Pathology Exam 3

Front 1

what are the functions of the kidney?

Back 1

-eliminate waste
-regulate plasma osmolality
-regulate blood acid base balance
-stimulate red blood cell production

Front 2

explain the difference between glomerular filtratrate & urine

Back 2

->glomerular filtrate is the large volume of UNPROCESSED fluid that crosses from the blood into the urinary space of the glomerulus
->renal tubules absorb 99% of the water in the glomerular filtrate, adding/subtracting electrolytes, acid & other substances
REMAINDER = urine

Front 3

distinguish between renal disease & syndromes of renal disease
(give example)

Back 3

disease = pathological process
(like an autoimmune reaction, infarction, inflammation, or edema

syndrome = a clinical picture, a collection of clinical signs & syx
(ex: poststreptococcal glomerulonephritis is an autoimmune glomerular disease that usually presents clinically as the clinical syndrome of acute nephritis)

Front 4

what is the difference between azotemia and uremia?

Back 4

AZOTEMIA: renal failure only evident by abnormal lab tests
UREMIA: renal failure w/ clinical sx

Front 5

what is meant by occult hematuria?

Back 5

intact red blood cells in the urine in amts too small to be noticed by gross exam only

Front 6

NEPHROTIC syndrome

Back 6

nephrotic syndrome:
-marked proteinuria (>3.5g/day)
-hypoalbuminemia, severe generalized edema, hyperlipidemia, lipiduria

Front 7

NEPHRITIC syndrome

Back 7

nephritic syndrome: acute syndrome of hematuria, proteinuria, HTN associated with acute glomerulonephritis

Front 8

what is the pathogenic mechanism for most primary glomerular disease?

Back 8

autoimmunity

Front 9

name the most common type of glomerulonephritis>

Back 9

IgA glomerulonephritis (Berger disease)

Front 10

name the most common cause of renal failure in the US

Back 10

diabetic glomerulosclerosis

Front 11

give the name of the vascular disease found in virtually ALL elderly people

Back 11

-benign nephrosclerosis

Front 12

why do pts with acute tubular necrosis (ATN) have a period of very high urine output?

Back 12

-ATN is a syndrome of death of renal tubular epithelial cells

-lack of renal tubular epithelial cells means the tubules cannot absorb the normally very large volume of glomerular filtrate, which is then able to pass through the tubules with little alteration & into the collecting system as urine

Front 13

what are several causes of tubulointerstitial nephritis?

Back 13

-renal ablation nephropathy, acute and chronic pyelonephritis, urinary obstruction or reflux, toxin damage, and chronic analgesic nephropathy

Front 14

what are the consequences of urinary obstruction & reflux?

Back 14

-obstruction and reflux encourage infection & stone formation and contribute directly to hydronephrosis & tubulointerstitial nephritis

Front 15

2 types of microorganisms that cause most acute pyelonephritis

Back 15

-most acute pyelonephritis is caused by ascending infection by E. coli and other fecal bacteria that ascend to the kidney from the bladder

Front 16

list some important facts about chronic pyelonephritis

Back 16

1- the presence or absence of bacteria in the urine is not helpful in making the diagnosis
2-it is often assoc. w/ obstruction or reflux
3- it may be asyx for a long time
4- it may be characterized by repeated episodes of fever & other evidence of urinary infxn
5-it is responsible for about 10% of pts on chronic dialysis
6-it is one of the main causes of chronic tubulointerstitial nephritis

Front 17

what's the most common type of urinary stone?
-what are some conditions associated with it?

Back 17

-most urinary stones: CALCIUM stones (occur in pts with high urinary calcium)
--ex: hyperparathyroidism, hypercalcemia
-urinary stones often present w/ urinary bleeding (hematuria) or flank pain (renal colic)
--stones predispose to obstruction & infection and chronic tubulointerstitial nephrtis

Front 18

name the 2 most important malignancies of the kidney

Back 18

-renal cell carcinoma; transitional cell carcinoma of the renal pelvis

Front 19

list some important facts about chronic pyelonephritis

Back 19

1- the presence or absence of bacteria in the urine is not helpful in making the diagnosis
2-it is often assoc. w/ obstruction or reflux
3- it may be asyx for a long time
4- it may be characterized by repeated episodes of fever & other evidence of urinary infxn
5-it is responsible for about 10% of pts on chronic dialysis
6-it is one of the main causes of chronic tubulointerstitial nephritis

Front 20

what's the most common type of urinary stone?
-what are some conditions associated with it?

Back 20

-most urinary stones: CALCIUM stones (occur in pts with high urinary calcium)
--ex: hyperparathyroidism, hypercalcemia
-urinary stones often present w/ urinary bleeding (hematuria) or flank pain (renal colic)
--stones predispose to obstruction & infection and chronic tubulointerstitial nephrtis

Front 21

name the 2 most important malignancies of the kidney

Back 21

-renal cell carcinoma; transitional cell carcinoma of the renal pelvis

Front 22

what is the gold standard test for determining how rapidly glomerular filtrate is being formed?

Back 22

-inulin clearance test
-involves IV injection of inulin, timed collection of urine output, and measurement of blood and urine inulin levels
-is filtered and NOT reabsorbed

Front 23

what is another test of glomerular function (more common) ?

Back 23

-creatinine clearance test:
-much more widely used, because creatinie occurs naturally in the plasma
--however:; not as accurate as inulin b/c some creatinine does not get into the urine through the glomerulus (secreted into urine by renal tubules)

Front 24

things abnormally found in the urine:

Back 24

-bacteria
-bile pigments/urobilinogen
-bilirubin
-color/clarity (abnormal)
-glucose
-hemoglobin (RBCs/free Hgb)
-ketones
-casts
-cells
-odor
-pH
-protein
-specific gravity >1.022

Front 25

how is renal failure defined?

Back 25

-loss of the ability of the kidneys to excrete waste, concentrate urine, and conserve electrolytes

Front 26

abnormal stuff in the urine:
bacteria (indications of)

Back 26

-nitrate - produced by gram negative bacterial metabolism, suggests infection

-leukocyte esterase - suggests high numbers of leukocytes/indicator of infection

Front 27

abnormal stuff in the urine:
bile pigments (urobilinogen)
(or the absence thereof)

Back 27

-produced in gut by digiestion of bilirubin secreted by liver
-jaundice of biliary obstruction is assoc with decreased amounts which disappears in the urine

Front 28

abnormal stuff in the urine
bilirubin

Back 28

not normally present in the urine, associated with jaundice (most types are assoc with bilirubin in urine)

Front 29

abnormal stuff in urine:
-color and clarity
(abnormal color, turbidity)

Back 29

-most common cause of abnormal color is medication, large volume of red cells makes urine dark red/opaque. lysed red cells make it red and clear.
BEETs can make urine discolored.
CLOUDY: caused by precipitated chemicals/cells.

Front 30

abnormal stuff in urine:
glucose

Back 30

-normal urine --> NO glucose
-DM most common cause
-congenital galactosemia can cause false pos for glucose

Front 31

abnormal stuff in urine:
Hemoglobin

Back 31

-blood in urine occurs as: intact red cells (hematuria) or free Hgb (hemoglobinuria)

-Free Hgb: none normally, could inidicate hemolytic anema
RBCs: one or two maybe normally, gross: you can see them
microscopic: can't see w/ naked eye

Front 32

abnormal stuff in urine:
ketones

Back 32

-diabetic ketoacidosis most common cause

Front 33

abnormal stuff in urine:
-centrifuged urinary sediment:
casts, cells, crystals

Back 33

-casts- cylinders formed by compaction of protein, red/white cells, epithelial cells in lumen of renal tubules always indicates disease

-cells-incr mean bleeding in urinary tract or contamin. w. vag blood. vaginal inflammatory exudate

crystals: in urine sediment, normal vary according to pH

Front 34

abnormal stuff in urine:
-protein

Back 34

-normally excrete less than 150 mg protein q day
-indicates renal disease

Front 35

abnormal stuff in urine:
specific gravity

Back 35

normal: 1.016-1.022
first thing in morning >1.022
high can be from dehydration, low spec gravity from excessive fluid intake
-alcohol

Front 36

patients with uremia also typically have:

Back 36

-accumulation of metabolic waste in blood
-HTN
-anemia
-edema
-oliguria
others: pericarditis/gastroenteritis, bleeding/coagulation defects, PND,

Front 37

what is the most serious implication of occult proteinuria?

Back 37

-glomerular disease or renal damage from HTN

Front 38

acute renal failure

Back 38

-combination of acute oliguria and anuria (assoc w/ azotemia)
-most common cause is damage to renal tubules (that occurs during vascular collapse/shock)
-toxic damage, or drugs
-severe hemolysis
-muscle disorders that liberate large amounts of myoglobin into blood
-acute glomerular/vascular dz

Front 39

chronic renal failure

Back 39

-combo of lo urine output/prolonged S&S of renal failure (uremia)
-progresses to ESRD
(obliterates original cause of diseae)
-DM, chronic glomerulonephritis & HTN account for 75% of CRF

Front 40

UTI (urinary tract infection)

Back 40

-combo of bacteriuria/pyuria caused by infection anywhere in urinary tract (kidney to urethra)
-acute bladder inflammation is comon manifestation. fever & dysuria or asx

Front 41

Urinary tract obstruction

Back 41

-may be acute or chronic
-acute: usually complete obstructin
in men w/ prostate diz
-chronic: usually partial, caused by tumors, scars, stones, also assoc with stagnation of urine, dilation of the collecting system & 2ndary bacterial infection
-severe chronic obstrctn --> renal damage/failure

Front 42

nephrolithiasis

Back 42

-kidney stones
-can cause hematuria, presents with severe pain as stone passses through ureter
-some pts have them over&over
-hyperparathyroidism is suspect

Front 43

PKD
polycystic kidney disease

Back 43

-adult: autosomal dominant: 10% of pts with CRF, does not become symptomatic until after 30.
-1000's of cysts, damage parenchyma & causes severe interstitial inflammation/fibrosis
-come to medical attention from hematuria, chronic UTI & hypertension
Childhood PKD: autosomal recessive, appears at birth/late childhood. assoc with liver cysts & biliary ductal hyperplasia: most affected infants die in perinatal period

Front 44

glomerular disease

Back 44

-all PRIMARY glomerular disease is autoimmune
-secondary: can be to lupus*
-one of 2 types:
-deposition in glomerulus of circulating antigen-antibody complexes formed elsewhere (type 3 rxn)
-direct antibody attack (type 2) on glomerular basement membrane by antiglomerular basement membrane antibody

Front 45

renal dysplasia

Back 45

in utero obstruction of urinary flow
-usually caused by obstruction of the ureter
-glomeruli fails to develop and the kidney enlarges b/c of dilation of renal tubules into cysts

Front 46

cystic disease

Back 46

-simply cysts: found at autopsy, a normal variation
-larger ones can be discovered incidentally; have to be investiagated

Front 47

acute glomerulonephritis
(what happens after in some)

Back 47

-in pts that develop actue glomerular disease, often recover fully but some progress: 2 ways:
->focal scarring/atrophy (focal segmental glomerulosclerosis)
->tubulointerstitial nephritis: chronic progressive imflammation w/ scarring & destruction of renal tubules

Front 48

glomerulonephritis

in general

Back 48

inflammation of the glomerulus
->may be acute/chronic
-and 1ary/2ndary to another disease
->alternative names, usual presenting clinical syndrome
-etiology/pathogenesis
-pathologic findings at glomerulus

Front 49

poststreptococcal glomerulonephritis

Back 49

>is: acute glomerularnephritis caused by autoimmune glomerular injury initiated by beta-hemolytic strep
>other names: acute proliferative glomerulonephritis
>usual CP: acute nephritic syndrome
>etiology: strep pharyngitis/skin infex, causes formatin of circulating antibody complexes that deposit in the glomerulus
>pathologic findings: incr cellularity of glomerulus, caused by proliferation of glomerular cells & presence of inflammatory cells, clumps of immune complex on basement membrane
-->hematuria, incr BUN/Cr, low urine output, edema,

Front 50

rapidly progressive glomerulonephritis

Back 50

-form of glomerulonephritis that may arise from unknown causes/2ndary to poststrep GLMNPH. no single mechanism.
**charactrized by arcs (crescents) of cells that proliferate in urinary space & collapse the glomerulus
>alt. names: crescentic glomerulonephritis
>usual CP: acute nephritic sydrm, or renal failure
>etiology: deposition of circulating antigen/antibody complexes in glomerulus, others no immune component. idiopathic or underlying disease.
>path findings: crescent shaped masses of proliferating cells inside the Bowman space
>prognosis bad: most progress to RF & dialysis

Front 51

membranous glomerulonephritis

Back 51

autoimmune dz: thickening of glomerular basement membrane caused by deposits of autoimmune antibody. MOST COMMON cause of nephrotic syndrome in adults.
>alt names: antiglomerular basement membrane GLMNPHT
>usual CP: nephrotic syndrome
>etology: autoimmune antigen/antibody deposits on the basement membrane. cause unknown most of time. or HBV, malaria, drugs, malignancy.
>path findings: very thick glomerular basement membrane caused by deposits of immune complexes. course slow unpredict. 10% progress to RF in 10 years. slow progression.

Front 52

minimal change glomerulnephritis

Back 52

diz that affects glomerular epithelial cells w/ very subtle changes that are not visible by convent microscp.
>alt names: lipoid nephrosis
>usual CP: nephrotic syndrome
>etiology: unknown. probably autoimmune. *responds to steroids well*
>path: nothing by light microscopy: epithethilial cell lesions ID by EM.
>relatively benign: in children 2-6. can occur in adults. most COMMON nephrotic syndrome in children.

Front 53

IgA glomerulonephritis

Back 53

autoimmune glomerular disease assoc w/ immunoglobulin A deposits in mesangial cells of glomerulus. most COMMON worldwide.
>alt names: Berger disease
>usual CP: hematuria
>etiology: autoimmune, often p respiratory GI infxn
>path: IgA immune complex deposits in glomerular mesangial cells. occurs in young men, 20-30 y/o. rucurrent bouts of hematuria. some progress to dialysis. should be suspected with someone who has several bouts of hematuria.

Front 54

chronic glomerulonephritis

Back 54

dx applied to 'burned out' chronic glomerular disease. can be from these previous diseases.
most from unknown cause.
half of people on dialysis have this.
>alt names: none
>usual CP: chronic renal failure/occult proteinuria
>etiology: abou half of pts have been dx prev with other GLMNPHTS. others unknown.
>path: some pts have resid microscopic evidence of particular type of GMLPHNT, most glomeruli are shriveled to nodular bits of scar.
>anemia & fatigue, wt loss, occult proteinuria. HTN.

Front 55

secondary glomerular disease:
diabetic glomerulosclerosis

Back 55

>most common cause of 2ndary glomerular disease, most common cause of RF in US.
>glycoproteins deposit in basement membrane of small blood vessels
>caused by vascular disease
>can become self-perpetuating due to renal ablation glomerular nephropathy: vicious circle of renal destruction, which makes remaining ones work harder. bloow flow through each increases, filtrate increases (workload incr). stresses, kills more off. leads to burnout.

Front 56

diseases of renal vasculature:
>benign nephrosclerosis

Back 56

characteristic change in renal blood vessels & glomeruli: part of getting old, consequence of BP.
>changes also happen in hypertensive pts much younger

Front 57

diseases of renal vasculature:
malignant nephrosclerosis

Back 57

>much more severe form of nephrosclerosis, seen in pts with malignant HTN.
-assoc with high BP. (>160/110)
>mechanism of damage similar to to benign, but more rapid progression.
>CP: renal failure, vascular stress presenting as MI, CHF, storke. incr intracranial pressure (seizures, HA, N&V, visual impariements, coma, mental aberration). papilledema, high blood renin. 25% die in 5 yrs

Front 58

diseases of renal vasculature:
renovascular hypertension

Back 58

-elevated blood pressure 2ndary to renal ischemia. (impaired blod flow to kidney caused by narrowing of renal artery, usually by atherosclerosis).
->over half are cured by restoring blood flow or excision of bad kidney

Front 59

acute tubular necrosis

Back 59

-extensive necrosis of tubular epithelial cells
-most common cause of ACUTE renal failure.
-ischemic acute tubular necrosis is usually a consequence of vascular collapse (from severe hemorrhage). nephrotoxic acute tubular necrosis is caused by a variety of chemicals that include antibiotics, mercury, other heavy metals, IV contrast.
>progress thru 3 clinical phases: one: hemorrhage/poisoning, UO falls. 2:maintenance: usually w/in first few days as pts are given supportive care/dialysis to let tubular epithelium regrow.
3: reovery: incr renal output, flood of dilute urine. as kidney regrows tubular epithelium regrows & regains its ability to process glomerular filtrate.

Front 60

diseases of renal vasculature:
malignant nephrosclerosis

Back 60

>much more severe form of nephrosclerosis, seen in pts with malignant HTN.
-assoc with high BP. (>160/110)
>mechanism of damage similar to to benign, but more rapid progression.
>CP: renal failure, vascular stress presenting as MI, CHF, storke. incr intracranial pressure (seizures, HA, N&V, visual impariements, coma, mental aberration). papilledema, high blood renin. 25% die in 5 yrs

Front 61

diseases of renal vasculature:
renovascular hypertension

Back 61

-elevated blood pressure 2ndary to renal ischemia. (impaired blod flow to kidney caused by narrowing of renal artery, usually by atherosclerosis).
->over half are cured by restoring blood flow or excision of bad kidney

Front 62

acute tubular necrosis

Back 62

-extensive necrosis of tubular epithelial cells
-most common cause of ACUTE renal failure.
-ischemic acute tubular necrosis is usually a consequence of vascular collapse (from severe hemorrhage). nephrotoxic acute tubular necrosis is caused by a variety of chemicals that include antibiotics, mercury, other heavy metals, IV contrast.
>progress thru 3 clinical phases: one: hemorrhage/poisoning, UO falls. 2:maintenance: usually w/in first few days as pts are given supportive care/dialysis to let tubular epithelium regrow.
3: reovery: incr renal output, flood of dilute urine. as kidney regrows tubular epithelium regrows & regains its ability to process glomerular filtrate.

Front 63

tubulointerstitial nephritis

Back 63

most common causes: chronic urinary obstruction, urinary reflux, chronic bacterial infection, adverse reaction to chronic ingestion of certain therapeutic drugs, reaction to renal toxins.
-renal ablation glomerulopathy is one of most common causes

Front 64

normal urine flow can be imparied by:

Back 64

-urinary obstruction
-ineffective ureteral peristalsis
-reflux of urine from bladder into the ureter

Front 65

urinary obstruction

Back 65

may occur at any point from the kidney to urethra
-may develop suddenly or slowly, partial or complete, unilat or bilat.
>can be imparied by pregnancy,

Front 66

urinary reflux

Back 66

regurgitation from the bladder through the uretero vesical junction also prevents smooth continuous flow of urine

Front 67

what can cause urinary stasis?

Back 67

obstruction, ineffective peristalsis, and reflux
(reflux nephropathy or obstructive nephropathy)
-secondary to increase urine pressure in renal pelvis
-stagnant, high pressure urine invites infection & damages the kidney directly

Front 68

hydronephrosis

Back 68

-a dilation of the renal pelvis and calyces caused by the increased urinary pressure assoc with physical obstruction or reflux.
-chronic obstruction promotes stagnation, stone formation, and infection & is accompanied by tubulointerstitial nephritis & renal atrophy.
>most assoc with undx chronic unilateral physical obstruction in the ureter or renal pelvis.
>bilateral obstruction is rare,

Front 69

pyelonephritis & UTI

Back 69

-bacterial infx of kidney (one of most important diz of kidney)
*gram neg fecal bacteria are usual culprits: E coli 80% of cases. common in women
>acute: assoc with S&S of acute infx.
>chronic: assoc with chronic urinary reflux/obstruction. CP: silent/present for many years, ultimately presenting as CRF. or sypmtomatic with flare-ups & acute pyelonephritis with quiet periods

Front 70

acute pyelonephritis

Back 70

-almost always 2ndary to lower UTI, but can occur in kidney from blood borne bacteria.
-obstruction/reflux less common causes
>presents as sudden onset of flank pain, assoc w/ hi fever, high peripheral white count, and other S&S of acute infx.
>urine packed with white cells, & bacteria, frequency/urgency w/ urination, painful urination
>abx effective

Front 71

chronic pyelonephritis

Back 71

chronic bacterial infx of kidney
-assoc with chronic urinary reflux, obstruction. CP as recurrent episodes of acute PYNPHRTis.
-scars and shrinks the kidney. dilates the collecting system. thins the cortex. a serious problem. pts usually dx late.

Front 72

acute interstitial nephritis

Back 72

caused by adverse rxn to drug, a type IV immune reaction (T-cell, delayed hypersensitivity) that begins 2 weeks after drug exposure
>abx, NSAIDS, diuretics most common offenders
>clinically: fever, rash, peripheral blood eosinophilia, assoc with hematuria, proteinuria, leukocytes in the urine. ARF.

Front 73

chronic analgesic nephropathy

Back 73

>one of most common causes of chronic tubulointerstitial nephritis & renal insufficiency in parts of Austraila & western europe, rare in US.
>pt is an older woman who has been taking large doses of combo tylenol,codeine,NSAIDs, caffeine, ASA. >3 years
-can progress to HTN & CRF
-can be caused by stuff deposited in kidney too: protein, uric acid crystals, renal calcium

Front 74

renal stones: nephrolithiasis

Back 74

-can form anywhere in urinary tract, mostly in kidney
-numerous or can grow big enough to fill the renal pelvis
-fairly common. most occur in young adults, men affected more than women. hereditary predisposition strong correlate.
>3 categories: calcium, infection, uric acid.

Front 75

3 kinds of stones (elaborated)

Back 75

calcium: most stones are like this. composed mainly of Ca+. have incr levels of urinary ca levels. 75% of stones
Infex stones: bact infx urine pH from acidic to alkaline. mainly composed to Mg. 15% of stones.
Uric acid: pts with gout.

Front 76

renal colic

Back 76

S&S - hematuria, as a fragment of stone passes down ureter it hurts like hell
>cramping & flank pain.
-one too large to pass can become a staghorn calculus
>always assoc with hydronephrosis & chronic infextion. large ones can remain silent for a long time

Front 77

tumors of the kidney:
renal cell carcinoma

Back 77

most kidney tumors are malignant.
>-clear cell carcinoma, hypernephroma, renal adenocarcinoma)
>malignancy of renal tubular epithelium & is 90% renal of malignancies. most in older adults. 1/3 linked to tobacco.
>first sx is hematuria.
>have a variety of paraneoplastic syndromes. fever, polycythemia, HTN, cushing, hypercalcemia, feminization of men, virilzation of women.
>mets to lung & bone common. may be first sign of renal cell carcinoma. survival: okay. surgical excision preferable.

Front 78

renal pelvis carcinoma

Back 78

-account for 10% of malignancies
-arise from lining of epithelial cells of urinary tract.
-neoplasms of these cells are called transitional cell carcinomas.
-tend to occur at multiple points in urinary tract.
-about half are accompanied by invasion by concurrent transitional cell of the bladder or hx of one.
-ones of renal pelvis are papillary & friable. bleed.
-are invasive, small and nephrectomy is best. 5 yr survival in 2/3rds pts.

Front 79

what are the component parts of the lower urinary system, and the male genital system?

Back 79

-lower US: ureters, bladder, & urethra.
male GS: testis, epididymis, vas deferens, seminal vesicles, prostate & penis

Front 80

what is the importance of the ureterovesicle junction in the flow of urine in the urinary tract?

Back 80

uretrovscl junction: acts as one-way gate to prevent reflux of urine from bladder into uereter.

Front 81

what are the consequences of malfunction of flow of urine in the ureterovesicle juntion?

Back 81

reflux of urine causes urinary stasis & creates stagnant, high-pressure urine in the collecting system, which damages the kidney & encourages infection, stone formation, and tubulointerstitial nephritis

Front 82

why do women have more cystitis than men?

Back 82

women have a shorter urethra, and in women the uretrha opens onto a mucosal surface that frequently contains pathogenic bacteria

Front 83

what are the pathologic & clinical differences between low grade and high grade transitional cell carcinomas of the bladder

Back 83

LOW grade tumors: always papillary, and are formed of cells with minimally atypical features. 10 yr survival >95%

HIGH grade tumors: tend to be flat, nodular, or ulcerated & have an aggressive microscopic appearance characterized by marked cellular atypia. high grade lesions have a much higher tendancy to recur than do low-grade lesions. have a 10 yr survival of ~50%

Front 84

what is the cause of most erectile dysfucntion?

Back 84

abnormally low blood arterial flow into the penis, or abnormally rapid venous blood flow out ward.
causes: DM, atherosclerosis, neurologic disease, hormone imbalances, therapeutic drugs

Front 85

what is the importance of undescended testis?

Back 85

-undescended testis that remains in the abodmen will not produce sperm (of course)
and is at greatly increased risk for testicular malignancy

Front 86

what are the 2 most common malignant tumors of the testis, and briefly discuss the avg five-year survival figure for pts with malignant tumors of the testis

Back 86

-semioma & embryonal cell carcinoma are the 2 most common malignant tumors
-5 year survival confined to nuts = 98%. 5 yr w/ distant mets = ~75%

Front 87

what is the most common type of prostatitis, what is its cause?

Back 87

> chronic nonbacterial prostatitis is most common
>cause is usually not clear, but chlamydia is often suspect

Front 88

describe the anatomy of the bladder & prostate critical to the pathologic effect of nodular hyperplasia of the prostate

Back 88

-the prostate encircles the neck of the bladder at its connection to the urethra.
-enlargement of the prostate by nodular hyperplasia squeezes the urethra and obstructs the free flow of urine

Front 89

what is the location of most prostate cancers?
why is the location important?

Back 89

>prostatic carcinoma: usually occurs in the POSTERIOR part of the gland. (accessible to diagnostic palpation by digital rectal exam)
> posterior location means they do not cause symptomatic urinary obstruction until late in the disease

Front 90

describe the Gleason scoring system for histologic grading of prostate cancer

Back 90

>Gleason's score is based on the histologic grade of the tumor
the most (best) differentiated and least (poorest) differentiated areas are graded on 1-5 scale. 1= very well differentiated (w/minimal cell atypia) and 5= poorly differentiated (w/ marked cellular atypia.)
scores are summed so best possible is 2 and worst is 10.

Front 91

discuss the role of prostate specific antigen (PSA) in the diagnosis & mgmt of prostate cancer.

Back 91

-many prostate carcinomas are discovered by finding an elevated blood PSA.
-problem: many of these cancers might have been discovered earlier by DRE. it is unwise to rely on PSA as SOLE screening test: a negative PSA (normal blood PSA) conveys false sense of security.
>PSA may also be incr in nodular hyperplasia, prostatitis, and other prostatic disease. it is best used as an additional test w/ DRE of prostate.

Front 92

discuss why syphilis is difficult to diagnose

Back 92

1) caregivers fail to think of it
2) lab tests don't become pos+ until after hallmark chancre is gone
3) darkfield exam of fluid expressed from a chanchre is not readily available outside public health facilities
4)lesions of 2ndary syphilis mimic many other skin diseases
5)if not dx in 1r/2ndry stages, syphilis enters long quiet stage (latent) that has few S&S
6)tertiary syphilis mimics many other diseases
7)blood tests remain positive after initial infx & successful treatment, blood tests have limited usefulness in detecting current infxn.

Front 93

what are some lesions of tertiary syphilis?

Back 93

-aortic aneurysm
-aortic valvular insufficiency
-chronic meningitis
-brain atrophy with dementia

Front 94

what is the most common cause of non-gonoccocal urethritis?

Back 94

Chlamydia

Front 95

explain the role of STDs in the spread of AIDS in Africa & Asia

Back 95

STDs are common in Africa/Asia
genital lesions are assoc with STD offer easy entry of HIV into the bloodstream of affected persons

Front 96

describe the clinical appearance of genital herpes

Back 96

>usually a localized crop of small blisters that are mildly irritating, disappear in about a week
>recurrences tend to be at same site & with time become less frequent & less intense

Front 97

what are sertoli cells good for?
leydig cells?

Back 97

regulate and sustain sperm production.

leydig: make testosterone in response to stimulation by luteinizing hormone (LH).

Front 98

cystocele

Back 98

-a downward protrusion of the bladder into the anterior vagina
-caused by stretching of vaginal wall from multiple births
-prevents complete empyting of bladder & can be cause of urine stagnation & inflammation (cystitis)

Front 99

cystitis

Back 99

inflammation of the bladder, very common
>bacterial: attributable to GN infex by fecal orgs like E.coli: product of urinary stasis, cystoscopy or surgery.
>Viruses, chlamydia, mycoplasma are uncommon causes
Clinically Char: by frequency of urination, painful/burning urination, dull low abd pain. fever doesn't happen unless it gets to kidneys

Front 100

non-bacterial cystitis

Back 100

bladder inflammation without infection.
>severe type: interstitial cystitis: very painful & chronic, involving all layers of bladder wall.
-occurs in women, unknown cause but AID is suspect (assoc with SLE). resistent to tx

Front 101

urethritis

Back 101

inflammation of urethra
>STD most common cause
-2 general types:
>gonococcal: by gonorrhea
>nongonococcal: chlamydia
-cystitis common complication.
-recurrent infx in men can produce scarring in urethra: stricture/chronic urinary obstruct

Front 102

bladder carcinomas
-interesting fact

Back 102

-tend to recur
-kill by infiltrative obstructino of ureters & adjacent pelvic structures & not by distant metastases

Front 103

most important problems of male genitalia are:

Back 103

-ED & infertility
-prostate cancer
-infections

Front 104

varicocele

Back 104

-most common anatomic problem for male infertility
-is a dilation of the veins in spermatic cord & testis.
-surgery is effective

Front 105

hypospadius/epispadius

Back 105

-urethral opening as elongated slit on underside (hypospadius) of penis
or the top side of penis (epispadius)

Front 106

phimosis

Back 106

inability to retract foreskin over the glans
-promotes poor hygiene, infx, inflammation, scarring. may encourage development of squamous carcinoma.
-trapped foreskin:paraphimosis.

Front 107

balanitis xerotica obliterans

Back 107

-an inflammatory disease of unknown cause assoc with a white sclerotic patch of skin at tip of glans which may constrict urethral opening

Front 108

peyronie disease

Back 108

fibrosing condition of tunica albugenia

Front 109

priapism

Back 109

painful persistent erection in absence of sexual desire
-RBC trapped in corpus cavernosum, as in sickle cell disease, or if venous outflow from penis is obstructed. (prostatitis, cystitis)

Front 110

Bowen disease

Back 110

squamous carcinoma in situ that has distinctive clinical & microscopic appearance identical to Bowen of nipple & vulva/oral cavity. untreated 10% progress to invasive carcinoma

Front 111

inguinal hernia

Back 111

-protrusion of bowel into the inguinal canal or scrotum

Front 112

varicoele

Back 112

scrotal varicose veins
-can cause scrotal enlargement/infertility

Front 113

spermatocele

Back 113

cyst of the epididymus that contains sperm and is formed by dilation of the epididymal tubule.
enlarges gradually with continued sperm production.

Front 114

orchitis

Back 114

-rare inflammation of testis
-mumps is most common cause. 25% of adult males with mumps will get this

Front 115

epididymitis

Back 115

-more common that orchitis
-acute bacterial is complication of UTI, prostatitis, or urethritis
(esp ghonorrhea or other STDs)
-nonbacterial is common and etiology unknown

Front 116

testicular neoplasms

Back 116

-most are malignant
2-classes:
-tumors of germ (sperm producing cells) almost all bad
-tumors of others, almost all benign
-tumors of nuts are most common cause of painless enlargement of testis. occur in ages 15-40 y/o.

Front 117

what is the most common type of testicular malignancy?

Back 117

-seminoma: a tumor of germ cells
-are most primitive, and grow really slow and metastasize late
-are held in check by immune system
respond well to radtx

Front 118

embryonal carcinoma

Back 118

-almost as common as seminoma
-composed of primitive embryonic cells
-met earlier, both to lymph nodes
-tx: depends on hormone, chemo & rad tx

Front 119

prostatitis

Back 119

3 kinds:
acute bacterial
-chronic bacterial
-chronic nonbacterial

Front 120

prostatic adenocarcinoma

Back 120

malignancy of prostate gland epithelial cells: most common prostate ca.
>in 2005 prostate CA was the most common of all CA in the US
-hormones play role, genetics, environment

Front 121

tabes dorsalis

Back 121

-sensory defect & abnormal gait in pts with syphilis
-affects posterior/dorsal nerve roots of spinal cord

Front 122

when is it easiest to spread syphilis?

Back 122

-in primary & secondary syphilis.
-transmission is rare after 5 years.
it can however cross the placenta to cause congenital syphilis

Front 123

gonorrhea

Back 123

gram negative (red staining) diplococcocus
-incubate 2-14 days
-urethral discharge with paniful frequent urination
-in men can lead to prostatitis, or epididymitis. urethral strictures.
-can be congentially acquired
-chlamydia FREQUENTLY occurs with it

Front 124

The role of Estrogen

Back 124

-develops & maintains female reproductive structures
-causes female secondary sex characteristics to develop
--fat deposits in breasts & everywhere else
--axillary & pubic hair
--mammary glands
--broadened pelvis

Front 125

the role of progesterone

Back 125

-prepares endometrium for implantation
-prepares mammary glands for lactation

Front 126

squamous carcinoma of the cervix

Back 126

-->possible consequence of repeated HPV infection
-->can cause dysplasia of cervical epithelium, causes precancerous change

Front 127

chlamydia

Back 127

-->nongonoccocal infections
-->many pts are asymptomatic
-->difficult to culture

Front 128

trichomoniasis

Back 128

-->caused by ameba-like organism
-->normally present in 10% of pts
-->symptomatic infx causes burning discharge, changes in vagina that precipitate: pregnancy, & loss of normal vagina flora

Front 129

molluscum contagiousum

Back 129

-virus,
-white nodules; well defined borders, look like small white abscesses, no redness/tenderness
-contain pearly cheesy material

Front 130

vaginitis

Back 130

common transient inflammation. uncomfortable but not serious
->caused by native bugs in vagina
->sometimes from candida or monilasis

Front 131

boosters at 15-18 months

Back 131

DTaP

Front 132

lichen sclerosus

Back 132

-chronic atrophic vulvitis
->non-neoplastic condition that leads to chronic atrophy, scarring and contracture of vulva.
->char by: whitish, parchment like skin dotted with patches of leukoplakia
-occurs most in postmenopausal women. can lead to shrinking & constriction of vulva
-2% can go on to get vulvar squamous carcinoma

Front 133

vulvar intraepithelial neoplasia

Back 133

-most common type of vulvar neoplasia
->uncommon. mainly in women >60
-most are squamous dysplasia
-tend to be aggressive & poorly differentiated squamous carcinomas
-early dx & surgery are effective

Front 134

Why do women tend to develop osteoporosis after menopause?

Back 134

⇒ estrogen is necessary for healthy strong bones.
⇒ Lack of estrogen is important in the thinning & brittlness of bones (osteoporosis) that occurs with age, which is a major health risk for menopausal women because it dramatically increases the risk of bone fractures in elderly women

Front 135

What are the most common sexually transmitted diseases of women and the problems associated with them?

Back 135

⇒ HPV: most common STD. Less aggressive strains are responsible for condyloma accuminatum (genital warts), more aggressive can cause dysplasia and carcinoma of the vulva, vagina, and cervix.

Front 136

Describe the developmental characteristics of the transformation zone of the cervix and its importance in cervical pathology

Back 136

⇒ Transformation zone: is an area extending from the cervical os outward for a short distance onto the ectocervix. In puberty: it is temporarily covered by glandular epithelium, but in adults it is re-covered by squamous cells.
⇒ Almost all dysplasia and cancer of the cervix arise in the transformation zone.

Front 137

What is the importance of HPV in cervical dysplasia and carcinoma?

Back 137

⇒ repeated infection with HPV is the cause of dysplasia and carcinoma of the cervix

Front 138

What is the importance of annual Pap smear screening?

Back 138

⇒ Pap smears are highly effective in detecting early, premalignant lesions of the cervix. Because it takes many years for premalignant lesions to become fully malignant, annual smears offer multiple opportunities for detection of lesions before they become potentially lethal.

Front 139

What is the difference between pathologic and functional uterine bleeding?

Back 139

⇒ Functional uterine bleeding is: abnormal bleeding not attributable to a particular anatomic disorder.
⇒ Pathologic uterine bleeding is: bleeding caused by endometrial hyperplasia, adenocarcinoma, or other anatomic disorders.

Front 140

Why would failure to ovulate cause dysfunctional uterine bleeding?

Back 140

⇒ If ovulation does not occur, no corpus luteum is formed and no progresterone is produced to convert proliferative endometrium to secretory endometrium. The result is a premature bleeding as the proliferative endometrium dies and sloughs away early for lack of progesterone support.

Front 141

Why does endometriosis cause infertility?

Back 141

⇒ Deposits of endometrium may obstruct the fallopian tube and impede movement of sperm, ovum, or conceptus. That prevents conception or implantatin of the endometrium.

Front 142

Define: Fibroid tumor of the uterus

Back 142

⇒ it is a benign smooth muscle tumor of the myometrium. A leiomyoma.

Front 143

What is the ‘cell of origin’ of most ovarian tumors and the 3 main types of carcinoma of the ovary?

Back 143

⇒ most arise from surface epithelial cells
⇒ serous, mucinous, endometroid carcinomas

Front 144

Why is an ectopic pregnancy dangerous?

Back 144

⇒ Because it may produce serious, even fatal intra-abdominal hemorrhage.

Front 145

What are 3 diagnostic components of preeclampsia (toxemia)? Explain how eclampsia is different.

Back 145

⇒ Preeclampsia/toxemia: consists of hypertension, proteinuria, and edema
⇒ Eclampsia is preeclampsia plus seizures

Front 146

What is the key difference between nonproliferative and proliferative fibrocystic change of the breast? Explain the differences/importance thereof.

Back 146

⇒ Epithelial hyperplasia occurs in proliferative but not in nonproliferative disease.
⇒ Epithelial hyperplasia is associated with an increased risk of breast cancer

Front 147

What is the most common tumor of the breast?

Back 147

-->fibroadenoma

Front 148

What is the name of the cell from which most breast cancers arise?

Back 148

-->breast duct epithelial cell

Front 149

How is the behavior of the lobular carcinoma different than that of ductal carcinoma?

Back 149

⇒ Lobular carcinoma: frequently occurs at multiple sites in affected breast. Has tendency to be accompanied by *cancer in the opposite breast. * is assoiated with an increased risk for subsequent development of a SECOND breast cancer.
⇒ Also, lobular carcinoma is difficult to diagnose by mammography because its multifocal, diffuse growth pattern is less likely than ductal carcinoma to form a detectable mass.

Front 150

What are the most important pathological factors that affect the prognosis of patients with breast cancer?

Back 150

⇒ 1 carcinoma in situ or invasive carcinoma
⇒ 2 lymph node mets
⇒ 3 tumor size
⇒ 4 invasion of skin or chest wall

Front 151

squamous columnar junction

Back 151

-vagina & ectocervix are lined by flat squamous epithelium
-> where they meet is the squamous columnar junction
-> changes during puberty to tall glandular cells. the junction is displaced outward.
->sexual maturity the glandular epithelium reverts to squamous & the junction goes to its original spot
-known as the transformation zone. (temporarily transformed ectocervical epithelium)

Front 152

ectropion

Back 152

"turning outward" of the cervix
->because it resembles ulcerated/eroded mucosa it got its old name "cervical erosion"
->a normal variant
->no role in develop of cancer/dysplasia

Front 153

endocervical polyps

Back 153

-not neoplasms
-protrusions of endocervical mucosa into endocervical canal/often visible on speculum exam. less than 2cm
occur in chronically inflamed cervices.
NOT premalignant

Front 154

acute cervicitis v. chronic cervicitis

Back 154

-acute; rare, uncommon: caused by gonococcal/chlamydial infx, post part infex with staph/strep.

-chronic; common, asymptomatic. irritated by trauma (childbirth, tampons, intercourse), vaginal microbes. mild can cause mildly abnormal but benign cells to appear on Pap smears.
BOTh: assoc with prurulent discharge.

Front 155

dysplasia

Back 155

-premalignant state of cervical epithelium that features cells with abnormal nuclei but that is not yet malignant.
BIOPSY report language: cervical intraepithelial neoplasia

Front 156

risk factors for cervical carcinoma

Back 156

-early age at first intercourse
-multiple sexual partners
-male partner with multiple female partners

Front 157

invasive squamous carcinomas

Back 157

-takes 10 years to develop
-earliest sign: vaginal bleeding not during menses or inbetween menses
-it is rare: could be prevented almost entirely by Pap smear, but there is still sample error with these.

Front 158

endometriosis

Back 158

-occurs post partum/post abortion
-retained fragments of placenta after delivery or retained products of conception causes acute inflammation of the endometrium

Front 159

amenorrhea

Back 159

absense of menstruation:
-primary: failure of the ovary itself/from genetic disease (Turner syndrome)
-secondary: failure of ovarian hormonal support: can be caused by Hypothalamic pituitary disorders, severe wt loss, too much exercise

Front 160

dysmenorrhea

Back 160

-painful menstruation
-clinical types of abnormal menstrual bleeding:
->menorrhagia - too much at normal time
->metrorrhagia - irregular bleedin between cycles
->polymenorrhea - frequent short cycles <3 wks
->oligomenorrhea - few long ccyles, >6 wks
->ovulatory bleeding -

Front 161

pathologic uterine bleeding

Back 161

-relatively uncommon
-complications of preganancy
-tumors, hyperplasia etc.

Front 162

2 categories of abnormal endometrial bleeding

Back 162

-pathologic uterine bleeding
-dysfunctional uterine bleeding

Front 163

dysfunctional uterine bleeeding

Back 163

-abnormal bleeding NOT associated with specific anatomic cause.
4 categories it falls into:
--ovulatory failure
--inadequate progesterone production by corpus luteum
--pill-induced bleeding
--long-term estrogen replacement

Front 164

endometriosis

Back 164

-deposits of endometrium outside of uterine cavity
-accumulations of normal endometrium in abnormal places (mostly in the ovaries 80% of cases), the fallopian tubes, or pelvic peritoneal surfaces. sometimes in lungs, liver and lymph nodes.
common cause of dysmenorrhea

Front 165

adenomyosis

Back 165

-endometrium may be found deep in the wall of the uterus
-extension of endometrium deep into myometrium.
rarely causes symptoms. mostly incidental discovery

Front 166

endometrial polyp

Back 166

neoplasm of endometrial stroma (supporting non-glandular cells)
-not premalignant, common close to menopause but can occur througout life.

Front 167

endometrial hyperplasia

Back 167

-overgrowth of endometrial glandular epithelium that can proceed to endometrial adenocarcinoma
-can happen in women with high blood estrogen:
-things that give you high estrogen: -obesity, ERT, irregular periods, estrogen secreting tumors of ovary. DM and HTN are risk factors unrelated to estrogen

Front 168

3 types of endometrial hyperplasia

Back 168

-simple hyperplasia: cells not atypical, untreated can progress to uterine cancer in 10 yrs
-complex hyperplasia: glands folded & tightly packed. individual cells show no atypia. progress to endometrial adenocarcinoma in 10 yrs.
-atypical hyperplasia: glands twisted complex, crowded. untreated cancer in 4 years.

Front 169

leiomyomas

Back 169

-benign smooth muscle tumors (aka - fibroids).
-most common benign tumors of women.
-1/3 women have them
-genetic influence: AA's. shrink after menopause. sometimes can get WAY out of control (100 lbs)

Front 170

leiomyosarcoma

Back 170

-rare malignant smooth muscle tumor that can arise from smooth muscle anywhere in the body.
-in uterus it arises directly from uterine smooth muscle cells. not from preexisting leiomyoma.
-are quite large, advanced when found and are often fatal.

Front 171

pelvic relaxation syndrome

Back 171

uterine prolapse, sometimes so far that the cervix protrudes from the external vaginal opening (introitus)
-rectocele: when rectum bulges forward into vagina
-cystocele: when vagina can bulge forward into bladder

Front 172

PID (pelvic inflammatory disease)

Back 172

-inflammation of the fallopian tubes
-also known as salpingitis
-almost always infectious & STD
-chlamydia & mycoplasma most common causes
-repeated infections can cause a tuboovarian abscess
-inflammation can impede progress of sperm/slow progression of fertilized ovum --> ectopic pregnancy. lower abd pain most common sympt.

Front 173

follicle cysts

Back 173

enlarged, unruptured graafian follicles (where the ovum is ejected)
->luteal cysts are formed of graafian follicles too, are VERY common

Front 174

PCOS

Back 174

-occurs in 5% of women, hormonal abnormalities
-excessive androgenizing agents
-insulin resistant, infertility

Front 175

normal cells of the ovary

Back 175

-contain 3 kinds of cells:
-germ cells (for reproduction)
-hormone-producing stromal cells (bulk of ovarian mass/support ovulation/pregnancy)
-surface epithelial cells, derived from peritoneum

Front 176

general rules of thum on ovarian masses

Back 176

-ovarian carcinomas are silent, lethal neoplasms
(-mass not equal to neoplasm)
-most ovarian MASSES are benign cysts
-about 65% of ovarian NEOplasms arise from the surface epithelium
-about half of ovarian NEOplasms are bilateral
-about 90% of ovarian MALIGNANCIES are carcinomas of the surface epithelium

Front 177

tumors of the surface epithelium
cystadenoma/cystadenocarcinoma

Back 177

-compose 65% of all ovarian tumors
-usually cystic,(called cystadenoma), benign or malig
-often bilat, rare hormonal activity
-3 main types:
serous- papillary growth pattern, mucinous - papillary growth , endometrioid - resemble epithelium-forming endometrial glands

Front 178

neoplasms of the surface epithelium classified by:

Back 178

-their potential to spread. 3 categories:
-benign
-borderline malignant

Front 179

teratoma

Back 179

-tumor that contains tissues not normally found in the organ from which it arises
-ovarian teratomas arise from germ cells, comprise 20% of all ovarian neoplasms. most are cystic, and contain skin, hair, hence common name 'dermoid cyst'. unilateral & benign.
-other germ cell tumors: dysgerminoma & choriocarcinoma

Front 180

ovarian stromal cells

Back 180

10% of ovarian tumors. most are ovarian fibromas
-solid, white, unilateral,benign
-not very aggressive (sluggish), can invade locally but doesn't met

Front 181

Krukenberg tumor

Back 181

-tumor formed by metastatic spread to the ovary from cancer in another organ
-ovary is site of metastasis rather than origin, from breast, lung, and GI cancers mets

Front 182

anti-CA-125

Back 182

-antibody to cancer antigen secreted by ovarian tumors
-not suitable for screening though

Front 183

facts on ovarian cancer in general

Back 183

-4 cause of cancer death in women
-5% assoc with BRCA gene
-slow symptom notice: there's room for them to grow
-1/3 discovered during routine gyn exam
-S&S: feeling of pelvic heaviness/fullness, dysuira, frequency of urination, painful defecation
clinical stating best guide to tx

Front 184

causes of female infertility

Back 184

-obstruction of fallopian tube: by crhonic salpingitis
-large uterine leiomyomas
-abnormal cervical mucus
-ova resistant to conception (older women)
-irregular/infrequent ovulation
-hypothalamic/pituitary disease
-immune factors

Front 185

abortion

Back 185

-interruption of pregnancy before 20 weeks or 500 grams fetal weight.
-spontaneous or induced
-further classifiable as:
--complete: all products are expelled from uterus
--incomplete: some expelled some not
--threatened: bleeding through undilated cervical os raising fear that spontaneous abortion might occur
--missed: fetus dies but is not expelled

Front 186

placenta previa

Back 186

-placenta implants in lower segment of uterus,
prone to hemorrhage because lower uterus doesn't expand with fetal growth

Front 187

placenta accreta

Back 187

-when placenta burrows too deep, when delivery occurs isn't expelled
massive bleeding can happen
placenta needs to be manually extracted

Front 188

hydatidiform mole

Back 188

abnormal fertilization: produce neoplastic/semineoplastic change in chorionic epithelium
--all secrete hCG
-benign tumor like overgrowth of placental cells caused by abnormal combinations of ovum/sperm
-produced by ovum with no nucleus, or one or more sperm. conceptus with 2 or more sperm and no female material

Front 189

invasive mole

Back 189

middle ground between hydatifiform mole and choriocarcinoma
may invade thru uterine wall into pelvis. difficult to remove, may require hysterectomy & chemo

Front 190

choriocarcinoma

Back 190

-malignant proliferation of epithelial cells that cover normal chorionic villi
-similar to tumor of same name arising from testis
-can arise from any form of normal or abnormal pregnancy
-can metastasize widely. most spread widely (lungs, brain, liver, kidneys)

Front 191

acute mastitis

Back 191

-acute infection of breast
-uncommon, almost all cases occur during lactation
-staph infx: produces abscess
-strep infx: more diffus, generalized swelling, tenderness pain. chronic inflammation an lead to fibrocystic change

Front 192

fat necrosis

Back 192

unusual type of necrosis
occurs only in fat
-esp. likely to cause local calcium deposits
-cause unknown, most traced to trauma: most often in women with large fatty breasts

Front 193

fibrocystic change

Back 193

consists of breast scarring, chronic inflammation, cystic dliation of breast ducts.
-from hormone changes all the time thru menstrual cycle
-no symptoms

Front 194

nonproliferative fibrocystic change

Back 194

-not assoc with incr risk of br.ca.
-if nuclei are normal: is called proliferative fibrocystic change
-if abnormal: dx is proliferative fibrocystic change with atypia: moderate incr risk of br. ca.

Front 195

epithelial hyperplasia

Back 195

-of any kind, whether by fibrocystic change or some other condition is associated with a small but definite increased risk for development of breast cancer

Front 196

proliferative breast disease

Back 196

-term that includes conditions, other than fibrocystic change, assoc with epithelial hyperplasia
-ex: intraductal papillomas are cauliflower-like polyps in breast dutcts.
-risk of cancer is proportional to degree/extent of epithelial hyperplasia

Front 197

fibroadenoma

Back 197

-benign tumor of breast stroma
(supporting tissue)
-women in 20's. solitary round mass 1-5 cm. not premalignant. surgical excision curative

Front 198

Phyllodes tumor

Back 198

uncommor much larger somewhat aggressive version of fibroadenoma
-mets rare
some recur after excision

Front 199

intraductal papillioma

Back 199

occurs in milk ducts near nipple
-is palpable, bleeds, causes nipple discharge
-soliatry papilloas are most common are not premalignant, but multiple papillomas (intraductal papillomatosis) are variety of proliferative breast disease, incr risk for breast carcinoma

Front 200

what are 2 of the most common types of breast cancer?

Back 200

90% of breast cancers are either:
-ductal carcinoma 75-80%
-lobular carcinoma 10-15%
-both exist first as carcinoma in situ before becoming invasive, if discovered can be removed/cured.

Front 201

lobular carcinoma (in more detail)

Back 201

-distinctive in several ways:
-it occurs in multiple sites
-appears to have greater tendancy than other types to have ca in opposite breast
-assoc with incr risk of development of second breast cancer.
-difficult to dx with mammography, less likely to form detectable mass

Front 202

ductal carcinoma (in more detail)

Back 202

-most common
-most aggressive when invasive
-in situ seen more common b/c of mammography
-less likely for opposite breast to be involved
-2/3 are invasive ductal carcinoma

Front 203

factors affecting development of breast cancer

Back 203

-sex: women have 100x risk
-lobular carcinoma in other breast:
-family hx/genetics, 2 genes linked but are responsible for small percent of breast cancers
-age: uncommon <30y/o
-estrogen: prolong exposure incr risk

Front 204

prognostic factors for pts with breast cancer

Back 204

-2 gravest clinical prognostic signs: distant mets or inflammatory carcinoma
pathological factors:
-in situ v. invasive
-lymph node mets
-tumor size
-invasion of skin/chest wall
less important: histologic type/grade, rate of cell division/ploidy of cells, presence/absence of estrogen/progesterone

Front 205

clinical presentation/behavior of breast cancer

Back 205

-half present in upper outer quadrant
-80% discovered by pt (1/3 will have lymph node mets by this time)
2 unusual CPs: inflammatory carcinoma- breast/skin swollen
-paget disease- nipple/areola involved: red, tender, cracked, oozing. breast cancers spread nearest lymph nodes. then blood later.

Front 206

diagnosis & treatment of breast cancer

Back 206

-mammography has limitations
-self breast exam has limitations
-professional exam catches stuff the mammogram misses
-tx depends on all the various factors listed previously: radiation/chemo/surgery

Front 207

gynecomastia

Back 207

-male breasts
-usually bilat
-can be from incr blood estrogen from cirrhosis, drugs (anabolic steroids, digitalis, theophylline, CCB, chronic marijuana use)
-1% breast cancers occur in men.

Front 208

What's the difference between the osteoblast and an osteoclast?

Back 208

osteoblast: bone-forming cell

osteoclast: bone dissolving cell

Front 209

what is the role of osteiod in bone formation?

Back 209

-osteiod, a specialized protein produced by osteoblasts, is transformed into bone by deposition of calcium, phosphate, & other minerals

Front 210

why do patients with achondroplasia have short stature?

Back 210

-bones grow from the epiphyseal cartilaginous plate at the end of long bones.
-in achondroplasia, epiphyseal bone growth is genetically defective & bones are abnormally short

Front 211

discuss the pathogenesis of osteoporosis

Back 211

-bones are continually being remade by a delicate balance between osteoblastic bone formation and osteoclastic bone dissolution
-> bone-forming capability is estrogen dependent & declines each year as estrogen production declines, ultimately tipping the balance toward bone dissolution. bone mass is also influenced by other factors: age, genetics, physical activity, diet & hormones, most notable of which are hormones (estrogen) & genetic factors. ex: AA's have greater bone mass than causasians, thus less osteoporosis, women more than men

Front 212

what's the difference between osteoporosis and osteomalacia?

Back 212

-osteomalacia: is a qualitative defect of bone microstructure: bone mass is normal, but it is defectively mineralized. most osteomalacia is caused by disturbed calcium, phosphate, or vitamin D metab.

osteoporosis: is a quantitative defect; bone microstructure is normal but less bone mass is present

Front 213

where do 80% of primary bone tumors occur?

Back 213

-the knee

Front 214

explain the pathogenesis of osteoarthritis, and describe the pathologic changes in affected joints

Back 214

-primary osteoarthritis: is associated with a genetic predisposition & age-related mechanical wear & tear
-affected joints rarely show inflammatory change
-joint cartilage is thin, frayed, or worn completely away
-the underlying bone surfaces become dense & sclerotic. further stress & degeneration produce subcortical bone cysts & joint spurs (osteophytes) which project into adjacent soft tissue to cause swelling, inflammation & pain.

Front 215

explain the pathogenesis of rheumatoid arthritis & describe the pathologic changes in affected joints

Back 215

-RA is caused by an autoimmune reaction that begins in response to some unidentified foreign agent, perhaps the EBV that triggers an immune reaction in the synovium. inflammation & neovascularization of the joint cause release of lytic enzymes that destroy joint cartilage.

Front 216

define rheumatoid factor (RF)

Back 216

-RF is an autoimmune antibody complex that circulates in the blood of most (but not all) patients with rheumatoid arthritis
-RF may also be found in some other autoimmune diseases

Front 217

explain how the seronegative spondyloarthropathies differ from RF

Back 217

1)spondyloarthropathies: are usually confined to the vertebrae & sacroiliac joints
2) inflammation also involves ligaments where they attach to bone;
3)rheumatoid factor is absent from blood
4)most pts carry the HLA-B27 antigen

Front 218

what are the distinguishing features that separate fibromyalgia from arthritis and other painful muskuloskeltal syndromes

Back 218

-fibromyalgia: differs from polymyalgia rheumatica & arthritis in that fever, wt loss, anemia increased erythrocyte sedimentation rate & other measurable abnormalities are not present in fibromyalgia.
-in fibromyalgia, no pathologic findings are detectable in the affected tissues, and no objective evidence of disease is present

Front 219

what's the difference between disuse atrophy and neurogenic atrophy? give examples of each

Back 219

disuse atrophy: occurs in inactive muscle innervated by an intact lower motor neuron. ex: muscle atrophy that occurs in bedridden pts

denervation atrophy: occurs in muscle whose innervating neuron is diseased or dead. ex: atrophy in pts with diabetic peripheral neuropathy/peripheral nerve injury

Front 220

what's the difference between Duchenne muscular dystrophy and Becker muscular dystrophy?

Back 220

-Duchenne muscular dystrophy is a severe form of muscular dystrophy caused by a genetic defect that results in the absence of dystrophin, a muscle cell structural protein

Becker MD: is a less severe form of MD in which dystrophin is present but molecularly abnormal

Front 221

what's the difference between myositis and myopathy?

Back 221

-myositis is muscle inflammation

-myopathy is generalized noninflammatory muscle disease that is not muscular dystrophy

Front 222

what's the molecular pathogenesis of myasthenia gravis?

Back 222

-in myasthenia gravis autoimmune antibodies attach to Ach receptors on the muscle side of the neuromuscular synapse
-this prevents reuptake of Ach (a necessary step in nerve impulse transmission to muscle)

Front 223

what is soft tissue?
what are some tumors/tumor-like conditions of soft tissue?

Back 223

-soft tissue is nonepithelial tissue that is not bone, cartilage, brain or nerve, meninges, bone marrow, or lymphoid tissue
-it includes fibrous tissue, skeletal & smooth muscle & fat. some soft tissue lesions are lipoma, fibroma, fibromatosis, & various sarcomas

Front 224

osteogenesis imperfecta

Back 224

-brittle bone disease: spectrum of inheritable disorders caused by genetic defects in collagen formation
-brittle bones that are easily fractured. defective middle ear bones cause deafness. defective collagen also causes abnormal tooth development, floppy heart valves, and thin sclerae (which make them look blue)

Front 225

Paget disease

Back 225

-osteitis deformans
-common bone disease of unknown cause but viruses strongly implicated.
-bone is formed&destroyed really rapdily. causes irregular thick/dense bone. any bone can be affected. usually asymptx, incidentally discovered. increased blood alkaline phosphatase. can develop osteosarcomas.

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biggest risk factors for fractures:

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->80 y/o
->wt less than 130#
->long term use of benzos
->no walking for exercise
->poor vision
->brain disease that affects stability

Front 227

what is a pathologic fracture?

Back 227

-fracture that results from a disease that has weakened the bone locally so that fracture occurs with normal stress

Front 228

osteomyelitis

Back 228

-bacterial infection of bone
-traumatic or direct implantation of bacteria in bone is the main cause of osteomyelitis in adults
-kids get it from another infection that spreads (ear infection for ex)
Staph aureus accounts for 80% of id'ifiable bacteria. accompanied by bone necrosis and inflammation

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bone infarct:
-aseptic necrosis

Back 229

-produce bone necrosis, often called asceptic necrosis
or avascular necrosis, many infarcts are caused by impaired blood flow
-steroids are a common cause
-some bones more vulnerable: femur & carpal bones of wrist
-kids growing have this problem & older b/c of vascular diz
-pain is most common complaint

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osteoporosis

Back 230

-increased bone porousness/bone mass.
-results from declining blood estrogen levels, postmenopause
-age genetics physical activity have effects
-2ndary causes: Cushings, diet deficiency, immobilization from bed rest, lack of wt bearing activity. 1/3 of women >65 will suffer a fracture from osteoporosis

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osteomalacia

Back 231

-soft bones. defective mineralization of bone protein. is a 'qualitative' defect. osteocytes make a normal/near normal amount of osteoid (protein). but it doesn't mineralize right. usually results from insufficient intake/diet or poor intest absorp of Ca, PO4, and vit D. in childhood: rickets. small bowel disease (Crohns) and CRF (called renal osteodystrophy). (because kidneys can't excrete phosphate blood lets go of Ca+)

Front 232

osteosarcoma

Back 232

-is a malignant tumor that forms neoplastic bone. excluding tumors of bone marrow, osteosarcoma is the most common primary tumor of bone. occurs in metaphysis of long bones. half occur in tibia/femur near the knee. 75% are in pts <20 y/o. presents as painful, enlarging mass.

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osteochondroma

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benign -a mushroom shaped bony protruberance capped by cartilage that arises in children & grows on surface of metaphysis of long bones.

Front 234

enchondroma

Back 234

-benign cartilage-forming tumor that tends to grow in medullary cavity of bones

Front 235

chondrosarcoma

Back 235

-malignant tumor of bone that forms a neoplastic cartilage. half as common as osteosracoma. favors spine, ribs, pelvis/vertebrae. adults 40-60. microscopic grade in chondrosarcoma is paramount in predicting tumor behavior

Front 236

fibrous cortical defect

Back 236

-tumor-like condition of bone that occurs in 1/3 kids >2 y/o. not true neoplasm, not a real cancer
-nodule of benign fibrous tissue near knee. asymptx. when large is called a nonossifying fibroma.

Front 237

fibrous dysplasia

Back 237

-benign nodular growth of fibrous & bone tisue that affects growing bones in children/teens
-probably developmental abnorm, all components of bone are present
-do not grow in coordinated manner. produce tumor-like masses of bone in fibrous matrix
-monstotic; in more than one bone. -polystotic fibrous dysplasia affects multiple bones.

Front 238

-aneurysmal bone cyst

Back 238

-forms tumor like masses in bone. is not a tumor
-composed of large richly vascular cysts containing pools of blood that expand/erode normal bone, can get big

Front 239

giant cell tumor

Back 239

-contains large cells w/ multiple nuclei that have microscopic apperance similar to normal ostoeclasts. are uncommon. most occur near the knee in epiphysis of femor/tibia. can be locally destructive. some met to lungs

Front 240

ewing sarcoma

Back 240

-malignant tumor that occurs mainly in kids 10-15 y/o. genetic factors important. AA *rarely* affected. occurs mainly in long bones & spreads quickly by blood-borne mets. surgery combined with radxtx/chemotx cures half of pts

Front 241

multiple myeloma

Back 241

-tumor of plasma cells (B lymphocytes) grows as localized bone lesions in cranium, ribs, sternum

Front 242

osteoarthritis
kinds

Back 242

-degenerative joint disease
-mechanial wear-&-tear condition, most common type of arthritis
-primary osteoarthritis: is osteoarthritis that can't be attributed to some specific circumstance (DIP joint) being old. wt bearing joints
-2ndaryOA: attributed to specific circum-->abnormal stress on a joint, physical malformations/nerve disease

Front 243

osteoarthritis:
pathological changes

Back 243

-most changes are minimal
-rarely show inflammation
-cartilage becomes thin, frayed, or completely worn away
-most importnt clinical char. activity related joint pain is is relieved by short rest. pain of most other tyes lasts an hour or so despite rest. early diagnosis is difficult. most affected joints: hip, knee, cervical and lumbar spine. in the foot is bunion joint.

Front 244

RA

Back 244

-chronic systemic autoimmune disease of synovial joints that affects 1-2% of adult population
-EBV suspect. -80% of RA occurs in women
-immune reaction stimluates growth of blood vessels into synovium & cartilage. a pannus grows over the cartilage surface & oozes destructive enzymes. causes papillary overgrowth of synovium leads to anklyosis. causes "Z-deformity". develop 'rheumatoid nodules'.(not found in other types of arthritis

Front 245

what is the fundamental immune reaction in RA?

Back 245

-involves T-lymphocytes, but B lymphocytes also play a role
-75% of pts have circulating antibody coplex in blood 'rheumatoid factor'.

Front 246

secondary amyloidosis

Back 246

-a condition related to the large volumes of antibody (immunoglobulin) produced in response to the autoimmune reaction. the immunoglobulins are broken down & can be deposited as amyloid protein in kidneys, liver,spleen & adrenals. RA is comon cause of 2ndary amyloidosis

Front 247

diagnosis of RA

Back 247

-joint fluid diagnostic for RA shows chronic inflammatory cells, is free of bacteria & uric acid
-rhuematoid nodules/detection of RF in blood confirm clinical dx
-anti-CCP is autoantibody present in half of RA pts.

Front 248

juvenile RA

Back 248

-differs from adult RA in several ways:
--onset sudden
--systemic, toxic
high fever & prostration. few joints involved, those which are are large (knee/hips). majority recover fully. few develop chronic deforming arthritis.

Front 249

spondyloarthropathy

Back 249

several related types of autoimmune, genetically influenced vertebral arthritis that occurs in pts who DO NOT HAVE RF antibody in their blood. called 'seronegative'
-->distinct from RA in that: --arthritis is confined to vertebrae, inflammation involves tendons where they attach to bone, RF is absent from blood, cells of most pts carry HLA-B27 antigen

Front 250

anklyosing spondylitis, reactive arthritis, psoriatic arthritis:
common things:

Back 250

-majority of pts are young
-males affected more than female
-infection seems to affect onset/trigger disease
-many pts have extra-articular inflammatory conditions like iritis/vasculitis

Front 251

ankylosing spondylitis

Back 251

-(rheumatoid spondylitis) is chronic relapsing arthritis, primarily affecting the spine/sacroiliac joints
-pts suffer from spinal rigidity/chronic back pain. otherwise are fine

Front 252

reactive arthritis

Back 252

-occurs w/in one month of infection somewhere in body other than joints (GU, GI) most common
-low back, feet, ankles often involved

Front 253

psoriatic arthritis

Back 253

-seen in 10% with psoriasis
-small joints of hands & feet are usually first affected. but spine & sacroiliac joints often involved later

Front 254

primary gout

Back 254

-chronic metabolic disease assoc w/ high uric acid levels; joint deposits of uric acid crystals, & inflammatory nodular subQ deposits (tophi) of uric acid crystals
-can cause kidney failure if deposited in kidney
-almost all are men. great toe in 90% of cases. called podagra.
-uric acid accelerates atherosclerosis.
-tx; diet & drugs

Front 255

acute septic arthritis

Back 255

-uncommon. happens if left untreated. adults caused by gonohorrhea. steroids & autoimmune, IVDA. infected IV/cath lines. people with RA are at higher risk. children with bacterial infections.

Front 256

Lyme disease

Back 256

-bacterial infx: Borrelia burgdorferi
-joint related: arthritis is sign of chronic infection
-meningitis & endocarditis can also occur

Front 257

Polymyalgia rheumatica and (giant cell arteritis)

Back 257

-PMR dx made in absence of other dxs. pain, stiffness in shoulders, neck & hips. fever, malaise, wt loss.
-moodiness, mild wt loss.
-dx confirmed by incr levels of CRP or ESR. 20% have/will devlop giant cell arteritis. (autoimmune vasculitis that affects temporal, retinal, and cranial arteries). steroids are good for this.

Front 258

dislocation

Back 258

-displacement of bone point such that articular surfaces no longer meet.
-subluxation: lesser degree of separation.

Front 259

sprain:

Back 259

-injury to ligament induced by stretching too far

strain: same injury to a strain. may stretch or tear away from attachment.

Front 260

spondylolisthesis

Back 260

-locking mechanism of vertebrae failure. (b/c of degeneration or disc disease)
-occurs in lower back, often asymptomatic.

Front 261

bursitis

Back 261

-inflammation of bursa, typically caused by direct trauma or stress of repetitive motion.
-bursa fills with inflammtory fluid

Front 262

herniated intervertebral disc

Back 262

-nucleus propulsus bulges/ruptures thrugh the annulous fibrosis

Front 263

tendonitis

Back 263

-inflammation/pain in tendon.

Front 264

fibromyalgia

Back 264

-clinical syndrome of muscle & periarticular tendon & ligament pain, tenderness, & stiffness that is not associated with objective signs of diasease. we don't know why it happens. psychological?
CANNOT be treated with NSAIDS/pain meds

Front 265

ganglion cyst

Back 265

-small smooth fluctuant fluid-filled simple cyst
arises near a joint/tendon sheath.
-focal myxoid degen of connective tissue. innocuous.

Front 266

pigmented villonodular synovitis

Back 266

-benign neoplasm
-pts 20-40 y/o.
-surgical excision curative.
-related neoplasm is giant cell tumor of tendon sheath.

Front 267

myositis

Back 267

-most commonly caused by virus
-trichinella spiralis, a worm form pork can cause it.

Front 268

anaerobic muscle infections

Back 268

-gas gangrene - C. perfringens, causes crepitus to wound.
-tetanus
-ludwig angina
-peritonsillar/retropharyngeal abscess

Front 269

dermatomyositis

Back 269

-AI diz of skin & skeletal muscle in which first sign is usually characteristic rash of eyelids
-muscle inflammation/weakness follow

Front 270

polymyosisits

Back 270

similar to dermatomyositis
-no skin involvement
-most pts are adults.
-in both diz: proximal msucles are most seriously affected. sx: soreness, weakness, muscle atrophy. in polymyositis: muscle inflammation is causd by direct muscle damage by T-cells.

Front 271

rhabdomyalsis

Back 271

-tern used to describe sudden necrosis of skeltal muscle.
-release of large amounts of myoglobin into circulation
-myoglobin is toxic to kidneys
-always 2ndary to some underlying medical condition. burns, heat stroke, crush injury, binge drinking, muscle contractions during seizures, drug OD. poisoning, electircal shock.

Front 272

liposarcoma

Back 272

-malignant tumor of fat cells
-arise in deep tissues and are sluggishly malignant
-locally aggressive

Front 273

sarcomas of fibrocyte cells and their forms

Back 273

-a fibromatosis; confined prolif of fibrous tissue
ex: >malignant fibrous histiocytoma- most common in adults, thigh & retroperitoneum, half met
>fibrosarcoma: mostly around knee & thigh & behaves much same as MFH
>synovial sarcoma: malignant tumor microscopicly similar to fibrosarcoma. half met.

Front 274

leiomyoma

Back 274

-benign tumor of smooth muscle, most often in uterus
-does not become malignant
a leiomyosarcoma does become malignant

Front 275

how is CSF produced, circulated and absorbed?

Back 275

-CSF is made by the choroid plexus of the lateral (1st&2nd) and 3rd ventricles. CSF flows downward to the 4th ventricle and exits the ventricular system through openings in the dorsum of the 4th ventricle (the foramina of Luschka & Magendie) into the subarachnoid space, where it bathes the surface of the brain & spinal cord. CSF is resorbed by arachnoid granulations over the cerebral hemispheres

Front 276

explain the meaning of the terms gray matter and white matter

Back 276

->the cortex and other collections of neuronal cell bodies are gray and are called gray matter.
->myelinated nerve fibers are white and are called white matter
-in the CNS the axons of neurons are gathered to form tracts; in the peripheral nervous system nerves carry incoming and outgoing motor signals

Front 277

name the parenchymal and ancillary cells of the CNS

Back 277

-parenchymal (main functional) cell of the CNS is the neuron
-ancillary cells are astrocytes, which form the structural framework.
-oligodendrocytes which contain myeling and wrap the neuronal axons
-microglia: are the macrophages of the CNS

Front 278

explain by increased intracranial pressure is dangerous

Back 278

-it can force the brain to herniate (protrude) through any available opening in in internal membranes or through skull openings
-herniated brain may undergo direct pressure necrosis, or may impede vascular flow that results in brain hemorrhage/infarction
-ex: herniation of cerebellar tissue thru the foramen magnum in a pt with massive intracranial hemorrhage

Front 279

compare & contrast the location, cause & effect of subdural & epidural hematomas

Back 279

-subdural hematomas: usually cased by mild head injury that breaks small venous channels & allows slow accumulation of blood in the subdural space & slow onset of symptoms
Epidural Hematoma: usually caused by more severe injury, sufficient to cause skull fracture & tear in an epidural artery. blood accumulates rapidly in the epidural space & sx occur promptly

Front 280

what is the cause of the most spontaneous subarachnoid hemorrhage?

Back 280

-berry (saccular) aneurysms are the most common cause of spontaneous subarachnoid hemorrhage

Front 281

explain the anatomic & pathologic differences between white & red stroke?

Back 281

white stroke: a bloodless infarct of brain tissue usually caused by arterial ischemia 2ndary to atherosclerotic blood vessels supplying the brain
red stroke: spontaneous bleeding into brain tissue & is usually caused by hypertension

Front 282

explain the cause of laminar cortical necrosis

Back 282

laminar cortical necrosis: is necrosis of a layer of cells in the cerebral cortex, caused by generalized cerebral hypoxia.
>when deprived of oxygen, this cell layer suffers the most & undergoes necrosis in circumstances that may not cause permanent injury to other brain cells.
->global ischemia may produce temp. coma or other neurologic deficit, but laminar cortical lesions is irreversible & is usually assoc. with permanent coma or death.

Front 283

what's the difference between concussion & contusion?

Back 283

->concussion: period of temporary brain dysfunction following head injury. is not associated with anatomically demonstrable brain lesions & radiographic images of the brain are normal.10% of concussion vitcims are rendered unconscious, frequent symptoms: dizziness, confusion, amnesia, nausea & blurred vision.
Contusion: superficial hemorrhage (bruise) in the brain caused by head injury.
->

Front 284

what is the cause of most epidemic bacterial meningitis & the population at risk?

Back 284

-bacterium: is Neisseria meningitidis. population at risk is young adults living in close quarters

Front 285

explain the biochemical dysfunction in Parkinson's & some of the conditions causing it

Back 285

->Parkinsonism is caused by motor control abnormalities in the basal ganglia of the midbrain.
->the affected cells do not transmit signals properly b/c they do not release normal amounts of dopamine.
Parkinsonism may be caused by vascular disease, toxins, encephalitis, or repeated head injury. usually cause is unknown

Front 286

recite some important facts about Alzheimer's disease

Back 286

-> causes over half of all cases of adult dementia
->usually in elderly, women more than men.
1% of people 60-64 are affected
->prevalence rises rapidly with advancing age & affects 1/3 >85
cause is unknown, 10% of cases have familial assoc

Front 287

probable cause of multiple sclerosis

Back 287

-MS is probably an autoimmune diseaze triggered by an as-yet undetected microbe

Front 288

why do alcoholics develop chronic brain disease?

Back 288

-ETOH = empty calories, no vitamins
-chronic alcoholism: develop variety of neuro disorders as result of deficiency of essential nutrients/vitamins

Front 289

what are the most common causes of metastatic brain tumors?

Back 289

-in descending order of frqy:
->lung,
-breast
-malignant melanoma of skin

Front 290

explain why it is difficult to completely remove most gliomas surgically

Back 290

-because they extend into normal tissue: 'fingers of neoplastic tissue'
-excision cannot be done without cutting out a wide margin of normal tissue as well and that is unacceptable.

Front 291

what are 2 diseases associated with peripheral neuropathy

Back 291

-> DM
-chronic alcoholism

Front 292

how can Guillain-Barre syndrome be fatal?

Back 292

-if nerves innervating respiratory muscles are severely affected then ventillation is compromised

Front 293

cerebral palsy

Back 293

->permanent nonprogressive motor problems (spasticity/paralysis) that arise owing to an insult to brain before it reaches a certain maturity inutero-age 2
->75% arise from prebirth unkown causes
->some assoc with birth trauma
risk factors: low birth wt, intrauterine growth retardation.

Front 294

different types of brain herniations:

Back 294

-subfalcine
-tentorial
-tonsillar

Front 295

differentiate between dermis, epidermis, subcutis

Back 295

-epidermis: surface squamous epithelium of skin

-dermis: fibrocollagenous layer of skin beneath the epidermis, separated from epidermis by basement membrane & containes skin appendages like sweat glands and hair follicles

-subcutis: layer of fat immediately beneath the dermis

Front 296

define eczema,
offer examples

Back 296

-eczema is dermatitis expressed as itchy, papulovesicular oozing crusted lesions
-most common type is allergic contact dermatitis,: poison ivy for example

Front 297

what are several systemic diseases with important skin findings?

Back 297

-systemic lupus erythematosus,
-systemic sclerosis
-AIDS, hyperthyroidis, hypopthyroidsm
-hyperlipidemia
-DM, neurofibromatosis

Front 298

explain the pathogenesis of psoriasis

Back 298

-psoriasis is casued by an over-proliferation of epidermal cells in genetically inclined persons
-it is probably automimmune

Front 299

define lichen simplex chronicus

Back 299

-a common pattern of skin reaction caused by chronic rubbing or scratching of skin affected by disease, usually allergic dermatitis, which stimulates epidermal growth & produces thick rough skin with exaggerated normal skin lines

Front 300

name 2 characteristics of diseases of the basement membrane zone, & list several examples

Back 300

-disease of the basement membrane zone usually produces vesicles or bullae & most are autoimmune
-some diseases are epidermolysis bullosa, bullous pemphigoid, deramtitis herpetiformis, erythema multiorme, lupus erythematosus, & lichen planus

Front 301

-explain the pathogeneis of allergic contact dermatitis
give example

Back 301

-it is a type-4 delayed hypersensitivity (T-cell) reaction
-the rash of poison ivy, which occurs only a few days after skin contact with the plant is an example

Front 302

-explain the pathogenesis of atopic dermatitis & name 1 characteristic of susceptible persons

Back 302

-atopic dermatitis is a very common allergic skin disease caused by type 1 (anaphylaxis) IgE dependent hypersensitivity reaction occuring in people with other allergic conditions such as hay fever/asthma

Front 303

-explain how acne vulgaris differs from rosacea

Back 303

-acne vulgaris is a disease of teenagers with oily skin and comedones that lead to scarring
-rosacea is a disease found in fair-skinned women aged 30-50 of norther european descent & usually does not cause scarring

Front 304

define impetigo

Back 304

-ipmetigo is a common superficial skin infection that forms pustules
-it occurs most often in infants/children usually caused by Staph or Strep infection

Front 305

explain the pathogenesis of epidermoid cysts

Back 305

-epidermoid cysts are formed of epidermis trapped beneath the surface, often in association with a hair follicle, the cells continue to proliferate and produce a cyst filled with keratin debris

Front 306

-name the cause of skin warts

Back 306

--infection by HPV

Front 307

name the skin cancer that may originate in a solar keratosis

Back 307

-squamous carcinoma

Front 308

-name the most common skin cancer & discuss the behavior of skin cancers

Back 308

-basal cell carcinoma: the most common
-the great majority of skin cancers are basal or squamous cell carcinoma
-they almost never metastasize or cause death of the pt.
-malignant melanoma, however is highly malignant & frequently metastasizes & causes death

Front 309

list several neoplasms or neoplasm like leions of the dermis

Back 309

-lipoma, dermatofibroma
-angioma, xanthoma, keloid
-kaposi sarcoma
-skin appendage tumors

Front 310

name the most common benign tumor of melanocytes

Back 310

nevus
melanocytic nevus)

Front 311

list several features of malignant melanoma that may be clues to early clinical diagnosis

Back 311

-most important clinical feature: change in color or pigmentation of preexisting pigmented lesion.
other warning signs: enlargement of existing pigmented lesion, a nodule in an otherwise flat pigmented lesion, itching or pain in a previously silent pigmented lesion, development of a new pigmented lesion in adult life, irregular borders, satellite areas of pigmentation, & varied coloration, esp: ares of pink or gray discoloration or unusually dense black coloration

Front 312

explain the importance of accurate microscopic measurements of the thickness of a malignant melanoma

Back 312

tumor thickness (depth of invasion) is a good guide to therapy and is closely correlated with survival