PATHOLOGY 1 Flashcards
weight loss
85F
Gallbladder carcinoma is uncommon, with a poor prognosis. Five year survival is less than 5%.
It may present insidiously with weight loss or a palpable mass or with jaundice.
Case Discussion
Large distended gallbladder, which is entirely occupied by a solid internal mass, with internal haemorrhage.
Histopathology confirmed the radiological suspicion of a gallbladder carcinoma
https://radiopaedia.org/cases/gallbladder-carcinoma-8
Intrahepatic cholangiocarcinoma
https://radiologyassistant.nl/abdomen/biliary-system/biliary-duct-pathology
There are four basic patterns of chlangiocarcinoma: (illustration on the left).
Cholangiocarcinoma is an uncommon tumor, that is mostly seen in patients with underlying benign bilairy disease.
The incidence in the U.S. is 2000 to 2500 cases per year (coloncancer 150.000 per year).
In Asian countries the incidence is ten times greater due to more chronic biliary infection.
High risk groups are patients with:
Autoimmune diseases
PSC, ulcerative colitis, primary biliary cirrhosis
Congenital anatomic anomalies
Caroli, choledochal cyst, anomalous pancreaticobiliary junction
Abnormal tumor suppressor genes, FAP, NF1
Infection
Biliary parasites, recurrent pyogenic cholangitis
Clinical presentation:
Jaundice
Pain
Fever if secondary cholangitis
These arise in the very small peripheral ducts.
These tumors have abundant fibrous stroma that can cause retraction of the liver capsule.
The tumor typically enhances in the equilibrium and delayed phases (5-10 minutes).
Although these tumors are usually quite heterogeneous because the contrast uptake is delayed and can be irregular.
The key findings to look for are:
Delayed enhancement
Peripheral biliary dilatation
Capsular contraction
Etoh Abuse
Case courtesy of Dr Henry Knipe, Radiopaedia.org, rID: 27870
Ectatic ducts, fibrosis and dystrophic calcifications of the pancreatic parenchyma.
Case Discussion
Case reproduced with permission, courtesy of Dr. Katharina Glatz, Basel, Switzerland, Pathorama.ch (original case at is here). All rights reserved; please see original case for copyright information.
Pancreatic carcinoma
Coronal section of ‘Whipple’s’ specimen (pancreatico-duodenectomy). There is an irregular, stellate, white to yellow pancreatic mass (35mm) in the head of the pancreas. Note the patent pancreatic duct visible traversing the tumour
Pancreaticoblastoma
https://pubs.rsna.org/doi/10.1148/rg.264065012
Most common pancreatic tumour in children
The liver of a Caroli’s disease patient with CHF. Multiple cystic dilatations of the intrahepatic bile ducts are grossly (a) and histologically (b) visible. Hematoxylin-eosin staining (b).
Caroli’s disease belongs to a group of hepatic fibropolycystic diseases and is a hepatic manifestation of autosomal recessive polycystic kidney disease (ARPKD). It is a congenital disorder characterized by segmental saccular dilatations of the large intrahepatic bile duct and is frequently associated with congenital hepatic fibrosis (CHF). The most viable theory explaining its pathogenesis suggests that it is related to ductal plate malformation.
https://www.hindawi.com/journals/ijh/2012/107945/
a Overview of the abdomen with the accessory spleen (black arrow) in its original position within the greater omentum and anterior-inferior to the main spleen (white arrow). b , c Anterior and posterior view of the resected spleen. Red arrows indicate the artery and blue arrows indicate the vein of the accessory spleen. The asterisk indicates the (main) splenic artery, and the pound sign indicates the (main) splenic vein.
what is this?
what are the associations?
What is the pathology?
Splenic Haemangioma
- Case Discussion
The case was operated laparoscopically and the surgeon extended the incision to deliver the enlarged spleen. It is proved to be a bleeding splenic haemangioma. Splenic haemangioma is regarded as the commonest benign splenic tumour and the second commonest focal lesion involving the spleen.
- Splenic haemangiomas, also known as splenic venous malformations, splenic cavernous malformations, or splenic slow flow venous malformations, while being rare lesions, are considered
- the second commonest focal lesion involving the spleen after simple splenic cysts 5,12 and the
- most common primary benign neoplasm of the spleen 6.
They are usually found incidentally and have imaging appearances similar to hepatic haemangiomas.
Please refer to the main article for a general discussion on cavernous venous malformation.
Terminology
It is important to note that according to newer nomenclature (ISSVA classification of vascular anomalies) these lesions are merely known as slow flow venous malformations. Having said that it is probably helpful in reports to include the word ‘haemangioma’ as this term is ubiquitous in the literature and most familiar to many clinicians. The remainder of this article uses the term ‘splenic haemangioma’ for consistency with the majority of the existing literature.
Epidemiology
Their autopsy prevalence rate is thought to range around 0.1-14% 7,8,13. Most haemangiomas tend to be discovered in adults from the mid-30s to the mid-50s years of age 8.
Clinical presentation
The vast majority are asymptomatic and are incidentally discovered. Occasionally they may be associated with splenomegaly, abdominal pain, dyspnoea, diarrhoea, or constipation [ref needed].
Pathology
Splenic haemangiomas are comprised of non-encapsulated non-neoplastic vascular channels of varying sizes ranging from capillary to cavernous, containing slow flowing blood. These vessels are lined with a single layer endothelium 2,8.
Associations
- splenic haemangiomatosis: the presence of multiple splenic haemangiomas
- splenic manifestations of a systemic angiomatosis syndrome such as
- Klippel-Trénaunay-Weber syndrome
- Beckwith-Wiedemann syndrome
- Radiographic features
Most lesions tend to be small in size (< 2 cm 12). Calcification if present, either central punctate or peripheral curvilinear, can be detected on radiographs or CT scans.
Splenic Lymphoma
Splenic Lymphoma
- Splenic lymphoma, also termed as lymphomatous involvement of the spleen, represents the most common malignancy to involve the spleen. They are commonly secondary, rarely being primary (referred as primary splenic lymphoma).
This article focuses on the location-specific primary and secondary lymphomas involving the spleen, for a broader and systemic discussion, please refer to the main article on lymphoma.
Epidemiology
The spleen is involved in about 30% of all Hodgkin lymphoma and 30-40% of patients with systemic non-Hodgkin lymphoma (NHL) 2,4. The primary splenic lymphoma is rarer, representing about 2% of all lymphomas 2.
- Pathology
Primary splenic lymphomas are in general due to diffuse large B-cell lymphoma (DLBCL) 4. Please refer to the main article on lymphoma for further discussion in the secondary involvement of the spleen.
found in close proximity to the carotid artery
Gross pathology of a carotid body tumour.
https://radiopaedia.org/cases/carotid-body-tumour-gross-pathology-2
Gross section of a carotid body tumour resected from an adult patient with a familial history of similar tumours. Grooves on either side represent impressions left by internal and external carotid artery branches. Deeply congested lymph nodes attached to the specimen were negative for tumour.
Author: AFIP
Obtained from the Pathology Information Educational Resource (PEIR) website (http://peir.net/) PEIR This image is labelled as a non-copyrighted image from a publication of the Armed Forces Institute of Pathology, a government agency.
Image# 413570
Modifications: added black to top and bottom to make square.
License: U.S. Government works may be used without restriction. This work is in the public domain in the United States because it is a work of the United States Federal Government under the terms of Title 17, Chapter 1, Section 105 of the US Code. See Copyright.
If you believe your copyright has been infringed, please write to license@radiopaedia.org giving details of why you believe this is so.
Follicular thyroid adenoma
Section of follicular adenoma of the thyroid gland.
Case courtesy of Ed Uthman, Radiopaedia.org, rID: 77605
PATHOLOGICAL SPECIMEN
- What is the inheritance pattern?
- What is the incidence?
- What are the clinical findings?
- What is the treatment?
- What is the malignancy risk?
Adult Polycystic Kidney Disease (Apkd) ( Fig. 4.5 )
- Intro:
- Cystic dilatation of collecting tubules, as well as nephrons
- (unlike MCD and infantile polycystic kidney disease in which only the collecting tubules are involved).
- AD trait (childhood type is AR).
- Incidence:
- 0.1% (most common form of cystic kidney disease; accounts for 10% of patients on chronic dialysis).
- Clinical
- Slowly progressive renal failure.
- Symptoms usually begin in 3rd or 4th decade, but clinical onset is extremely variable, ranging from palpable cystic kidneys at birth to multiple cysts without symptoms in old age.
- Enlarged kidneys may be palpable.
- Treatment
- Treatment is with dialysis and transplant.
- Malignancy
- No increased risk of malignancy.
PATHOLOGY SPECIMEN
What are the associated findings of this condition?
Associated Findings
- Hepatic cysts, 70%
- Intracranial berry aneurysm, 20%
- Cysts in pancreas and spleen, <5%
Michaelis-Gutmann bodies
Malacoplakia
Rare inflammatory condition that most commonly affects the bladder.
Yellow-brown subepithelial plaques consist of mononuclear histiocytes that contain Michaelis-Gutmann bodies.
On IVP, multiple mural filling defects with flat or convex border are seen, giving a cobblestone appearance.
Obstruction is a rare complication.
Malacoplakia is an uncommon chronic granulomatous inflammatory disease that can affect essentially any part of the body but most frequently involves the bladder wall.
Epidemiology
Malacoplakia has a peak incidence in middle age and has a reported female-to-male ratio of 4:1 1. Other risk factors include immunosuppression, AIDS and diabetes mellitus.
Clinical presentation
Presenting symptoms depend on the region involved.
In the most common setting, when the bladder is the site of diseases, patients present with gross haematuria, lower urinary tract symptoms and recurrent urinary tract infection (most commonly with Escherichia coli ). Papules, plaques and ulceration on direct visualisation during flexible cystoscopy have been described 5.
Pathology
In the urinary system, although infection with E. coli is very often observed, impaired host bactericidal defences and defective phagocytosis are considered an important part of the pathogenesis 1.
Histology
Von Hansemann cells (ovoid histiocytes) which contain calcific Michaelis-Gutmann bodies are a histologic hallmark which are pathognomonic for this diagnosis 2,5. Identification may require special stains.
Location
The urinary bladder is the most frequently affected organ (40% of patients with malacoplakia).
Radiographic features
Imaging characteristics of malacoplakia are varied and depend on the region involved.
Urinary system
Malacoplakia is most commonly observed within the bladder, although plaques may also occur in the ureters.
It may present as multiple, polypoid, vascular, solid masses or as circumferential wall thickening, associated with vesicoureteral reflux and dilatation of the upper urinary tract. These masses vary in size from a few millimetres to several centimetres. Occasionally, malacoplakia can be locally aggressive and invades surrounding structures even causing bone erosions 1.
Treatment and prognosis
Although malacoplakia may be extremely aggressive, invading the adjacent spaces and even causing bone destruction, non-surgical medical management is the mainstay of treatment. As such, biopsy for accurate diagnosis is essential.
Treatment of urinary involvement usually includes antibiotics, ascorbic acid, and a cholinergic agonist 1.
Case courtesy of Dr Michael P Hartung, Radiopaedia.org, rID: 83974
https://www.pathologyoutlines.com/topic/bladdermalakoplakia.html
Last revised by Dr Michael P Hartung◉ on 26 Nov 2020
https://radiopaedia.org/articles/malacoplakia-1
What is the definition of
Epithelium.
1: a membranous cellular tissue that covers a free surface or lines a tube or cavity of an animal body and serves especially to enclose and protect the other parts of the body, to produce secretions and excretions, and to function in assimilation
https: //www.merriam-webster.com/dictionary/epithelium
What is the definition of mesothelium
mesothelium: epithelium derived from mesoderm that lines the body cavity of a vertebrate embryo and gives rise to epithelia (as of the peritoneum, pericardium, and pleura), striated muscle, heart muscle, and several minor structures
Howell–Jolly bodies are found on blood smear in a patient. What does this mean?
- Which of the following is most likely a cause of diabetes insipidus
* A. Craniopharyngioma
* B. Rathke cleft cyst
* C. Lymphocytic hypophysitis
* D. Macroadenoma
* E. Empty sella
- Which of the following is most likely a cause of diabetes insipidus
- Which of the following is most likely a cause of diabetes insipidus A. Craniopharyngioma Based of Stat Dx.
B. Rathke cleft cyst C. Lymphocytic hypophysitis D. Macroadenoma E. Empty sella
D insipidus from ADH deficiency is designated as central to differentiate it from nephrogenic diabetes insipidus, which is a result of renal tubular unresponsiveness to circulating ADH. The clinical manifestations of the two diseases are similar and include the excretion of large volumes of dilute urine with an inappropriately low specific gravity. Serum sodium and osmolality are increased as a result of excessive renal loss of free water, resulting in thirst and polydipsia. Patients who can drink water can generally compensate for urinary losses; patients who are obtunded, bedridden, or otherwise limited in their ability to obtain water may develop life-threatening dehydration. Lymphocytic hypophysitis Dr Mostafa El-Feky◉ and Assoc Prof Frank Gaillard◉◈ et al. Lymphocytic hypophysitis is an uncommon non-neoplastic inflammatory condition that affects the pituitary gland. It is closely related to other inflammatory conditions in the region, namely orbital pseudotumour and Tolosa-Hunt syndrome. Epidemiology Lymphocytic hypophysitis is seen most frequently in women, with a F:M of ~ 9:1, and often in the postpartum period or the third trimester of pregnancy. Clinical presentation Clinical presentation is varied depends on the part of the pituitary affected and the size of the lesion. Lymphocytic hypophysitis can thus be classified as: anterior pituitary: lymphocytic adenohypophysitis most common mimics a pituitary adenoma endocrine hormone deficits are common, including hypopituitarism mass effects on adjacent structures (e.g. optic chiasm) posterior pituitary: lymphocytic infundibular neurohypophysitis rare diabetes insipidus both anterior and posterior pituitary: lymphocytic infundibular panhypophysitis Pathology It is characterised by infiltration of the pituitary stalk with lymphocytes, as the name would suggest. Importantly, there is a paucity of plasma cells or granulomas, differentiating it from IgG4-related hypophysitis and granulomatous hypophysitis (e.g. due to neurosarcoidosis) respectively. Associations autoimmune conditions such as autoimmune thyroiditis pernicious anaemia ipilimumab: monoclonal antibody drug Radiographic features CT Coronal CT and multiplanar reconstructions can visualise the pituitary region reasonably well. Lymphocytic hypophysitis appears as an enhancing soft tissue mass involving the pituitary and extending into the suprasellar region. MRI MRI, as is the case with other pituitary lesions, is the best modality for assessing this condition which appears as a pituitary region mass. T1 affected area is isointense with slight signal heterogeneity normal posterior pituitary bright spot may be absent 8 T1 C+ (Gd) can variably enhance, usually homogeneously 7 dural enhancement may be present 8 infundibulum may be thickened 8 T2 hypointensity in parasellar region can be present and may be useful in differentiating from a pituitary adenoma 4 Treatment and prognosis Lymphocytic hypophysitis is usually self-limiting and spontaneous recovery can occur. Corticosteroids are sometimes given and deficient hormones can be replaced 8. Differential diagnosis The differential diagnosis is primarily that of other pituitary region masses. Considerations include: pituitary adenoma macroadenomas are expected to enlarge the sella turcica craniopharyngioma (papillary type) suprasellar meningioma dural-based usually follows the cerebral cortex intensity pituitary metastasis Langerhans cell histiocytosis (LCH) IgG4-related hypophysitis granulomatous hypophysitis (idiopathic or secondary to systemic illness e.g. sarcoidosis, syphilis, and tuberculosis) xanthomatous hypophysitis necrotising hypophysitis
- HCC, least likely risk factors
- Alcohol
- NASH
- Hep A
- Hep B
- Hep C
- HCC, least likely risk factors
- Alcohol
- NASH
- Hep A
- Hep B
- Hep C
Hepatocellular Carcinoma (p. 870 Robins)
- HCC accounts for approximately 5% of all cancers worldwide,
- with a 3 to 8:1 male predominance.
- It occurs most commonly in developing countries with high rates of HBV infection, particularly where infection starts in infancy and there is a high associated carrier rate.
- Half of such cases are not associated with cirrhosis; rather there may be important adjunct exposure to aflatoxin (a mycotoxin produced by Aspergillus species that contaminates staple food crops).
- In Western populations, increased rates of hepatitis C infection are also driving HCC incidence.
-
Pathogenesis (p. 870)
- HCC usually arises in the background of chronic liver disease.
- Major etiologic factors are
- chronic viral infection (HBV or HCV),
- chronic alcoholism,
- NASH,
- and food contaminants (e.g., aflatoxins);
- lesser causes include
- hemochromatosis,
- tyrosinemia, and
- α1-AT deficiency.
- Activating mutations of β-catenin occur in 40% of HCC, and p53 inactivation is present in 60% of HCC.
- Chronic inflammation is associated with genotoxic products, cytokine production, and hepatocyte regeneration; such changes—along with an underlying genetic susceptibility—presumably underlie tumorigenesis.
- L-6 can suppress hepatocyte differentiation and promote hepatocyte proliferation by regulating the function of the transcription factor HNF4-α.
- Morphology (p. 872)
- HCC can present as
- a solitary mass,
- multifocal nodules, or
- a diffusely infiltrative cancer with massive liver enlargement,
- often (although not necessarily) in a background of cirrhosis;
- intrahepatic spread and vascular invasion are common.
- Histologically lesions may range from well differentiated to highly anaplastic and undifferentiated.
- A distinctive variant is fibrolamellar carcinoma.
- Constituting 5% of HCC, it usually presents as a single scirrhous, hard tumor occurring in 20- to 40-year-olds in the absence of chronic liver disease.
- The cells are well-differentiated cells in cords or nests separated by dense lamellar collagen bundles.
- Clinical Features (p. 873)
- Features include
- hepatomegaly,
- right upper-quadrant pain,
- weight loss, and
- elevated serum α-fetoprotein.
- Features include
- Prognosis depends on
- the resectability of the tumor;
- mortality is secondary to cachexia,
- GI or esophageal variceal bleeding,
- liver failure with hepatic coma, or
- tumor rupture and fatal hemorrhage.
- HCC can present as
- Hepatitis A Virus (p. 831)
Hepatitis A virus (HAV) is a single-stranded RNA virus that causes a benign, self-limited disease; fulminant HAV is rare (fatality rate 0.1% to 0.3%). It is not directly cytopathic; hepatocyte damage is due to CD8+ T-cell responses. HAV accounts for 25% of acute hepatitis worldwide; it has a fecal-oral route of spread. Acute infection is marked by anti-HAV immunoglobulin M (IgM) in serum; IgG appears as IgM declines (within a few months) and persists for years, conferring long-term immunity. An effective vaccine is available.
- Hepatitis B Virus (p. 831)
Hepatitis B virus (HBV) can cause the following (Fig. 18-3):
- Acute, self-limited hepatitis
- Nonprogressive chronic hepatitis
- Progressive chronic disease culminating in cirrhosis (and increased risk of HCC)
- Fulminant hepatitis with massive liver necrosis
- Asymptomatic carrier state
- Which is true regarding pituitary adenomas
- Thyrotroph is the most common microadenoma
- Microadenoma is usually non-functioning
- X
- Somatotrophs can lead to Cushing’s disease
- Lactotrophs are more readily identified in males due to galactorrhea
- Which is true regarding pituitary adenomas
- Thyrotroph is the most common microadenoma - false its rare.
- Microadenoma is usually non-functioning - ? True. Clinically silent. From Robbins: The prevalence of pituitary adenomas is 14%, with a peak incidence from age 35 to 60 years; the vast majority are clinically silent microadenomas.
- X
- Somatotrophs can lead to Cushing’s disease - false
- Lactotrophs are more readily identified in males due to galactorrhea - False
* Lactotroph Adenoma (p. 1078)- Prolactinomas are the most common functional pituitary tumor (30%).
- Even microadenomas can secrete sufficient PRL to cause hyperprolactinemia;
- moreover, serum PRL concentrations tend to correlate with adenoma size.
- Hyperprolactinemia can produce amenorrhea (25% of cases), galactorrhea, loss of libido, and infertility.
- Hyperprolactinemia is normal during pregnancy.
- In addition to adenomas, pathologic hyperprolactinemia can be caused by lactotroph hyperplasia, occurring when the normal dopamine inhibition of PRL secretion is blocked.
- This can result from damage to the hypothalamic dopaminergic neurons, pituitary stalk transsection (e.g., head trauma), or drugs that block dopamine receptors; any suprasellar mass can potentially disturb the normal hypothalamic inhibitory pathways.
- Consequently, mild PRL elevations—even in the presence of a pituitary adenoma—do not necessarily indicate a PRL-secreting tumor.
* Somatotroph Adenomas (p. 1079) - GH-secreting tumors are the second most common functioning adenoma.
- Hypersecretion of GH stimulates hepatic production of insulin-like growth factor 1 (IGF-1), which causes many of the clinical manifestations; the effects depend on the age of onset.
- If somatotroph adenomas appear before epiphyseal closure, elevated GH results in gigantism characterized by a generalized increase in body size and disproportionately long arms and legs.
- If increased GH appears after epiphyseal closure, patients develop acromegaly, with enlargement of head, hands, feet, jaw, tongue, and soft tissues.
- GH excess is also associated with
- gonadal dysfunction,
- diabetes mellitus,
- muscle weakness,
- hypertension,
- arthritis,
- congestive heart failure, and
- increased risk of gastrointestinal (GI) cancers.
- Diagnosis relies on documenting elevated serum GH and IGF-1 levels; failure to suppress GH production by an oral glucose load is the most sensitive assay.
- Tumors can be surgically removed, or GH secretion can be reduced by drug therapy with somatostatin analogues or GH receptor antagonists.
- Effective control of GH levels leads to gradual recession of the tissue overgrowth and resolution of the metabolic abnormalities.
* Corticotroph Adenomas (p. 1079) - Corticotroph cell adenomas are typically microadenomas at the time of diagnosis because ACTH production leads to early symptoms related to adrenal hypercortisolism (Cushing disease).
- In addition to adenomas, a wide variety of conditions can also cause elevated cortisol levels (Cushing syndrome, discussed under adrenal pathology).
- Surgical removal of the adrenals results in loss of inhibitory feedback to the pituitary corticotrophs and can induce the formation of large, destructive adenomas (Nelson syndrome);
- these can also cause hyperpigmentation through effects on melanocytes of other products of the ACTH precursor.
* Other Anterior Pituitary Adenomas (p. 1080)
•Gonadotroph adenomas
* (10% to 15% of pituitary adenomas) * typically occur in middle-aged men and women. * Because they produce hormones somewhat variably and the secretory products do not cause recognizable symptoms, most tumors are detected only when they become large enough to cause neurologic symptoms. * Impaired LH production is the most common gonadotroph deficiency; in men the resulting low serum testosterone manifests as decreased energy and libido, whereas in premenopausal women the outcome is amenorrhea. * Thyrotroph adenomas * (1% of pituitary adenomas) are rare causes of hyperthyroidism. * Nonfunctioning pituitary adenomas * (25% to 30% of pituitary adenomas) * include nonsecretory (“silent”) variants of functioning adenomas, as well as true hormone-negative adenomas; the latter are unusual. * Patients with nonfunctioning adenomas typically present with mass effects. * Pituitary carcinomas * are quite rare (\<1%); * most are functional (secreting PRL or ACTH most commonly). * Diagnosis of carcinoma requires the demonstration of metastases. * CLINICAL PRESENTATION * https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3853872/
The predominant physiologic consequence of hyperprolactinemia is hypogonadotropic hypogonadism (HH) which is due to suppression of pulsatile GnRH. The clinical manifestations of conditions vary significantly depending on the age and the sex of the patient and the magnitude of the prolactin excess. Clinical presentation in women is more obvious and occurs earlier than in men. Women can present with symptoms of oligomenorrhea, amenorrhea, galactorrhea, decreased libido, infertility, and decreased bone mass.
It is worth noting that many premenopausal women with hyperprolactinemia do not have galactorrhea, and many with galactorrhea do not have hyperprolactinemia. This is because galactorrhea requires adequate estrogenic or progesterone priming of breast. Conversely, isolated galactorrhea with normal prolactin levels occurs due to increased sensitivity of the breast to the lactotrophic stimulus.[14,15,16] Thus, galactorrhea is very uncommon in postmenopausal women. Approximately 3-10% women with PCOS have coexistent modest hyperprolactinemia.[17]
Prolonged hypoestrogenism secondary to hyperprolactinemia may result in osteopenia.[18] Spinal bone mineral density (BMD) is decreased by approximately 25% in such women and is not necessarily restored with normalization of prolactin levels.[19] Women with hyperprolactinemia and normal menses have normal BMD.[20,21] Hyperprolactinemic women may present with signs of chronic hyperandrogenism such as hirsutism and acne, possibly due to increased dehydroepiandrosterone sulfate secretion from the adrenals,[22] as well as reduced sex hormone binding globulin leading to high free testosterone levels.
Men with hyperprolactinemia may present with erectile dysfunction, decreased libido, infertility, gynecomastia, decreased bone mass, but rarely galactorrhea. Over time, the patient may have diminished energy, reduced muscle mass, and increased risk of osteopenia.[23]
