Introduction to Allergic purpura

Allergic purpura, or anaphylactoid purpura, is a type of nonthrombocytopenic purpura. It’s characterized by allergy symptoms and acute or chronic vascular inflammation affecting the skin, joints, or GI or genitourinary (GU) tract. When allergic purpura primarily affects the GI tract with accompanying joint pain, it’s called Henoch-Schönlein syndrome or anaphylactoid purpura. However, the term allergic purpura applies to purpura associated with many other conditions, such as erythema nodosum. An acute attack of allergic purpura can last for several weeks and is potentially fatal (usually from renal failure); however, most patients do recover.
Fully developed allergic purpura is persistent and debilitating, possibly leading to chronic glomerulonephritis (especially following a streptococcal infection). Allergic purpura affects more males than females and is most prevalent in children ages 3 to 7. The prognosis is more favorable for children than for adults.
Causes
The most common identifiable cause of allergic purpura is probably an autoimmune reaction directed against vascular walls, triggered by a bacterial infection (particularly streptococcal infection). Typically, an upper respiratory tract infection occurs 1 to 3 weeks before the onset of symptoms. Other possible causes include allergic reactions to some drugs and vaccines, allergic reactions to insect bites, and allergic reactions to some foods (such as wheat, eggs, milk, and chocolate).
Signs and symptoms
Allergic purpura is characterized by purple skin lesions that are macular, ecchymotic, and varying Continue reading “Introduction to Allergic purpura”

Brief Summary on Snakebites, poisonous

Poisonous snakebites are most common during summer afternoons in grassy or rocky habitats. Poisonous snakebites are medical emergencies. With prompt, correct treatment, they need not be fatal.
Causes
The only poisonous snakes in the United States are pit vipers (Crotalidae) and coral snakes (Elapidae). Pit vipers include rattlesnakes, water moccasins (cottonmouths), and copperheads. They have a pitted depression between their eyes and nostrils and two fangs, ¾? to 1¼? (2 to 3 cm) long. Because fangs may break off or grow behind old ones, some snakes may have one, three, or four fangs.
Because coral snakes are nocturnal and placid, their bites are less common than pit viper bites; pit vipers are also nocturnal but are more active. The fangs of coral snakes are short but have teeth behind them. Coral snakes have distinctive red, black, and yellow bands (yellow bands always border red ones), tend to bite with a chewing motion, and may leave multiple fang marks, small lacerations, and much tissue destruction.
Signs and symptoms
Most snakebites happen on the arms and legs, below the elbow or knee. Bites to the head or trunk are most dangerous, but any bite into a blood vessel is dangerous, regardless of location.
Most pit viper bites that result in envenomation cause immediate and progressively severe pain and edema (the entire extremity may swell within a few hours), local elevation in skin temperature, fever, skin discoloration, petechiae, ecchymoses, blebs, blisters, bloody wound discharge, and local necrosis.
Because pit viper venom is neurotoxic, pit viper bites may cause local and facial numbness and Continue reading “Brief Summary on Snakebites, poisonous”

Special considerations in Case Of Skull Fracture

  • Establish and maintain a patent airway; nasal airways are contraindicated in patients with possible basilar skull fractures. Intubation may be necessary.
  • Suction the patient through the mouth, not the nose, to prevent the introduction of bacteria in case a CSF leak is present.
  • Be sure to obtain a complete history of the trauma from the patient, his family, any eyewitnesses, and ambulance personnel.
  • Ask whether the patient lost consciousness and, if so, for how long. The patient will need further diagnostic tests, including a complete neurologic examination, a CT scan, and other studies.
  • Check for abnormal reflexes such as Babinski’s reflex.
  • Look for CSF draining from the patient’s ears, nose, or mouth. Check bed linens for CSF leaks, and look for a halo sign. If the patient’s nose is draining CSF, wipe it—don’t let him blow it. If an ear is draining, cover it lightly with sterile gauze—don’t pack it.
  • Position the patient with a head injury so secretions can drain properly. Elevate the head of the bed 30 degrees if intracerebral injury is suspected.
  • Cover scalp wounds carefully with a sterile dressing; control any bleeding as necessary.
  • Take seizure precautions, but don’t restrain the patient. Agitated behavior may stem from hypoxia or increased ICP, so check for these symptoms. Speak in a calm, reassuring voice, and touch the patient gently. Don’t make any sudden, unexpected moves.
When a skull fracture requires surgery:

Acute respiratory failure in COPD

In patients with essentially normal lung tissue, acute respiratory failure (ARF) usually means a partial pressure of arterial carbon dioxide (PaCO2) greater than 50 mm Hg and a partial pressure of arterial oxygen (PaO2) less than 50 mm Hg. These limits, however, don’t apply to patients with chronic obstructive pulmonary disease (COPD), who commonly have a consistently high PaCO2 and low PaO2. In COPD patients, only acute deterioration in arterial blood gas (ABG) levels and corresponding clinical deterioration indicate ARF.
Causes
ARF may develop in COPD patients from any condition that increases the work of breathing and decreases the respiratory drive. Such conditions include respiratory tract infection (such as bronchitis or pneumonia), which is the most common precipitating factor; bronchospasm; or accumulating secretions secondary to cough suppression. Other causes include:
  • central nervous system (CNS) depression—head trauma or injudicious use of sedatives, narcotics, tranquilizers, or oxygen
  • cardiovascular disorders—myocardial infarction, heart failure, or pulmonary emboli
  • airway irritants—smoke or fumes
  • endocrine and metabolic disorders—myxedema or metabolic alkalosis
  • thoracic abnormalities—chest trauma, pneumothorax, or thoracic or abdominal surgery.
Signs and symptoms
In COPD patients with ARF, increased ventilation-perfusion mismatching and reduced alveolar ventilation decrease PaO2 (hypoxemia) and increase PaCO2 (hypercapnia). This rise in carbon Continue reading “Acute respiratory failure in COPD”

Introduction to Retinal Detachment

When the sensory retina splits from the retinal pigment epithelium, retinal detachment occurs, creating a subretinal space. This space then fills with fluid, called subretinal fluid. Retinal detachment usually involves only one eye but may involve the other eye later.
Surgical reattachment is often successful. However, the prognosis for good vision depends on the area of the retina that’s been affected.
Causes
Any retinal tear or hole allows the liquid vitreous to seep between the retinal layers, separating the retina from its choroidal blood supply. In adults, retinal detachment usually results from degenerative changes of aging, which cause a spontaneous retinal hole.
Predisposing factors include myopia, cataract surgery, and trauma. Perhaps the influence of trauma explains why retinal detachment is twice as common in males.
Retinal detachment may also result from seepage of fluid into the subretinal space (because of inflammation, tumors, or systemic diseases) or from traction that’s placed on the retina by vitreous bands or membranes (from proliferative diabetic retinopathy, posterior uveitis, or a traumatic intraocular foreign body).
Retinal detachment is rare in children but occasionally can develop as a result of retinopathy of prematurity, tumors (retinoblastomas), or trauma. It can also be inherited, usually in association with myopia.
Signs and symptoms
Initially, the patient may complain of floating spots and recurrent flashes of light. But as detachment progresses, gradual, painless vision loss may be described as a veil, curtain, or Continue reading “Introduction to Retinal Detachment”

Male Infertility

Male infertility may be suspected whenever a couple fails to achieve pregnancy after about 1 year of regular unprotected intercourse. Between 40% and 50% of infertility problems in the United States are totally or partially attributed to the male.
Causes
Factors that cause male infertility include:
  • varicocele, a mass of dilated and tortuous varicose veins in the spermatic cord
  • semen disorders, such as volume or motility disturbances or inadequate sperm density
  • proliferation of abnormal or immature sperm, with variations in the size and shape of the head
  • systemic disease, such as diabetes mellitus, neoplasms, liver or kidney disease, or viral disturbances, especially mumps orchitis
  • genital infection, such as gonorrhea, tuberculosis, or herpes
  • disorders of the testes, such as cryptorchidism, Sertoli-cell–only syndrome, varicocele, ductal obstruction (caused by absence or ligation of the vas deferens or infection), hydrocele (collection of fluid in the testes), or infection (orchitis and epididymitis).
  • genetic defects, such as Klinefelter’s syndrome (chromosomal pattern XXY, eunuchoidal habitus, gynecomastia, and small testes) or Reifenstein’s syndrome (chromosomal pattern 46XY, reduced testosterone, azoospermia, eunuchoid-ism, gynecomastia, and hypospadias)
  • immune disorders, such as autoimmune infertility and allergic orchitis
  • endocrine imbalance (rare) that disrupts pituitary gonadotropins, inhibiting spermatogenesis, testosterone production, or both; such imbalances occur with Kallmann’s syndrome, panhypopituitarism, hypothyroidism, and congenital adrenal hyperplasia
  • chemicals and drugs that can inhibit gonadotropins or interfere with spermatogenesis, such as arsenic, methotrexate, medroxyprogesterone acetate, nitrofurantoin, monoamine Continue reading “Male Infertility”

Granulocytopenia and lymphocytopenia

In granulocytopenia, a marked reduction in the number of circulating granulocytes occurs. Although this implies that all the granulocytes (neutrophils, basophils, and eosinophils) are reduced, granulocytopenia usually refers only to decreased neutrophils.
This disorder, which can occur at any age, is associated with infections and ulcerative lesions of the throat, GI tract, other mucous membranes, and skin. Its most severe form is known as agranulocytosis.
Lymphocytopenia (lymphopenia), a rare disorder, is a deficiency of circulating lymphocytes (leukocytes produced mainly in lymph nodes).
In granulocytopenia and lymphocytopenia, the total white blood cell (WBC) count may reach dangerously low levels (less than 500/µl), leaving the body unprotected against infection. The prognosis in both disorders depends on the underlying cause and whether it can be treated. Untreated, severe granulocytopenia can be fatal in 3 to 6 days.

Causes
Granulocytopenia and lymphocytopenia have several causes.
Granulocytopenia
Granulocytopenia may result from decreased production of granulocytes in bone marrow, increased peripheral destruction of granulocytes, or greater utilization of granulocytes.
Decreased production of granulocytes in bone marrow generally stems from radiation or drug therapy; it’s a common adverse effect of antimetabolites and alkylating agents and may occur in the patient who is hypersensitive to phenothiazines, sulfonamides (and some sulfonamide derivatives such as chlorothiazide), antibiotics, or antiarrhythmic drugs.
Drug-induced granulocytopenia usually develops slowly and typically correlates with the dosage and duration of therapy. Production of granulocytes also decreases in such conditions as aplastic anemia and bone marrow cancers and in some hereditary disorders such as infantile genetic agranulocytosis.
Loss of peripheral granulocytes is due to increased splenic sequestration, diseases that destroy peripheral blood cells (viral and bacterial infections), and drugs that act as haptens (carrying antigens that attack blood cells and causing acute idiosyncratic or non-dose-related drug Continue reading “Granulocytopenia and lymphocytopenia”

Introduction to Bell’s palsy

Bell’s palsy is a neurologic disorder that affects the seventh cranial (facial) nerve, producing unilateral facial weakness or paralysis. Onset is rapid. Although it affects all age-groups, it’s most common in persons younger than age 60. In 80% to 90% of patients, it subsides spontaneously, with complete recovery in 1 to 8 weeks; however, recovery may be delayed in older adults. If recovery is partial, contractures may develop on the paralyzed side of the face. Bell’s palsy may recur on the same or opposite side of the face.

Causes
The seventh cranial nerve is responsible for motor innervation of the facial muscles. With Bell’s palsy, the nerve is blocked by an inflammatory reaction around the nerve (usually at the internal auditory meatus). This is commonly associated with infections (most likely herpes simplex) and can result from hemorrhage, tumor, meningitis, or local trauma.
Signs and symptoms
Bell’s palsy usually produces unilateral facial weakness, occasionally with aching pain around the angle of the jaw or behind the ear. On the weak side, the mouth droops (causing the patient to drool saliva from the corner of his mouth), and taste perception is distorted over the affected anterior portion of the tongue. In addition, the forehead appears smooth, and the patient’s ability to close his eye on the weak side is markedly impaired. When he tries to close this eye, it rolls upward (Bell’s phenomenon) and shows excessive tearing. The patient also has hypersensitivities to sound.
Although Bell’s phenomenon occurs in those without Bell’s palsy, it isn’t apparent because the eye closes completely and covers this eye motion. In Bell’s palsy, incomplete eye closure makes this upward motion obvious.
Diagnosis
Patients with Bell’s palsy typically have a distorted facial appearance and inability to raise the Continue reading “Introduction to Bell’s palsy”