Is it worth listening to Goljan audio if I'm doing Pathoma? Filesharing is prohibited in this subreddit. These drugs also pr od uc e me th em og lo bin. Popular Posts This Week Sorry. I have heard that there are 'new' Goljan audio lectures since I took Step 1.
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Penis Embryo: what is the embryology of hypospadias? Opening on the undersurface you pee and it goes on your shoes failure of closure of urethral fold Epispadias? Opening on upper surface pee and goes in face ; defect in genital tubercle Peyronies dz: like Dupuytrens contracture Priapism permanent erection, seen commonly in SCDz bc of the RBCs and sickle cells trapped in the vascular channels. I t is more commonly seen in an uncircumscribed pt they usually do not clean poor hygiene predisposes the smegma is carcinogenic.
Testicle Cryptorchid testis testicle doesnt want to come down. There are two phases in the decent of a testicle: transabdominal migration down to inguinal canal.
MIF mullerian inhibitory factor is responsible for taking all the mullerian struct. The second part of the trip is androgen dependent. This includes testosterone and dihydrotestosterone. So, the first phase is from MIF and the second phase is androgen dependent.
Need testicle down by two years of age bc if not, has a risk of seminomas. Still at risk if you get it down. Lets say you went in, and it look atrophic and other testicle looks normal, have to take normal one out, too bc it is also at risk. So, must have testes examines to make sure you dont have a seminoma. Analogy: in turners, they are infertile and have menopause before menarche, bc by two years of ages, they have no follicles in their ovaries, and this is called a streak gonad.
This is an ovary without any follicles. This is analagous to cryptorchid testes: just like the cryptorchid testes predisposes to seminomas which is a germ cell tumor , so does the streak gonad predispose to a germ cell tumor however, do not call them seminomas in women, but dysgerminomas. So, in pts dxd with Turners syndrome, they surgically remove both ovaries bc of the great risk. They dont keep them in there bc lead to cancer. Would develop a varicocele. So, if you block the left renal vein, you will increase the pressure in the spermatic vein and will lead to a varicocele.
Torsion spermatic cord twisting; when there is a torsion of the spermatic cord, it shortens it. This means that the testicle will go up into the inguinal canal. This is painful. You will lose your cremasteric reflex in normal male, if you scatch the scrotum, it will contract, which is lost in torsion of the testicle.
Hydrocele persistence of tunica vaginalis; when you have big scrotum, you dont know whether its big bc there is fluid in it, or its big bc there is a testicle in it. So, what do you do? If it transilluminates, it is hydrocele. If it doesnt its cancer. Seminoma Note the yellow-tan tumor that does not completely replace the testicle usually they do, but not in this case. Seminoma The microscopic appearance of this tumor shows collections of germ cells in nests or cords with a stroma that has scattered lymphocytes present.
This is the same histologic pattern that you would see in a dysgerminoma of the ovary. MC best prognosis ; huge cells with lymphocyctic infiltrate. They are the counterpart of a womans dysgerminoma. These will melt with radiation, have little beta hcG; met to paraortic lymph nodes why? Bc they came from the abdomen, and thats where they will go. MC testicular tumor in child?
Yolk sac tumor; tumor marker? Alpha feto protein What is worst testicular cancer? Chest xray reveals multiple nodular masses in the lung. So, gynecomastia and mets dz, - what is the primary cancer? Source of gynecomastia: BHCG is like LH, and therefore it stimulates progesterone in the male, which increases duct growth and breast tissue and leads to gynecomastia Example:: same scenario, but older man will lead to malignant lymphoma.
This is why you get dribbling and urinary retention as the most common symptom. Prostate cancer is in the periphery of the prostate gland within the periphery of your finger. So, when you press on it, you feel hardness. Example 75 yo man with urinary retention and bladder is up the umbilicus and has dribbling what is the most likely cause?
NOT prostate cancer. What male hormone is totally responsible for prostate? Dihydrotestosterone in embryogenesis, this hormone fuses the labia to form a scotrum, extends the clitoris to form a penis and makes a prostate gland.
If you use a 5 alpha reductase inhibitor, that will increase testosterone. Carcinoma of the prostate This slide shows the cross-section through a prostate gland with scattered foci of yellow-tan areas which represent the carcinoma. Carcinoma of the prostate arises in the posterior lobe and produces a firm or hard prostate gland on rectal exam. PSA is increased. Carcinoma of the prostate This slide is a microscopic section of a prostatic adenocarcinoma showing well-formed glands that are fairly monotonous in appearance.
Adenocarcinoma of the prostate This slide shows a nerve with perineural invasion by a carcinoma of the prostate. Most testosterone in a woman is from the ovary. Therefore, if a pt has hirstuism, have to get two tests get a testosterone level have to fractionate it bc sometimes the total can be normal, but the free test can be increased, and you get a DHEA sulfate test.
So, if testeterone is predominantly elevated, it is coming from the ovary and if DHEA is elevated, it is coming from the adrenals.
If it is adrenal orgin, it consists of hydroxylase def adrogenital syndrome , Cushings, etc.. Hirstuism from the ovaries is a common phenomenon. So, when you are evaluating hirsutism, look at DHEA levels adrenal origin and testosterone levels ovarian origin. One of the common causes of ovarian origin are polycystic ovarian syndrome. If you know what LH does, it makes the pathophys easy. In a woman, LH is responsible for synthesis of theca interna which is around the developing follicle.
During the proliferative phase of the cycle, what is predominantly being synthesized is the 17 keto steroids DHEA and androstenedione. The androstenedione is converted by oxydoreductase into testosterone. Then, the test goes across the membrane of the developing follicle into the granulosa cells, where there is aromatase. FSH is put in there.
Then, the aromatase in the granulosa cell converts test into estrodiol and this is where the woman gets her estradiol from the aromatization process. LH is responsible for synthesis of 17 keto steroids and testosterone in the ovaries. This is why we will see hirstuism in a woman with polycystic ovarian syndrome bc increase of 17 ketosteroids, DHEA, androstendione, and testosterone. Obesity is a common correlation with this dz. Androstenedione is aromatized into estrone a weak estrogen.
Testosterone is aromatized into estradiol, which is a strong estrogen. So, we have a paradox have a woman with signs of excess androgens hirsutism, acne not signs of virulization. At the same time, these are being converted to estrogens so will have endometrial hyperplasia and therefore have a risk of endometrial caricinoma. So, there is a combo of increased androgens and increased estrogens.
So, bc increased estrogens, pt is constantly suppressing FSH and constantly increasing LH, so the cycle repeats itself. So, why do they have cysts? Functions of FSH is to prepare the follicle. Also, they increase the aromatase activity. If the FSH is constantly suppressed, the follicle degenerates and leaves behind a cystic spaces where the follicle used to be. Can feel these by pelvic exam and seen with ultrasound.
The MC secondary cause is endometriosis. So, in other words, it is not bleeding from an endometrial polyp, its not bleeding from a cancer; this type of bleeding is a hormone imbalance that causes abnormality in bleeding. So, if a young lady is bleeding, that is the usual cause. What is occurring? There is a persistent estrogen stimulation that is occurring on the mucosa, and not enough progesterone stimulation. So, they develop a lil hyperplasia, there is a build up of mucosa as the month progresses, and then eventually the stroma sloughs off and leads to significant bleeding.
So, its mainly an estrogen primed uterus, without the effect of progesterone and they do not ovulate related to this. This is the MCC. In other words, is the hypothalamus putting out GnRH or not? So, is it a hypothalamic-pit abnormality? Is it an ovarian prob? Maybe the ovary is not making enough estrogen. Is its an end organ prob?
This is anatomically related maybe she doesnt have a vagina - Rokitansky-KusterHauser syndrome, or maybe she has an imperforate hymen shes been having periods all along, and has blood built up behind it, or cervical stenosis DES exposure these are all anatomical reasons for the amenorrhea. Ashermans syndrome secondary amenorrhea, woman has repeated dilatation and curotoshes? So, amenorrhea is primary or secondary : hypothalamic-pit problem, ovarian prob, or end organ prob.
Goljan - Audio Transcript
Penis Embryo: what is the embryology of hypospadias? Opening on the undersurface you pee and it goes on your shoes failure of closure of urethral fold Epispadias? Opening on upper surface pee and goes in face ; defect in genital tubercle Peyronies dz: like Dupuytrens contracture Priapism permanent erection, seen commonly in SCDz bc of the RBCs and sickle cells trapped in the vascular channels. I t is more commonly seen in an uncircumscribed pt they usually do not clean poor hygiene predisposes the smegma is carcinogenic. Testicle Cryptorchid testis testicle doesnt want to come down. There are two phases in the decent of a testicle: transabdominal migration down to inguinal canal. MIF mullerian inhibitory factor is responsible for taking all the mullerian struct.
Goljan Audio Transcript Notes PDF
Goljan Transcripts - MODIFIED With SLIDES 5