How to Removed Cyst on Face

Sebaceous cysts are common noncancerous cysts of the skin. Cysts are abnormalities in the body that may contain liquid or semiliquid material.

Sebaceous cysts are mostly found on the face, neck, or torso. They grow slowly and are not life-threatening, but they may become uncomfortable if they go unchecked.

Doctors usually diagnose a cyst with only a physical examination and medical history. In some cases, a cyst will be examined more thoroughly for signs of cancer.

Causes of a sebaceous cyst:

Sebaceous cysts form out of your sebaceous gland. The sebaceous gland produces the oil called sebum that coats your hair and skin. Cysts can develop if the gland or its duct, the passage where oil is able to leave, becomes damaged or blocked. This usually occurs due to a trauma to the area.

The trauma may be a scratch, a surgical wound, or a skin condition, such as acne. Sebaceous cysts grow slowly, so the trauma may have occurred months or weeks before you notice the cyst.

Other causes of a sebaceous cyst may include:

  • a misshapen or deformed duct
  • damage to the cells during a surgery
  • genetic conditions, such as Gardner’s syndrome or basal cell nevus syndrome

Blackheads Removal

What are blackheads?

Blackheads are small bumps that appear on your skin due to clogged hair follicles. These bumps are called blackheads because the surface looks dark or black. Blackheads are a mild type of acne that usually form on the face, but they can also appear on the following body parts:

Acne affects nearly 50 million Americans and is the most common skin disorder in the United States, according to the American Academy of Dermatology.

What causes blackheads?

Blackheads form when a clog or plug develops in the opening of hair follicles in your skin. Each follicle contains one hair and a sebaceous gland that produces oil. This oil, called sebum, helps keep your skin soft. Dead skin cells and oils collect in the opening to the skin follicle, producing a bump called a comedo. If the skin over the bump stays closed, the bump is called a whitehead. When the skin over the bump opens, exposure to the air causes it to look black and a blackhead forms.

Some factors can increase your chances of developing acne and blackheads, including:

  • producing too much body oil
  • the buildup of the Propionibacterium acnes bacteria on the skin
  • irritation of the hair follicles when dead skins cells don’t shed on a regular basis
  • undergoing hormonal changes that cause an increase in oil production during the teen years, during menstruation, or while taking birth control pills
  • taking certain drugs, such as corticosteroids, lithium, or androgens

Some people believe that what you eat or drink can affect acne. Dairy products and foods that increase blood sugar levels, such as carbohydrates, may play a part in triggering acne, but researchers aren’t convinced that there’s a strong connection.

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Frostbite management

Frostbite is the condition in which living human tissues freeze and are damaged because of exposure to low temperatures. Frostbite will most likely affect the hands, feet, nose, and ears. Frostbite can be a very serious injury.

source: imgur.com

Exposure of bare or poorly protected skin, hands, and feet to freezing temperatures will cause frostbite. Increased wind speed, known as wind chill, is often a factor. Drinking alcohol, being dehydrated, taking beta-blockers (medicine for heart disease), smoking, and having diabetes, peripheral vascular disease (of arteries), peripheral neuropathy (nervous system disorder), and Raynaud’s syndrome increase the risk of frostbite.

source: imgur.com

Symptoms include a pins-and-needles feeling, numbness, pain, decreasing ability to sense touch, and red skin. If the problem is recognized and treated at this stage, mild swelling and peeling of the skin may be the only effects. As the process gets worse, the affected area becomes pale and firm. As the area is rewarmed, large blisters, blood blisters, and dead tissue that looks black, blue, or dark gray (from gangrene) can occur.

The doctor will diagnose frostbite on the basis of the history of exposure to freezing temperatures and a physical examination.

source: imgur.com

The best treatment is prevention! Dress properly for the weather and make sure children are protected and watched closely. Drink plenty of nonalcoholic and noncaffeinated liquids. Plan ahead and limit exposure to cold when possible. If frostbite is possible, get to shelter and warmth immediately. Immersing the injured area in warm water (104° F) is best.

Asthma Management

DEFINITION

  • Chronic inflammatory airway disease characterized by variable reversiblemairway obstruction, airway hyper-responsiveness and bronchial inflammation.

AETIOLOGY

  • Genetic factors: Positive family history, twin studies. Almost all asthmatic patients show some atopy (tendency of T lymphocyte (Th2) cells to drive production of IgE on exposure to allergens). Linkages to multiple chromosomal locations point to ‘genetic heterogeneity’.
  • Environmental factors: House dust mite, pollen, pets (e.g. urinary proteins, furs), cigarette smoke, viral respiratory tract infection, Aspergillus fumigatus spores, occupational allergens (isocyanates, epoxy resins).

PATHOLOGY/PATHOGENESIS

  • Early phase (up to 1 h): Exposure to inhaled allergens in a presensitized individual results in cross-linking of IgE antibodies on the mast cell surface and release of histamine, prostaglandin D2, leukotrienes and TNF-a. These mediators induce smooth muscle contraction (bronchoconstriction), mucous hypersecretion, oedema and airway obstruction.
  • Late phase (after 6–12 h): Recruitment of eosinophils, basophils, neutrophil and Th2 lymphocytes and their products results in perpetuation of the inflammation and bronchial hyper-responsiveness.
  • Structural cells (bronchial epithelial cells, fibroblasts, smooth muscle and vascular endothelial cells), may also release cytokines, profibrogenic and proliferative growth factors, and contribute to the inflammation and altered function and proliferation of smooth muscle cells and fibroblasts (‘airway remodeling’).

EPIDEMIOLOGY

  • Affects 10% of children and 5% of adults. The prevalence of asthma appears to be increasing. ,¼<. Acute asthma is a very common medical emergency and still responsible for 1000–2000 deaths/year in the UK.

HISTORY

  • Episodes of wheeze, breathlessness, cough; worse in the morning and at night.
  • Ask about interference with exercise, sleeping, days off school and work.
  • In an acute attack it is important to ask whether the patient has been admitted to hospital because of his/her asthma, or to ITU, as a gauge of potential severity.
  • Precipitating factors: Cold, viral infection, drugs (b-blockers, NSAIDs), exercise, emotions.
  • May have a history of allergic rhinitis, urticaria, eczema, nasal polyps, acid reflux and family history.

EXAMINATION

  • Tachypnoea, use of accessory muscles, prolonged expiratory phase, polyphonic wheeze, hyperinflated chest.
  • Severe attack: PEFR <50% predicted, pulse > 110/min, respiratory rate > 25/min, inability to complete sentences.
  • Life-threatening attack: PEFR < 33%, silent chest, cyanosis, bradycardia, hypotension, confusion, coma.

INVESTIGATIONS

  • Acute : Peak flow, pulse oximetry, ABG, CXR (to exclude other diagnoses, e.g. pneumothorax, pneumonia), FBC (” WCC if infective exacerbation), CRP, U&Es, blood and sputum cultures.
  • Chronic : PEFR monitoring: There is often a diurnal variation with a morning ‘dip’.
  • Pulmonary function test: Obstructive defect, with improvement after a trial of a b2-agonist.
  • Blood: Eosinophilia, IgE level, Aspergillus antibody titres (see allergic Aspergillus lung disease).
  • Skin prick tests: May help in the identification of allergens.

MANAGEMENT

 

Acute:

 

  • Resuscitate, monitor O2 sats, ABG and PEFR.
  • High-flow oxygen.
  • Nebulized b2-agonist bronchodilator salbutamol (5 mg, initially continuously, then 2–4hourly), ipratropium (0.5mg qds).
  • Steroid therapy (100–200mg IV hydrocortisone, followed by 40mg oral prednisolone for 5–7 days).
  • If no improvement : IV magnesium sulphate. Consider IV aminophylline infusion or IV salbutamol.
  • Summon anaesthetic help if patient is getting exhausted (PCO2 increasing).
  • Treat any underlying cause (e.g. infection, pneumothorax). Give antibiotics if there is evidence of chest infection (purulent sputum, abnormal CXR, ” WCC, fever). Monitor electrolytes closely (bronchodilators and aminophyline).
  • May need ventilation in severe attacks. If not improving or patient tiring, involve ITU early.
  • Discharge : When PEF >75% predicted or patient’s best, diurnal variation < 25%, inhaler technique checked, stable on discharge medication for 24 h, patient owns a PEF meter and has steroid and bronchodilator therapy. Arrange follow-up.
  • Chronic ‘stepwise’ therapy: Start on the step appropriate to initial severity and step up or down to control symptoms. Treatment should be reviewed every 3–6 months.

COMPLICATIONS

  • Growth retardation, chest wall deformity (e.g. pigeon chest), recurrent infections, pneumothorax, respiratory failure, death.

Pharyngitis/Tonsillitis

Inflammation of the pharynx or tonsils. Pharyngitis accounts for 1% to 2% of visits to outpatient clinics, physicians’ offices, and emergency rooms.
Between 10% and 20% of these cases are caused by infection with group A β-hemolytic streptococcus (GABHS).

OTHER DEFINITION

_ Streptococcal tonsillitis is manifested as acute onset of fever, headache, neck pain, odynophagia, sore throat, otalgia, red tongue with enlargement of papillae, sore throat, red swollen uvula, and tender anterior cervical adenitis.

_ Peritonsillar abscess (accumulation of pus between the tonsil and its capsule) is the most common complication of acute tonsillitis. Clinical signs include deformed posterior pharynx, medial displacement of the uvula, trismus, and muffled voice (hot-potato voice).

SEVEN DANGER SIGNS IN PATIENT WITH SORE THROAT

  1. Persistence of symptoms longer than 1 wk without improvement
  2. Respiratory difficulty, particularly stridor
  3. Difficulty in handling secretions
  4. Difficulty in swallowing
  5. Severe pain in the absence of erythema
  6. A palpable mass
  7. Blood, even in small amounts, in the pharynx or ear

CAUSES

VIRUSES

  • Respiratory syncytial virus
  • Influenza A and B
  • Epstein-Barr virus
  • Adenovirus
  • Herpes simplex

BACTERIA

  • Group A streptococci (GAS)
  • Neisseria gonorrhoeae
  • Fusobacterium necrophorum (10% of pharyngitis)

OTHER ORGANISM

  • Mycoplasma pneumoniae
  • Chlamydophila pneumoniae
  • Arcanobacterium haemolyticum

PHYSICAL & CLINICAL FINDING

  • May appear normal to severely erythematous
  • Tonsillar hypertrophy and exudates commonly seen but do not indicate etiology
  • Rhinorrhea
  • Conjunctivitis
  • Cough
  • High fever
  • Systemic signs of infection
  • Herpes simplex or enterovirus infection: vesicles
  • Streptococcal infection

WORKUP

The Centor criteria to identify patients at risk for GAS consists of:

  1. Fever subjective or measured >38.1° C (100.5° F)
  2. Absence of cough
  3. Tonsillar exudates
  4. Tender anterior cervical lymphadenopathy

Rapid streptococcal antigen test

LABORATORY TESTS

  • CBC
  • Viral cultures, serologic studies rarely needed
  • Monospot if diagnosis is unclear

TREATMENT

NONPHARMACOLOGIC THERAPY

  • Fluids
  • Salt water gargles

PHARMACOLOGIC THERAPY

  • Analgesics: aspirin (adults) or acetaminophen or ibuprofen (adults and children)
  • If streptococcal infection proven or suspected: (1). Penicillin V 500 mg PO bid for 10 days or benzathine penicillin 1.2 million U IM once (adults). Children: penicillin V 250 mg bid or tid. (2). Erythromycin 500 mg PO bid or 250 mg qid for 10 days or azithromycin if penicillin allergic.
  • If gonococcal infection proven or suspected: ceftriaxone 250 mg IM once
  • Amoxicillin 500 mg tid for 10 days is the primary antibiotic treatment of streptococcal tonsillitis. Macrolides or clindamycin can be used in penicillin allergic patients.
  • Treatment of peritonsillar abscess is drainage through needle or incision

Lumbar Puncture

Indications

  • Dx CNS disease, administer CNS treatment or treat hydrocephalus

Contraindications

  • ⁄Intracranial pressure (ICP); intracranial mass effect (r/o mass lesion: head CT when signs of ⁄ICP)
  • Bleeding dysfunction
  • Infection near site
  • Elderly: avoid fast and large volume withdrawals.

Equipment

  • Skin preparation: sterile sponges, povidone-iodine swabs, and EtOH swabs
  • Mask, sterile field (towels and drapes), and gloves
  • Local anesthetic, usu. lidocaine 1% plain
  • Syringe (3 mL) and needles (22-G x 1.5”, 25-G x  5/8”)
  • Spinal needles (both 18- and 20-G, 3” length)
  • Three-way stopcock, sterile collection tubes, and manometer
  • Gauze dressings and adhesive bandage


Preparation

  • Sterile technique; skin preparation
  • Find L4-5 space (L4 at iliac crest level)
  • Local anesthesia : infiltrate skin (25-G needle), then Δ to 22-G needle and advance † infiltrate deeper tissue

Patient Positioning

  • Lateral decubitus: (preferred): Lateral decubitus position at edge of bed, while maximally flexing knees (near chest), hips, and back (opens L3/L4 space) pt. shoulders and hips
    perpendicular to bed
  • Sitting: (easier for obese or spinal dz/deformity): Pt. sits at bed edge, leans over two pillows, flexes head

Technique

  • Insert spinal needle into skin and slowly advance (keep perpendicular to skin, hold w/two hands, keep stylet in place); feel “pop”; perforate ligamentum flavum; withdraw stylet,
    and look for CSF drainage
  • If no CSF and needle advanced < 4 cm (in adult), advance 2 mm, remove stylet, and check for CSF drainage; repeat until get CSF or needle advanced  > 4 cm (then withdraw and redirect needle)
  • Connect three-way stopcock, and attach manometer; measure opening pressure (normal 70-180 mm CSF)
  • Send fluid for studies; remove needle and dress wound; pt. remains supine > or = 12 h (minimize headaches)

Complications

  • Brain herniation (⁄ ICP and mass), infection (meningitis or empyema), subdural hematoma (rapid withdrawal of large volume CSF), bloody tap, spinal epidural hematoma, headache, dry tap † needle may be too lateral or deep
  • For CSF interpretation see Labs Tab.

De Quervain Disease

De Quervain disease is a stenosing tenosynovitis of the abductor pollicis longus and the extensor pollicis brevis tendons at the styloid process of the radius.

  • It is most common in women between 30 and 50 years of age. The cause remains uncertain but may be related to friction between the tendons, their fibrous sheath, and the underlying bony groove caused by movement of the thumb and wrist.
  • The resulting inflammation causes thickening and stenosis of the synovial sheath of the first compartment of the extensor retinaculum (dorsal carpal ligament).

CLINICAL EXAMINATION

 Pain develops over the styloid process of the radius, radiating up the forearm and down the thumb. Occasionally, the pain occurs suddenly after a strain of the wrist. The aching pain, aggravated by use of the hand, gradually intensifies and may sometimes cause considerable weakness and disability.

Physical examination

 A sharp tenderness over the styloid process of the radius, and a visible swelling and palpable thickening of the fibrous sheath may be detected. Sharp pain at this site is often produced by active extension and abduction of the thumb against resistance. The Finkelstein test usually causes severe pain. The Finkelstein test exacerbates the pain, it is performed by flexing the thumb and the placing the wrist in ulnar deviation.

MANAGEMENT AND PROGNOSIS

  • Symptoms are relieved by injecting a corticosteroid into the sheath or placing the forearm, wrist, and thumb in a cast or removable splint for about 1 month, or both.
  • Surgical with the use of local anesthesia, a short transverse incision is made over the sheath on the lateral aspect of the wrist; care must be taken to avoid the sensory branches of the superficial branch of the radial nerve.
  • The thickened sheath is opened with a longitudinal incision through the first compartment, freeing the involved tendons.
  • The incision is then closed. Prognosis is excellent.

Endometrial Biopsy

Endometrial biopsy is an office technique for obtaining tissue samples from the lining of the uterus.

INDICATIONS

Dysfunctional uterine bleeding, postmenopausal bleeding, menorrhagia, infertility (selected cases), endometrial or pelvic infections (e.g., tuberculosis), or other situations in which a tissue diagnosis is indicated. Because it is associated with some discomfort and a small but not insignificant risk of perforation or infections and carries not only the cost of the procedure but also the cost of histologic diagnosis, this procedure is best suited for diagnosis, not screening.

CONTRAINDICATION

Pregnancy, active pelvic inflammatory disease, significant vaginal infection, profuse bleeding, blood dyscrasia. Endometrial biopsy should generally be performed during the first 14 to 16 days of the menstrual cycle to avoid inadvertent disruption of an undiagnosed pregnancy. (Biopsies performed within 10 to 14 days beyond a temperature rise or luteinizing hormone surge will generally not interfere with implantation during that cycle.)

EQUIPMENT

  • Disposable endometrial sampling device (e.g., Accurette, Explora, Gynocheck, Pipelle, Z-Sampler, and others) or reusable curette (Novak or other curette)
  • Sterile single-tooth tenaculum (optional)
  • Sterile uterine sound (optional)
  • Sterile lacrimal duct probe (optional)
  • Skin preparation materials (generally an iodine-based antibacterial solution such as Betadine)
  • Suitable tissue preservation/transportation medium (10% formalin solution or similar)
  • Pelvic examination equipment (examination gloves, lubricant, speculum, light source)

TECHNIQUE

The discomfort of endometrial biopsy may be decreased by premedicating with a single oral dose of a nonsteroidal anti-inflammatory agent given in doses usually used to treat dysmenorrhea. Although this is an office procedure, informed consent is generally considered necessary. The patient is prepared and positioned as for a routine pelvic examination. After the cervix has been visualized, it is disinfected with a topical antiseptic (e.g., Betadine).

When the patient is parous, endometrial sampling often may be accomplished without stabilizing or dilating the cervix; both of these procedures produce mild to moderate discomfort and should be avoided when possible. The sampling device is gently introduced into the uterine cavity and the depth is noted. For suction devices such as the Pipelle or Z-Sampler, the piston is withdrawn (producing a vacuum), and the curette itself is gradually withdrawn by use of a spiral or twisting motion. If an adequate tissue sample is obtained, it should be placed in fixative, completing the procedure. If additional tissue is needed, the piston may be advanced to a point just short of expelling the sample, the device again advanced into the uterine cavity, and the procedure repeated. (If tissue already obtained is to be expelled before attempting a second or subsequent try, care must be taken to avoid contact with the fixative solution or any bacterial contamination.)

Open curettes, such as the Novak, or rigid suction cannula should be gently inserted to the apex of the uterine cavity and then withdrawn in a straight line, using light pressure against the uterine wall. Tissue obtained may be removed from the opening of the curette using the point of a broken (but still sterile) wooden cotton-tipped applicator.

If significant cervical stenosis is encountered (or there is significant patient discomfort) a paracervical block using a few milliliters of 1% lidocaine (or similar) may be appropriate. The use of a lachrymal duct probe may assist in finding the path of the endocervical canal, but its fine size also increases the risk of a “false passage.”

COMPLICATION

Uterine perforation (1 to 2/1000), infection (endometrial, myometrial, pelvic). Vasovagal syncope during the procedure may occur but is generally transient.

Tubal Occlusion Procedure: A Nonsurgical form of Permanent Birth Control

Procedures can be performed either postpartum (during cesarean  section or immediately after vaginal delivery) or interval (remote from a pregnancy). An interval tubal occlusion should be performed in the follicular  phase of the menstrual cycle in order to avoid the time of ovulation and possible pregnancy.

LAPAROSCOPIC TUBAL OCCLUSION

Eighty to ninety percent of tubal occlusions are done laparoscopically. All methods occlude the fallopian tubes bilaterally.

ELECTROCAUTERY

  • This involves the cauterization of a 3-cm zone of the isthmus. It is the most popular method (very effective but most difficult to reverse).


CLIPPING

  • The Hulka-Clemens clip (also Filshie clip), similar to a staple, is applied at a 90-degree angle on the isthmus. It is the most easily reversed method but also has the highest failure rate.

BANDING

    • A length of isthmus is drawn up into the end of the trocar, and a silicone band, or Fallope ring, is placed around the base of the drawn-up portion of fallopian tube.
    •  Small polyester/nickel/titanium/steel coil implant is placed in the proximal  fallopian tube.

  •  Minimally invasive.
  •  Two-year data shows 99.8% efficacy.
  • Alternative contraception needed until tubal occlusion proved by hysterosalpingogram 3 months after implant placed.
  • Mechanism of action: Scarring forms around implant over 3 months and prevents sperm to enter the fallopian tube.

POSTPARTUM TUBAL OCCLUSION

  • Pomeroy method: A segment of isthmus is lifted and a suture is tied around the approximated base. The resulting loop is excised, leaving a gap between the proximal and distal ends. This is the most popular method.
  • Parkland method: A window is made in the mesosalpinx and a segment of isthmus is tied proximally and distally and then excised.
  • Madlener method: Similar to the Pomeroy but without the excision, a segment of isthmus is lifted and crushed and tied at the base.
  • Irving method: The isthmus is cut, with the proximal end buried in the myometrium and the distal end buried in the mesosalpinx.
  • Kroener method: Resection of the distal ampulla and fimbriae following ligation around the proximal ampulla.
  • Uchida method: Epinephrine is injected beneath the serosa of the isthmus. The mesosalpinx is refl ected off the tube, and the proximal end of the tube is ligated and excised. The distal end is not excised. The mesosalpinx is reattached to the excised proximal stump, while the long distal end is left to “dangle” outside of the mesosalpinx.

PARTIAL OR TOTAL SALPINGECTOMY

Removal of part or all of the fallopian tube.

LUTEAL-PHASE PREGNANCY

A luteal-phase pregnancy is a pregnancy diagnosed after tubal sterilization but conceived before. Occurs around 2–3/1000 sterilizations. It is prevented by either performing sensitive pregnancy tests prior to the procedure or performing the procedure during the follicular phase.

REVERSIBILITY OF TUBAL OBSTRUCTION

Around one-third of tubal ligations can be reversed such that pregnancy can result. Pregnancies after tubal ligation reversal are ectopic until proven otherwise.

Renal Cell Cancer in Management

  • Renal Cell Cancer or Hypernephroma is a serious pathological condition of the kidney. Renal cell cancer originates from small renal tubules of the kidney. Kidney tubule functions as a filtering apparatus of the body. The survival rate of the advanced renal cell carcinoma or cancer is usually five years. Renal cell carcinoma is often resistant to radiation and chemotherapy treatment. In this article, we will discuss in detail about the various causes, symptoms, and treatment options for Renal Cell Cancer.

How Do We Define Renal Cell Cancer Or Hypernephroma?

  • Renal Cell Cancer is also known by the name of Hypernephroma.
  • Cancer of Proximal Convoluted Tubule
  • The cancer of the kidneys stems from the lining of proximal convoluted tubule.

Renal Filter

  • Renal symptoms are caused by abnormalities of electrolytes, metabolites and water retention.
  • Capillaries surround the tubule. Capillaries are integrated with proximal tubule. The excessive electrolytes, metabolites and water are filtered in proximal convoluted tubule from capillary blood.
  • Most of the electrolytes and water are reabsorbed into blood.
  • Excessive water and unwanted metabolites are discharged as urine.

Common Cancer

  • Renal Cell Cancer or Hypernephroma is one of the commonest forms of cancer of the kidneys and constitutes for more than 75% of cases of kidney cancer.

Fatal Cancer Growth

  • Renal Cell Cancer or Hypernephroma is also termed to be one of the most lethal tumors of the Genitourinary System.

Non-Metastasize Cancer

  • Non-metastasize cancer is treated by removal of kidney.
  • Survival rate is over 5 years in over 65% of the cases.

Treatment Resistant

  • Renal Cell Cancer is resistant to chemotherapy and radiation treatment, thus metastatic spread is often difficult to treat.
  • Incidental Asymptomatic Renal Cell Tumor.
  • The disease is asymptomatic during initial stage and diagnosis is delayed until cancer is spread in distant organ.

Causes Of Renal Cell Cancer Or Hypernephroma

Age Factor

  • It is usually known to occur in adults in the age range of 50-70.

Hereditary Factor

  • The exact cause of Renal Cell Cancer/Hypernephroma is unknown.
  • Family history of Renal Cell Cancer/Hypernephroma
  • Hereditary is one of the causes not yet eliminated.
  • NSAIDs (Non-Steroidal Anti-Inflammatory Drugs)
  • Long-term use of NSAIDs is associated with cancer of the kidney.

Occupational Hazards

  • Exposure to chemicals- asbestos, cadmium, lead, chlorinated solvents and petrochemicals.

Dialysis

  • Several years of dialysis may be triggering the cancerous activities of the renal cells.
    Risk Factors Of Renal Cell Cancer Or Hypernephroma
  • Hypertension
  • Horseshoe Shaped Kidney
  • Polycystic Renal Disease
  • Tobacco abuse and Obesity.

Symptoms Of Renal Cell Cancer Or Hypernephroma

Nonspecific Symptoms of Renal Cell Cancer Or Hypernephroma

  • Weakness and fatigue
  • Loss of weight
  • Loss of appetite
  • Specific Symptoms of Renal Cell Cancer Or Hypernephroma

Pain

  • Moderate to severe flank pain often radiates to lower back
  • Severe abdominal pain, intensity becomes severe following abdominal examination.

Abdominal Mass

  • Abdominal mass is felt during examination on right or left side of the umbilicus.

Urine Discoloration

  • Urine may be dark brown or red because of bleeding from cancer in to renal tubule.
  • Increased Erythropoietin Secretion
  • Deep vein thrombosis
  • Polycythemia
  • Decreased Erythropoietin Secretion

Pale skin

  • Anemia
  • Increased Angiotensin Secretion

Vision problems

  • Hypertension
  • Night sweating
  • Diagnosis Of Renal Cell Cancer Or Hypernephroma

Urine Examination

  • Hematuria
  • Proteinuria
  • Frank Blood in urine
  • Bacteria in urine

Blood Examination

  • Complete Blood Cell Count (CBC)-
  • White Blood Cell Count- Elevated, if renal cell cancer is associated with kidney or bladder infection.
  • Red Blood Cell Count- Elevated, secondary to increased erythropoietin secretions.
  • Platelet Count- Elevated, secondary to increased secretion of erythropoietin hormone.
  • Hemoglobin
  • Decreased hemoglobin results in anemia secondary to decreased secretion of erythropoietin in few cases.
  • Erythrocyte Sedimentation Rate (ESR)-
  • ESR is elevated.

Kidney Function Test

  • Blood urea nitrogen- Elevated
  • Creatinine- Elevated
  • Liver Enzyme Test- (Elevated If Cancer is Metastasized in Liver)
  • Aspartate Aminotransferase (AST)- Elevated
  • Alanine Aminotransferase (ALT)- Elevated