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168 Cards in this Set
- Front
- Back
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Where is Vitamin D derived from in the human body?
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In the human body it is derived from two sources.
1. Skin is the major source of Vitamin D3. 2. Diet is the other major source: Vitamin D3 is absorbed by the small intestine in association with chylomicrons |
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How is Vitamin D3 transported in the blood?
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Vitamin D3 binds to vitamin D binding protein
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Where does the first hydorxylation of Vitamin D3 occur?
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The first hydroxylation occurs in the liver. Vitamin D3 forms 25-OH Vitamin D3 then it is released into the bloodstream
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Where does the second hydroxylation of Vitamin D3 occur
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Hydroxylation occurs in the kidneys
-It is hydroxylated to a highly active 25-(OH)2 vitamin D3 |
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How is the process regulated by plasma calcium concentration?
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The process is regulated indirectly by an increase in plasma calcium concentration, which triggers secretion of PTH, or directly by a decrease in circulating phosphates, which in turn stimulates activity of 1-alph-hydroxylase which is responsible for the conversion of 25-OH vitamin D3 to active 1,25-(OH)2 vitamin D3
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What stimulates intestinal absorption of calcium and phosphate?
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Active 1,25-(OH)2 vitamin D3 stimulates intestinal absorption of calcium and phosphate and mobilization of calcium from bones
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True or False.
Active 1,25-(OH)2 Vitamin D3 is necessary for normal development and growth of bones and teeth |
True
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Does vitamin D2 undergo the same conversions as vitamin D3 and produce the same biological effects?
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YES
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What does Vitamin D3 deficiency result in?
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Deficiency in Vitamin D3 will result into rickets, a disease that causes abnormal bone ossification
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If a patient has prolonged renal hemodialysis what are you going to supplement them with? Why?
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Patients on prolonged renal hemodialysis are often supplemented with vitamin D3 and calcium to avoid severe disturbance of calcium homeostasis as a result of secondary hyperparathyroidism, a condition prevalent in these patients.
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What is the pre-cursor to Vitamin D3 in the skin?
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7-dehydrocholesterol
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What is vitamin D3 converted to in the liver?
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25-OH Vitamin D3
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What is 25-OH Vitamin D3 converted to in the kidneys?
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1,25 (OH)2 Vitamin D3
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An electron micrograph of a biopsy of kidneys was produced your patient's kidneys appear to have
1. an accumulation of immune complexes in the subepithelial zone of the glomerular capillaries. 2. Glomular basement membrane materials project around the subepithelial deposits 3. Glomeruli are normocellular What is the possible diagnosis of your patient? |
Stage II membranous glomerulopathy
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Describe what happens in Stage I glomerulopathy.
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Stage I: There are no basement membrane projections adjacent to deposits
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Describe stage II glomerulopathy.
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There are GBM projections between deposits
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Describe stage III glomerulopathy
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The deposits become incorporated into the basement membrane
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Describe stage IV glomerulopathy.
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The deposits start to fade away leaving lucent gaps and a thickened basement membrane
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Describe Stage V glomerulopathy
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The lesion, paradoxically, has normal subepithelial zone of the basement membrane, which has been repaired and the disturbance has been pushed to the subendothelial zone.
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In Diabetic glomerulosclerosis what part of the nephron thickens?
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Glomerular basement membrane thickening and widening and expansion of the mesangial matrix, and mild mesangial hypercellularity occur.
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What appears in Kimmelstiel-Wilson nodules? What disease are these present in?
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Sometimes focal, segmental, nodular lesions appear. These occur in Diabetic glomerulosclerosis
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What happens to the capillaries and mesangial cells in Kimmelstil-Wilson ?
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Capillaries and mesangial cells are pushed to the periphery
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What is the leading cause of end-stage renal disease in the United States
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Diabetic Glomerulosclerosis
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What disease is indicated with proliferation of the parietal cells of Bowman's capsule and also inflitration of macrophages, producing a crescent like mass in most glomeruli?
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Crescenteric glomerulonephritis
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The proliferation of parietal cells in the glomerulous can cover approximately ________ of the entire urinary space.
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50%
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What are some components of the crescents in Cresenteric glomerulonephritis?
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Fibrin and macrophages are components of the cresents
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Is cresenteric glomerulonephrtiis a disease or a component of a disease?
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It is a morphological component of an active disease.
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Describe the nephron in Mesangial glomerulonephritis?
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Also known as type I membanoproliferative glomerulonephritis.
Hypercellularity (increase in mesangial cells) and subendothelial deposits, glomeruli are enlarged. |
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What is caused by a mutation of the nephrin gene leading to the absence or malfunction of the podcyte slit filtration diaphragm.
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Congenital nephrotic Syndrome
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A child that is affected by congenital nephrotic syndrome will suffer from massive ___________ and ____________.
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massive proteinuria and edema
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What does the mutation of the nephrin gene cause in congenital nephrotic syndrome?
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The mutation in the nephrin gene leading to absence or structural malformation of the slit diaphragm, leads to proteinuria and edema.
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What is water permeability regulated by in the collecting duct?
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Water permeability of the epithelium of the collecting duct is regulated by antidiuretic hormone (ADH/vasopressin)
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Where is ADH produced? Where is ADH released from?
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ADH is a hormone produced in the hypothalamus and released from the posterior lobe of the pituitary gland.
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If the permeability of the collecting duct is increased by ADH, is the urine more/less concentrated?
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The urine will be more concentrated
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Where are the actions of the collecting duct more significant throughout the nephron?
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The action of ADH is more significant in the collecting tubules and collection ducts.
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Where does ADH bind?
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ADH binds to receptors on the collecting duct cells.
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What does the binding of ADH trigger?
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1. Translocation of AQP-2 containing intracytoplasmic vesicles into the apical cell surface-a short term effect
2. Synthesis of AQP-3 and their insertion into the apcial cell membrane -long term effect |
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What stimulates the release of ADH?
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An increase in plasma osmolarity or a decrease in blood volume, as well as nicotine
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What occurs in the absence of ADH?
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copius, dilute urine is produced. Central diabetes insipidus (CDI)
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What is responsible for the form of CDI called nephrogenic diabetes insipidus?
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A recent study indicates that a mutation of two genes encoding AQP-2 and ADH receptors are responsible
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Do the kidney respond to ADH in nephrogenic diabetes insipidus?
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No, the kidney does NOT respond to ADH because of the defecitve AQP-2 and ADH receptor proteins synthesized by the collecting tubule and duct epithelial cells.
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Can excess water consumption in nephrogenic diabetes insipidus inhibit ADH release? If so what does it cause?
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Excess water consumption can also inhibit ADH release thereby promoting the production of a large volume of hyposmotic urine.
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True or False.
In Nephrogenic Diabetes insipidus, an increased secretion of ADH can produce an extremely hyperosmotic urine, thereby conserving water in the body. |
True
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What physical activities can stimulate the release of ADH?
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Inadequate consumption of water or loss of water because of sweating, vomiting, or diarrhea stimulates release of ADH.
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What mutation has been linked to congenital nephrogenic diabetes insipidus?
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Mutation of AQP-2 gene
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Where is AQP-2 located at in the nephron?
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AQP-2 is present in the terminal portion of the DCT and in the epithelium of the collecting tubules and ducts.
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What is regulating AQP-2?
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AQP-2 is under the regulation of ADH and is thus known as an ADK-regulated water channel
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In nephrogenic diabetes insipidus what does the kidney not respond to and why?
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Kidney does not respond to ADH because of the defective AQP-2 and ADH receptor proteins synthesized by the collecting duct epithelial cells.
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A failure of tubular function due to poor oxygenation, following a fall in blood pressure and cells swelling as a result of failure of the NaK ATPase pump, leading to inadequate excretion of water into the intersitium is a sign of what?
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Acute Tubular Necrosis
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What physiological symptoms are present in Acute Tubular Necrosis.
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1. Oliguria/anuria
2. Hyperkalemia: raised potassium in blood 3. Acidosis: raised H+ in blood |
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A mutation in either PKD1 or PKD2 endcoding polycystin1 and polycystin2 proteins causes _________________.
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Autosomal Dominant Polycystic Kidney Disease (ADPKD)
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Where are polycystin1 and polycystin2 proteins found in ADPKD?
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The proteins are found predominantly in the cilium of the principle cells of the collecting ducts.
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True or False.
Polycystin1 and Polycystin2 are mechanosensors. |
True
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What does the loss of P1 or P2 lead to?
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A complete loss of P1 or P2 leads to extensive cyst formation
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What are the cyst in ADPKD derived from?
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Cysts are derived from dilation of the collecting ducts
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A patient presents with hypertension and renal failure. What is the diagnosis?
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Autosomal Dominant Polycystic Kidney Disease is clinically presented with hypertension and renal failure
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Most common bladder cancer, male dominant, replacement of normal epithelial cells with ones that are enlarged, crowded with enlarged hyperchromatic nuclei and prominent mitotic figures, but the epithelium is not thickened are presentation of what disease?
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Transitional Cell Carcinoma (TCC)
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98% of affected fetuses result in a miscarriage, this accounts for 10% of all spontaneous abortions in the U.S. and affects 1:2500 live female births.
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Turner Syndrome
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Turner Syndrome is the result of a full or partial loss of _______________.
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The X chromosome
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A patient present with short stature, lymphoedema, broad chest, low hairline, low-set ears, webbed neck, gonadal dysfunction including amenorrhea and infertility. What is a possible diagnosis?
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Turner Syndrome
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A teenager, 17 years old, from Bow Legs Oklahoma presents with having difficulty with visual-spatial relationships and math issues (this has been a problem throughout life), has a webbed neck, and has not yet started to menstruation. What is a possible diagnosis? What would you treat this patient with?
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Turner Syndrome
No cure: treat with GH, estrogen replacement, thyroid replacement |
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A patient has Turner Syndrome. What are going to be other medical complications that this person could deal with?
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1/3 thyroid disorders
-hyperthyroidism 1/3 kidney malformation 5-10% constricted aorta Lymphedema |
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Characterized by bilaterally enlarged ovaries due to fluid-filled follicular cysts and abnormally large tunica albuginea
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Polycystic Ovarian Disease
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True or False.
A patient that has polycystic ovarian disease will not be infertile and will ovulate. |
False
A patient that has polycystic ovarian disease will be infertile due to lack of ovulation. |
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Describe the morphology of polycystic ovarian disease.
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ovaries resemble small, white balloons filled with marbles.
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What is the cause of polycystic ovarian disease?
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Fluid filled follicular cysts and atrophic secondary follicles beneath an unusally thick tunica albuginea.
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What is the pathogenesis behind polycystic ovarian disease
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it is unclear but related to defect in regulation of androgen synthesis which leads to excess production of estrogen
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Abnormal selection process in follicle maturation, progesterone not produced which leads to failure of mature follicle to transform into progesterone producing corpus luteum is what occurs in this disease.
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Polycystic Ovarian Disease
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What is the treatment of choice for polycystic ovarian disease?
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Hormone to stabilize and reconstruct estrogen; progesterone ratio; surgical intervention-incision into ovary cortex to allow oocyte exit following hormonal treatment
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What are Teratomas?
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Teratomas are germ cell tumors
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What is an Ectopic (tubal) pregnancy?
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1. implantation of embryo in abnormal site
2. Ooctyes fail to enter uterine tube can implant on surface of ovary, intestine or inside the rectouterine pouch: ~95% implant in uterine tube wall |
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Do ectopic pregnancies develop past early fetal stages? Can ectopic pregnancies be fatal?
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Most ectopic implantations do not develop past the early fetal stages
-Yes an ectopic pregnancy can be fatal. It may need to be surgically removed |
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Define Endometriosis.
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Presence of uterine endometrial tissue in the pelvic peritoneal cavity.
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As endometrium is shed, bleeding occurs in peritoneal cavity, causing sever pain, formation of cysts, and scar tissue and adhesions. This occurs in what disease.
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Endometriosis
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Why could endometriosis lead to sterility?
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The ovaries and uterine tube become deformed and embedded in scar tissue
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What does the treatment of endometriosis involve?
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Treatment involves decreasing pain symptoms with medications, shrinking and/or slowing endometrial growths by blocking ovulation with hormones; restoring fertility by removal of growths by conservative surgery and hormonal treatment; prevention of recurrence by complete removal of growths and ovaries by hysterectomy.
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What is a non-cancerous growth frequently appearing in childbearing years?
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Uterine Fibroid
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Describe how the polyp of the uterine friboid grows?
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Non-cancerous growths of uterine tissue forming mass or polyp protruding into uterine cavity; sensitive to estrogen so an increase in estrogen during cycle leads to an increase in growth of the polyp.
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The symptoms of irregular bleeding, bleeding between menstrual cycles, excessively heavy bleeding during menstruation, and post-menopause bleeding are signs of what?
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Uterine Fibroid
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What makes a patient at higher risk of a uterine fibroid?
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If a patient is obese, on tamoxifen, has high blood pressure, or have cervical polyps they are at higher risk of having a uterine fibroid.
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If a uterine fibroid is removed, can it reoccur?
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Yes it can reoccur even if it is surgically removed.
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Describe what occursi n Erythroblastosis fetalis.
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AKA Rh (D antigen) isoimmunization
-If a mom is Rh- and a baby is Rh+, blood from the baby can enter mom's circulation by passing through the placenta -mom makes Abs against baby's RBCs (Rh Antigen) and antibodies (IgG) can pass thru placenta & cause hemolysis of baby's RBC -Baby suffers from jaundice, anemia, & can stillbirth or death of baby shortly after birth |
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What are the symptoms of Erythroblastosis fetalis?
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Baby has low muscle tone, developmental delays, increase in amniotic fluid.
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How do you diagnose a baby with Erythroblastosis fetalis?
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Diagnosis is fetal/newborn hemolysis, increase in bilirubin levels, direct Coombs test detects presence of antibodies on surface of RBC.
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What may be the complications of a baby that has erythroblastosis fetalis?
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1. Hydrops fetalis: fluid accumulation in the brain
2. Kernicterus: brain damage due to high levels of bilirubin. 3. Neurological issues |
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How is Erythroblastosis fetalis prevented?
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It is prevented by injections of RhoGam mid-term pregnancy and within a few days following birth
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When must a mother get RhoGam injections?
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must get RhoGam injections during every pregnancy, following miscarriages,, abortions, amniocentesis or chorionic villus biopsy, or following abdominal injury during pregnancy.
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How many babies were lost every year prior to RhoGam?
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approximately 10,000 babies were lost every year in the U.S.
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What is RhoGam?
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RhoGam is a solution to IgG directed against D antibodies. This alpha-D antibody binds & kills any fetal RhD(+) RBC that crosses the placenta preventing mom from making antibodies against the Rh+ fetal RBCs.
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What is a cervical carcinoma?
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Carcinoma of the cervix that originates from stratified squamous wet epithelial cells.
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What causes cervical cancer?
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HPV infection now recognized as main cause.
16 strains of HPV considered high-risk for development of cervical cancer |
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If a carcinoma in-situ is diagnosed what does that mean?
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A carcinoma-in-situ is contained within epithelium and does not invade the underlying stroma
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A carcinoma that penetrates basal lamina and metastasizes to other regions of body is called a ________/
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Invasive carcinoma
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What percentage of cervical cancers occur from cervical glands?
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10-20% originate from cervical glands
these are called adenocarcinomas |
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How many women die each year from cervical cancer?
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In 2006-approximately 10,000 women in US were diagnosed and 4,000 women died
worldwide approximately half a million were diagnosed and a quarter of a million died. |
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True or False
Cervical lesions may exist in noninvasive forms of cervical cancer for as long as 20 years. |
True
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What is used to detect a variation in cells (from cervical to vagina) with stages of menstrual cycle?
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Pap smear
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Is there a cure for cervical cancer?
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Yes it can be treated with surgery if it is found before it becomes invasive
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Where does breast cancer originate from?
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Breast cancer originates from the epithelium lining the ducts and the terminal ducts of the breast.
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What is the difference between a ductal carcinoma and a lobular carcinoma?
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Ductual carcinoma originates from epithlium lining ducts.
Lobular carcinoma originates from epithelium lining the terminal ductules |
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Where do breast cancer tumors metastasize to if not found early?
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they metastasize to lymphatic vessles to axillary nodes near affected breast and into the bloodstream. Via the bloodstream they will pass to the lungs, bone and brain
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how many cases of breast cancer are diagnosed per year?
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180,000 new cases diagnosed annually in the US and ~2000 are men
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How many people die each year from breast cancer?
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43000 women and 400 men die yearly
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What is the mutation that causes breast cancer?
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Deficiency of mutation in BRCA1 shown to decrease stability or elevate incidence of mutation rate of tumor suppressor gene (p53)
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Mutations in the ______________ incapacitate checkpoint G2-M of cell cycle and concurrently, number of centrosomes of these cells is increased.
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BRCA1 gene
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How many women with breast cancer have the BRCA1 mutation?
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5-10% of women with breast cancer posses this mutation
If you have this mutation it confers very high lifetime risk of breast and ovarian cancer |
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If there is a presence of estrogen or progesterone receptors when breast cancer is present, is this good or bad for the prognosis? why?
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This is a good prognosis.
Tamoxifen an estrogen receptor blocker which is the treatment of choice can be used |
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What does the presence of c-erb B2 oncoprotein on the cell surface indicative of for breast cancer?
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This is a poor prognosis
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The loss of ovarian function prior to the age of 40 is called ______________.
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Premature ovarian failure
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What is the number of women affected with premature ovarian failure?
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1:250 @ age 25
1:100 @ age 40 *Can occur at any age prior to 40 |
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What are the first symptoms of premature ovarian failure?
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The first symptom is usually a missed period and the later symptoms are similar to menopause
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What are the 2 causes of Premature ovarian failure?
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1. loss of follicles from ovaries
2. Autoimmune destruction of maturing follices but no effect on primordial follicles |
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How is premature ovarian failure diagnosed?
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Diagnosed by
- determination of blood FSH: abnormally high due to lack of release of estrogen from mature follicle -Low estrogen & LH levels in blood |
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Ostoeporosis, infertility, and depression are complications of ______________.
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Premature ovarian failure
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Is there a treatment for premature ovarian failure?
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NO TREATMENT
-treat symptoms with Hormone Replacement Therapy til age 50 |
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The improper descent of the testis is called ____________.
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Cryptorchidism
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What is the most common genital problem encountered with pediatrics?
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Cryptorchidism
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What is the frequency of cryptorchidism in premature boys? full term boys?
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30% in premature boys
3% in full term |
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What are the main causes of Cryptorchidism?
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1. hypothalamus-pituitary-gonadal axis
2. Epididymis 3. Gubernamculum and genitofemoral nerve |
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When are the testis suppose to descend?
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Descent is at 28 weeks
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Does Cryptochordism have an effect on spermatogenesis?
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Yes, there is an effect.
If the testis do not descend the increase in temperature will decrease spermatogenesis. |
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What is the desired temperature for proper spermatogenesis?
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35'C
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True or False.
Cryptorchidism affects testosterone synthesis. |
False.
Cryptorchidism does NOT effect testoterone synthesis because it does NOT EFFECT the LEYDIG CELLS |
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What is a germ cell tumor of the testes called?
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Seminoma
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This is the most prevalent testicular cancer in men with peak incidence at 30-35 years of age.
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Seminoma
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Will a male develop a seminoma before puberty?
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NO
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What does the appearance of tumor cells appear as in seminoma?
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Tumor cells have a fried egg appearance and lymphocytes infiltrate around the Stubules
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Describe aging testes.
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1. involves interstitial fibrosis and hyalinization of the seminiferous tubules.
2. Leydig cell numbers decrease but testoterone levels are maintained 3. Leydig cells are influenced enough in number enough to influence sperm production |
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What is the ratio of germ cells to Sertoli cells in young healthy men?
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held relatively constant at about 13:1
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What is considered normal in a cross section of seminephorous tubules when looking for Sertoli cells and germ cells?
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10-12 Sertoli cells per tubule section and approximately half of the germ cell elements within the tubule should be spermatid stage
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What is looked for in developing fertility of a male?
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Counting mature spermatids per tubule cross section and seminal fluid count
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What is Orchitis?
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Orkhis is Greek for testile
-an acute inflammatory response of the testis secondary to an infection. |
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What are most cases of Orchitis associated with?
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Most cases are associated with viral mumps infection, however other viruses and bacteria can cause orchitis
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How many prepubertal patients with mumps develop orchitis?
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20%
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In bacterial orchitis, most cases are associated with ______________ and they occur in sexually active males older than 15 years or in men older than 50 years with _______ _________ _______.
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Associated with the epididymis
men older than 50 years of age with benign prostatic hypertrophy |
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What is a Varicocele?
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Dilation of the veins of the pampiniform plexus, "bag of worms" appearance
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What testis is the varicocele associated with?
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A varicocele is usually associated with the left testes due to blockage of the left renal vein and thus increased venous pressure.
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Is a Leydig cell tumor common?
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NO!
It is not as common as a seminoma |
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What is a Leydig cell tumor secreting?
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The Leydig cell tumor is a functionally acitve tumor it secretes:
1. androgens 2. estrogens 3. or both |
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Are Leydig cells benign or malignant?
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they are mostly benign
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What is the characteristic inclusion of a Leydig Cell Tumor?
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The Reinke crystal is a characteristic rectangular, eosinophilic, cytoplasmic inclusion.
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Describe BPH.
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BPH: Benign Prostatic Hypertrophy
-enlarged mucosal and submucosal glands ---> can be palpated -increase in PSA and PAP -DRE for detection |
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What is the routine treatment for BPH?
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TURP (Transurethral Procedure)
-Remove the glands in the submucosa |
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Quanterra and enzyme 5-alpha-reductase are ______________ medicines for treatment of BPH.
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Alternative herbal medicines
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Where does BPH almost always occur?
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occurs almost exclusively in the transitional and periurethral zones leading to partial or total obstruction of the urethra.
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_________ is synthesized in the stromal cells by conversion from circulating testosterone in the presence of ______________.
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1. DHT
2. 5-alpha-reductase |
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Once synthesized DHT acts as a autocrine/paracrine agent on the stromal cells and as a autocrine/paracrine hormone on the glandular epithelial cells, causing them to proliferate.
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1. Autocrine
2. Paracrine |
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True or False.
BHP is believed to occur in all males at anytime throughout life. |
False.
BHP is believed to occur to some extent in all men by age 80 |
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What characterizes Prostatic Carcinoma?
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1. Enlarged main or peripheral glands
2. Increased PSA and PAP 3. Increased osteoblastic activity related to increase in bone formation |
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True/False
Prostate Cancer is one of the most common cancers in male, affecting approximately 1 in 20. |
True
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Tumors usually develop in the ___________ zone in prostate cancer.
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Peripheral zone
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What has dramatically increased the diagnosis of prostate cancer?
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Prostate-specific antigen (PSA) testing for prostate cancer has dramatically increased early diagnosis of this disease, with annual digital rectal examine.
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What is considered one of the best biomedical markers currently available in the field of oncology?
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PSA
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What is the Gleason score used for?
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The Gleason score is used to predict tumor behavior and patient survival rate.
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What does the ranking of 1 indicate as a Gleason score?
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a ranking of 1 indicates well differentiated cells, which form the slowest growing and least aggressive form of cancer.
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A patient has had a prostate biopsy and has a Gleason score of 5. What does this mean?
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The ranking of 5 is given to poor differentiated areas, no glands, lots of cells. This is the greatest growing cancer.
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Two biopsies are taken in different areas of the prostate and added together. What will be the range of the score for both area?
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2-10
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What are the treatment options for prostate cancer?
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Treatments include:
1. Surgery & radiation 2. Hormonal therapy is the treatment of choice for advanced cancer with metastases. |
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Why is hormonal therapy the treatment of choice for advanced prostate cancer?
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Deprive the cells of testoterone by orchiectomy (removal of testis) or by administration of estrogen or GnRH agonist to suppress testotserone.
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An autosomal recessive sex-limited condition with inability to convert testosterone to DHT is called ____________.
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5-alpha-reductase deficiency
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What is DHT required for?
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DHT is required for masculinization of the external genetalia in utero.
---> genetic males will be born with ambiguous genitalia ---> male pseudohermaphroditism |
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Why are the uterus and fallopian tubes not present in 5-alpha-reductase deficiency?
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The uterus and fallopian tubes are absent because of the normal secretion of the Mullerian-inhibiting factor.
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Are the testes and wolffian structures intact in a male with 5-alpha-reductase deficiency?
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YES
The wolffian system is the epididymis, ductus deferens, seminal vesicles |
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Kleinfelter syndrome is observed in males with _________ _________ chromosome.
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with an extra X chromosome
---> 47 chromosomes XXY |
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Are Kleinfelter syndrome males phenotypically or genotypically males?
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Phenotypically & genotypically they are males because of the presence of the Y chromosome.
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Do males with Kleinfelter syndrome have high FSH levels?
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Yes, because of Sertoli cell function is abnormal
--Sertoli cells fail to produce INHIBIN |
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What are the estrogen: testosterone ratio in males with Kleinfelter syndrome?
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These males have low testosterone levels and high estradiol levels
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What can the high estradiol levels do to males that have Kleinfelter Syndrome?
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Males with Kleinfelter syndrome have small testis and few spermatogenic cells present.
Increased levels of Estradiol can lead to phenotypic feminization. |
