These things you must know about Male and Female Epispadias

These things you must know about Male and Female Epispadias

Epispadias is a rare congenital abnormality that involves the opening of the urethra. It can occur in male as well as in female.
In Male – The urethra opens in the top of the penis rather than the tip.


In Female – The urethral opening is towards the clitoris or even in the belly area.

Frequency – It occurs more commonly in males than in females, with a prevalence of 1 case in 10,000 – 50,000 persons.
The male to female ratio is 2.3 : 1


Epispadias from Front View
Epispadias from Front View





Etiology – There are more than one hypothesis about epispadias.
1. Defective migration of paired primordia of  the genital tubercle that usually fuse on the midline to form the genital tubercle at the fifth week of embryonal development.
2. Another hypothesis relates the defect to the abnormal developement  of the cloacal membrane.
Classification – Usually Epispadias are of three types.
1. Glandular – Malformation affects the distal part of the urethra.
2. Penile – Entire penile urethra is affected, with an external meatus on the dorsal shaft of the penis.
3. Complete or Penopubic type – total deficiency of the dorsal wall of the urethra.

How epispadias are diagnosed ?
Epispadias is most often noticed at birth during physical examination. If the defect is mild, it might not be detected at first.
In some cases, it might not be noticed until the child has been toilet trained and presents with urine leak. This is most common eith girls.

Epispadias from Lateral View
Epispadias from Lateral View

Treatment – Surgery is the treatment of choice for epispadias.
The main goals of the treatment are –
1. Make sure the penis works properly
2. Make the penis of a good length.
3. Fix bends in the penis ( dorsal bend and chordae)
4. Make the penis look normal
5. If the bladder and bladder neck are affected, surgery will be needed to make sure that the child can control his urine
6. Surgery might also be needed to preserve fertility.

You must know these things about Embolism

You must know these things about Embolism


  • An embolus is a detached intravascular solid, liquid, or gaseous mass that is carried by the blood from its point of origin to a distant site, where it often causes tissue dysfunction or infarction.
  • The vast majority of emboli are dislodged thrombi, hence the term thromboembolism.
  • Other rare emboli are composed of fat droplets, nitrogen bubbles, atherosclerotic debris (cholesterol emboli), tumor fragments, bone marrow, or even foreign bodies.
  • Emboli travel through the blood until they encounter vessels too small to permit further passage, causing partial or complete vascular occlusion.

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Types of Emboli

Some important types of embolism

  • Pulmonary Embolism:
  1. Pulmonary emboli originate from deep venous thromboses and are the most common form of thromboembolic disease.
  2. Incidence since the 1970s of roughly 2 to 4 per 1000 hospitalized patients in the United States.
  3. PE causes about 100,000 deaths per year in the United States.
  4. In more than 95% of cases, PEs originates from leg DVT.
  5. Course of embolus causing Pulmonary Embolism

  1. Rarely, a venous embolus passes through an interatrial or interventricular defect and gains access to the systemic arterial circulation (paradoxical embolism).
  2. Most pulmonary emboli (60% to 80%) are clinically silent because they are small. With time they become organized and are incorporated into the vascular wall; in some cases organization of the thromboembolus leaves behind a delicate, ridging fibrous web.
  3. Sudden death, right heart failure (cor pulmonale), or cardiovascular collapse occurs when emboli obstruct 60% or more of the pulmonary circulation.
  4. Embolic obstruction of medium-sized arteries with subsequent vascular rupture can result in pulmonary hemorrhage but usually does not cause pulmonary infarction. This is because the lung is supplied by both the pulmonary arteries and the bronchial arteries, and the intact bronchial circulation is usually sufficient to perfuse the affected area. Understandably, if the bronchial arterial flow is compromised (e.g., by left-sided cardiac failure), infarction may occur.
  5. Embolic obstruction of small end-arteriolar pulmonary branches often does produce hemorrhage or infarction.
  6. Multiple emboli over time may cause pulmonary hypertension and right ventricular failure.

Figure- Embolus from a lower extremity deep venous thrombosis,

lodged at a pulmonary artery branchpoint.

Systemic Thromboembolism

  1. Most systemic emboli (80%) arise from intracardiac mural thrombi, two thirds of which are associated with left ventricular wall infarcts and another one fourth withleft atrial dilation and fibrillation. The remainder originates from aortic aneurysms, atherosclerotic plaques, valvular vegetations, or venous thrombi (paradoxical emboli);10% to 15% are of unknown origin.
  2. Arterial emboli are in contrast to venous emboli, the vast majority of which lodge in the lung, arterial emboli can travel to a wide variety of sites; the point of arrest depends on the source and the relative amount of blood flow that downstream tissues receive.
  3. The emboli are arterial and invariably cause infarction at the sites of lodgement . These sites, in descending order of frequency are: lower extremities (75%) or the brain (10%), internal visceral organs; the intestines, kidneys, spleen, and upper extremities, may be involved on occasion.
  4. The consequences of systemic emboli depend on the vulnerability of the affected tissues to ischemia, the caliber of the occluded vessel, and whether a collateral blood supply exists; in general, however, the outcome is tissue infarction.

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Fat and Marrow Embolism

  1. Microscopic fat globules—sometimes with associated hematopoietic bone marrow—can be found in the pulmonary vasculature after fractures of long bones or, rarely, in the setting of soft tissue trauma and burns. Presumably these injuries rupture vascular sinusoids in the marrow or small venules, allowing marrow or adipose tissue to herniated into the vascular space and travel to the lung.
  2. Fat and marrow emboli are very common incidental findings after vigorous cardiopulmonary resuscitation and are probably of no clinical consequence. Indeed, fat embolism occursin some 90% of individuals with severe skeletal injuries but less than 10% of such patients have any clinical findings.
  3. Fat embolism syndrome is the term applied to the minority of patients who become symptomatic. It is characterized by pulmonary insufficiency, neurologic symptoms, anemia, and thrombocytopenia, and is fatal in about 5% to 15% of cases. Typically, 1 to 3 days after injury there is a sudden onset of tachypnea, dyspnea, and tachycardia; irritability and restlessness can progress to delirium or coma.
  4. Thrombocytopenia is attributed to platelet adhesion to fat globules and subsequent aggregation or splenic sequestration; anemia can result from similar red cell aggregation and/or hemolysis.
  5. A diffuse petechial rash (seen in 20% to 50% of cases) is related to rapid onset of thrombocytopenia and can be a useful diagnostic feature.
  6. Fat microemboli and associated red cell and platelet aggregates can occlude the pulmonary and cerebral microvasculature.
  7. Release of free fatty acids from the fat globules exacerbates the situation by causing local toxic injury to endothelium, and platelet activation and granulocyte recruitment (with free radical, protease, and eicosanoid release) complete the vascular assault. Because lipids are dissolved out of tissue preparations by the solvents routinely used in paraffin embedding, the microscopic demonstration of fat microglobules typically requires specialized techniques, including frozen sections and stains for fat.

Figure– Bone marrow embolus in the pulmonary circulation. The cellular elements on the left side of the embolus are hematopoietic cells, while the cleared vacuoles represent marrow fat. The relatively uniform red area on theright of the embolus is an early organizing thrombus.

Air Embolism

  1. Gas bubbles within the circulation can coalesce to form frothy masses that obstruct vascular flow and cause distal ischemic injury.
  2. For example, a very small volume of air trapped in a coronary artery during bypass surgery, or introduced into the cerebral circulation by neurosurgery in the “sitting position,” can occlude flow with dire consequences.
  3. A particular form of gas embolism, called decompression sickness, occurs when individuals experience sudden decreases in atmospheric pressure.
  4. Scuba and deep sea divers, underwater construction workers, and individuals in unpressurized aircraft in rapid ascent are all at risk. When air is breathed at high pressure (e.g., during a deep sea dive), increased amounts of gas (particularly nitrogen) are dissolved in the blood and tissues. If the diver then ascends (depressurizes) too rapidly, the nitrogen comes out of solution in the tissues and the blood.
  5. The rapid formation of gas bubbles within skeletal muscles and supporting tissues in and about joints is responsible for the painful condition called the bends
  6. In the lungs, gas bubbles in the vasculature cause edema, hemorrhage, and focal atelectasis or emphysema, leading to a form of respiratory distress called the chokes. A more chronic form of decompression sickness is called caisson disease (named for the pressurized vessels used in bridge construction; workers in these vessels suffered both acute and chronic forms of decompression sickness).
  7. In caisson disease, persistence of gas emboli in the skeletal system leads to multiple foci of ischemic necrosis; the more common sites are the femoral heads, tibia, and humeri. Individuals affected by acute decompression sickness are treated by being placed in a chamber under sufficiently high pressure to force the gas bubbles back into solution. Subsequent slow decompression permits gradual resorption and exhalation of the gases, which prevents the

obstructive bubbles from reforming.

Amniotic Fluid Embolism

  1. Amniotic fluid embolism is the fifth most common cause of maternal mortality worldwide; it accounts for roughly 10% of maternal deaths in the United States and results in permanent neurologic deficit in as many as 85% of survivors.
  2. Amniotic fluid embolism is an ominous complication of labor and the immediate postpartum period.
  3. Although the incidence is only approximately 1 in 40,000 deliveries, the mortality rate is up to 80%. The onset is characterized by sudden severe dyspnea, cyanosis, and shock, followed by neurologic impairment ranging from headache to seizures and coma.
  4. If the patient survives the initial crisis, pulmonary edema typically develops, frequently accompanied by disseminated intravascular coagulation.
  5. The underlying cause is the infusion of amniotic fluid or fetal tissue into the maternal circulation via a tear in the placental membranes or rupture of uterine veins.
  6. Classicfindings at autopsy include the presence of squamous cells shed from fetal skin, lanugo hair, fat from vernix caseosa, and mucin derived from the fetal respiratory or gastrointestinal tract in the maternal pulmonary microvasculature
  7. Other findings include marked pulmonary edema, diffuse alveolar damage and the presence of fibrin thrombi in many vascular beds due to disseminated intravascular coagulation.

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Figure-Amniotic fluid embolism. Two small pulmonary arterioles are packed with laminated swirls of fetal squamous cells. There is marked edema and congestion. Elsewhere the lung contained small organizing thrombi consistent with disseminated intravascular coagulation. (Courtesy Dr. Beth Schwartz, Baltimore, Md.)

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Explain Why Adrenaline is used in Anaphylactic Shock

Explain Why Adrenaline is used in Anaphylactic Shock

Explain why Adrenaline is used in Anaphylactic Shock. Anaphylaxis is a severe form of life threateing allergic reaction that causes swelling of  mouth and tongue, breathing problems, flushing, collapse and a loss of consciousness. Adrenaline is used as a treatment for anaphylaxis.


Adrenaline is the life saving drug for the treatment of anaphylactic shock. Adrenaline 0.3 – 0.5 ml of 1:1000 solution (1 mg/ml) is administered intramuscularly.

◙ Causative agents of Anaphylactic Shock : Anaphylaxis or anaphylactic shock can be triggered by these agents peanuts, shellfish, and insect bites or stings. These can cause severe anaphylactic reaction or allergic reaction lead to anaphylactic shock.

◙ Symptoms of Anaphylaxis :

►Vasodilation → Peripheral Resistance↓ → BP↓


►Hypotension – BP ↓

►Increased vascular permeability↑

►Activation of vagal pathways

◙ Mechanism of Action:

Adrenaline produces the following effect :

►ß1- medicated cardiac stimulation → HR↑ + FOC↑

►α1 – mediated vasoconstriction → Peripheral Resistance↑ →BP↑

►α1 – mediated vasoconstriction → Mucosal Oedema ↓

►ß2 stimulation → Bronchodilation + ↓Release of mediators from Mast cells

►Physiologic Antagonist of Histamine → ↓Release of mediators from Mast cells

That explains Why Adrenaline is used in Anaphylactic Shock.

Uses of Adrenaline as Treatment of Anaphylactic Shock:

A patient with a history of allergic attack should be considered for Adrenaline. This is available in the market as a auto-injector or pen. Administration of adrenaline on certain attack will eliminate the chances of death.

Type of medicine Sympathomimetic
Used for Anaphylactic Shock
Medicine Name Emerade®; EpiPen®; Jext®
Available as Auto-injection device or ‘pen’

Questions Type : Explain Why

Chapter : Autonomic Nervous System

Explain Why Adrenaline is used in Anaphylactic Shock.

Information can be seen from Essential of Medical Pharmacology by KDT and Shanbhag 

Explain Why Propanolol should be avoided in bronchial asthma

Difference between Hypertrophy and Hyperplasia

Difference between Hypertrophy and Hyperplasia

The question is Comment on the Difference between Hypertrophy and Hyperplasia.

Hypertrophy and Hyperplasia are two related terms often both occurs together causing enlargement of the organ or tissue. But they are not similar terms. Both are caused by increase functional demand or by hormonal influence. They has a basic difference.


Hypertrophy – Increase in the size of the cell . Number of cells unchanged.

Hyperplasia – Increase in the number of cells. Size of the cells unchanged.

Morphological Changes:-

Hypertrophy – Increase synthesis of DNA, RNA. Increase protein Synthesis. Increase number of cell organelles like mitochondria.

Hyperplasia – Increase number of cells due to increase rate of DNA synthesis

Types: – 


a. Physiological :

Enlarged size of uterus in pregnancy.

Increased muscle mass in Body Builders.

b. Pathological : 

i) Adaptive: Hypertrophy of Cardiac, Smooth and Skeletal Muscle

ii) Compensatory: Hypertrophy of compensatory organ on removal of contralateral organ. Nephrectomy of one kidney causes hypertrophy of the other.


a. Physiological : 

i) Hormonal –

1. Hyperplasia of breast at puberty, during lactation and pregnancy

2. Hyperplasia of prostate in Old age,

3. Hyperplasia of pregnant uterus.

ii) Compensatory: Hyperplsia occurs when a part of an organ or the contralateral organ in case of paired organ is removed.

  1. Regeneration of liver following partial hepatectomy.
  2. Hyperplasia of the other kidney following nephrectomy on one side.
  3. Regeneration of epidermis after skin abarasion

b. Pathological : 

i) Hormonal –

  1. Endometrial Hyperplasia
  2. Benign Prostaic hyperplasia
  3. Hyperplasia of thyroid in thyrotoxicosis

ii) Irritation –

  1. Hyperplasia of lymphoid tissue in infections
  2. Intraductal epithelial hyperplasia in fibrocystic changes in breast.
  3. Epidermal Hyperplasia – Skin warts due to HPV, Pseudocarcinamatous hyperplasia at the margin of non-healing ulcer.
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