found on portion of body surface (except nipples, external genitalia, under nails)
eccrine (merocrine) sweat glands
` simple, coiled tubular exocrine gland
` secretory portion in dermis
`pore: opening of duct on skin surface
`produce sweat: exocytotic product of secretory cells
`regulated by ANS
`prevent over heating
`acidic secretion-acid mantel of skin
Apocrine sweat glands
axillary and anogenital areas
`larger than eccrine
`ducts empty into hair follicles
`components=true sweat + fatty substances + proteins
`odorless (until bacteria metabolise fatty acid and protein)
`regulated by Sympathetic nervous system-little role in T homeostasis (turned on at puberty)
Other sweat glands
1. ceruminous glands
2. mammary glands
1. modified apocrine in external ear canal, secrete cerumen-wax
2. secrete milk
what gland is two glands in one?
adrenal (suprarenal glands)
Sebaceous (oil) glands
`simple alveolar glands
`none on palms, soles, or fingernails
` secrete sebum-holocrine class secretion
`sebum= lipids + cell fragments
secreted into hair follicle or pore on skin surface
` stimulated by androgens
`helps w/ waterproofing and antibacterial skin
Articular disease typically involves swelling and tenderness of the . It limits both active and passive range of motion due to stiffness or pain.
Extra-articular disease typically involves _____________ of joints and types of movement.
What is the extent of movement in a synovial jt?
What is the extent of movement in a cartilaginous jt?
What is the extent of movement in a fibrous jt?
What are some common or concerning symptoms?
Low back pain
Monoarticular or polyarticular jt pain
Inflammatory or infectious jt pain
Jt pain with systemic fevers such as fevers, chills, rash, anorexia, wt loss, weakness
Jt pain with symptoms from other organ systems
For midline back pain, what do you assess for?
Spinal cord metastases
Epidural abscess (rare)
If a pt complains of pain off midline, what do you assess for?
Renal conditions like polynephritis or stone
What is radicular gluteal and posterior leg pain in the S1 distribution that increases with cough or Valsalva?
Leg pain that resolves with rest and/or lumbar forward flexion occurs in
Cauda equina syndrome from S2-S4 midline disc or tumor should be considered if a patient has
bowel or bladder dysfxn (usually urinary retention with overflow incontinence), especially if there is saddle anesthesia or perineal numbness
What are some key warning signs or red flags for serious underlying systemic disease?
Age older than 50 y/o
Hx of cancer
Unexplained wt loss
Pain last more than 1 month or not responding to txment
Pain at night or present at rest
History of IV drug use
Presence of infection
Radicular pain arises from
spinal nerve compression, most commonly C7 C6
Unlike low back pain, radicular pain is usually caused by
foraminal impingement from degenerative jt changes rather than disc herniation (low)
Pain in one jt suggests
monoarticular arthritis, possibile tendinitis, or bursitis
Lateral hip pain near the greater trochanter suggests
Migratory pattern of spread in jt pain is seen in
rheumatic fever or gonococcal arthritis
A progressive additive pattern of involvement with symmetric jt involvement is seen in
Generalized aches and pains in the muscles
Generalized aches and pains in the jt with no evidence of arthritis
Severe pain of rapid onset in a red, swollen jt suggests
acute septic arthritis or gout
If a child has severe pain of rapid onset in a red, swollen joint you should consider ____________ in bone contiguous to a jt.
Fever, chills, warmth, and redness are seen in
septic arthritis--also consider gout or rheumatic fever
Fever, chills, warmth, redness are seen in ___
fever, chills, warmth, redness are seen in septic arthritis; also consider gout or possible rheumatic fever.
Pain, swelling, loss of active and passive motion, or "locking" suggest
articular jt pain
Pain, swelling, loss of active and passive motion, or "locking" suggest __
articular joint pain
Loss of active but not passive motion and tenderness outside of the jt are seen in
Gelling, stiffness & limited motion after inactivity, occurs in _________ and lasts only a few minutes
degenerative jt disease
Stiffness lasting 30 minutes or more is seen in
Stiffness also occurs in
fibromyalgia and polymylagia rheumatica
Some jt problems have systemic features such as fever, chills, rash, anorexia, wt loss, and weakness. What are some jt problems these are common in?
RA, systemic lupus erythematous (SLE), PMR. High fever and chills suggest infectious cause
A butterfly rash on the cheeks is commonly seen in
systemic lupus erythematous (SLE)
A scaly rash and pitted nails of psoriasis is seen in
Few papules, pustules or vesicles on reddened bases, located on distal extremities are seen in
An expanding erythematous patch early in an illness is seen in
Hives are commonly seen in
serum sickness or drug rxn
Erosions or scaling on the penis and crusted, scaling papules on the soles and palms is seen in
Reiter's syndrome--includes arthritis, urethritis, and uveitis
The maculopapularrash of rubella may be indicative of
arthritis of rubella
Clubbing of fingernails can be seen in
Red, burning, itchy eyes (conjunctivitis) can be seen in what jt disorders
Reiter's syndrome, Behcet's syndrome
These diseases have a preceding sore throat
acute rheumatic fever or gonoccocal arthritis
Diarrhea, abdominal pain, cramping are seen in
arthritis with ulcerative colitis (MARLA'S DISEASE), regional enteritis, slceroderma
Symptoms of urethritis
Reiter's syndrome or possibly gonococcal arthritis
Mental Status change, facial or other weakness, stiff neck
Lyme disease with central nervous system involvement
Risk factors for osteoporosis and fracture part 1
Prior fragility fracture
Postmenopausal status in women
Low dietary Ca
Vitamin D deficency
Tobacco and alcohol use
Risk for osteoporosis and fracture part 2
Use of corticosteriods
Medical conditions--thyrotoxicosis, celiac sprue, chronic renal disease, organ transplantation, diabetes, HIV, 1 or 2 hypogonadism, multiple myeloma, and anorexia nervosa
Medications such as aromatase inhibitors, methotrexate, anti seizure meds, immunosupressive, antigonadal therapy
Inflammatory disorders of MS, pulmonary, GI, including RA
A T score less than -2.5 is indicative of
A T score of -2.5 to 1.5 is indicative of
Peak bone mass is reached by age 30. Bone loss is due to age-related declines in
Estrogen and testosterone
Osteoporsis is also common in ________ and __________ disease
renal and hepatic
The entire plasma volume (3L) is filtered 60x per day. This equates to _____ L of filtrate
How much of the filtrate is excreted at urine?
1% or 1.5L/day
There are 3 processes that occur before urine is created. What are they?
What kind of process is glomerular filtration?
Passive (no ATP), nonselective (everything is filtered) cause its pressure driven
What pressure powers glomerular filtration?
Hydrostatic pressure-forces fluids & solutes thru filtration membrane
What the is the net filtration pressure?
Difference between the glomerular hydrostatic pressure and forces that drive fluid back into glomerulus (colloid osmotic aka oncotic pressure of glomerular blood and capsular hydrostatic pressure
The presence of what creates the colloid osmotic (oncotic) pressure?
The proteins present in the blood. Opposes filtration by holding water and ions in capillaries
What does a positive net filtration pressure of 10 mean? What if it's 0 or negative?
10 means that fluid is moving out of the capillaries into the blood stream and urine is being created. 0 means things aren't moving and there's no pee production and this is BAD
What does GFR measure?
The volume of filtrate per minute by all glomeruli in kidneys approx 120-125ml/min
GFR is governed by 3 factors. What are the 3 factors and which is the most important one?
Total surface area for filtration, filtration membrane permeability (not probz in healthy ppl)
NFP--big factor! a small drop in NFP is enough to stop filtration which is bad bad bad!
GFR and NFP are have a direct or indirect relationship?
Direct--move in same direction.
How does the body control GFR?
By changing NFP and probably other ways too
Instrinic controls to regulate GFR in the kidney work by....
renal autoregulation--adjusting resistance of blood flow to maintain steady rate of blood flow
One type of intrinsic control is myogenic mechanism. How does this mechanism work?
The stretch or lack of stretch in smooth muscle will cause either vasoconstriction or vasodilation.
Myogenic mechanism example--your blood pressure is high so your afferent arteriole is stretched. The stretch of smooth muscle will cause ______________. Why?
Vasocontriction in order to reduce the amount of blood going in, in an attempt to lower the BP
Tubuloglomerular mechanism is another type of intrinsic control involving the macula densa cells of JGA. What is the role of the macula densa cells?
Secrete vasoconstrictor in response to changes in osmolarity and filtrate flow in distal convoluted tubule (DCT)
In the tubuloglomerular mechanism, they macula densa cells secrete vasoconstrictor in response to changes. Why do they do this?
When the flow is increased, it constricts and says hey don't put so much in here.
If the afferent arteriole vasodilates, what does this do to the glomerular capillary BP, NFP, and GFR? Why is the afferent arteriole vasodilating?
Increases them. Myogenic mechanism in response to lack of stretch of smooth muscles
If the afferent arteriole vasoconstricts, what does this do to the glomerular capillary BP, NFP, and GFR? Why is the afferent arteriole vasoconstricting?
Decreases it. Myogenic mechanism in response to stretch of smooth muscles (seen in high BP or systole)
There is also extrinsic controls that regulate GFR. They change GFR by modifiying
systemic blood pressure
In cases of extreme stress, sympathetic nervous system controls override local renal control. What happens to the afferent arterioles initially and why?
The afferent arterioles constrict so blood can go to the skeletal muscles
The decrease blood flow to the kidneys is sensed by
macula densa cells
The macula dense cells stimulate juxtaglomerular cells to secrete
The secretion of renin triggers the renin-angiotensis system which increases
blood volume and blood pressure
In the RAAS system, renin catalyzes angiotensin to
What catalyzes angiotensin I to angiotensin II?
Angiotensin II is a potent vasoconstrictor that stimulates the release of _________ & _________.
Aldosterone--increased Na & H2O reabsorption
ADH-increased H2O reabsoprtion
Both aldosterone and ADH cause increases in
blood volume, blood pressure, and GFR
Renin is released by the JG cells. What causes this release?
reduced stretch of JG cells
stimulation of JG cells-MD, SNS, angiotensin II
What is tubular reabsorption?
movement of molecules from filtrate to blood
In the paracellular route of tubular reabsorption, reabsorption occurs through
tight jxns and into peritubular capillaries
In the transcellular route, a specific transporter protein is used to move substance b/t tubular filtrate and interstitial fluid. There are 3 barriers to this. What are they?
Luminal membrane of tubule cell, basolateral membrane of tubule cell, peritubular capillary wall
What ion creates the gradients in tubular reabsorption in PCT?
What does sodium drive?
Reabsorption of other substances in PCT b/c of the gradient that's created
How does sodium move through the luminal membrane?
Facilitated diffusion coupled with cotransport
How does sodium move thru the basolateral membrane?
Active transport (need energy, Na/K pump)
How does glucose and other organics move across the luminal membrane?
Contransport with Na
How does glucose and other organics move across the basolateral membrane?
Ions, water, and organics get across by
passive diffusion (sorry for weird wording in the ?)
Water follows sodium from the filtrate to blood so what does this create?
Concentration gradient so other ions follow
In the loop of Henle, what is reabsorbed?
Sodium, chloride, potassium, water
The reabsorption in the DCT is controlled by
Aldosterone targets what type of cells?
Principal cells-sodium ion reabsorption/obligatory water reabsorption.
Aldosterone causes Na ion reabsorption which causes H2O reabsorption. What does this do to the urine?
Concentrates it (not very much though)
ADH targets what cells?
What does ADH cause? What does this do to the urine?
Open or synthesize water channels. This increases water reabsorption. Concentrates it
What hormone decreases sodium and water reabsorption? How does it do so?
ANP by inhibiting the secretion of aldosterone
Some substances are not reabsorbed or incompletely reabsorbed. What are they?
Urea, uric acid, and creatine.
Each substance (except sodium) has a transport maximum aka saturation. This reflects what?
The number of carriers avaliable
What is tubular secretion?
Movement of molecules from blood into filtrate
What molecules are prevalent in tubular secretion?
Certain drugs, urea/uric acid, K+, H+, HCO3-
The kidneys are vital for maintaining body fluid concentration. What is the normal concentration? It is hormonally controlled by
To vary the concentration of urine, filtrate in the DCT & collecting ducts must be
To vary the urine concentration, an osmotic gradient must be
created and maintained in medulla
To vary urine concentration, loops of hence and vasa recta. Why?
Cause they control the reabsorption of water, Na, Cl, K, Ca, and Mg
What happens to the concentration as you move from the cortex to the medulla?
It increases-- 300,400,600,900,1200
The high interstitial osmolarity provides a gradient for water reabsorption from the collecting ducts as they pass thru the medulla on their way to the renal pelvis
The ascending limb actively transports NaCl to the interstitial fluid. What about water?
It is impermeable to water.
What happens to the filtrate concentration in the ascending limb?
The concentration decreases. But the ISF concentration increases with depth (b/c there's no H20 to dilute it)
The descending limb is permeable to H2O but impermeable to _____. What does this do to the filtrate concentration?
NaCl. Filtrate concentration increases
The cycle repeats and reaches a steady state. What is the concentration of the filtrate when it leaves?
The filtrate leaves less concentrated
The ISF of the medulla has solute concentration gradient correlated of the depth. What does this mean?
That picture! As you get deeper, the conc increases
The vasa recta are important because they help to make sure the ISF concentration gradient isn't destroyed by equilibration with blood. How do they do this?
Vasa recta walls freely permeable to H2O and NaCl. Blood equilibrates with ISF along length
Urine varies in concentration from 100mOsm to 1400mOsm, what is this dependent on?
Pee can vary in color. It can also have an odor that develops from?
Bacterial transformationof urea to ammonia
What is the pH of urine?
What is the specific gravity of urine?
Urine is ___% water?
Urine is also made up of solutes. What are some of them?
Urea, Na, K, Phosphate, Sulfate, Creatine, Uric Acid, and Others
The presence of other solutes may indicate
Glycosuria is the presence of glucose in the urine. This can be a sign of what pathology?
Ketonuria is the excessive formation and accumulation of ketone bodies. This is seen in
Starvation and untreated diabetes mellitus
Pyuria is pus (leukocytes) in the urine. It is commonly seen in
STDs and UTIs
To localize the cause of UT pain, you must asses
location, onset, quality, quantity, pattern (CA duh)
UT pain in the bladder localizes to
suprapubic to upper thich
UT pain in the ureteral is localized to
groin or genital region
UT pain renal pain is localized to
costovertebral angle in back
Renal and ureteral pain are not changed by
changing body position
Renal pain is known as
Most UT pain is referred, why?
The kidney has no pain receptors--damage occurs without nephralgia. But the capsule is innervated
Pain in lower portions of the UT are normally
A urinalysis is a starting point for a differential diagnosis. What 3 factors do you note?
Color, odor, turbidity
Dark, strong smelling odor indicates
decreased renal fxn
Cloud and pungent urine indicates
What are 2 types of congenital renal disorders?
Polycystic kidney disease
What is renal a genesis?
Absence of one of both kidneys. May be random or clearly hereditary. Can be an isolated problem or associated with other unrelated disorders
Can you survive with bilateral agenesis?
NAH... well it's usually fatal
In unilateral renal agenesis, the remaining kidney will have to compensate. How does it do so?
Compensatory hypertrophy occurs. (side note, single kidney may be abnormally formed)
Bilateral renal agenesis aka Potter Syndrome is commonly seen in males (75%). There is abnormal development of the kidneys or they just fail to develop. The infants present with ____ ________ and eventually die of ______________ ________
Specific group of facial anomalies. Infants die of respiratory distress
Polycystic kidney disease is a result of
multiple dilations of collecting ducts so they appear as fluid-filled cysts.
ARPKD is polycystic kidney disease when it is diagnosed in
infants and young children
ADPKD is polycystic kidney disease when it's diagnosed in
ARPKD is autosomal recessive polycystic kidney disease. What chromosome is affected and what is the survival rate?
Begins in utero-chromosome 6 is affected. Low survivability-but it varies in number of collecting ducts dilated. ARPKD is accompanied by hepatic fibrosis
ADPKD is a defect of chromosome __ or ___. The pathology isn't well understood but where do they think the problem stems?
9-10% of dialysis requiring kidney failure. Defect on chromosome 16 or 4. Tubular epithelial cell hyperplasia--primary cause--cysts involve entire nephron
ADPKD is seen in adults of what ages and what symptoms do they present with?
UTIs, back or flank pain, hematuria, HTN, bilaterally enlarged kidneys, renal fxn may or may not be impaired.
Eventually their poor kidneys will fail when they're in their 70s-80s
Our kidneys are normally protected from infectious disorders by
acidic pH, prevention of reflux, prostatic secretions
Infections agents are normally introduced by
retrograde flow of urine--pyelonephritis
Pyelonephritisis an infection of. Some pathways of infection are
renal pelvis and interstitium. pathways of infection are hematogenous, lympathic, urinary
Some risk factors for pyelonephritisare
vesicoureteral reflux, pregnancy, neurogenic bladder, instrumentation, obstruction, sexual trauma
Acute pyelonephritisis acute infection of . How is the infection probably spread>
one or both upper urinary tracts, severity increases with age. Infection probably spread by ascending microorganisms.
What is the inflammatory process like in acute pyelonephritis?
Focal and irregular. Seen in pelivs, calyces, medulla
The infection in acute pyelonephritis causes
medullary infiltration of WBCs with renal inflammation, edema, purulent urine
The inflammatory mediators in acute pyelonephritis cause damage to . What may also occur?
tubule cells. Necrosis of renal papillae may occur. Healing--deposition of scar tissue, atrophy of affected tubules
Chronic pyelonephritis is characterized by persistent or recurring episodes of acute that lead to
shrunken, fibrotic kidney. Parenchyma mostly replaced by fibrotic tissue. More likely when infection is related to obstruction.
Obstructive disorders (congenital or acquired) interfere with urine flow. Dilation of the proximal tract leads to
Changes in the tract depend on....
degree of obstruction, duration, timing
Hydrostatic pressure will increase where in obstructive disorders?
Know this too
i = V/ r
Ohm's law :
Complete obstruction causes hydroureter. What does this affect? What happens after 4-6 weeks?
Pressure in pelvis and tubules increases. GFR falls. BF drops-parts become ischemic. After 4-6wks-tubular atrophy and medullary destruction
What is a renal calcus?
Kidney stone-crystals of combine organic material
Kidney stones can migrate down the urinary tract and cause
pain, obstruction, infection
What is nephroliathiasis?
Presence of stone anywhere in tract
What are some factors that influence formation of a calculus?
Supersaturation, abnormal urine pH, low urine volume
The pathophy of a renal calculus isn't well understood. But we do know that there are conditions conducive to crystallization, cellular response to crystals, matrix to enhance mineralization, standard normal activity, and hypercalciuria
There are no symptoms of a renal calculus in pelvis. But there is a ureteral colic, which is
pain when in ureter. ureter distends behind stone
There are 3 groups of renal tumors. What are they?
Benign, primary neoplasms, secondary neoplasms. Distor kidney and renal architecture
Benign renal tumors make up a small % of renal tumors. There are 4 types. What are they?
Oncocytomas, mesoblastic nephroma, renal angiomyolipoma (hemartoma), renal adenoma
This type of benign renal tumor is genetic and slow growing. It is asymptomatic-incidental discovery
This benign renal tumor is a congenital tumor of infancy
This benign renal tumor is seen in adults-abdominal BV, adipocytes, smooth muscle, others
Renal angiomyolipoma (hemartoma)
This benign renal tumor is common. It may be a pre-malignant adenocarcinoma. "Renal neoplasm of low malignant potential"
Renal cell carcinoma (renal adenocarcinoma) usually affects adults (males) 50-70y/o. Some risk factors are occupation exposures, high protein diet, smoking, obesity, HTN, family. Where does it form? And what are some symptoms?
From epithelium of PCT. Hematuria, flank pain, mass
Urothelial tumors are malignant and affect
lining of renal pelvis, calyces, ureter, bladder.
In the bladder. urothelial tumors are
transitional cell carcinomas and squamous cell carcinomas and adenocarcinomas
Some risk factors for urothelial tumors are
smoking, excessive coffee intake (Lindsey...), aromatic and amine exposure, UTI history, family, etc
Nephroblastoma aka Wilms tumor is the most common abdominal tumor in children. There is a defect on chromosome ____. What results due to this defect? What are some signs and symptoms?
Defect on chromosome 11. There is no normal differentiation of tubules and glomeruli. Tumor or mass of flank or abdomen. Abdominal pain, HTN, microscopic hematuria
Glomerular abnormalities result from...
alteration in structure and fxn of glomerular capillaries.
There are primary and secondary glomerulopathies. What is the difference?
In 1*, the kidney is only or predominant organ affected.
In 2*, drug exposure or infection causes glomerular injury in setting or multi system or vascular abnormalities.
Glomerulonephritis is . What is the most common cause of it?
inflammation of the glomerulus. there are a variety of causes, but the most common is chronic renal disease and end-stage renal failure
Acute glomerulonephritis is caused after an infection with. What symptoms are seen? What does the inflammation do to the glomerular membrane?
Group A post-streptococcal infection. Symptoms-hematuria, red cell casts, proteinuria, decreased GFR, oliguria, edema, HTN.
Inflammation thickens glomerular membrane
Rapidly-progressing glomerulonephritis is subacute, cresentic, extracapillary glomerulonephritis. It is seen primarily in adults and is idiopathic or with other proliferative glomerular disorders. What does crescentic refer to?
Cellular proliferation in Bowman's space-crescent lesions
Goodpasture syndrome is an anti-glomerular basement membrane disease. What happens? What is apparent at diagnosis?
Antibody formation against capillaries. At diagnosis-renal insufficeny is apparent. Injury is accompanied by rapid decline in glomerular fxn
There are several glomerular diseases that lead to chronic renal failure. What ares some pathological changes that occur?
Proliferation of meangial cells, tubular dilation and atrophy, tubulointersitial injury
In chronic glomerulonephritis, the mechanism is related to glomerulosclerosis and interstitial injury. But the primary cause is difficult to establish. What deposit or form within glomerular capillary filtration membrane?
Antigen-anitbody complexes deposit or form within glomerular capillary filtration membrane
In chronic glomerulonephritis, the glomerular cells respond to inflammatory mediators and this leads to
cell proliferation, sclerosis, chronic impaired renal fxn
The severity of chronic glomerulonephritis is based on
size, number, location, duration of exposure, and type of antigen-anitbiody complexes. Clinically-urine changes
In nephrotic syndrome, there is an excretion of ___ g or more of protein in urine per day. It is characteristic of __________ _______. There is hypoalbuminemia, edema, hyperlipidemia, lipiduria. There are primary and secondary forms.
Characteristic of glomerular injury
In nephrotic sydrome, what will you see clinically?
Proteinuria and other symptoms related to loss of serum proteins
Pts with nephrotic syndrome will have edema. Why?
Plasma levels elevate in pts with nephrotic syndrome. This is known as
Pts will also exhibit hypocalcemia and hyper coagulability
Renal dysfxn classification. It can be
acute & rapidly progressing
chronic, progressing to end-stage renal failure over months or years
Renal insufficiency is a decline in renal fxn to __% of normal
Renal failure is a significant loss of renal fxn. End stage renal failure is < ___%
In renal failure, there is
azotemia, acidosis, impaired urine dilution, severe anemia, electrolyte imbalances, and GFR <20%
Therapeutic dietary intervention that includes a nutrition assessment, nutrition intervention and monitoring progress is called?
Medical Nutrition Therapy (MNT)
What are the six nutrients necessary for proper body fxn?
carbs, proteins, fats, vitamins, minerals, & water
energy yielding nutrients that are needed in higher amounts?
Macronutrients (carbs, lipids & proteins)
nutrients needed in smaller amounts?
vitamins and minerals
what are phytochemicals?
non-nutrient compounds that contribute to health
A substance that significantly reduces the adverse effects of free radicals?
How many kcals/gram do Carbs provide?
What are simple carbs?
Monosacharides (glucose, fructose & galactose)
disaccharides: (maltose, sucrose, lactose
what are complex carbs?
polysacharides,(starch, fiber & glycogen)
what is the difference between dietary fiber & functional fiber?
dietary found in foods naturally (soluble & insoluble)
Fxnable is added to food
what is glycogen?
storage form of glucose stored in the liver & muscle cells
Whole grains have what 3 parts of the grains intact?
germ, endosperm, bran
Milling (refined grains) removes what from the grain?
Bran & Germ
What is added to enriched grains?
how many kcals/gram are in proteins?
what is found in complete proteins?
9 essential amino acids + 11 nonessential =20 aa
what is the only complete protein found in plants?
what is an incomplete protein?
low is one or more essential amino acid (such as plant proteins)
How many kcals/gram are found in Fats?
what are the 4 categories of fats?
What are the types of fatty acids?
What is trans fat?
made by hydrogenation, which makes it harder to digest and your body recognize it as a saturated fat
Trans fats do what?
raise LDL lower HDL
what is so bad about Trans Fats? they taste great!
well they raise your LDLs and lower your HDLs
What is linoleic acid?
a type of fat, or fatty acid (omega 6), found in vegetable oils, nuts, seeds and animal products. (we get plenty of this one)
what is alpha-linoleic acid?
omega 3s. used to make EPA and DHA
what are the fat souble vitamins?
What are the Major minerals?
Ca, Phospherous, magnesium, potassium, sodium, chloride
what are the best ways to reach your nutrient needs?
well balanced diet with variety, portion control, energy balance & nutrient dense foods
what is energy density?
energy value of a food in relation to the foods weight
what are your dietary reference intakes?
What is different about the new nutrition labels coming out?
-Calories are in bigger letters
-Vitamin D, C & Potassium are now at the bottom
-calories from fat removed
what are the 5 mjr food groups?
fruits, veggies, proteins, grains, dairy
how do you integrate nutrition into care?
look at PMH, FH, SH, & diet histroy
how does 24 hour dietary recall work?
recall from last food eaten to 24 hours ago, includes quantities
What is a "usual intake" type of diet history?
helpful for elderly or kids. reflects long term dietary habits
what is a food frequency questionaire
used to determine trends of certain foods
what are some nutrition related concerns?
Amenorrhea (No period)
what parts of the PE does nutrition focus on?
Vitals, skin head, hair, eyes, mouth, nails, extremeties, abdomen, skeletal muscle, fat stores
What are some nutrition indicator vital signs?
BP, Height/weight, BMI, waist circumference, % wt change, general observation
How do you calculate BMI?
703 X wt (lbs)/ (height^2)
what is an underweight BMI?
18.5 or less
What is an overweight BMI?
What is a class 1 Obesity BMI?
What is an extreme obesity BMI? ( Class 3)
What is a healthy boy fat % for men?
What is an overweight body fat % for men?
What is an extremely obese Body fat % for men?
Elderly men with a BMI < ___ have a higher mortality?
How is BMI done for Peds?
same way, but plot BMI on growth charts by the CDC
What are some of the interventions for obesity?
wt loss clinics with reduced calorie diets
what are some obesity related concerns?
heart dz, stroke, type 2 diabetes, & some cancers
What groups have the highest rates of obesity?
African american and hispanics
higher income blacks and Hispanics are less likely to become obese T or F?
higher income women are less likely to be obese than low income women, T or F?
There is no significant relationship between obesity and education among women, T or F?
FALSE, no relation for men, but there is for women
which states have an obesity prevalence of less than 20%?
None. We have all turned into fat asses
What area of the US has the highest obesity rate currently?
a high waist circumference shows an increased risk for what?
Type 2 diabetes
waist circumference is a predictor of what?
where should the waist circumference be taken?
upper hip bone and top of right iliac crest
what are the 5 indicators of Metabolic Syndrome?
Lg waist circumference
impaired fasting blood glucose
what is a high waist circumference for men? women?
can you have a change in waist circumference without significant change in wt or BMI?
What is a syndrome of renal failure?
uremia--represents numerous consequences related to renal failure
What is increased serum urea levels known as?
Azotemia-usually increase creatinine levels
Both uremia and azotemia indicate
an accumulation of nitrogenous wastes in blood
Acute renal failure is an abrupt reduction in renal fxn. What is it associated with?
Oliguira--BUN and creatinine levels elevated
Is acute renal failure reversible?
Yes if caught early
Acute renal failure is caused by different clinical conditions. What are the 3 classifications of acute renal failure?
Prerenal, intrarenal, or postrenal
In prerenal ARF, there is pre renal azotemia due to
impaired renal blood flow and cause of this the GFR drops
The failure to restore BV or BP in pre renal ARF may lead to
acute tubular necrosis or acute cortical necrosis
Intrarenal failure is characterized by what kind of azotemia?
There are several causes of infrarenal ARF. What is the most common?
Acute tubular necrosis- can be postischemic or nephrotoxic.
What form of infrarenal ARF is most often after surgery?
Ischemia releases ROS and inflammatory mediators which lead to
cell swelling and necrosis
Necrosis patchy refers to
any part of nephron
Nephrotoxic ATN is produced by
numerous antibiotics that accumulate in cortex.
Necrosis uniform occurs
in proximal tubules
In acute renal failure, why is the GFR reduced?
Tubular obstruction, tubular back leak, alterations in renal blood flow
Is postrenal ARF common?
uh no, it's rare
When does post renal ARF occur?
Occurs with UT obstructions that affect kidneys bilaterally
In post renal ARF, there is an increase in intraluminal pressure proximal to the obstruction which leads to
decrease in GFR
There are 3 phases in AFR. What are they?
Initiation, maintenance, recovery
In what phase is there reduced perfusion or toxicity--evolving injury?
In what phase is there an established injury and dysfxn--urine output is lowest, serum creatinine and BUN increase
In what stage in the renal injury repaired?
Chronic renal failure occurs when there is
irreversible loss of renal fxn--affects nearly all organ systems
Chronic renal failure will progress steadily to
end stage renal disease
The most common causes of chronic renal failure are
diabetes mellitus and HTN
Chronic renal failure progresses in stages that correlate with specific signs and symptoms. What are the 4 stages?
Reduced renal reserve, renal insufficiency, renal failure, end stage renal disease
What are some specific signs and symptoms of reduced renal reserve?
GFR reduced to 50%, no clinical symptoms but BUN elevated
In this stage of CRF, the GFR is severely reduced and there are mild clinical symptoms of renal dysfxn
In end stage renal disease,
the GFR is nearly absent, severe alteration in H2O, electrolyte, acid/base balance
The skeletal and bone systems will be altered due to renal disease. What happens to them?
Hypocalcemia and bone disease due to lack of vitamin D
In the cardiovascularsystem, you will see ____________ in chronic renal failure.
HTN--may lead to CHF due to increase in fluid volume & dyslipidemia
What are some neural effects of CRF?
Neural fxn-progressive and non-specific
Mild sleep disorders, impaired conc, memory loss, impaired judgement
Hiccups, muscle cramps, twitching
Azterixis, seizures, coma
Some endocrine/reproductive effects due to CRG include
drop in circulating sex steroids, hyperinsulinemia
main (largest) portion of the brain, occupying the upper part of the cranial cavity; its two hemispheres, united by the corpus callosum, form the largest part of the CNS in humans.
Main (largest) portion of teh brain, occupying the upper part of teh cranial cavity; its two hemispheres, united by the corpus callosum, form the largest part of the CNS in humans
situated on the back of the brain stem; consisting of a media lobe(vermis) and two lateral lobes (the hemispheres)
Situated on the back of the brain stem; consisting of a median lobe (vermis) and two lateral lobes (the hemispheres)
the stemlike portion of the brain connecting the cerebral hemispheres with the spinal cord and comprising the pons, medulla oblongata, and midbrain.
located between the cerebrum and midbrain, it contains the thalamus, hypothalamus, and pineal gland; involved in controlling body temperature, sleep, appetite, blood pressure, and sexual activity.
comprising the forebrain, midbrain, and hindbrain
White matter: inner portion
Gray matter: outer portion
that part of the central nervous system lodged in the spinal column
White matter: outer portion
Gray matter: central portion
the three membranes covering the brain and spinal cord: dura mater, arachnoid, and pia mater.
inflammation of the meninges caused by bacteria, viral, or fungal infection
the outermost, toughest of the three meninges membranes of the brain and spinal cord
the delicate membrane interposed between the dura mater and pia mater
the innermost of the three meninges covering the brain and spinal cord
fluid within the ventricles of the brain, the subarachnoid space, and the central canal.
the 12 pairs of nerves emerging from the cranial cavity through various openings in the skull.
sense of smell
movements of the eye
muscles of the eyes
hernial protrusion of the meninges through a bone defect in the cranium or vertebral column; may be repaired surgically
brain and cord contain areas of degenerated myelin. Symptoms of lesions include weakness, incoordination, speech disturbances, and visual complaints.
What is multiple sclerosis?
Chronic demyelinating disease of CNS--problems getting impulses out where they need to be
Inflammation and sclerosis of myelin sheaths on nerves
Unpredicatable, symtoms vary
a progressive neuromuscular disorder characterized by chronic fatigue and muscle weakness; considered to be an autoimmune disease. Antibodies block and destroy receptors at the myoneural junction because of a deficiency of acetylocholine.
see pg 214 in medical terminology book
lack of muscle strength
a progressive neuromuscular disorder characterized by chronic fatigue and muscle weakness; considered to be an autoimmune disease. Antibodies block and destroy receptors at the myoneural junction because of a deficiency of acetylcholine. The onset of symptoms is gradual, with drooping eyelids, difficulty speaking and swallowing, and weakness of the facial muscles; the weakness may then extend to other muscles enervated by cranial nerves, especially the respiratory muscles. The disease occurs most often in women than men, with onset between ages 20 and 40 years in women, and in older men between ages 50 and 60 more often than in younger men
disease of cranial and peripheral nervous system; motor, sensory, and reflex impairment.
organic brain syndrome (chronic brain syndrome)
any mental disorder caused by impairment of brain tissue function; may be acute and reversible, caused by injury, infection, and nutritional deficiency, or chronic, resulting from relatively permanent organic impairment of brain tissue function.
a slowly progressive, degenerative, neurologic disorder characterized by resting tremor.
petit mal seizures
also called absence seizure, the petit mal is a minor seizure lasting only a few seconds. The person has a momentary clouding of consciousness, may have a blank facial expression, and blink the eyes rapidly; the duration of the seizure is 5-10 seconds. The individual may not be aware of the episode. It is more frequent in children.
petit mal seizures
also called absence seizure, the petit mal is a minor seizure lasting only a few seconds. The person has a momentary clouding of consciousness, may have a blank facial expression, and blink the eyes rapidly; the duration of the seizure is 5-10s. The individual may not be aware of the episode. It is more frequent in children
an acute viral disease with fever, sore throat, headache, vomiting, and often stiffness of the neck and back; may be minor or major; can be prevented by vaccination.
severe pain in the leg along the course of the sciatic nerve; also pain radiating into the buttock and lower limb, most commonly caused by herniation of a lumbar disk.
radicular gluteal and posterior leg pain in the S1 distribution that increases with cough or valsalve.
severe pain in the leg along the course of the sciatic nerve; also pain radiating into the buttock and lower limb, most commonly caused by herniation of a lumbar disc
ie using a catheter to drain fluid from brain cavities to the spinal cord.
to bypass, e.g., using a catheter to drain fluid from brain cavities to the spinal cord
spinal cord injuries
a traumatic disruption of the spinal cord, with extensive musculoskeletal involvement; spinal fractures and dislocations are common in car accidents and airplane crashes can cause varying degrees of paraplegia and quadriplegia.
see pg 214
beneath the dura mater, usually a result of a closed head injury, acceleration-deceleration injury, use of anticoagulants, contusions, or chronic alcoholism; they are largely a result of venous bleeding
see page 215
an inherited inborn error of metabolism in which there is an enzyme deficiency causing altered lipid metabolism; deficiency of this enzyme results in accumulation of a specific lipid in the brain, which leads to physical and mental retardation
benign or malignant, primary or metastatic; may be classified by location, tissue type, or degree of malignancy ie gliomas, neuromas.
tumors (cord, brain)
benign or malignant, primary or metastatic; may be classified by location, tissue type, or degree of malignancy
a popular term for an acute cervical sprain; acceleration extension injury of the cervical spine.
a radiopaque substance is injected into arteries in the neck, then x-ray films are taken.
reflex response; when sole of foot is stroked, the big toe turns up instead of down ( normal in newborn, but pathological later on)
holes made with a drill creating openings in bone to permit access for biopsy, insertion of drains for relieving pressure, or for monitoring devices.
holes made with a drill creating openings in bone to permit access for biopsy, insertion of drains for reliving pressure, or for monitoring devices
3D view of brain tissue obtained as x-ray beams pass through layers of the brain. A CT scan will show areas of tumors, hemorrhage, blood clots, aneurysms, MS, and brain abscess; contrast medium may also be injected by IV to better visualize abnormalities.
cutting of nerve fibers to relieve intractable pain.
any operation on the cranium, ie puncture of the skull and removal of its contents to decrease the size of the head of a dead fetus and aid in delivery.
use of ultrasound to show displacement of brain structures.
record of electrical activity of the brain
examination of cerebrospinal fluid (cell counts, culture, blood)
excision of the posterior arch or a vertebra to view the spinal cord or to relieve pressure
magnetic resonance imaging (MRI)
see pg 216
the film produced by myelography; ie injection of a dye into the subarachnoid space to detect tumors or herniated disks
the film produced by radiography of the spinal cord after injection of a dye into the spinal cavity
injection of anesthetic into a nerve to produce the loss of sensation
nerve cells (neurons)
conducting cells of the nervous system, consisting of a cell body containing the nucleus and its surrounding cytoplasm, and the axon and dendrites; specialized cells for transmitting impulses.
the radiograph obtained by visualization of the fluid-containing structures of the brain after cerebrospinal fluid is intermittently withdrawn by lumbar puncture and replaced by air, oxygen, or helium.
positron emission tomography (PET) scan
images of various structures show how the brain uses glucose and gives information about brain function; PET scans are used to asses Alzheimer's, stroke, epilepsy, and schizophrenia as well as study and diagnose brian tumors.
positron emission tomography (PET) scan
images of various structures show how the brain uses glucose and gives information about brian function; PET scans are used to assess ALzheimer's, stroke, epilepsy, and schizophrenia as well as study and diagnose brain tumors
cutting the roots of spinal nerves to relieve incurable pain
a test of the sense of balance, ie the patient may lose balance when standing erect, feet together, and eyes closed.
a test of the sense of balance, e.g., the patient may lose balance when standing erect, feet together, and eyes closed
drilling a hole in the skull to evacuate clots or injet air for a diagnostic procedure.
drilling a hole in the skull to evacuate clots or inject air for a diagnostic procedure
surgical transection of the fibers of the vagus nerve
radiography of the cerebral ventricles after introduction of air or other contrast medium
the feeling experienced in connection with an emotion
hostile attitude; may be caused by insecurity or inferiority feeling
conflicting emotional attitudes toward a goal
conflicting emotional attitudes toward a goal, e.g., hate or love
loss of memory
developmental disorder characterized by the inability to form social relationships and communicate with others.
brain disorder in which the individual experiences extremes in energy, mood, and behavior- between mania and depression that interfere with the ability to carry out day to day activities; also called manic depressive illness.
brain disorder in which the individual experiences extremes in energy, mood, and behavior between mania and depression that interfere with the ability to carry out day-to-day activities; also called maniac-depressive illness
excessive violent motor activity or lack of reaction and movement; observed in schizophrenia
a mental disturbance of relatively short duration, ie illusion, hallucinations, and excitement
a mental disturbance of relative short duration, e.g., illusions, hallucinations, and excitement
in psychiatry, a morbid sadness, dejection, or melancholy; a decrease of body functions
a false personal belief
automatic repetition by a patient of what is said to him or her.
introducing convulsions by means of electricity; used on patients with affective disorders.
hearing or seeing things not really present.
extremely emotional state
disabling brain disorder that interferes with normal activities of working, eating, sleeping, and enjoying usual activities; most patients require treatment (medications and/or therapy) to improve after a depressive episode
disabling brain disorder taht interferes with normal activities of working, eating, sleeping, and enjoying usual activities; most patients require treatment (medications and/or therapy) to improve after a depressive episode
make believe, i.e. pretending to be ill.
make believe, e.g., pretending to be ill
belief in one's own extreme greatness, goodness, or power.
mental and physical exhaustion as a result of psychological stress, conflict, or depression; similar to chronic fatigue syndrome.
an emotional disorder caused by unresolved conflicts, anxiety being its chief characteristic; person is still in touch with reality.
a person who is overly suspicious with feelings of being persecuted or having delusions of his or her abilities or power that are not consistent with reality.
any persistent abnormal dread or fear
a major mental disorder with a loss of contact with reality; characterized by delusions and hallucinations; often part of schizophrenia and severe depressive disorders.
rapid eye movements (REM)
occur during periods of dreaming
a chronic, severe, and debilitating brain disorder characterized by visual and auditory hallucinations and delusions as well as disordered thoughts. Most individuals with schizophrenia are not able to hold a job or care for themselves.
loss of the ability to speak owing to injury or disease of the brain centers
failure of muscular coordination
the process of furnishing a person with information on the state of one or more physiologic variables, such as heart rate, blood pressure, or skin temperature, often enabling the person to gain some voluntary control over the body function.
the collection of spinal roots descending from the lower spinal cord and supplying the rectal area
in deep stupor; cannot be aroused
denoting an injury to the brain, occurring at a site opposite to the point of impact.
deep tendon reflex
a reflex elicited by a sharp tap on the appropriate tendon or muscle to induce brief stretch of the muscle, followed by contraction
many meanings; one refers to a deep furrow in the brain
many meanings; one refers to a deep furrow in teh brain