Wednesday, July 20, 2016

polymorphic eruption of pregnacy

polymorphic eruption of pregnacy is the commonest dermayological condition

in 3rd trimester
vertically abdoman over abdoman ane thigh

pemphigoid gestations/herpes gestations(earlier)
serious vondition usually in 3rd trimester
 cause perinatal motality
intense pluritis,begin periumbilical area and spred limbs and hands
stat with papul and became vesicals and bullus
may be several months post partum

dagnosis by skin Bx and direct immunoflorescence =
C3 compliment depositin the basement membraneof skin

probably due to autoimmune  condition due to fetal antigen

treat with topical or systemic 40mg daily prednisolone






mx of women with heart dx
avid induction of labour if posssible
use prophylactic Ab
ensure fluied balance
avoid supine position
epidural aneasthesia
keep 2nd stage short
use synto judiciusly



if mitral balve area less than 2cm2 , antisipated problems more



Eisenmenger syndrome
associate with very high maternal moatality (50%)
with VSD left to tight shunt and pulmonary HTN
eventually pulmknary HTN/right ventrical pressure goesup more than Left ventrical

cshunt reverse to  right to left

major risk at delivery
with sudden reduction of systemic vasculer ressistanceat delivery leading to right to left huntand desaturation

very high motality

so termination of the pregnacy carefullly discuss wity mother



diabetics in pregnancy
homons affect Carbohydrate(CHO) metabolism


inpregnac6 human placentalnlacyogen and cortisol level are  incresed

both these homones are insuline antagonist and there for mother develops relative insuline resistence

thesechanges are more in 3rd trimester

 to balnce during normal pregnancy maternal pancrease secreate more insuline

how ever in CHO chalange level of glucase is higher tham non pregnant level


glucase gose through the placenta via facilitated diffusion

so when maternal glucause level incease cause to increase fetal glucause

WHO Definition is FBS >7.8 or bld suger 2 hours following a 75g oral glucause  >11.1 mmol/l

impair glucose tolarence is 7.8 to 11.1

HbA1c is good indicater

fetal complication

neural tube defect, congenital HD, all other abnormality



neonayal comlications are respiratory destress syndrom,hypoglyceamia,hypomagneaceamia,polycythemia, hyperbilirubinaemia



diuratic should not use in HTN in pregnancy



Diazoxide (INN; brand name Proglycem[1]) is a potassium channel activator, which causes local relaxation in smooth muscle by increasing membrane permeability to potassium ions.



if pat came with antipartum haemorrage ,rectal and vaginal examination is CONTRAINDICATED before uss examination

if placenta previa sympathomimatics are contraindicated unless woeman is actually labour


cervical dialatation is the bestindication of progression of labour.


rotation of the fetal head (occipito transverse to occipito anterior ) occur in labour



rectocel and cystocel not cause to obstruct labour while anh type of melvic mass does



hydrops fetalis - Google Search



hydrops fetalis
hydrops fetalis - Google Search



Hydrops fetalis is a condition in the fetus characterized by an accumulation of fluid, or edema, in at least two fetal compartments. By comparison, hydrops allantois or hydrops amnion are an accumulation of excessive fluid in the allantoic or amniotic space respectively.



causes for shoulder dystocia - Google Search


lower forcep dilivery vs NVD

cause vaginal tear and , epis
but fetal wise ficep delivery is much better



pudendal nerve block - Google Search



pudendal nerve arise s234,  it cont4ibute to motor fibers to anus,perineal muscle and supply sensory fibers to labia
pudendal nerve block - Google Search


primary pulmonary hypertention has high chance of having maternal death



staphylococcus aureus
postpartum mastitis most commonly vause by coagulase positive staphylococcus aureus



just after birth closer of ductus umbilicalnvein and ductus venosus occur



just after birth increse venous return to right atrium cause increase pressure in RA and closed flap valve of foraman ovale



abotion
spontaneous abotion after choronic villus sampling (at 10weeks ) 1 in 100

2nd trimester aminocenyissis cause abotion 1in 200



Danzole is a progestogen derived from testosterone
it had androgenic side efect

1.weight gain
2,acne
3.fluid retention
4.voice changes


5.it can be adrogenise female uterus if given during pregnacy
cause clitoromegaly and labial fusion

use for effective treatment for endometriosis and menorrhagia

it ruduce the fibrosistic pain in the brest



Isotretinoin
isotretinoin is the best longterm treatment for adolecent uncontrol acne which no respond to OCP or teracyclin. but b4 the treatment pregnacy should be exclused as it is teratogenic




ocp
risks of endometrial and ovarian cancer appear to be reduced with the use of oral contraceptives,

whereas the risks of breast, cervical, and liver cancer appear to be increased
but it reduced the benign brest disease



primary dysmenorrhea
pain usually commencing prior  to menses and persisting for the 1 and 2 days of the period



secondory dysmenorrhes is due to fibrois,endometrosis,adenomyosis,or PID



mis cyvle bleeding, mucus prductiom is due to inccrese eostrogen level at obulation



there are 3 type of decelaration.. early decelaration, late decelaration and variable decelarations

early decelaration not pathalogical

late decelaration may be pa5hological

variable decelarations always  pathological



If  clearr, elastic  mucus at cervice in day 14 what can u say?.

she has adequate oestrogen production

withovulation prgestron level goes high and mucus become thick, celluler, and non elastic



causes for hyperprolactimeamia
1.deficienvynof releasing hypoyhalamic dopamine in70%
2.pitiutary or supra pitiutary adenoma or tumpurprimary25% 3.hypothyroidism
4.suing phenothiazine
5.polycystic kvaries
6.stress


most common site for endometriosus are  ovaries, ut
most common sites for endometriosis are ovaris, utero cervical ligament,pelvic peritonium,slecially pouch of Douglas
sever liver dx is a absolute contraindication of HRT


vaginitis
florid vagonitis with a propuse,yellow, irritating, frothy,offensive discharge is due to
1.trichomonal vaginitis
2.bacterial vaginosis(gardanella infection)

tp confirm do KOH smear and wet smear



adenomysis.. endometrial tissue in myometrium and present with dysmenorrhea and menorrhagia
danazole, gestrinone and GnRh analog use to treat for adenomysis.
generaly treatment induce amenorrhea help to relive pain


anovulatory  cycle =? dysfunctional uterine bleeding


Postpartum fever is defined as a temperature of 38.7 degrees C (101.6 degrees F) or greater for the first 24 hours or greater than 38.0 degrees C (100.4 degrees F) on any two of the first 10 days postpartum.[2]



However, the most common cause of postpartum fever is endometritis, which is inflammation in the lining of the uterus,
endometritis, especially after surgical delivery, parental clindamycin and gentamycin are recommended along with appropriate fluid resuscitation and supportive care.[7]


Other significant causes of postpartum fever (in order of temporal occurrence after delivery) include atelectasis, urinary tract infection/pyelonephritis, surgical wound infection (the case of surgical delivery), septic thrombophlebitis and mastitis.[5] Finally, unusual causes of acute abdominal pain should be considered if clinically appropriate,



erythema toxicum is normal! milia,positional talipis are normal and desaper


neonsttal urticaria=nenatal toxicum


GA in the first trimester is usually calculated from the fetal crown-rump length (CRL). This is the longest demonstrable length of the embryo or fetus, excluding the limbs and the yolk sac.


The GA estimate has a 95% confidence interval of plus or minus 6 days, and it is most accurate between 7 and 10 weeks' amenorrhea


Zyprexa, Zyprexa Relprevv (olanzapine) dosing, indications, interactions, adverse effects, and more


Trigeminal neuralgia (TN), also known as tic douloureux, is a distinctive facial pain syndrome that may become recurrent and chronic


trigeminal neuralgia
TN presents as attacks of stabbing unilateral facial pain, most often on the right side of the face. The number of attacks may vary from less than 1 per day to 12 or more per hour and up to hundreds per day.




Carbamazepine is the best studied drug for TN and the only one with US Food and Drug Administration (FDA) approval for this indication
Lamotrigine and baclofen are second-line therapies
Gabapentin has demonstrated effectiveness in TN, especially in patients with multiple sclerosis
Features of surgical treatment include the following:

Three operative strategies now prevail: percutaneous procedures, gamma knife surgery (GSK), and microvascular decompression (MVD)
Ninety percent of patients are pain-free immediately or soon after any of the operations, [2] but the relief is much more long-lasting with microvascular decompression
Percutaneous surgeries make sense for older patients with medically unresponsive trigeminal neuralgia
Tr7geminal neuralgia




ms
A mid-diastolic rumbling murmur with presystolic accentuation will be heard after the opening snap.[2][9] The murmur is best heard at the apical region and is not radiated. Since it is a low-pitch sound, it is heard best with the bell of the stethoscope.[2] Its duration increases with worsening disease.[2] Rolling the patient toward left as well as isometric exercise will accentuate the murmur. A thrill might be present when palpating at the apical region of the



3rd heart sound - Google Search



polyhydroamniosis
diagnosed when the amniotic fluid index (AFI) is greater than 24 cm

morethan 97 centile



acute and chronic polyhydramnios - Google Search



acute and chronic polyhydramnios - Google Search


osteoma - Google Search



tb lymphadenopathy

emedicine.medscape.com/article/358610-images?imageOrder=4



male uti
Initial inpatient treatment includes intravenous (IV) antimicrobial therapy with a third-generation cephalosporin, such as ceftriaxone; a fluoroquinolone, such as ciprofloxacin; or an aminoglycoside. Antipyretics, analgesics, and adequate IV fluids to restore appropriate circulatory volume and promote adequate urinary flow are also important.

Follow-up urine cultures are warranted in males with UTIs; however, follow-up urethral cultures are not routinely warranted unless the man is symptomatic, in which case the symptoms are likely to be the result of exogenous reinfection.


anemia recognition by serum iron ferritin tibc - Google Search



Keratoacanthoma (KA) is a relatively common low-grade tumor that originates in the pilosebaceous glands and closely resembles squamous cell carcinoma (SCC). In fact, strong arguments support classifying keratoacanthoma as a variant of invasive SCC.[1, 2] In most pathology/biopsy reports, dermatopathologists refer to the lesion as "squamous cell carcinoma, keratoacanthoma-type."

Keratoacanthoma is characterized by rapid growth over a few weeks to months, followed by spontaneous resolution over 4-6 months in most cases. Keratoacanthoma may progress rarely to invasive or metastatic carcinoma. Whether these cases were SCC or keratoacanthoma, the reports highlight the difficulty of distinctly classifying individual cases.[3, 4, 5, 6]




uti mx
All infants <3 months old with suspicion of a UTI or if seriously ill should be referred immediately to a hospital. They require intravenous antibiotic therapy (e.g. cefotaxime) until the temperature has settled, when oral treatment is substituted (see Case History 18.2.)
Case History 18.2

Urinary tract infection
Infants >3 months and children with acute pyelonephritis/upper urinary tract infection (bacteriuria and fever 38oC or bacteriuria and loin pain/tenderness even if fever is <38oC) are usually treated with oral antibiotics with low resistance patterns (e.g. co-amoxiclav for 7–10 days); or else intravenous antibiotics, e.g. cefotaxime is given for 2–4 days followed by oral antibiotics for a total of 7–10 days. The choice of antibiotic is adjusted according to sensitivity on urine culture.
Children with cystitis/lower urinary tract infection (dysuria but no systemic symptoms or signs) can be treated with oral antibiotics for 3 days.



uti prevention
Monday, February 8, 2016
5:08 PM
Antibiotic prophylaxis, although this is controversial. It is often used in those under 2 years of age with a congenital abnormality of the kidneys or urinary tract or who have had an upper urinary tract infection and those with severe reflux. Trimethoprim (2 mg/kg at night) is used most often, but nitrofurantoin or cephalexin may be given. Broad-spectrum, poorly absorbed antibiotics such as amoxicillin should be avoided.




Infection with HCV is self-limited in only a small minority of infected persons. Chronic infection develops in 70-80% of patients infected with HCV.[6] Cirrhosis develops within 20 years of disease onset in 20% of persons with chronic infection.[17] The onset of chronic hepatitis C infection early in life often leads to less serious consequences.
In immunocompetent adults, less than approximately 4% of HBV infections become chronic, whereas up to 90% of perinatally infected infants will have chronic disease.[11] Among children who acquire HBV infection between ages 1 and 5 years, 30-50% become chronically infected




polycythemia vera
Polycythemia vera (PV) is a stem cell disorder characterized as a panhyperplastic, malignant, and neoplastic marrow disorder. Its most prominent feature is an elevated absolute red blood cell mass because of uncontrolled red blood cell production.

Signs and symptoms

Impaired oxygen delivery due to sludging of blood may lead to the following symptoms:

Headache
Dizziness
Vertigo
Tinnitus
Visual disturbances
Angina pectoris
Intermittent claudication
Bleeding complications, seen in approximately 1% of patients with PV, include epistaxis, gum bleeding, ecchymoses, and gastrointestinal (GI) bleeding. Thrombotic complications (1%) include venous thrombosis or thromboembolism and an increased prevalence of stroke and other arterial thromboses.

Physical examination findings may include the following:

Splenomegaly (75% of patients)
Hepatomegaly (30%)
Plethora
Hypertension
Practice Essentials
Polycythemia vera (PV) is a stem cell disorder characterized as a panhyperplastic, malignant, and neoplastic marrow disorder. Its most prominent feature is an elevated absolute red blood cell mass because of uncontrolled red blood cell production.

Signs and symptoms

Impaired oxygen delivery due to sludging of blood may lead to the following symptoms:

Headache
Dizziness
Vertigo
Tinnitus
Visual disturbances
Angina pectoris
Intermittent claudication
Bleeding complications, seen in approximately 1% of patients with PV, include epistaxis, gum bleeding, ecchymoses, and gastrointestinal (GI) bleeding. Thrombotic complications (1%) include venous thrombosis or thromboembolism and an increased prevalence of stroke and other arterial thromboses.

Physical examination findings may include the following:

Splenomegaly (75% of patients)
Hepatomegaly (30%)
Plethora
Hypertension
Diagnosis

According to 2008 revised World Health Organization (WHO) guidelines, diagnosis of PV requires the presence of both major criteria and one minor criterion or the presence of the first major criterion together with two minor criteria.

Major WHO criteria are as follows:

Hemoglobin > 18.5 g/dL in men and > 16.5 g/dL in women, or other evidence of increased red blood cell volume
Presence of JAK2617V F or other functionally similar mutation, such as JAK2 exon 12 mutationMinor WHO criteria are as follows:
See the list below:

Bone marrow biopsy showing hypercellularity for age with trilineage growth (panmyelosis) with prominent erythroid, granulocytic, and megakaryocytic proliferation
Serum erythropoietin level below the reference range for normal
Endogenous erythroid colony formation in vitro
Management

Treatment measures are as follows:

Phlebotomy – To keep hematocrit below 45%
Aspirin – 81 mg daily
Cytoreductive therapy – For patients at high risk for thrombosis
Splenectomy in patients with painful splenomegaly or repeated episodes of splenic infarction
Hydroxyurea is the most commonly used cytoreductive agent. If hydroxyurea is not effective or not tolerated, alternatives include the following:

Interferon alfa
Busulfan – In patients older than 65 years
Ruxolitinib (Jakafi)








Leprosy
Leprosy is a chronic infection caused by the acid-fast, rod-shaped bacillus Mycobacterium leprae. Leprosy can be considered 2 connected diseases that primarily affect superficial tissues, especially the skin and peripheral nerves. Initially, a mycobacterial infection causes a wide array of cellular immune responses. These immunologic events then elicit the second part of the disease, a peripheral neuropathy with potentially long-term consequences.
Although both lepromatous leprosy and tuberculoid leprosy involve the skin and peripheral nerves, tuberculoid leprosy has more severe manifestations. Nerve involvement results in loss of sensory and motor function, which may lead to frequent trauma and amputation. The ulnar nerve is most commonly involved.

Damage in the following nerves is associated with characteristic impairments in leprosy:
Ulnar and median - Clawed hand
Posterior tibial - Plantar insensitivity and clawed toes
Common peroneal -Foot drop
Radial cutaneous, facial, and greater auricular nerves (may also be involved; as seen in the image below)
Infiltration by bacteria may lead to destruction of nasal cartilage (lepromatous leprosy), ocular involvement, and diffuse thickening of the skin. Advanced cases of leprosy involve the loss of eyebrows and lashes, but these deformities are less common today.
Worldwide, leprosy is considered the most common cause of crippling of the hand, which is caused by ulnar nerve involvement. [6] Peroneal nerve involvement can lead to foot drop
Painless skin patch accompanied by loss of sensation but not itchiness (Loss of sensation is a feature of tuberculoid leprosy, unlike lepromatous leprosy, in which sensation is preserved.
Lagophthalmos, iridocyclitis, corneal ulceration, and/or secondary cataract due to nerve damage and direct bacillary skin or eye invasion
The incubation period of leprosy is long, ranging from a few months to 20-50 years. The mean incubation time is estimated to be 10 years for lepromatous leprosy and 4 years for tuberculoid leprosy.
Lepromatous leprosy
This form is characterized by extensive bilaterally symmetric cutaneous involvement, which can include macules, nodules, plaques, or papules. Multiple flat hypopigmented lesions are seen in the image below.
Unlike lesions in tuberculoid leprosy, those in lepromatous leprosy have poorly defined borders and raised and indurated centers. As in all forms of leprosy, lepromatous lesions are worst on cooler parts of the body. Common areas of involvement include the face, ears, wrists, elbows, buttocks, and knees.
Hoarseness, loss of eyebrows and eyelashes, and nasal collapse secondary to septa perforation may occur in advanced cases of disease. Involvement of the eye may include keratitis, glaucoma, or iridocyclitis as seen in the image below.
Hypopigmented or reddish skin lesions with loss of sensation
Involvement of the peripheral nerves as demonstrated by their thickening and associated loss of sensation
Skin smear positive for acid-fast bacilli
Laboratory studies include the following:

Skin biopsy, nasal smears, or both are used to assess for acid-fast bacilli using Fite stain. Biopsies should be full dermal thickness taken from an edge of the lesion that appears most active. [8]

serologic assay
Medical Care
In response to the increased incidence of dapsone resistance, the WHO introduced a multidrug regimen in 1981 that includes rifampicin, dapsone, and clofazimine. Some clinical studies have also shown that certain quinolones, minocycline, and azithromycin have activity against M leprae. The WHO recently recommended single-dose treatment with rifampin, minocycline, or ofloxacin in patients with paucibacillary leprosy who have a single skin lesion. However, the WHO still recommends the use of the long-term multidrug regimens whenever possible because they have been found to be more  efficacious.


CTG deceleration
A deceleration is a decrease in the fetal heart rate below the fetal baseline heart rate.
1.early decelaration
2late decelarationa
3.varible decelaration

1. An early deceleration is defined as a waveform with a gradual decrease and return to baseline with time from onset of the deceleration to the lowest point of the deceleration (nadir....nimnaya) >30 seconds. The nadir of the early deceleration occurs with the peak of a contraction.
Early decelerations appear to be caused by vagal discharge produced when the head is compressed by uterine contractions. The onset and depth of early decelerations mirror the shape of the contraction, and tend to be proportional to the strength of the contraction.
2. A late deceleration also has a waveform with a gradual decrease and return to baseline with time from onset of the deceleration to nadir >30 seconds. However, the late deceleration is “shifted to the right” of the contraction.
Late decelerations occur when a fall in the level of oxygen in the fetal blood triggers chemoreceptors in the fetus to cause reflex constriction of blood vessels in nonvital peripheral areas in order to divert more blood flow to vital organs such as the adrenal glands, heart, and brain. Constriction of peripheral blood vessels causes hypertension that stimulates a baroreceptor mediated vagal response which slows the heart rate. The time consumed in this two step process accounts for the delay in the timing of the deceleration relative to the contraction
Late decelerations with good variability (“reflex lates”) are sometimes caused by excessive uterine contractions or maternal hypotension which may be alleviated by correcting the underlying cause. In conditions with reduced placental exchange such as intrauterine growth restriction (IUGR) measures to improve blood flow and oxygen delivery to the fetus may not be as effective.
3 Variable Decelerations

Variable decelerations are irregular, often jagged dips in the fetal heart rate that look more dramatic than late decelerations. Variable decelerations happen when the baby’s umbilical cord is temporarily compressed. This happens during most labors. The baby depends on steady blood flow through the umbilical cord to receive oxygen and other important nutrients. It can be a sign that the baby’s blood flow is reduced if variable decelerations happen over and over. Such a pattern can be harmful to the baby.




Somatization disorder (also Briquet's syndrome) is a mental disorder characterized by recurring, multiple, and current, clinically significant complaints about somatic symptoms. It was recognized in the DSM-IV-TR classification system, but in the latest version DSM-5, it was combined with undifferentiated somatoform disorder to become somatic symptom disorder, a diagnosis which no longer requires a specific number of somatic symptoms


Cyanosis in a newborn infant with respiratory distress (respiratory rate >60 breaths/min) may be due to:
Cardiac disorders – cyanotic congenital heart disease
Respiratory disorders, e.g. surfactant deficiency, meconium aspiration, pulmonary hypoplasia, etc.
Persistent pulmonary hypertension of the newborn (PPHN) – failure of the pulmonary vascular resistance to fall after birth
Infection – septicaemia from group B streptococcus and other organisms
Metabolic disease – metabolic acidosis and shock.
Whether the presentation of congenital heart disease is with a heart murmur, heart failure, cyanosis or shock depends on the underlying anatomic lesion causing:
left to right shunt
right to left shunt
common mixing
outflow obstruction in the well or sick child.



Acute treatment of proven crystal-induced arthritis is directed at relief of the pain and inflammation. Nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, colchicine, and adrenocorticotropic hormone (ACTH) are treatment options. The choice is based primarily on whether the patient has any concomitant health problems (eg, renal insufficiency or peptic ulcer disease). Colchicine, a classic treatment, is now rarely indicated.



gout tx
Therapy to control the underlying hyperuricemia generally is contraindicated until the acute attack is controlled (unless kidneys are at risk because of an unusually heavy uric acid load). Starting therapy to control hyperuricemia during an acute attack may intensify and prolong the attack. If the patient has been on a consistent dosage of probenecid or allopurinol at the time of the acute attack, however, the drug should be continued at that dosage during the attack.

Furthermore, control of hyperuricemia generally is not pursued for a single attack. If attacks are recurrent or evidence of tophaceous or renal disease is present, therapy for control of hyperuricemia is indicated.[1



treat for uric acid stone
1.hydration
2.urine alkalization
3.Llopurinol

Preeclampsia is defined as the presence of (1) a systolic blood pressure (SBP) greater than or equal to 140 mm Hg or a diastolic blood pressure (DBP) greater than or equal to 90 mm Hg or higher, on two occasions at least 4 hours apart in a previously normotensive patient, OR  (2) an SBP greater than or equal to 160 mm Hg or a DBP greater than or equal to 110 mm Hg or higher (In this case, hypertension can be confirmed within minutes to facilitate timely antihypertensive therapy.).[1]

In addition to the blood pressure criteria, proteinuria of greater than or equal to 0.3 grams in a 24-hour urine specimen, a protein (mg/dL)/creatinine (mg/dL) ratio of 0.3 or higher, or a urine dipstick protein of 1+ (if a quantitative measurement is unavailable) is required to diagnose preeclampsia.[1]

Preeclampsia with severe features is defined as the presence of one of the following symptoms or signs in the presence of preeclampsia[1] :

SBP of 160 mm Hg or higher or DBP of 110 mm Hg or higher, on two occasions at least 4 hours apart while the patient is on bed rest (unless antihypertensive therapy has previously been initiated)
Impaired hepatic function as indicated by abnormally elevated blood concentrations of liver enzymes (to double the normal concentration), severe persistent upper quadrant or epigastric pain that does not respond to pharmacotherapy and is not accounted for by alternative diagnoses, or both.
Progressive renal insufficiency (serum creatinine concentration >1.1 mg/dL or a doubling of the serum creatinine concentration in the absence of other renal disease)
New onset cerebral or visual disturances
Pulmonary edema
Thrombocytopenia (platelet count <100,000/μL)
In a patient with new-onset hypertension without proteinuria, the new onset of any of the following is diagnostic of preeclampsia:

Platelet count below 100,000/μL
Serum creatinine level above 1.1 mg/dL or doubling of serum creatinine in the absence of other renal disease
Liver transaminase levels at least twice the normal concentrations
Pulmonary edema
Cerebral or visual symptoms
Eclampsia is defined as seizures that cannot be attributable to other causes in a woman with preeclampsia. HELLP syndrome (hemolysis, elevated liver enzyme, low platelets) may complicate severe preeclampsia.



ACE inhibitors are probably second-line antihypertensives for patients with unilateral renal artery stenosis and two kidneys. First-line antihypertensives are diuretics, beta-blockers and calcium-channel blockers. Bilateral renal artery stenosis, or a unilateral stenosis in a patient with only one kidney, is an absolute contraindication to ACE inhibition



Antiphospholipid syndrome is an autoimmune disease, in which "antiphospholipid antibodies" (anticardiolipin antibodies and lupus anticoagulant) react against proteins that bind to anionic phospholipids on plasma membranes.
IgM is the immediate antibody that is produced once a human body is exposed to a bacteria, virus or a toxin
2. IgG is found throughout the body, mainly in most of the bodily fluids, while IgM is found mainly in the blood and lymphatic fluids.
3. IgM is larger in size compared to IgG
4. IgM is temporary and disappears after a few weeks. It is then replaced by IgG.



Autism spectrum disorder (ASD) manifests in early childhood and is characterized by qualitative abnormalities in social interactions, markedly aberrant communication skills, and restricted repetitive behaviors, interests, and activities (RRBs).



Siblings of children with autism are at risk for developing traits of autism and even a full-blown diagnosis of autism. Therefore, siblings should also undergo screening not only for autism-related symptoms but also for language delays, learning difficulties, social problems, and anxiety or depressive symptoms.[1



Sideroblastic anemia or sideroachrestic anemia is a form of anemia in which the bone marrow produces ringed sideroblasts rather than healthy red blood cells (erythrocytes).[1] In sideroblastic anemia, the body has iron available but cannot incorporate it into hemoglobin, which red blood cells need to transport oxygen efficiently. The disorder may be caused either by a genetic disorder or indirectly as part of myelodysplastic syndrome,[2] which can evolve into hematological malignancies (especially acute myelogenous leukemia).





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