nursesrevision@gmail.com - Nurses Revision

DISEASE OF LYMPH VESSELS

Lymphoedema/lymphatic dysfunction

Lymphoedema refers to swelling in the tissues due to obstruction of lymph drainage

Lymphedema is also defined as the interstitial collection of protein-rich fluid due to disruption of lymphatic flow.

When lymph vessel is obstructed, lymph accumulates in the distal parts leading to low grade inflammation and lymph vessels

Lymphatic dysfunction means that lymphatic system is not working well

Physiologic basis of lymphedema — Lymphedema occurs when the lymphatic load exceeds the transport capacity of the lymphatic system, which causes filtered fluid to accumulate in the interstitium. As opposed to generalized edematous states, the rate of capillary filtration is normal in patients with lymphedema

Causes of lymphoedema

Causes of Lymphoedema can be:

Primary: is due to a congenital and or inherited condition associated with pathologic development of the lymphatic vessels.
Secondary: This occurs as the result of other conditions or treatments

Congenital lymphatic obstruction (Milroy’s disease): failure for the lymph vessel especial in lower limb to develop. This is also called hereditary or primary lymphoedema
Surgical removal of lymph vessel and lymph nodes due to cancer to prevent secondary tumors and further disease spread i.e. removal of axillary nodes during mastectomy may lead to lymphoedema of the affected arm
Tumours can compress lymph vessel blocking lymph flow and tissue drainage
Filariasis: It is a disease caused by tissue dwelling nematode, transmitted by mosquito bite
Malignant metastasis of lymph node and lymph vessel

Signs and symptoms of lymphoedema

Typical signs and symptoms of lymphedema include:

The onset of lymphedema is usually insidious. Affected patients may initially experience aching pain at the affected area and a sense of heaviness or fullness of the limb. Over time, the skin becomes dry and firm with less pitting and is fibrous to palpation.
Two-thirds of cases of lymphedema are unilateral, although the laterality depends on the precipitating event. For example, an axillary node dissection will increase the risk of lymphedema in the ipsilateral arm while a pelvic node dissection increases the risk of bilateral lower extremity edema.
At onset, swelling in the affected limb is typically characterized as “soft” and “pitting”. Pitting is variable in patients with lymphedema and reflects movement of the excess interstitial water in response to pressure. It is generally absent with progressive lymphedema, reflecting the evolution of fibrosis and adipose tissue deposition.
For patients who had previously undergone a lymph node dissection and radiation, lymphedema is typically characterized by slowly progressive ipsilateral swelling of an arm following axillary node dissection or a leg following inguinal node dissection. The swelling may first be apparent only in the proximal portion of the limb, or it can affect only a portion of the distal limb including the digits.
Among patients with breast cancer, there may also be swelling over the ipsilateral breast and/or upper chest wall. Other manifestations include a feeling of heaviness, tightness, aching or discomfort in the limb, and restricted range of motion.
Skin changes — With worsening lymphedema, dermal thickening becomes clinically apparent, which is manifested by cutaneous fibrosis. The overlying skin of the affected limb also becomes hyperkeratotic, which can lead to verrucous and vesicular skin lesions.
Discomfort — A feeling of heaviness, tightness, aching or discomfort in the affected limb commonly accompanies swelling.
Restricted range of motion — With later stages of lymphedema, patients may develop restricted range of motion in the affected limb as a result of the increased weight, which may limit their ability to perform activities of daily living (ADLs).

Summary of Clinical Features

Swelling in arms and legs
Tissues of the neck and head may be affected also.
Reduced mobility due to swelling
Heaviness of the affected area
Skin changes i.e discoloration
Blister formation
Leaking of fluid from the skin
Infections
Poor vision, ear pain and nasal congestion in case of head and neck lymphoedema
Difficult in swallowing
Difficulty in breathing and talking
Salivating
Lymphangitis and cellulitis occur as complications which presents as streaky red patch on area affected, fever, chills and itching

Diagnosis and Investigation of lymphoedema

History: Components of history that should be addressed include:

Age of onset
Area(s) of involvement
Associated symptoms (e.g., pain)
Medications — While none is directly associated with an increased risk of lymphedema, some are associated with edematous states (e.g., NSAIDs agents) or are contraindicated in the treatment of lymphedema (e.g., diuretics)
Progression of symptoms
Past medical history, including of medical conditions associated with lymphedema, any prior travel, infections, surgery or prior RT
Family history

2. Physical Examination.

The physical exam should evaluate the vascular system, skin, and soft tissue, and palpation of the lymph nodes.

If primary lymphedema is suspected, evaluation should include documentation of any physical signs or congenital anomalies associated with an inherited condition. Examples include:

Short stature (Turner Syndrome)
Port wine stains or hemangiomas (Klippel-Trenaunay-Weber Syndrome)
Shield chest (Turner Syndrome, Noonan Syndrome)
A positive Stemmer sign is indicative of lymphedema. It is characterized by the examiner’s inability to lift the skin of the affected limb compared to the contralateral limb. It is also described as difficulty lifting the skin of the dorsum of the fingers or toes of the affected limb. A positive Stemmer sign can be found in any stage of lymphedema. While it is possible to have a false negative Stemmer sign, a false positive sign is rare.
Opto electronic volume try — Volume can be assessed utilizing an infrared, optoelectronic measurements. This technique utilizes infrared beams to scan the limb and calculate a volume.
Circumferential measurements — Circumferential measurements on the affected and contralateral arm are a simple and inexpensive method to estimate edema. Measurements can be taken at any point in the arm or leg, or circumferentially around the head, neck, or trunk, as long as the clinician is utilizing anatomic landmarks to reproduce the measurements. Measurements in the arm are made at four points in both the affected and contralateral arm:
Metacarpal-phalangeal joints
Wrists
Ten centimeters distal to the lateral epicondyles
Fifteen centimeters proximal to the lateral epicondyles
Water displacement detects changes in volume of less than 1 percent. For patients with limb lymphedema, volume difference of 200 mL or more between the affected and opposite limbs is typically considered as a cutoff point to define lymphedema.
Bioimpedance spectroscopy — Bioimpedance spectroscopy (BIS) is a reliable and accurate tool to determine volume. Using electrical current, resistance measurements are used to compare the composition of fluid compartments.

4. Imaging

Computed tomography (CT) scan can demonstrate accumulation of fluid within soft tissue with good sensitivity
MRI has also been used in the evaluation of lymphedema.
Lymphoscintigraphy — Lymphoscintigraphy is a technique used to image the flow of fluid from the skin to the lymph nodes, particularly in the extremities.
X-ray of lymphatic system by introducing a dye between toes or in the groin
Genetic testing — For patients diagnosed with primary lymphedema or suspected of lymphedema tarda, referral to a medical geneticist or genetic counselling service is suggested for evaluation of the family history and recommendations for further work-up.
Blood smear to isolate filarial worms

Stages of Lymphedema.

Staging — Lymphedema is staged using the criteria of the International Society of Lymphology. It involves two criteria to diagnose and classify lymphedema: the “softness” or “firmness” of the limb (reflecting fibrotic soft tissue changes) and the outcome after elevation:

Stage 0 — Stage 0 lymphedema is a subclinical or latent condition where swelling is not evident despite impaired lymphatic transport. Most patients are asymptomatic, but some report a feeling of heaviness in the limb. Stage 0 may exist for months or years before the onset of overt lymphedema occurs (stage I to III).
Stage I – There is accumulation of fluid that subsides with 24-hour limb elevation. The appearance is that of soft edema that may pit, with no evidence of dermal fibrosis. This is sometimes called reversible edema.
Stage II – Stage II lymphedema does not resolve with 24-hour limb elevation alone. This reflects the evolution of dermal fibrosis. As the fibrosis progresses, the limb may no longer pit on examination. This is sometimes called spontaneously irreversible lymphedema.
Stage III – Stage III lymphedema is characterized by lymphostatic elephantiasis. On exam, pitting is absent, and the skin reveals trophic skin changes such as fat deposits, acanthosis, and warty overgrowths.

Classification of lymphedema

Several classification systems are used, including the American Physical Therapy Association (APTA) & National Cancer Institute’s Common Terminology Criteria for Adverse Events (CTCAE). Of these, we prefer the APTA classification system. Both schemas are described below.

APTA uses girth as an anthropometric measurement to classify lymphedema. The maximum girth difference between the affected and unaffected limb is used to determine the class of lymphedema. See ‘Circumferential measurements‘ below):

Mild lymphedema — maximum girth difference <3 cm
Moderate lymphedema — 3 to 5 cm difference
Severe lymphedema — difference >5 cm

National Cancer Institute Common Terminology Criteria for Adverse Events (CTCAE) — categorizes lymphedema based upon exam findings & the presence of functional impairment:

Grade 1 — Trace thickening or faint discoloration
Grade 2 — Marked discoloration; leathery skin texture; papillary formation; limiting instrumental activities of daily living (ADL)
Grade 3 — Severe symptoms limiting self care ADL

Management of lymphoedema

Compression of the affected limb to promote lymph drainage
Wrapping the affected limb in elastic bandage to maintain continuous pressure on swollen limb to reduce the size and improve mobility
Use of compression garments (special designed socks), stockings, or sleeves that have a comfortable fit over the swollen limb (manual lymphatic drainage/lymphatic drainage massage)
Exercise can help fluid move from the vessels and reduce on swelling such as knee bending, wrist rotation, swimming, walking, etc for 20 to 30 minutes daily
Routine skin care
Liposuction in advanced stages of lymphedema when other options fail
Anti biotic are prescribed prevent spread of infections
Treat secondary fever with analgesics
Ensure good diet to improve immunity
Lymphatic venous anastomosis
Massaging
Elevation
Apply pressure on the affected areas
Complete decongestive therapy
Surgery due to obstruction

Lymphangitis

Lymphangitis refers to inflammation of lymph vessels due bacterial infection.

Microbes in the lymph, draining the area infected, spread along the walls of lymph vessel. This may be stopped in the first lymph node or continue involving whole lymph drainage network to even blood.

Potential pathogens include

bacteria,
mycobacteria,
viruses,
Fungi
parasites.

Lymphangitis commonly develops after cutaneous inoculation of microorganisms into the lymphatic vessels through a skin wound or as a complication of a distal infection.

Pathophysiology of Lymphangitis

The major function of the lymphatic system is to resorb fluid and protein from tissues and extravascular spaces. The absence of a basement membrane beneath lymphatic endothelial cells affords the lymphatic channels a unique permeability, allowing resorption of proteins that are too large to be resorbed by venules.
Lymphatic channels are situated in the deep dermis and subdermal tissues parallel to the veins and have a series of valves to ensure one way flow. Lymph drains via afferent lymphatics to regional lymph nodes and then by efferent lymphatics to the cisterna chyli and the thoracic duct into the subclavian vein and venous circulation.
Lymphangitis develops after cutaneous inoculation of microorganisms that invade the lymphatic vessels and spread toward the regional lymph nodes. Organisms may invade lymphatic vessels directly through a skin wound or an abrasion or as a complication of a distal infection.

Pathophysiology of Edema

Circulation of lymph is a complex process. All body tissues are bathed in interstitial fluid and when in excess, it accumulates leading to oedema.

Therefore edema occur due to;

Excessive production of interstitial fluid as in increased capillary permeability due to inflammation, colloid osmotic pressure in hypoproteinemia, high venous pressure in thrombosis
Inadequate removal/ transport of interstitial fluid by lymphatic system lead to accumulation of interstitial fluids a condition called lymphoedema

Normally 2-4 liters of interstitial fluids is filtered per day and is returned to vascular circulation. Fluid flux across capillary depend on hydrostatic and oncotic pressure (positive in arterial end and negative in the venular end)

Causes

Extremity oedema is due to right sided heart failure, constrictive pericarditis, renal diseases, liver cirrhosis and hypoproteinemia
Acute or chronic obstruction in the venous system
Abnormalities in lymphatic system
Allergic disorders

Clinical Manifestation of Lymphangitis

Characterized by erythematous streaks with pain and rapid spread, or by nodular swellings along the course of the lymphatic vessels.

Acute lymphangitis – occur in skin abrasion with infection at a distal site, such as interdigital dermatophyte infection or cellulitis of the lower leg. This may be accompanied by lymphangitis with red, tender streaks extending proximally with involvement of regional lymph nodes (lymphadenitis). Fever may also be present as a systemic symptoms.
In individuals with normal immunity the cause is Streptococcus pyogenes; can also occur in Staphylococcus aureus infection. In immunocompromised patients, gram-negative organisms are important causes of lymphangitis following lower limb cellulitis.
Pasteurella multocida from dog and other animal bites can result in localized infection with concomitant lymphangitis. It occurs in up to 30 percent of Erysipelothrix infections, a zoonosis occurring in persons in contact with fish and some animals. Cutaneous anthrax can present with extensive edema, regional lymphadenopathy, and lymphangitis.
Lymphangitis associated Rickettsiosis has been described with the causative organism R. sibirica mongolotimonae and in African tick bite fever due to R. africae. The presence of an inoculation eschar suggests tick-transmitted infection.
Nodular lymphangitis
- Nodular lymphangitis (also known as sporotrichoid lymphangitis, sporotrichoid spread, or lymphocutaneous syndrome) presents as painful or painless nodular subcutaneous swellings along the course of the lymphatic channels.
- Sporotrichosis has been described in the setting of gardening trauma or injury due to a thorn or wood splinter. It can have an incubation period of up to three months and presents in a cutaneous or a lymphocutaneous form accompanied by lymphangitis; painless ulcers may also be observed. Lesions on the upper limbs are the most common presentation
- lesions may ulcerate with accompanying regional lymphadenopathy. The incubation period between exposure and the onset of nodular lymphangitis can be prolonged and the presentation may be indolent with few or no systemic symptoms.
- Causes of nodular lymphangitis include: Sporothrix schenckii, Nocardia (most often N. brasiliensis), M. marinum, leishmaniasis, tularemia, and systemic mycoses:
- M. marinum has been described to cause “fish tank granuloma,” an entity that can occur following a hand injury while cleaning a fish tank. It has an incubation period of up to eight weeks. Infection due to rapidly growing mycobacteria can also occur in the setting of thorn or splinter injury. Other mycobacterial causes of lymphangitis include M. kansasii, M. chelonae, and M. fortuitum.
- Nocardia infections may present with cutaneous, subcutaneous, or lymphocutaneous manifestations following traumatic injury. Although this may mimic the appearance and clinical course of acute staphylococcal or streptococcal infection, the clinical course is usually much more indolent.
- Cutaneous leishmaniasis can present with subcutaneous nodules with lymphangitis or lymphadenitis up to 24 weeks following exposure. This presentation is more frequent with New World leishmaniasis caused by L. braziliensis or L. mexicana than with Old World Leishmaniasis due to L. major or L. tropica.
- Nodular lymphangitis is a rare manifestation of Francisella tularensis and Burkholderia pseudomallei infection. The initial skin lesion of F tularensis infection may be a papule or an ulcer or contain an eschar. The systemic mycoses, including coccidioidomycosis, blastomycosis, and histoplasmosis, can present with nodular lymphangitis.
- Filarial lymphangitis — The presence of the parasite within the lymphatic channels causes inflammation and subsequent dilatation, thickening, tortuosity of the lymphatic channels with valvular incompetence. Often occurs in a retrograde progression with distal or peripheral spread away from the regional lymph nodes where the adult parasite resides. It can also occur as a result of inflammation due to dying parasites.
- Wuchereria bancrofti, B. malayi, and B. timori are the causes of lymphangitis due to lymphatic filariasis.

Diagnosis of Lymphangitis.

Clinical features, & laboratory analysis of clinical specimens.

Microbiological investigations

Swab, aspirate, and biopsy of the primary site, nodule, or distal ulcer for histology and microscopy (including gram, fungal and acid fast staining), as well as culture (including bacterial, fungal, and mycobacterial cultures).
Serology (e.g., F. tularensis, Histoplasma)
Blood film (e.g., filaria)
Imaging —Lymphangiography (using dye injection into the lymphatics) and lymphoscintigraphy (using intradermal technetium injection at distal site of affected limb) have been used to evaluate for lymphedema and lymphatic obstruction . This may be useful if surgical management of lymphedema is a consideration.

Treatment of Lymphangitis

Some cases of nodular lymphangitis require surgical debridement. In the setting of lymphedema with significant lymphatic obstruction, surgical intervention may also be appropriate. Pending diagnostic evaluation, empiric antibiotic therapy with activity against skin flora may be initiated.

DISEASES OF LYMPH NODES

Lymphadenitis/adenitis

Lymphadenitis refers to inflammation of lymph nodes due bacterial infection spreading from infected lymph vessels.

The lymph nodes become enlarged, tender, congested with blood and chemotaxins.

If the phagocytes and antibody production is overwhelmed abscess may form with in the node Neighboring tissues may become involved and infected materials may be transported to other nodes and blood

Lymphadenititis may be acute or chronic. In children cervical lymph nodes are more affected

Causes of acute lymphadenititis

Measles Typhoid
Cat-scratch fever Wound
Skin infections

Causes of chronic lymphadenititis

TB
Syphilis
Unresolved acute infections

Signs and symptoms of lymphadenitis

Tenderness of the affected nodes
Redness of the skin around the affected nodes
Fever in severe cases

Lymphadenopathy

This refers to enlargement of lymph nodes.

Causes of Lymphadenopathy

It may be local or generalized

Causes of generalized lymphadenopathy include;

Infection like TB, HIV, syphilis
Acute and chronic lymphoid leukemia
Lymphoma like Hodgkin’s and Non-Hodgkin’s lymphoma
Sarcoidosis

Causes of localized lymphadenopathy include

Localized infection ie scalp infection leads to cervical lymph nodes enlargement,
infection of the upper extremity lead to axillary lymph nodes enlargement, infection of the lower limbs lead to inguinal lymph nodes enlargement and infection of the throat or tonsils lead to mandibular lymph node enlargement
Carcinoma that spread to lymphatics lead to regional lymphadenopathy i.e. stomach cancer lead to supraclavicular lymphadenopathy, breast cancer lead to axillary lymphadenopathy.

DISEASES OF THE SPLEEN

Splenomegaly/ hypersplenism

Splenomegaly refers to enlargement of the spleen more than its normal size (12x 7 cm).

The enlarged spleen may be non palpable but it is detectable on scan. It becomes palpable only when enlarged more than two and half times its normal size.

The spleen may be infected by blood-borne microbes or local spread of infection Enlargement of the spleen is associated with problems which include;

Premature destruction of red blood cells
Sequestration of red cells, white cells and platelets (pancytopenia)
Valunabirity to traumatic rapture
Hyperplasia of bone marrow follows as a compensatory response

Causes of splenomegaly

Bacterial infection like endocarditic, tuberculosis, septicemia, brucellosis, syphilis and typhoid
Viral infection like hepatitis and AIDS
Protozoa infection like malaria, leishmaniasis and trypanosomiasis
Fungal like histoplasmosis
Inflammatory disorders like SLE, rheumatoid arthritis and sarcoidosis
Congestion due to portal hypertension, hepatic vein thrombosis, chronic CCF and pericardial effusion
Hemolytic disorders like sickle cell anemia and spherocytosis
Infiltrative diseases of the spleen like leukemia and lymphomas
Iron deficiency anemia and megaloblastic anemia
Idiopathic

Signs and symptoms of splenomegaly

Palpable spleen Fever
Jaundice
Other signs of underlying disease

Management of splenomegaly

Investigations helps in identifying the cause such as blood smear, CBC, radiological imaging and culture and biopsy.
Treat the cause accordingly
In severe persistent spleenism, splenectomy may be performed

Hyposplenism

This refers to lack or impairment of spleen function.

It is due to Trauma
Surgical removal of the spleen
Autoplenectomy as in sickle cell due to ischemic atrophy (microvascular occlusion) Splenic atrophy in celiac disease

Signs of hypoplenism

Recurrent bacterial infection such as streptococci, E-coli, Haemophilus influenza and Neisseria meningitides
Severe septicaemia Intravascular coagulation Multiorgan failure
Red cell abnomalities

DISEASE OF LYMPH VESSELS Read More »

Anatomy and Physiology of the Lymphatic System

ANATOMY AND PHYSIOLOGY OF LYMPHATIC SYSTEM

The lymphatic system is part of the circulatory system which begins with very small close ended vessels called lymphatic capillaries which is in contact with the surrounding tissues and interstitial fluid. The lymphatic system is almost a parallel system to the blood circulatory
system.

It consist of:

Lymph
Lymph vessel
Lymph nodes
Diffuse lymphoid tissue
Bone marrow

Lymph

This is a clear watery fluid which transports plasma proteins, bacteria, fat from ileum and damaged tissues to the lymph nodes for destruction which circulates in lymph vessels.

It has similar composition as plasma and contains lymphocytes and macrophages for defense.
Lymph is an ultra filtrate of blood from capillary ends due to pressure in the blood vessel into the tissue as interstitial fluid totaling approximately 2 liters (1 – 3 % of body weight). Lymph is identical to interstitial fluid

Lymph vessels/Lymphatics

They are similar to blood vessels and its where lymph circulates before it is returned to general blood circulation. They continue from lymph capillaries which originate as blind-ended tube in the interstitial spaces and join lymph nodes, tissues and organs

Lymph capillaries are anatomically similar to blood capillaries i.e. made of a single layer of endothelial cell except there is no basement membrane making them able to allow large molecules like plasma protein that leak into interstitial spaces pass through capillary cells

All body tissues have a network of lymphatic vessels except the brain, spinal cord, bones, conea of the eye and superficial layer of the skin.

Lymph vessles become larger as they join together eventually forming two large ducts that is;

Thoracic duct from cistern chyli in front of L1 & L2 draining lymph from legs, pelvis, abdomen, left of the chest, neck and left arm into the left subclavian vein in root of the neck
Right lymphatic duct in the root of the neck draining lymph from right chest, head, neck and right arm into right subclavian vein

Lymph circulation

The lymphatic system represents an accessory route through which fluid can flow from the interstitial spaces into the blood. The lymphatic’s can carry proteins and large particulate matter away from the tissue spaces.

This returns proteins to blood from the interstitial spaces and is an essential function, without this death occurs within about 24 hours.

Lymph flow is aided by;

Contraction of surrounding skeletal muscles
Movement of the parts of the body
Pulsations of arteries adjacent to the lymphatic
Compression of the tissues by objects outside the body
Rhythmic contraction of lymph large vessels

The lymphatic pump becomes very active during exercise, often increasing lymph flow. Conversely, during periods of rest, lymph flow is sluggish, almost zero.

Lymph nodes

These are oval bean-shaped organs that lie along the lymph vessel. Four or five afferent lymph can vessel enters one lymph node but leave through one vessel. Lymph passes to around 8 nodes before it returns to blood circulation

Lymph nodes consist of lymph tissue which is parked with lymphocytes and macrophages & reticular tissue that produce a network of fibers which provide internal structure with in the node

Large Lymph nodes are located in strategic positions in the body throughout the body arranged in deep and superficial groups’ i.e.

Cervical Lymph nodes drain lymph from the head and neck
Axillary Lymph nodes drain lymph from the upper limbs
Hillar nodes, aortic nodes, sternal nodes drain lymph from thoracic organs and tissues
Popliteal nodes and Inguinal nodes drain lymph from lower limbs
Cistern chyli drain lymph from the abdominal and pelvic cavities

Lymphoid Tissue

This includes lymph glands called lymph nodes i.e. pharyngeal tonsils (adenoids) near the posterior nares, palatine tonsils at the back of the mouth and lingual tonsils at the back and sides of the tongue, aggregated lymphoid follicles (peyer’s patches) in the small intestines

Lymphoid tissue is found in the bone marrow, spleen, liver, lungs and thymus gland

Spleen

This is the largest lymph organ located in the left hypochondriac region of the abdominal cavity between fundus of the stomach and diaphragm

The spleen has two roles i.e.

site of old blood cell destruction
monitoring body immune system

The spleen filters blood

Bone Marrow

This acts as a site of

B-cell and T-cell generation.
It also produces monocyte, granulocytes, RBCs and platelets.

The B-cells mature in the bone marrow. The bone marrow is responsible for generating stem cells where all blood cells arise

Thymus Gland

This is a grayish organ located in the chest between lungs just below the neck

It has two lobes each with outer cortex and inner medulla. The medullar contains mature lymphocytes. The cortex receive pre-T cell

In cortex cell recognize certain antigen, those which fail die. The live cell continues to medulla and general circulation. This gland secrets thymosin required for development of T-lymphocytes

Function of lymph

Transport of proteins and large particles that cannot be absorbed directly into circulation.
Transport of fatty acids and cholesterol from intestines.
Return of excess fluid from tissues into circulation.
Carry bacteria into nearest lymph node where they can be destroyed.
Carry antibodies
Transport vitamin K from intestine to blood stream

Anatomy and Physiology of the Lymphatic System Read More »

Benign Prostatic Hyperplasia (BPH)

BPH

BPH-Benign prostatic hyperplasia is the enlargement, or hypertrophy, of the prostate gland.

BPH is common in elderly men over 60 years and above

Common causes of BPH and Pathophysiology

The outcome of BPH depends on two major factors i.e.

Anatomical factors: These involve enlargement of the Prostate gland which produces a physical blockage at the neck of the bladder against urinary flow. This results in increased responsiveness of the prostate gland to androgens and estrogens.
Dynamic factors; These result from excessive sympathetic stimulation via alpha-1 receptors in the prostate gland leading to increased tone at the sphincters of urinary bladder and the prostate.

The pathophysiology of BPH is as follows:

Resistance. BPH is a result of complex interactions involving resistance in the prostatic urethra to mechanical and spastic effects.
Obstruction. The hypertrophied lobes of the prostate may obstruct the bladder neck or urethra, causing incomplete emptying of the bladder and urinary retention.
Dilation. Gradual dilation of the ureters and kidneys can occur.

Resulting symptoms of BPH.

Urinary frequency. Frequent trips to the bathroom to urinate may be an early sign of a developing BPH.
Urinary urgency. This is the sudden and immediate urge to urinate.
Nocturia. Urinating frequently at night is called nocturia.
Weak urinary stream. Decreased and intermittent force of stream is a sign of BPH.
Dribbling urine. Urine dribbles out after urination.
Straining. There is presence of abdominal straining upon urination.
Urinary retention
Decrease in force of urinary out put
Intermittency during urination

Investigations and Diagnosis of BPH

Digital rectal examination (DRE). A DRE often reveals a large, rubbery, and nontender prostate gland.

Urinalysis. A urinalysis to screen for hematuria and UTI is recommended.
Prostate specific antigen levels. A PSA level is obtained if the patient has at least a 10-year life expectancy and for whom knowledge of the presence of prostate cancer would change management.
Urinalysis: Color: Yellow, dark brown, dark or bright red (bloody); appearance may be cloudy. pH 7 or greater (suggests infection); bacteria, WBCs, RBCs may be present microscopically.
Urine culture: May reveal Staphylococcus aureus, Proteus, Klebsiella, Pseudomonas, or Escherichia coli.
Urine cytology: To rule out bladder cancer.
BUN/Cr: Elevated if renal function is compromised.
Prostate-specific antigen (PSA): Glycoprotein contained in the cytoplasm of prostatic epithelial cells, detected in the blood of adult men. Level is greatly increased in prostatic cancer but can also be elevated in BPH. Note: Research suggests elevated PSA levels with a low percentage of free PSA are more likely associated with prostate cancer than with a benign prostate condition.
WBC: May be more than 11,000/mm3, indicating infection if patient is not immunosuppressed.
Uroflowmetry: Assesses degree of bladder obstruction.
IVP with post voiding film: Shows delayed emptying of bladder, varying degrees of urinary tract obstruction, and presence of prostatic enlargement, bladder diverticula, and abnormal thickening of bladder muscle.
Voiding cystourethrography: May be used instead of IVP to visualize bladder and urethra because it uses local dyes.
Cystometrogram: Measures pressure and volume in the bladder to identify bladder dysfunction unrelated to BPH.
Cystourethroscopy: To view degree of prostatic enlargement and bladder-wall changes (bladder diverticulum).
Cystometry: Evaluates detrusor muscle function and tone.
Transrectal prostatic ultrasound: Measures size of prostate and amount of residual urine; locates lesions unrelated to BPH.

Classification of drugs for BPH

They are classified into 3 major groups;

5 alpha-reductase inhibitors
Alpha-1 selective blockers
Combined therapies

5 alpha-reductase inhibitors

They inhibit an enzyme 5 alpha – reductase in the prostate thus preventing the conversion of testosterone into active form thus suppressing the activity of androgens in the prostate. The overall effect is decreased growth of the prostate gland.

N.B the effects of these drugs is not prompt and don’t relieve urine retention.

Finasteride 5mg o.d.
Dutasteride 0.5mg o.d

Both are administered orally

Alpha – 1 selective blockers

They block alpha I receptors in the prostate and bladder leading to relaxation of sphincter and so improved urine flows.

These are grouped into two;

Short acting agent e.g. Prazosin, Indamine, and Alfuzosin.
Long acting agents e.g. Tamucurosin, Doxazocin and Terazosin.

Doses;

Prazosin 0.5-1mg o.d given at bed time after few days orally then maintained at 1mg b.d * 3/7
Terazosin 2-10mg o.d
Doxazocin 1mg o.d.
Tamucurosin 0.4 mg once daily given with meals orally.

NB: Tamucurocin is a long acting member best indicated since doesn’t interfere with blood pressure

Trazocin should be given at a lower dose then maintained later this is to avoid hypotension while standing

Their effects are faster thus usually combined with Finasteride

Adverse effects:

Postural hypotension
Tachycardia reflex

Others rarely used members include; Phentolamine and phenoxybenzamine

Medical Management

The goals of medical management of BPH are to improve the quality of life and treatment depends on the severity of symptoms.

Catheterization. If a patient is admitted on an emergency basis because he is unable to void, he is immediately catheterized.
Cystostomy. An incision into the bladder may be needed to provide urinary drainage.

Pharmacologic Management

Alpha-adrenergic blockers (eg, alfuzosin, terazosin), which relax the smooth muscle of the bladder neck and prostate, and 5alpha reductase inhibitors.
Hormonal manipulation with antiandrogen agents (ﬁnasteride [Proscar]) decreases the size of the prostate and prevents the conversion of testosterone to dihydrotestosterone (DHT).
Use of phytotherapeutic agents and other dietary supplements (Serenoa repens [saw palmetto berry] and Pygeum africanum [African plum]) are not recommended, although they are commonly used.
One herbal medication effective against BPH is Saw Palmetto.

Surgical Management

Other treatment options include minimally invasive procedures and resection of the prostate gland.

Transurethral microwave heat treatment. This therapy involves the application of heat to prostatic tissue.
Transurethral needle ablation (TUNA). TUNA uses low-level radio frequencies delivered by thin needles placed in the prostate gland to produce localized heat that destroys prostate tissue while sparing other tissues.
Transurethral resection of the prostate (TURP). TURP involves the surgical removal of the inner portion of the prostate through an endoscope inserted through the urethra.
Open prostatectomy. Open prostatectomy involves the surgical removal of the inner portion of the prostate via a suprapubic, retropubic, or perineal approach for large prostate glands.

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Erectile Dysfunction Medications

Erectile Dysfunction

Erectile dysfunction, ED is the inability of the male to attain and maintain an erection sufficient to permit satisfactory sexual intercourse.

Penile erectile dysfunction is a condition in which the corpus cavernosum does not fill with blood to allow for penile erection. This can result from the aging process and in vascular and neurological conditions.

So, what is impotence?

Impotence, a term often used synonymously with ED, many involve a total inability to achieve erection, an inconsistent ability to achieve or ability to sustain only brief erections.

Physiology of an Erection

This begins with stimulus such as sight and touch. This stimulates the parasympathetic nervous division that transmits nerve impulses to the erectile tissue of the penis (corpus carvernosum). The nerve endings release nitric oxide(NO) which binds on muscle cells in the penis leading to generation of cyclic GMP (Cyclic Guanosine monophosphate) which relaxes the muscle cells in the corpus cavernosum leading to creation of larger intracellular spaces and sinusoids. More blood flows into the erectile tissues, the tissue expands compresses the veins leaving the penis, thus increased blood volume in the organ and one erects.

Erection is continuously maintained during sexual intercourse by the release of NO, and prostaglandin E₁ (PGE₁).

Termination of erection( Detumescence ) is brought about by 2 events i.e.

Activity of enzyme phosphodiesterase type 5 enzyme (PDE-5) which catalyzes the breakdown of GMP into inactive form.
Stimulation of sympathetic nervous division to bring about the contraction of the penile muscles terminating ejaculation.

Pharmacology application of the above;

Erection relies on the penile blood flow thus an event that interferes with penile blood flow results into penile dysfunction.
Any factor which interferes with neuro-transmitters such as acetylcholine may end with Erectile Dysfunction.
Psychological factors e.g. stress may as well interfere initiation of erection.

Classification of Erectile Dysfunction.

Primary Erectile Dysfunction; is where a man has never been able to attain and maintain an erection for sexual intercourse

Secondary Erectile Dysfunction: is where impotence occurs in a man who has past history of satisfactory sexual performance.

Causes of Erectile Dysfunction

Erectile Dysfunction mainly occurs past middle age and is common after the age of 65 years.

A variety of vascular, Neurological, hormonal or endocrinal, pharmacological or psychological and genetic causes may underly the disorder, i.e.

Vascular diseases: Blood supply to the penis can become blocked or narrowed as a result of vascular disease such as atherosclerosis (hardening of the arteries).
Neurological disorders (such as multiple sclerosis): Nerves that send impulses to the penis can become damaged from stroke, diabetes, or other causes.
Psychological states: These include stress, depression, lack of stimulus from the brain and performance anxiety.
Trauma: An injury could contribute to symptoms of Erectile Dysfunction.
Cancer treatments; near the pelvis can affect the penis’ functionality.
Surgery and or radiation for cancers in the lower abdomen or pelvis can cause Erectile dysfunction. Treating prostate, colon-rectal or bladder cancer often leaves men with Erectile dysfunction.
Drugs; used to treat other health problems can negatively impact erections such as Cimetidine (Tagamet), Ranitidine (Zantac)

Classification of Drugs used to treat Erectile Dysfunction.

There are divided into 4 groups;

Central inhibitors
Peripheral inhibitors
Central conditioners
Peripheral conditioners

PDE 5 Inhibitors/Peripheral Inhibitors.

These are agents which act in the penile tissue to maintain the environment of erection. They include phosphodiesterase-5 inhibitors e.g. sildenafil, tadalafil, and vardenafil are selective PDE-5 inhibitors developed drugs in the past decade and found effective in a majority of patients with Erectile Dysfunction.

SILDENAFIL:

It is an orally active drug

Classification:

Therapeutic– ED agent, vasodilator

Pharmacological– phosphodiesterase type 5 inhibitor

Brand names:

Kamagra
Penegra
viagra
Caverta
Edegra 25, 50, 100mg tablets

Indications:

Erectile Dysfunction
Pulmonary Hypertension.

Mechanism of action;

Sildenafil acts by selectively inhibiting an enzyme phosphodiesterase-5 and enhancing nitric oxide action in corpus cavernosum thus preventing the breakdown of GMP produces smooth muscle relaxation of the corpus cavernosum which in turn promotes increased blood flow and subsequent erection hence sex intercourse and exercise tolerance is improved but it has no effect on penile (swelling) tumescence in the absence of sexual activity. It doesn’t cause priapism in most patient.

Dosage:

It is recommended in the dose of

50mg for men less than 65 years,
elderly 25mg if not effective then 100mg 1 hour by intercourse.

Duration and degree of penile erection is increased in 74-82% of men with Erectile Dysfunction including diabetic Neuropathy cases.

However, Sildenafil is effective in men who have lost libido or when ED is due to spinal cord injury or damaged Nervic eregantis since Nitric Oxide is an important regulator of pulmonary vascular resistance, PDE-5 inhibitor lower pulmonary circulation than vardenafil and is only PDE-5 inhibitor shown to improve arterial oxygenation in pulmonary Hypertension. It has now become the drug of choice for this condition

N.B.; it should be given once a day.

Adverse effects/ side effects:

These are mainly due to preservation of nitric oxide which causes vasodilatation in the brain.

Dizziness and headache
Nasal congestion
Hypotension and palpitation
Loose emotion
A feeling of dependency/ addiction
Flushing
Tachycardia
Muscle pain
Diarrhoea
Sildenafil in addiction, weakly inhibits the isoenzyme PDE-5 which is involved in photoreceptor transduction in the retina. As such impairment of colour vision especially, blue-green discrimination occurs in some recipients.
Hormones and related drug neuropathy among users of PDE-5 inhibitors have be reported.

Contraindications:

In patients with coronary heart diseases.
Those taking nitrates. Though sildenafil remains effective for less than 2hours, it is advised that nitrates should be avoided for 24hours
Presence of liver or kidney disorder
Peptic ulcer, bleeding disorder
Patients of leukemia, sickle cell anemia, myocardial infarction etc.

Drug interactions:

Sildenafil markedly potentiates the vasodilator action of nitrates, precipitates fall in Blood Pressure and myocardial infarction may occur.
Inhibitors of CYP3A4 like erythromycin, Ketoconazote, cemetidine may potentiate its action i.e. may increase Sildenafil plasma concentration.
Vitamin k antagonist may increase the risk of bleeding.
Concomitant use with alpha- blockers may lead to hypotension.

N.B: men even without Erectile Dysfunction are going for it to enhance sexual satisfaction.

Nursing implications:

Determine Erectile Dysfunction before administration.
Monitor hemodynamic parameters and exercise before and after therapy

Patient/ family teaching:

Instruct the patient to take drugs at least 1 hour before sexual activity
Not more than once a day.
Instruct the patient that sexual stimulation is required for erection to occur.
Advise the patient that the drug is not indicated for women.
Advise the patient not to concurrently take the drug with nitrates or alpha-adrenergic blockers
Instruct the patient if chest pain occurs after taking the drug to report to the PHC practioners immediately.
Advise the patient to avoid excess alcohol intake in combination with PDE-5 since it can increase the risk of orthostatic hypotension

TADALAFIL:

Brand names;

Megalis,
Tadarich,
Tadalis,
Cialis and Apcalis 10, 20mg tablets

It is a more potent and longer acting congener of Sildenafil, duration of action is 24-36 hours. It is claimed to act faster, though peak plasma levels are attained between 30-120minutes.

Indication;

Erectile Dysfunction

Mechanism of action

As for Sildenafil

Side effects, risks, contraindications and drug interactions are similar to Sildenafil

Because of its longer lasting action, nitrates are contraindicated for 36-48hours after Tadalafil.
Due to its lower affinity for PDE-6, visual disturbances occur less frequently

Dosage:

10mg o.d. at least 30minutes before sexual intercourse (max 20mg)

Peripheral Initiators of Erection

They include Alprostadil administered intra cavernously (injected) directly into the corpus cavernosum using a fine needle or introduced into the urethra as a small pellet, produces erection in few hours to permit intercourse . It is more used in patients taking anti-hypertensive drugs, those with cardiac diseases e.g Coronary artery disease and patients who do not respond to PDE-5 inhibitors.

Mode of Action

It is a prostaglandin E₁ analog thus relaxes the penile muscles bringing about erection.

Contraindications

Presence of any anatomical obstruction or condition that might predispose to priapism. The risk could be exacerbated by these drugs.
Penile implants.
Bleeding disorders, CV diseases, optic neuropathy, severe hepatic and renal disorders.

Adverse effects

Priapism
Thrombo-embolism
Local tenderness
Penile fibrosis

Central initiators:

These initiate neuronal path ways for erection e.g.

Apomorphine administered orally

Mechanism of action:

Apomorphine is a dopamine agonist which acts centrally to stimulate an erectile neuronal path way.

It is also for known for Parkinsonism and induction of vomiting thus rarely used for this indication

Adverse effect:

Nausea and vomiting
Head ache and dizziness
Decreased milk production if taken by lactating mothers for another use

Central conditioners:

These provide a central mood condition of erection. They include;

(a). Trazodone which is a CNS anti-depressant due to massive adverse effects

(b). Androgens: e.g. testosterone

Click here to read more about Androgens.

Erectile Dysfunction Medications Read More »

Androgens

Androgens are male sex hormones

Androgens include Testosterone, which is produced in the testes, and the Androgens, which are produced in the Adrenal glands.

Androgens are chiefly produced in the testes and small amounts in adrenal cortex. In female, small amounts are produced in the ovary and adrenal cortex.

Testosterone is the most important natural androgen and in adult male, 8-10mg is produced daily. Its secretion is regulated by gonadotropins and gonadotrophic releasing Hormone (GnRH). Inadequate production of androgens is due to pituitary malfunction or atrophy, injury to or removal of testicles. Androgens stimulate the development of male characteristics.

Naturally occurring androgens hormones are;

Testosterone, the principal androgenic hormone produced by the leydig cells of the testes.
Dehydroepiandrosterone (DHEA) produced by adrenal cortex.

Common Terms

Anabolic steroids: androgens developed with more anabolic or protein-building effects than androgenic effects.
Androgenic effects: effects associated with development of male sexual characteristics and secondary characteristics (e.g., deepening of voice, hair distribution, genital development, acne)
Androgens: male sex hormones, primarily testosterone; produced in the testes and adrenal glands
Hirsutism: hair distribution associated with male secondary sex characteristics (e.g., increased hair on trunk, arms, legs, face)
Hypogonadism: underdevelopment of the gonads (testes in the male)
Penile Erectile Dysfunction: condition in which the corpus cavernosum does not fill with blood to allow for penile erection; can be related to aging or to neurological or vascular conditions

Examples of Androgens

Drug Name	Usual Dosage	Usual Indications
danazol (Danocrine)	100–600 mg/d PO, depending on use and response	Prevent ovulation for treatment of endometriosis; prevention of hereditary angioedema
fluoxymesterone (Androxy)	5–20 mg/d PO for replacement therapy; 10–40 mg/d PO for certain breast cancers	Treatment of delayed puberty in male patients and certain breast cancers in postmenopausal women
testosterone (Androderm, Depo-testosterone)	50–400 mg IM every 2–4 weeks, dose varies with preparation (check more below)	Replacement therapy in hypogonadism (check more below)
methyltestosterone (Testred, Virilon)	Males: 10–50 mg/d PO Females: 50–200 mg/d PO	Replacement therapy in hypogonadism; treatment of delayed puberty in male patients and certain breast cancers in postmenopausal women

TESTOSTERONE (depo-testerone, androderm)

Classification:

Therapeutic: Hormone

Pharmacological: Androgen

Pregnancy; Category-x

Schedule: III controlled substance.

Dosage: 50–400 mg IM every 2–4 weeks, dose varies with preparation; some long-acting depository forms are available; dermatological patch 4–6 mg/day, replace patch daily.

Effects of Testosterones.

Anabolic Effects (Growth and Metabolic Functions)

Maintains bone density.
Regulates fat distribution.
Helps in Red Blood Cell production.
Supports muscle growth, strength and body mass.
Speeds up recovery from injury.
They act to increase the retention of nitrogen, sodium, potassium, and phosphorus.
They decrease the urinary excretion of calcium.
Testosterones increase protein anabolism and
decrease protein catabolism (breakdown).

Androgenic Effects ( Sexual Characteristics and Functions)

Enhances sex drive and libido.
Increases aggression.
Acne.
Beard and body hair.
Male pattern boldness.
Development and maintenance of male sex organs.
Spermatogenesis.
Increased size of the prostate.

Control of Testosterone Secretion.

Hypothalamus releases GnRH, which stimulates the Anterior Pituitary gland to secrete FSH an LH which in turn stimulate the Leydig cells to secrete testosterone. High levels of serum testosterone exerts a negative feedback i.e.

APG suppresses secretion of LH.
Hypothalamus suppresses the GnRH.

Indications of Testosterone.

Hypogonadism and impotence in males due to testicular/pituitary/hypothalamic deficiency.
Testosterone deficiency .
Breast cancer treatment in post menopausal women, who cant be operated.
Treatment of delayed male puberty.
Prevention of postpartum breast engorgement.
Illegally, sportsmen often use anabolic steroids for promoting their musculature and sporting abilities.
Blockage of follicle-stimulating hormone and luteinizing
response hormone release in women to prevent ovulation for
treatment of endometriosis.
Prevention of hereditary angioedema

Contraindications of Testosterone.

Allergy to androgens or other ingredients in the drug. Prevent hypersensitivity reactions.
Pregnancy, lactation. Potential adverse effects on the neonate. It is not clear whether androgens enter breast milk.
Presence or history of prostate or breast cancer . Aggravated by the testosterone effects of the drug.
Liver dysfunction, Cardiovascular disease. Can be exacerbated by the effects of the hormones.
Topical forms of testosterone have a Black Box Warning alerting user to the risk of virilization (Female develops male characteristics) in children who come in contact with the drug.
Danazol has Black Box warning regarding the risk of thromboembolic events, fetal abnormalities, hepatitis, and intracranial hypertension.
For use with caution in patients with Diabetes Mellitus, BPH and Sleep apnea.

Side Effects and Adverse Effects of Testosterone

In men,

Administration of an androgen may result in breast enlargement
(gynecomastia),
testicular atrophy,
inhibition of testicular function,
impotence,
enlargement of the penis,
nausea and vomiting,
jaundice,
headache,
anxiety,
male pattern baldness,
acne and depression,
fatigue,
abdominal cramps,
confusion,
deepening of the voice,
edema,
drug-induced hepatitis,
gingivitis.
hirsutism (increased hair distribution)

In women,

receiving an androgen preparation for breast carcinoma the most common adverse reactions are;
amenorrhea and virilization (acquisition of male sexual characteristics such as changes in body and facial hair, a deepening voice, acne, menstrual irregularities and enlargement of the clitoris).

Drug Interactions

May increase action of warfarin (anti-coagulants), oral hypoglycemic agents and insulin.
Concurrent use with corticosteroids may increase the risk of edema formation.

Nursing intervention/ involvement:

If the androgen is to be administered as a buccal tablet, the nurse demonstrates the placement of the tablet and warns the patient not to swallow the tablet but to allow it to dissolve in the mouth.
The nurse reminds the patient not to smoke or drink water until the tablets is dissolved. Oral and parenteral androgens are often taken or given by injection outpatient basis.
When given by injection, the injection is administered deep I.M into the gluteus muscle.
Oral testosterone is given with or before meal to decrease gastric upset.
When testosterone Trans -dermal system testostederm is prescribed, the nurse places the system on clean, dry scrotal skin. Optimal skin contact of the Trans dermal system is achieved by shaving scrotal hair before placing the system.
Monitor fluid input and output
Weigh the patient twice a week
Assess for edema and report
Monitor secondary sexual characteristics in men
Monitor menstrual irregularities, deepening of the voice, in females.
Monitor Hemoglobin and hematocrit periodically
Monitor urine and serum calcium levels

Patient/family teaching:

Advise the patient to report signs of priapism, difficulty in urinating, hypercalcemia, edema, unexpected weight gain, swelling of the fee, hepatitis, unusual bleeding.
Explain rationale for prohibiting use of testosterone for increasing athletic performance
Notify Doctor of pregnancy.
DM patients to monitor blood sugar.
Regular follow up, laboratory tests and physical examination
For ladies to notify doctor if signs of body hair distribution, deepening of voice menstrual irregularities occur.

ANABOLIC STEROIDS

These are agents that are not easily converted to the potent androgen 5 alpha o-dihydrotestosterone (DHT) hence their effects on sex are less but their anabolic effect are high.

Drugs commonly used by athletes include; nandolone, stanozolol, and mithenelone. All of this drugs are regulated as controlled substances, making their use by athletes illegal.

Clinical uses/indications of anabolic steroids.

Osteoporosis
Appetite improves and there is a feeling of well being.
To counteract osteoporosis seen in chronic glucocorticosteroid therapy.
Stimulates linear growth in prepubertal boys (height).
Used in renal diseases.

NANDROLONE

This is another steroid naturally produced by body, it is often synthesized and sold under the trade names Deca- Durabolin and Durbolin.

Professional athletes like Berry Bonds and Roger Clemens alleged used nandrolone to illegally enhance their performance.

STANOZOLOL:

This synthetic steroid goes by the brand name Winstrol. This steroid is unusual in that it can be taken orally. Base ball players like Rafael. Palmeiro have tested positive for illegal use of stanozolol and strength athletes often use it illegally to quickly get stronger.

OXANDROLONE:

Is a synthetic steroid retailed as the drug Anavar, which is approved for use in osteoporosis. Body builders use this steroid illegally to create greater muscle.

Contraindications:

Male patients with cancer of the breast or with known or suspected carcinoma of the prostate.
Carcinoma of the breast in female with hypercalcemia; androgenic anabolic steroids may stimulate osteolytic resorption of bones.
Pregnant because of masculinization of the fetus.
Nephrosis or the nephritic phase of nephritis.

Side effects of anabolic steroids:

Severe acne, oily skin and hair – hair loss.(virilization)
Liver diseases resulting into complications such as heart attack and stroke.
Altered mood, irritability, increased aggression, depression or suicidal tendencies.
Alteration in cholesterol and other blood lipids
High blood pressure
Gynecomastia- abnormal development of mammary glands in men causing breast enlargement.
Shrinking of testicles.
Azoospermia (absence of sperm in semen)
Menstrual irregularities in women
Infertility
Excess facial or body hair, deeper voice in women.
Stunted growth and heat in teens
risk of viral or bacterial un function due to unsterile injections
Edema
Prostate cancer
Injury from skin-to-skin transfer of topical testosterone

Drug interactions:

Anti-coagulants. Anabolic steroids may increase sensitivity to oral anti-coagulants. Dosage of the anti-coagulants may have to be decreased in order to maintain the prothrombin time at the desired therapeutic level. Patients receiving oral anti-coagulant therapy require close monitoring, especially when anabolic steroids are started or stopped.

Patient’s information:

The physician should instruct patients to report any of the following effects of androgenic anabolic steroids,
hoarseness,
acne,
changes in menstrual periods,
more hair on the face,
Nausea and vomiting,
changes in skin colour or ankle swelling.

ANTI ANDROGENS

Antiandrogens, also known as androgen antagonists or testosterone blockers, are a class of drugs that prevent androgens from mediating their biological effects in the body.

They act by blocking the androgen receptor and/or inhibiting or suppressing androgen production. They include:

Danzol
Finasteride
Spironolactone
Flutamide
Cyproterone
Ketoconazote
Bicalutamide and Nilutamide

Finasteride

Available preparations: Tablets 5mg

Available brands: Finest, Proscar

The androgen hormone inhibitor finasteride is a synthetic drug that inhibits the conversion of testosterone into the androgen 5 alpha o-dihydrotestosterone (DHT). The development of the prostate glands is dependent on DHT. The lowering of serum levels of DHT reduces the effect of this hormone on the prostate gland, resulting in decrease in the size of the gland and this synthesis associated with prostate gland enlargement.

Indications;

Benign Prostatic Hyperplasia(BPH)
Androgenetic alopecia (male pattern baldness) in men only

Mechanism of action:

It inhibits the enzyme 5-alpha-reductase which is responsible for converting testosterone to its potent metabolite 5-alpha dihydrotestosterone in prostate, liver and skin since 5-alphs dihydrotestosterone is partially responsible for prostatic hyperpiesia and hair loss.

Dose:

In BPH 5mg o.d
Alopecia 1mg/day for 3 months or more. Available in tablets of mg and 5mg

Side effects;

Decreased libido
Decreased volume of ejaculation
Erectile dysfunction/impotence
Breast tenderness and enlargement
Testicular pain

Contraindications/precautions;

Known hypersensitivity to finasteride
Use with caution on hepatic impairment

Nursing implications:

Assess for symptoms of prostatic hyperplasia e.g. feeling of incomplete bladder emptying, interruption of the urinary stream
Digital rectal examination should be done before and periodically during BPH therapy.
Laboratory tests of prostate specific antigen cancer concentration which is used to screen for cancer of prostate.
Take this drug without regard to meals.

Patient/ family teaching;

Finasteride possesses risk to male fetus; tell males not to have sex with pregnant women to avoid the risk of absorption
Inform the Doctor immediately if sexual partner is or may become pregnant because additional measures such as discontinuing the drug or use of condom may be necessary.

Androgens Read More »

Uterine Relaxants

Uterine Relaxants are drugs which inhibit uterine motility by decreasing the frequency and strength of contractions.

Uterine Relaxants are drugs that inhibit uterine contractions and prolong pregnancy to allow the fetus develop more fully, thereby increasing the chances of neonatal survival.

These drugs prevent premature labor. It can succeed if only the cervical dilatation is less than 4cm.
They include;

Salbutamol
Magnesium Sulphate
Nifedipine
Indomethacin
Terbutaline

SALBUTAMOL

Legal class; class B controlled drugs
Medical class; tocolysis
Form; tabs , sterile solution for injection
Dosage :tabs 4mg
Soluton for injection 50mg/ ml

Indications

Uncomplicated premature labour between 24 to 33 weeks of gestation
Asthma

Contraindications

Cardiac diseases
APH
Intra uterine fetal death.
Intra uterine infections
Raptured membranes
Eclampsia and pre-eclampsia
1st an 2nd trimester of pregnancy

Dose

For premature labour, intravenous, infusion 10mcg/ min, gradually increase according to response at 10 minutes intervals until contractions diminish, then increase rate until contractions have ceased, max dose : 45mcg/min
Maintain rate for 1hr then gradually reduce by intravenous or intramuscular injection 100-250mg repeated according to response, then orally 4mg every 6-8hrs
Do not use for more than 48minutes

Side effects

Hypoglycemia
Vomiting and nausea
Sweating
Tremors
Hypotension
Pulmonary oedema
Maternal and fetal tachycardia
Headache
Palpitations
Urticaria

Magnesium Sulphate ( MgSO4)

Legal class; class B controlled drugs
Medical class; tocolytic and anticonvulsant
Form; sterile solution for injection
Strength/dosage; 50% of 5 grams/10ml

Dosage

Loading dose (14g)

4g of MgSO are given slowly intravenously for over 15 to 20 minutes and is prepared as follows

Take a 20ml syringe and draw 8 mils if 50% MgSO4 (4g)
Add 12 mils of water for injection to make 20% of the solution
Give intravenously slowly over 15 minutes.

Immediately this is followed by 10g intramuscular and is prepared as follows;

Take 20mils syringe, draw 10mils of 50% MgSO4 (undiluted) which is equivalent to 5g in each syringe
Then add one mil of 2% lignocaine in each syringe to reduce pain
Give deep intramuscular on each buttock

Maintenance Dose

Give 5g of 50% MgSO4 deep intramuscular on alternate buttocks every 4hrs prepare as below.

Take 10ml syringe and draw 10ml of 50% of MgSO4 (5g).
Add 1ml of lignocaine 2% in a syringe and give deep intramuscular.
The dose can be repeated after every 4hrs of alternate buttock.
The treatment is continued for 24hrs from the time of starting treatment or last fit.
> Incase the mother gets fit before 4hours, she is given 2g slowly intravenous.

Useful Effects of MgSO4:

Prevent seizures which are associated with pre eclampsia and eclampsia
Reduces cerebral oedema
Relieves constipation by retaining some water in the lumen

Indications

Severe eclampsia and pre eclampsia
Patients with hypomagnesemia
Patients with severe asthma
Used in short term treatment of constipation
Patients with myocardial infarction

Contraindications

Patients with hypermagnesemia
Patients who are hypersensitive to MgSO4
Renal impairment
Hepatic failure
Hypotensive patients
Patients with epilepsy

Side effects

Drop in blood pressure
Flushing of the skin
Dizziness
Confusion
Muscle weakness
Loss of knee jack reflex
Prolonged bleeding time
Excessive bowel activity

Adverse effects

Shock in hypertensive patients
Hypermagnesemia
Respiratory depression and coma

NIFIDIPINE

Legal class; class B controlled drugs
Medical class; tocolytic and antihypertensive
Form; tablet

Dosage

20mg and the dose is repeated after 30minutes if contractions persists.
If contractions continue after 3hrs give 20mg every 3-8hrs until ceased and the maximum dose is 160mg/day

Indications

Threatened abortion
Preterm labour less than 34wks of pregnancy
Hypertension

Contraindications

Maternal conditions like cardiac diseases
Hypertension
Intrauterine infections
Any condition that make pregnancy to prolong
Fetal death

Side effects

Dizziness
Headache
Flushing
Oedema
Fatigue

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Drugs used in Labor

Drugs used in Labour

Drugs used in labour can be grouped according to the effect they have on the uterus.

Uterine Stimulants/Uterine Mortility drugs. (Oxytocics)
Uterine relaxants (Tocolytics)

Uterine Stimulants/Uterine Motility Drugs(Oxytocics)

Uterine motility drugs stimulate uterine contractions to assist labor (oxytocics) or induce abortion (abortifacients).

Oxytocics

Oxytocics stimulate contraction of the uterus, much like the action of the hypothalamic hormone oxytocin, which is stored in the posterior pituitary. These drugs include

Ergonovine (Ergotrate)
Methylergonovine (Methergine)
Oxytocin (Pitocin, Syntocinon).

Oxytocin

Legal class; class B controlled drugs
Medical class; oxytocic drugs
Form; sterile solution for injection
Strength; 10 IV per ampule.

Indications of Oxytocin

Induction of labor
Cases of inter-uterine fetal death.
Hypotonic uterine contractions
Mothers with hypertension
After delivery to control bleeding
Pre-eclampsia and eclampsia
Congestive cardiac failure
Post term
Prevent PPH
Incomplete or missed abortion.
Active management of third stage of labor.

Contraindications of Oxytocin

Hypertonic uterine
Fetal and maternal distress
Multiple pregnancy
Trial of labor
Mal presentation like breech, brow
Cephalo pelvic disproportion
Low blood pressure

Dose

Induction/argumentation of labour; 5 I.U into 500mls of solution for infusion, initially, 5 drops per min.
Preventing of PPH after delivery of the placenta; Slow I.V, 5 I.U, increase rate during 3rd stage.

Route

Intramuscular
Intravenously when mixed with normal saline or dextrose

Side Effects

Dizziness
Nausea and vomiting
Rashes
Fetal brandy cardia
Hypotension

Adverse Effects

Lead to ruptured uterus
Hypotension
Tachycardia
Intra uterine fetal anoxia and hypoxia to the fetus leading to birth asphyxia.

Pharmacokinetics

Absorption is immediate following IV injections
Drug is distributed throughout the extracellular fluid. Some amount enters the fetal circulation.
It is metabolized rapidly in kidney and liver in small amount and are excreted in urine

Abortifacients

Abortifacients are used to evacuate uterine contents via intense uterine contractions. These drugs include;

Misoprostol
Carboprost (Hemabate)
Dinoprostone (Cervidil, Prepidil Gel, Prostin E2)
Mifepristone ( Mifeprex).

Misoprostol

Legal class; class B controlled drugs
Medical class; oxytocic drugs/ cervical, rippening agent
Form; tablet
Strength; 200mcg/ 100mcg tablet

Indications

Induction of labour
Control post partum hemorrhage due to uterine atony
Before cervical dilatation
Intra-uterine fetal death
Gastric and deudenal ulcerations

Contraindications

Mal presentation
Placeta previa grade 3 and 4
Multiparous mothers
Cephalo pelvic disproportion
Hypersensitivity to misoprostol

Dose

Induction of labour; 100mcg vaginally every after 12hrs
NSAID ulcerations; 200mcg 4 times a day

Route

Sublingually
Rectally
Vaginally

Side Effects

Headache
Dizziness
Fever
Shivering
Vomiting
Uterine rupture
Fetal distress.
Constipation

Pharmacokinetics.

Absorbed in the GIT and distributed widely through out the body metabolised in the liver and is excreted in urine.

DINOPROSTOL

Available preparation – 3mg tab
Available brand – Prostin

Pharmacokinetics

Following vaginal insertion, it diffused slowly into the maternal blood.
There is also some local absorption into the uterus through the cervix
It is distributed widely in the molter, metabolized in the lungs, liver, kidney, spleen and other maternal tissues and excreted in urine with small amount in faeces.

Indications

Induction of labor
Missed abortion

Contraindications

Active cardiac diseases
Multiple pregnancy
Hypersentivity to dinoprostol
Untreated pelvic infection
Caesarian section

Dose : 3 mg vaginally

Side Effects

Abdominal pain
Nausea and vomiting
Hypotension
Shivering
Back pain
Rapid cervical dilatation

SYNTOMETRINE

Legal class; class B controlled drugs
Medical class; oxytocic drug
Form; sterile solution for injection
Strength; combination of ergometrine and Pitocin ( ergometrine 0.5 mg + Pitocin 5 IU) –It exists in an ampules of 1 mill

Dose

I ml as single dose but can be repeated where necessary if bleeding is not controlled

Route

Intramuscular
Intravenous

Indications

Give to multi gravidas after delivery
Mothers with a history of post partum hemorrhage
Multiple or twin delivery because of large placental site
Mothers with heavy lochia
Abortion when fundal height is less than 12 weeks

Contraindications

Mothers with cardiac disease, pre eclampsia, eclampsia and hypertension.

Adverse Effects

Retained placenta
IUFD in undiagnosed second twin
Lead to retained 2nd twin
Uterine rapture if given in abortion, above 20 weeks of gestation products of conception are not fully out.
Causes hypoxia and anoxia

Side Effects

Nausea and vomiting
Headache
Hypotension
Dyspnea
Muscle pain

ERGOMETRINE

Legal class; class B controlled drugs
Medical class; oxytocic drug
Form; tablet and sterile solution
Strength/dosage; tabs 0.25 to 0.5mg tab
Injection 200mcg/ml
0.5mg/ml
EFFECTS
It causes sudden prolonged intermittent uterine contraction
INDICATION
Contra indications
Side effects
Dangers
(Are the same as for syntometrine)

UTERINE RELAXANTS

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Fertility Drugs/Gonadotropin Drugs

Fertility Drugs

Fertility drugs are drugs that stimulate the female reproductive system.

Examples of Fertility drugs;

Cetrorelix (Cetrotide)
Chorionic gonadotropin (Chorex, Profasi, Pregnyl).
Chorionic gonadotropin alpha (Ovidrel).
Clomiphene (Clomid)
Menotropins
(Pergonal, Humegon).

Therapeutic Actions and Indications.

Women without primary ovarian failure who cannot get pregnant after 1 year of trying may be candidates for the use of fertility drugs. Fertility drugs work either directly to stimulate follicles and ovulation or stimulate the hypothalamus to increase FSH and LH levels, leading to ovarian follicular development and maturation of ova.

Indications

Given in sequence with human chorionic gonadotropin (HCG) to maintain the follicle and hormone production, these drugs are used to treat infertility in women with functioning ovaries whose partners are fertile.
Fertility drugs also may be used to stimulate multiple follicle development for the harvesting of ova for in vitro fertilization.
Menotropins also stimulate spermatogenesis in men with low sperm counts and otherwise normally functioning testes.
Cetrorelix inhibits premature LH surges in women undergoing controlled ovarian stimulation by acting as a GnRH antagonist.
Chorionic gonadotropin is used to stimulate ovulation by acting like GnRH and affecting FSH and LH release.

Contraindications of fertility drugs

Allergy to fertility drug: Prevent hypersensitivity.
Primary ovarian failure: These drugs only work to stimulate functioning ovaries
Thyroid or adrenal dysfunction. Drugs have effects on the hypothalamic-pituitary axis.
Ovarian cysts: Can be stimulated by the drugs and can become larger
Pregnancy: Due to the potential for serious fetal effects
Idiopathic uterine bleeding: Can represent an underlying problem that could be exacerbated by the stimulatory effects of these drugs.
Lactation: Risk of adverse effects on the baby
Thromboembolic disease. Increased risk of thrombus formation
Women with respiratory diseases: Alterations in fluid volume and blood flow can overtax the respiratory system.

Adverse effects of fertility drugs

Greatly increased risk of multiple births and birth defects
Ovarian overstimulation: abdominal plain, distention, ascites, pleural effusion
Headache
Fluid retention
Nausea
Bloating
Uterine bleeding
Ovarian enlargement
Gynecomastia
Febrile reactions possibly due to stimulation of progesterone release.

Fertility Drugs

Drug	Indication	Dose
Clomifene	Anovulatory infertility	50mg daily for 5 days, starting within 5 days of onset of menstruation (preferably on the second day) or at any time if cycles have ceased
Bromocriptine	Hyper prolactanaemic, infertility, Suppression of lactation, Hypogonadism, Galactorrhoea syndrome, Benign breast disease	Initially 1.25mg at bed time increased gradually to the usual dose of 2.5mg 3 times a day with food increased if necessary to a max. dose 30mgdaily

Nursing Diagnosis

Acute pain related to headache, fluid retention, or GI upset
Sexual dysfunction related to alterations in normal hormone control
Disturbed body image related to drug treatment and diagnosis
Deficient Knowledge regarding drug therapy
Risk for Impaired Tissue Perfusion (Cardiopulmonary, Peripheral) related to increased risk for thrombus formation
Situational Low Self-Esteem related to the need for fertility drugs.

Drugs used in labor

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Estrogen Receptor Modulators

Estrogen Receptor Modulators are agents that either stimulate or block specific estrogen receptor sites.

They are used to stimulate specific estrogen receptors to achieve therapeutic effects of increased bone mass without stimulating the endometrium and causing other less desirable effects i.e. these drugs stimulate the estrogen receptors in the body so as to produce estrogen as needed by the body.

Examples of Estrogen Receptor Modulators.

Two available estrogen receptor modulators are raloxifene (Evista) and toremifene (Fareston).

Raloxifene

Dose : 60 mg/day Orally.

Indications : –Used therapeutically to stimulate specific estrogen receptor sites, which results in an increase in bone mineral density without stimulating the endometrium in women; – reduces risk of invasive breast cancer in postmenopausal women with osteoporosis who are at
high risk for invasive breast cancer

Toremifene

Dose : 60 mg/day orally until disease progression occurs.

Indications: Used as an antineoplastic agent because of its effects on estrogen receptor sites for treatment of advanced breast cancer in postmenopausal women with estrogen receptor–positive and estrogen
receptor–unknown tumors

Contraindications of Estrogen Receptor Modulators

Allergy to estrogen receptor modulators.
Contraindicated in pregnancy and lactation because of potential effects on the fetus or neonate.
History of venous thrombosis or smoking. Increased risk of blood clot formation if smoking and estrogen are combined.

Adverse Effects of Estrogen Receptor Modulators

Raloxifene has been associated with GI upset, nausea, and vomiting.
Changes in fluid balance may cause headache, dizziness, visual changes, and mental changes.
Specific estrogen receptor stimulation may cause hot flashes, skin rash, edema, and vaginal bleeding.

Clinically Important Drug–Drug Interactions

Cholestyramine: reduced raloxifene absorption
Highly protein-bound drugs (e.g. diazepam, ibuprofen, indomethacin, naproxen): interference on binding sites
Warfarin: decreased prothrombin time if taken with raloxifene

Nursing Considerations

Assess for the mentioned cautions and contraindications (e.g. drug allergies, cardiovascular diseases, metabolic bone disease, history of thromboembolism, etc.) to prevent any complications.
Perform a thorough physical assessment (e.g. bowel sounds, skin assessment, vital signs, mental status, etc.) to establish baseline data before drug therapy begins, to determine effectiveness of
therapy, and to evaluate for occurrence of any adverse effects associated with drug therapy.
Assist with pelvic and breast examinations. Ensure specimen collection for Pap smear and obtain a history of patient’s menstrual cycle to provide baseline data and to monitor for any adverse
effects that could occur.
Arrange for ophthalmic examination especially for patients who are wearing contact lenses because hormonal changes can alter the fluid in the eye and curvature of the cornea, which can
change the fit of contact lenses and alter visual acuity.
Monitor laboratory test results (e.g. urinalysis, renal and hepatic function tests, etc.) to determine possible need for a reduction in dose and evaluate for toxicity.

Nursing Diagnoses

Ineffective tissue perfusion related to changes in the blood vessels brought about by drug therapy and risk of thromboemboli
Excess fluid volume related to fluid retention
Acute pain related to systemic side effects of gastrointestinal (GI) pain and headache

Implementation with Rationale
These are vital nursing interventions done in patients who are taking female sex hormones and estrogen receptor modulators:

Administer drug with food to prevent GI upset.
Provide analgesic for relief of headache as appropriate.
Provide small, frequent meals to assist with nausea and vomiting.
Monitor for swelling and changes in vision or fit of contact lenses to monitor for fluid retention and fluid changes.
Provide comfort measures to help patient tolerate drug effects.
Provide safety measures (e.g. adequate lighting, raised side rails, etc.) to prevent injuries.
Educate client on drug therapy to promote understanding and compliance.

Evaluation

Here are aspects of care that should be evaluated to determine effectiveness of drug therapy:

Monitor patient response to therapy (palliation of signs and symptoms of menopause, prevention of pregnancy, decreased risk factors for coronary artery disease, and palliation of certain cancers).
Monitor for adverse effects (e.g. GI upset, edema, changes in secondary sex characteristics, headaches, thromboembolic episodes, and breakthrough bleeding).
Evaluate patient understanding on drug therapy by asking patient to name the drug, its indication, and adverse effects to watch for.
Monitor patient compliance to drug therapy

Fertility Drugs/Gonadotropin Drugs

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Gonadotropin drugs

GONADOTROPINS

Gonadotropins are fertility medications given by injection that contain follicle-stimulating hormone (FSH) alone or combined with luteinizing hormone (LH).

Gonadotropins are hormones that stimulate the gonads, which are the sex organs in the body.

Gonadotropins are produced by the pituitary gland, which is a small gland located at the base of the brain. The release of gonadotropins is regulated by the hypothalamus.

In females, the gonads are the ovaries, and in males, they are the testes.

Gonadotropins are a class of medications used to treat infertility and disorders associated with reproductive functions.

Types of Gonadotropins

There are two main types of gonadotropins:

1. Follicle-stimulating hormone (FSH): This hormone stimulates the growth and development of follicles in the ovaries of females and sperm production in the testes of males.

Females

Males

– Normal Ovarian Function: FSH is useful for the development and maturation of follicles in the ovaries, which contain the eggs. This ensures regular ovulation and fertility.

– Estrogen Production: FSH stimulates the production of estrogen by the growing follicles. Estrogen is for the development of female secondary sexual characteristics, menstrual cycle regulation, and overall reproductive health.

– Improved Egg Quality: FSH contributes to the development of healthy eggs, increasing the chances of successful fertilization and pregnancy.

– Fertility Treatment: FSH is a key component of fertility treatments like in vitro fertilization (IVF) to stimulate multiple egg production.

– Sperm Production: FSH is essential for the production of sperm in the testes. It stimulates the Sertoli cells, which are responsible for nourishing and supporting sperm development.

– Improved Sperm Quality: FSH contributes to the production of healthy, motile sperm, increasing the chances of fertilization.

2. Luteinizing hormone (LH): This hormone triggers ovulation in females and testosterone production in males.

Females

Males

– Ovulation: LH triggers the release of the mature egg from the follicle (ovulation), which is essential for fertilization.

– Corpus Luteum Formation: After ovulation, LH stimulates the formation of the corpus luteum, which produces progesterone. Progesterone is for maintaining the uterine lining for potential pregnancy.

– Hormonal Balance: LH plays a role in regulating the production of estrogen and progesterone, contributing to hormonal balance in the female body.

– Fertility Treatment: LH is used in fertility treatments to trigger ovulation and support the development of the corpus luteum.

– Testosterone Production: LH stimulates the Leydig cells in the testes to produce testosterone. Testosterone is essential for male sexual development, sperm production, and overall health.

– Secondary Sexual Characteristics: LH-driven testosterone production is responsible for the development of male secondary sexual characteristics like facial hair, muscle mass, and deepening of the voice.

– Libido and Sexual Function: Testosterone, produced under the influence of LH, plays a crucial role in libido and sexual function.

GONADOTROPIN DRUGS (Fertility Drugs)

Gonadotropin Drugs/Fertility drugs are agents that stimulate the female reproductive system.

Fertility drugs are medications used to help women who are having trouble getting pregnant. They work by stimulating the ovaries to produce more eggs, increasing the chances of conception.

Indications for Fertility Drugs:

1. Treatment of infertility in women with functioning ovaries whose partners are fertile: This is a broad category encompassing various causes of infertility, including:

Anovulation: When a woman doesn’t ovulate regularly, fertility drugs can stimulate ovulation and increase the chances of pregnancy.
Polycystic Ovarian Syndrome (PCOS): PCOS often causes irregular ovulation. Fertility drugs can help regulate ovulation and improve fertility.
Endometriosis: This condition can affect ovulation and egg quality. Fertility drugs can help stimulate ovulation and improve chances of conception.
Premature Ovarian Failure: In some cases, women experience premature ovarian failure, leading to low egg reserves. Fertility drugs can help stimulate limited egg production.
Unexplained Infertility: When the cause of infertility is unknown, fertility drugs can be used to stimulate ovulation and see if it improves chances of pregnancy.

2. Used to stimulate multiple follicle development for harvesting of ova for in vitro fertilization (IVF): This is a crucial aspect of IVF, where multiple eggs are needed for fertilization and embryo transfer.

3. Menotropins are used to stimulate spermatogenesis in men with low sperm counts and otherwise normally functioning testes: While not directly related to female fertility, this highlights the broader application of fertility drugs in both men and women.

Contraindications for Fertility Drugs:

Allergy to fertility drug: Prevent hypersensitivity reactions.
Primary ovarian failure: These drugs only work to stimulate functioning ovaries.
Ovarian cysts: Can be stimulated by the drugs and can become larger.
Pregnancy: Due to the potential for serious fetal effects.
Idiopathic uterine bleeding: Can represent an underlying problem that could be exacerbated by the stimulatory effects of these drugs.
Lactation: Risk of adverse effects on the baby.
Thromboembolic disease: Increased risk of thrombus formation.
Women with respiratory diseases: Alterations in fluid volume and blood flow can overtax the respiratory system.

Adverse Effects:

Greatly increased risk of multiple births and birth defects.
Ovarian overstimulation: abdominal pain, distention, ascites, pleural effusion.
Others: headache, fluid retention, nausea, bloating, uterine bleeding, ovarian enlargement, gynecomastia, and febrile reactions possibly due to stimulation of progesterone release.

Fluid retention is a common side effect of fertility medications, because;

Hormonal Changes: Fertility drugs increase estrogen levels, which can lead to fluid retention. Estrogen promotes sodium retention in the body, and sodium attracts water, causing fluid buildup.

Increased Blood Flow: Fertility drugs increase blood flow to the ovaries and uterus, which can lead to fluid buildup in the pelvic area.

Drugs used in treatment of infertility

Name

Clinical uses and dosage

Contraindications

Clomifene

Available in tablet form of 50mg
Brand name Clomid

Infertility due to failure to ovulate.

Given 50 mg daily × 5/7

Starting from the 5th day of the cycle ,

Increase to 100mg ×5/7

From day 5-10 if no response.

Pregnancy.

Bromocriptine

Available in tablet form of 2.5mg

Female infertility associated with hyperprolactinemia

Dosage 1.25 – 2.5mg

Bid × 3-7 days with food.

Inhibition of lactation 2.5mg bid with meals × 14 days.

Severe ischemic heart disease

Uncontrolled hypertension

Pregnancy

Breast feeding.

FEMALE REPRODUCTIVE SYSTEM DRUGS

Drugs that affect the female reproductive system typically include hormones and hormonal-like agents.

These drug types include;

Gonadotropin Sites of Action

Female Sex Hormones

The female sex hormones can be used to replace hormones that are missing or to act on the control mechanisms of the endocrine system to decrease the release of endogenous hormones.
Drugs that act like estrogen, particularly at specific estrogen receptors, are also used to stimulate the effects of estrogen in the body with fewer of the adverse effects.

Female sex hormones include;

Estrogens
Progestins

Estrogens.

This hormone is naturally produced by the ovaries, placenta and adrenal glands. It stimulates the development of female sex characteristics, prepares the body for pregnancy, affects the release of FSH and LH, and is responsible for proliferation of the endometrial lining.

Low estrogen in the body is responsible for the signs and symptoms of menopause, in the uterus, vagina, breast and cervix.

Other Functions of estrogen include;

Breast development.
Increase cholesterol in bile, to prevent damaging effects of bile salts.
Increases fat storage, such as in breast tissue.
Maintains bone mineral density.
Maintains muscle strength.
Prevents atherosclerosis, by increasing HDL concentration and lowering LDL.
Estrogen is responsible for maintaining libido, memory, and mental health.
It stimulates ovulation, maintains the uterine walls and is important in vaginal lubrication.

Indications of Estrogen Therapy.

Estrogens are used for hormone replacement therapy (HRT) when ovarian activity is blocked or absent.
Is used to control the signs and symptoms of menopause.
They can also be used in therapy for prostate cancer and inoperable breast cancer, also as palliative care.
Treatment of female hypogonadism(when the body produces little or no hormones).
Treat ovarian failure.
Oral contraceptives (estrogen and progestin)
Morning after pill (emergency pills)
Endometriosis
Dysmenorrhea, used with progestin.

Progestin/Progesterone.

This promotes maintenance of pregnancy and it is called a pregnancy hormone.

Its functions include;

Transforms proliferative endometrium into secretory endometrium.
Prevents follicle maturation, ovulation and uterine contractions.
Used in contraceptives. It inhibits release of GnRH, FSH and LH, hence follicle development and ovulation are prevented.

Indications of Progestin.

Used as a contraceptive.
Maintains pregnancy and development of secondary sex characteristics.
Use to treat primary and secondary amenorrhea, and functional uterine bleeding.
Treatment of acne and premenstrual dysphoric disorder (PMDD).
For the relief of signs and symptoms of menopause .

Contraindications of Female Sex hormones.

Estrogen

Known allergies
Idiopathic vaginal bleeding.
Breast Cancer(Estrogen dependant cancer)
CVA since it increases clotting factor prodn.
Hepatic dysfunction.
Pregnancy.
Lactation.

Progestin/Progesterone

PID
STD
Endometriosis
Renal and hepatic disorders.
Epilepsy.
Asthma.
Migraine headaches
Cardiac Dysfunction —potential excerbation.

Adverse Effects.

Corneal Changes.
Photosensitivity.
Peripheral edema.
Chloasma ( patches on the face)
Hepatic adenoma.
Nausea
Vomiting.
Abdominal cramps.
Bloating.
Withdraw bleeding.
Changes in menstrual flow.

Important aspects/issues to remember.

Women receiving any of these drugs should receive an annual medical examination, including
breast examination and Pap smear, to monitor for adverse effects and underlying medical
conditions.
Women taking estrogen should be advised not to smoke because of the increased risk of
thrombotic events.
Women who are receiving these drugs for fertility programs should receive a great deal of psychological support and comfort measures to cope with the many adverse effects associated
with these drugs. The risk of multiple births should be explained.
Drugs are used in treatment of specific cancers in males and they should be advised about the
possibility of estrogenic effects.
Not indicated during pregnancy or lactation because of potential for adverse effects on the fetus
or neonate.

Examples of female sex hormones and dosages.

Estrogen

Estradiol, 1–2 mg/day orally or 1–5 mg IM every 3–4 weeks or 2–4 g intravaginal cream daily.
Estrogens, conjugated (C.E.S., Premarin), 0.3–1.25 mg/day orally.
Estropipate (Ortho-Est, Ogen), 0.625–5 mg/day orally.

Progestin/Progesterone.

Etonogestrel (Implanon) 68 mg implanted sub dermally for up to 3 yr, replaced or changed when needed.
Medroxyprogesterone (Provera) 5–10 mg/day PO for 5–10 days for amenorrhea or 400–1000 mg/week IM for cancer therapy or 150 mg of deep IM every 3 months (13 weeks) for contraception.

Clinically important Drug Interactions

Estrogen

Barbiturates, rifampin, tetracyclines, phenytoin: decreased serum estrogen levels
Corticosteroids: increased therapeutic and toxic effects of corticosteroids.
Nicotine: Increased risk of thrombi and emboli
Grapefruit juice: inhibition of metabolism of estradiols
St. John’s wort: can affect metabolism of estrogens and can make estrogen-containing
contraceptives less effective.

Progestins

Barbiturates, carbamazepine, phenytoin, griseofulvin, penicillin, tetracyclines, rifampin: reduced
effectiveness of progestins
St. John’s wort: can affect the metabolism of progestins and can make progestin-containing
contraceptives less effective..

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