pediagenosis: Health
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Showing posts with label Health. Show all posts
Showing posts with label Health. Show all posts

Wednesday, June 23, 2021

Shock

Shock

Shock

Clinical manifestations of shock.

Figure 2-1 Clinical manifestations of shock.

Shock is an acute clinical syndrome of circulatory dysfunction in which there is failure to deliver sufficient oxygen and substrate to meet metabolic demand. All practitioners who care for children must understand and identify shock promptly to initiate an effective treatment plan. This, in turn, can help prevent the progression and poor outcomes that characterize the natural clinical course of shock. The goal is to prevent end-organ damage; failure of multiple organ systems; and, ultimately, death.


ETIOLOGY AND PATHOGENESIS

Normal circulatory function is maintained by the interplay between the heart and blood flow with the purpose of delivering oxygen and nutrients to the tissues. Cardiac output is calculated by multiplying the stroke volume (volume of blood ejected by the left ventricle in a single beat) by the heart rate (ejection cycles per minute). Stroke volume is dependent on the filling volume of the ventricle (preload), resistance against which the heart is pumping blood (afterload), and myocardial contractility. During childhood, the heart rate is faster, and the stroke volume is smaller than during adulthood. In children, increasing the heart rate is the primary means to increase the cardiac output. Shock develops as the result of conditions that cause decreased intravascular volume, abnormal distribution of intravascular volume, or impaired cardiovascular function. Children effectively compensate for circulatory insufficiency by increasing their heart rate, systemic vascular resistance (SVR), and venous tone. Children can therefore maintain normal blood pressures despite significantly compromised tissue perfusion. Thus, in pediatric patients, it is especially important to recognize that hypotension is not part of the definition of shock.

The clinical manifestations of shock can be directly related to the abnormalities seen on the tissue, cellular, and biochemical levels. Microcirculatory dysfunction; tissue ischemia; and release of biochemical, vasoactive, and inflammatory mediators are all part of the spectrum of pathophysiologic aberrations seen in shock. Poor perfusion of vital organs results in impaired function. For example, inadequate perfusion of the brain and kidneys results in depressed mental status and decreased urine output, respectively. As poorly perfused cells switch to anaerobic metabolism to generate energy, lactic acid accumulates resulting in a metabolic acidosis that further interferes with cell function. Hypoperfusion also initiates inflammatory events, such as the activation of neutrophils and release of cytokines, that cause cell damage and microischemia.

The prevalence of causes of shock varies by patient age, as well as region of the world. Hypovolemic shock from diarrheal illness is the leading cause of pediatric mortality worldwide, but is very rare in the United States. Congenital lesions (including heart disease) and complications of prematurity are most common in neonates and infants. Malignant neoplasms (for whom infectious complications are prevalent), infectious causes, and unintentional injuries are more common in older children and young adolescents. Injury, homicide, and suicide become more prevalent in older adolescents.

 

Compensated (Early) Shock

In compensated shock, homeostatic mechanisms have temporarily balanced metabolic supply and demand. In this state, the systolic blood pressure is normal in the presence of inadequate tissue perfusion. The earliest symptoms of shock result from an effort to maintain cardiac output and perfusion of vital organs (heart, brain, and kidneys). The body’s initial mechanism to maintain cardiac output and compensate for low stroke volume is to increase heart rate (tachycardia). Other compensatory mechanisms include increasing SVR, cardiac contractility, and venous tone. As shock continues, the early compensatory mechanisms fail to meet the metabolic demands of the tissues, and uncompensated shock ensues. Here, as the microcirculation is affected, the child shows signs of brain, kidney, and cardiovascular compromise.

 

Uncompensated (Late) Shock

Uncompensated shock occurs when attempts to maintain blood pressure and perfusion are no longer successful, resulting in hypotension. When hypotension develops, the child’s condition may deteriorate rapidly to cardiovascular collapse and subsequent cardiac arrest. Eventually, the child in uncompensated shock develops multiple organ dysfunction syndrome (MODS) secondary to ongoing shock and exaggerated inflammatory responses. Irreversible shock implies irreversible damage to vital organs resulting in death, regardless of therapy.

 

CLASSIFICATION OF SHOCK

Hypovolemic Shock

The most common type of shock in children is hypovolemic shock. Hypovolemia is defined as a decrease in circulating blood volume. The most common cause of hypovolemic shock is fluid loss associated with diarrhea and vomiting. Other causes include blood losses (e.g., trauma and gastrointestinal disorders), plasma losses (peritonitis, hypoproteinemia, burns), and water losses (osmotic diuresis, heatstroke). In hypovolemic shock, preload is decreased, SVR may be increased as a compensatory mechanism, and cardiac contractility is typically normal or may be increased.

 

Distributive Shock

Distributive shock is the result of abnormal distribution of blood volume (i.e., poor flow to the splanchnic circulation with excessive flow to the skin) caused by vasodilatation from changes in vasomotor tone and peripheral pooling of blood, resulting in inadequate tissue perfusion. SVR can be low, producing increased blood flow to the skin that keeps the extremities warm (warm shock), as well as a widened pulse pressure and bounding peripheral pulses. Conversely, SVR may be increased, resulting in decreased blood flow to the skin, resulting in cool extremities, with a narrowed pulse pressure and weak pulses (cold shock). Generally, cardiac output is normal or increased. Distributive shock commonly occurs in anaphylaxis; central nervous system or spinal injuries; drug ingestions; and most commonly in children, sepsis.

 

Cardiogenic Shock

Cardiogenic shock results from myocardial dysfunction and can usually be distinguished from other forms of shock because of associated signs of congestive heart failure (i.e., rales, gallop rhythm, hepatomegaly, jugular venous distension). Pump failure, arrhythmias, and congenital heart disease may all contribute to the inadequate perfusion seen in cardiogenic shock. A patient may exhibit tachycardia, increased SVR, and signs of decreased cardiac output as a result of a decrease in myocardial contractility. Causes of cardiogenic shock in children include viral myocarditis, arrhythmias, drug ingestions, complications of cardiac surgery, trauma, metabolic derangements, and congenital heart disease. Cardiogenic shock can also occur with obstruction of blood flow, as seen with a tension pneumothorax, massive pulmonary embolism, or critical coarctation of the aorta or other obstructive vascular lesions. A patient may also show evidence of both intrinsic cardiac disease and obstruction of blood flow with a cardiac tamponade or ductal-dependent congenital abnormality. It is important to recognize that infants that present with shock caused by a ductal-dependent cardiac lesion require blood flow through the ductus arteriosus to maintain adequate oxygen delivery.

 

Neurogenic Shock

Neurogenic shock may occur in the setting of pediatric trauma. Spinal cord injury may produce hypotension caused by a loss of sympathetic tone. The classic picture of neurogenic shock is hypotension without tachycardia or cutaneous vasoconstriction. The pulse pressure is usually widened. Patients sustaining spinal injuries often have concurrent torso trauma. Therefore, patients with known or suspected neurogenic shock should be treated initially for hypovolemia.

 

Septic Shock

Sepsis is defined as the presence of the systemic inflammatory response syndrome (SIRS) caused by a presumed or confirmed infection (Box 2-1). Sepsis may occur because of bacterial, viral, fungal, or parasitic infections. Septic shock is defined as sepsis and cardiovascular dysfunction. Classifying septic shock may be difficult because of the developmental variability in physiologic response to sepsis. A clinical picture consistent with hypovolemic, distributive, or cardiogenic shock may be present in a child with sepsis. Additionally, studies have demonstrated that the cardiovascular pathophysiology of children with sepsis can evolve over time, and the adjustment of hemodynamic therapy is commonly necessary.

 


CLINICAL MANIFESTATIONS AND EVALUATION

Shock remains a clinical diagnosis (Figure 2-1). Early recognition of the clinical signs of shock (including familiarity with normal ranges for vital signs by age; see Chapter 1) should lead to directed management. An accurate history should be obtained from the family and, if possible, the child, simultaneously with treatment initiation.

A history of fluid loss, as with a gastrointestinal bleed, gastroenteritis, or diabetic ketoacidosis, is consistent with hypovolemic shock. A detailed trauma history is useful because an injured child may have hypovolemic shock from hemorrhage (i.e., with blunt abdominal trauma), neurogenic shock with spinal cord injury, or obstructive shock from tension pneumo- thorax. A child who has had fever or is immunocompromised may have features consistent with septic shock. Exposure to an allergen, such as a food or an insect bite, could suggest distributive shock caused by anaphylaxis. A history of ingestion or medications should always be included when speaking to the family because shock may be attributable to toxin exposure. Patients with underlying heart disease may present in cardiogenic shock. Patients with a history of adrenal insufficiency (i.e., chronic steroid therapy, congenital adrenal hyperplasia, or hypopituitarism) can present with adrenal crisis and shock.

A complete physical examination should be performed, including vital signs and pulse oximetry. When a child presents in shock, it is sometimes difficult to obtain an accurate weight, which can be essential for determining fluid requirements and medication doses. If the patient’s weight cannot be measured, one may be estimated using a length-based tape system (e.g., the Broselow tape) or the child’s age.

Children in shock tend to be tachypneic, as well as tachycardic. Blood pressure should be monitored closely. Remember, children with shock may have normal blood pressures. Narrow pulse pressure may occur as a result of a compensatory increase in SVR, as in hypovolemic or cardiogenic shock. Widening of the pulse pressure can be seen as the result of decreased SVR, as can occur with distributive shock. The child’s temperature should also be measured because fever—or in young infants, hypothermia—may suggest septic shock.

When first examining an ill child, one should do a rapid assessment of mental status. Change in the level of consciousness of a child may indicate decreased cerebral oxygenation or perfusion. Signs of diminished perfusion to the brain include confusion, irritability, lethargy, and agitation.

Examining the child’s skin is another way to assess perfusion and the degree of shock. A child with normal cardiorespiratory function should have warm and pink nailbeds, mucous membranes, palms, and soles. As shock progresses and poor perfusion develops, the skin may become cool, pale, or mottled. Capillary refill, although limited by clinician variability as well as ambient temperature and the child’s body temperature, can help to evaluate children in shock. Light pressure is applied to blanch the fingernail bed. The pressure is released, and the amount of time until color returns is measured. Normal is less than 2 seconds; volume depletion or poor perfusion can increase this time to greater than 3 seconds.

The evaluation of a child with poor perfusion and shock should always include an assessment of pulses. This includes the rate, strength, and regularity of the central and peripheral pulses. In healthy children, the carotid, brachial, radial, femoral, dorsalis pedis, and posterior tibial pulses are readily palpable. A rapid pulse is a nonspecific clinical sign of distress. An irregular pulse is a warning of cardiac dysrhythmia. A weak pulse raises the concern for shock and a severe hypovolemic state. An absence of central pulses indicates ineffective or absent cardiac contractions and signifies the need for immediate resuscitative action.

After the initial evaluation of airway, breathing, and circulation (the ABCs), a complete physical examination can help elucidate the type of shock. For example, central cyanosis, a gallop rhythm, crackles on lung examination, hepatomegaly, or heart murmur may indicate an underlying cardiac condition. Children with stridor, wheeze, urticaria, or edema may have anaphylactic shock. Purpura or petechiae can be seen in children with septic shock. Bruises and abrasions can be seen with traumatic injury and may give a clue to underlying hemorrhagic shock.

Algorithm for management of pediatric septic shock.

Figure 2-2 Algorithm for management of pediatric septic shock. 



MANAGEMENT

General Principles

Early recognition of compensated shock is critical to ensuring appropriate and expedient therapy. Initial therapy of shock is universal, regardless of the cause of the shock state, with the goals of optimizing blood oxygen content, improving cardiac output, reducing oxygen demand, and correcting metabolic abnormalities (Figure 2-2). General principles of resuscitation should be applied immediately on presentation to medical care (see Chapter 1). Ultimately, after initial management has commenced, correction of the underlying cause is essential (e.g., stopping blood loss in hemorrhagic shock, antibiotics for shock caused by bacterial infection).

Immediate attention to the ABCs is mandatory. Maintenance of a patent airway with positioning or endotracheal intubation should be performed immediately if airway compromise is present. Hypoxemia should be corrected without delay; all patients with compromised perfusion should receive supple- mental oxygen at 100% FiO2 (fraction of inspired oxygen). Insufficient respiratory effort should be addressed with positive-pressure ventilation.

Imminently life-threatening causes of shock should be identified and corrected. For example, a child with upper airway obstruction from anaphylaxis should receive epinephrine. If a child has severe respiratory distress, asymmetric breath sounds, and poor perfusion, a tension pneumothorax might need to be decompressed.

Vascular access is indicated in all cases. If possible, large-bore intravenous (IV) catheters should be inserted in peripheral veins. If an IV line is unable to be placed promptly, intraosseous (IO) cannulation should be performed. IV fluid boluses of 20 mL/kg of isotonic saline should be given rapidly and repeated as needed with reassessment occurring simultaneously. Rapid fluid administration should be actively performed using either a pressure bag or a push–pull system rather than using passive gravity flow for administration. IV fluids should be given with care in cardiogenic shock, so as to not worsen associated pulmonary edema.

Adequate hemoglobin is essential for optimal oxygen carrying capacity. Thus, in cases of hemorrhagic shock, O-negative packed red blood cells should be rapidly administered early in the resuscitation. Even in cases of nontraumatic shock, children who have cyanotic heart disease or neonates may require less fluid and higher hematocrit percentages to ensure adequate oxygen carrying capacity. Life-threatening metabolic abnormalities should be identified and corrected early. Hypoglycemia should be treated with 0.5 to 1 g/kg of IV dextrose. Hypocalcemia (especially decreased ionized calcium) is common in septic shock and can occur as acidosis resolves; it should be corrected with either calcium gluconate or calcium chloride.

 

Circulatory Support

Depending on the cause, patients in shock may require large volumes of fluid as well as vasoactive medications. Clinical studies of septic shock in children have demonstrated an association between higher volumes of fluid administration and survival. Current guidelines for septic shock recommend up to and over 60 mL/kg in the first 15 to 60 minutes. Every hour that goes by without implementation of this therapy is associated with a 1.5-fold increase in mortality. A retrospective chart review of 90 children with septic shock showed that those who received less than 20 mL/kg of fluid within the first hour had a mortality rate of 73%. Early fluid resuscitation was associated with a threefold reduction in the odds of death.

Vasoactive agents help improve cardiac output through their effects on myocardial contractility, heart rate, and vascular tone.

These drugs target at least three types of receptors. The β1- receptors mediate inotropic (contractility), chronotropic (rate), and dromotropic (increased conduction velocity) activity. The β2-receptors mediate vasodilatation and smooth muscle relaxation in blood vessels and bronchial tree. The α-receptors mediate arteriole constriction systemically and bronchial muscle constriction. The dopaminergic receptors mediate smooth muscle relaxation and increase renal blood flow and sodium excretion.

Table 2-1 outlines commonly used vasoactive agents, their targeted receptors, and their hemodynamic effects. Data are varied on the choice of initial agent; current recommendations from the American College of Critical Care Medicine state that dopamine, epinephrine, or norepinephrine may be appropriate first-line therapy for septic shock, provided they are administered through a central venous catheter. Dopamine or low-dose epinephrine may be given via a peripheral vein while central venous access is obtained.

 


Special Circumstances: Shock in Neonates

Neonatal physiology poses specific challenges regarding the management of shock. As mentioned previously, optimal oxygen-carrying capacity may demand a higher hematocrit in a newborn. Hypoxemia may occur more readily because of the presence of smaller and fewer alveoli, absent collateral channels of ventilation, and poor chest wall compliance; uncorrected hypoxemia may result in bradycardia in neonates. Additionally, myocardial performance is more drastically affected by acidosis and hypocalcemia in neonates. Prompt correction of hypoxemia, acidosis, and hypocalcemia is essential. Neonates are also more prone to hypoglycemia, which should be looked for and treated appropriately.

When faced with a neonate with shock, early consideration should be given to ductal-dependent congenital heart disease. Lesions marked by ductal-dependent systemic blood flow, such as aortic stenosis, hypoplastic left heart syndrome, coarctation of the aorta, and interrupted aortic arch, may present as shock in the neonatal period (see Chapter 44). Infants with these lesions depend on blood flow from the pulmonary artery across the ductus arteriosus into the aorta for perfusion of all or part of the systemic circulation. Although this is deoxygenated blood, the oxygen content is sufficient to meet the metabolic demands of the tissues. Therefore, when the ductus arteriosus closes, circulatory failure and tissue hypoxia occur.

Prostaglandin E1 (PGE1 or alprostadil) is the definitive initial therapy for neonates with ductal-dependent congenital heart disease who have not yet undergone surgical palliation or correction. An infusion at 0.1 µg/kg/min is required to reopen a closing ductus arteriosus. Side effects of prostaglandin include flushing, hypotension, pyrexia, bradycardia, seizures, and apnea. Emergent evaluation by a pediatric cardiologist should be pursued, but initiation of PGE1 therapy should not be delayed pending the evaluation.

 

FUTURE DIRECTIONS

Current research in shock in children is predominantly in the realm of septic shock. Goal-directed therapy of septic shock, an established concept in adults, is less well investigated in children and will continue to be an important topic in future investigations. Diagnostic laboratory studies, such as serum lactate and B-type natriuretic peptide levels, may hold promise in early detection and ongoing monitoring of children with shock. Newer noninvasive techniques for cardiac output measurement (e.g., pulse contour waveform analysis, partial carbon dioxide rebreathing) have begun to be used successfully in children and may be applied more broadly in the years to come. Massive transfusion therapy in children with hemorrhagic shock is another area in which advances in therapy for adults are beginning to be investigated in pediatric patients. Additional advanced critical care therapies, such as steroid or thyroid hormone replacement, renal replacement therapy, newer hemodynamic agents (e.g., levosimendan), and extracorporeal circulatory support, have been studied in pediatric patients, but their exact role remains unclear.

Tuesday, June 8, 2021

Resuscitation

Resuscitation

Resuscitation

Figure 1-1 Pediatric and adult airway anatomy.
Figure 1-1 Pediatric and adult airway anatomy.


Cardiopulmonary gency interventi or in respiratory extre PR)  is the series of emergency interventions provided to a person who appears dead or in respiratory extremis, with the goal of restoring vital functions through optimization of cardiac output and tissue oxygen delivery. The two main components are external cardiac massage (chest compressions) and assisted respirations.

Saturday, May 29, 2021

Sideroblastic Anaemia

Sideroblastic Anaemia


Sideroblastic Anaemia
This is a refractory anaemia defined by the presence of many pathological ring sideroblasts in the bone marrow (Fig. 3.14). These are abnormal erythroblasts containing numerous iron granules arranged in a ring or collar around the nucleus instead of the few randomly distributed iron granules seen when normal erythroblasts are stained for iron. There is also usually erythroid hyperplasia with ineffective erythropoiesis. Sideroblastic anaemia is diagnosed when 15% or more of marrow erythroblasts are ring sideroblasts. They can be found at lower numbers in a variety of haematological conditions.

Figure 3.14 Ring sideroblasts with a perinuclear ring of iron granules in sideroblastic anaemia.

Sideroblastic anaemia is classified into different types (Table 3.8) and the common link is a defect in haem synthesis. In the hereditary forms the anaemia is usually characterized by a markedly hypochromic and microcytic blood picture. The most common mutations are in the ALA‐S gene which is on the X chromosome. Pyridoxal‐6‐phosphate is a coenzyme for ALA‐S. Other rare types include an X‐linked disease with spinocerebellar degeneration and ataxia, mitochondrial defects (e.g. Pearson’s syndrome when there is also pancreatic insufficiency), thiamine‐responsive and other autosomal defects. The much more common form is refractory anaemia with ring sideroblasts, which is a subtype of myelodysplasia (see Chapter 16). Acquired reversible forms may be due to alcohol, lead and drugs, e.g. isoniazid.
Lead Poisoning

Lead Poisoning


Lead Poisoning
Haemoglobin synthesis in the developing red cell
Figure 2.7  Haemoglobin synthesis in the developing red cell. The mitochondria are the main sites of protoporphyrin synthesis, iron (Fe) is supplied from circulating transferrin; globin chains are synthesized on ribosomes. δ‐ALA, δ‐aminolaevulinic acid; CoA, coenzyme A.

       Lead inhibits both haem and globin synthesis at a number of points. In addition it interferes with the breakdown of RNA by inhibiting the enzyme pyrimidine 5′ nucleotidase, causing accumulation of denatured RNA in red cells, the RNA giving an appearance called basophilic stippling on the ordinary (Romanowsky) stain (see Fig. 2.17). 
Differential Diagnosis Of Hypochromic

Differential Diagnosis Of Hypochromic


Differential Diagnosis Of Hypochromic
Table 3.7 Laboratory diagnosis of a hypochromic anaemia.


anaemia
Table 3.7 lists the laboratory investigations that may be neces­ sary. The clinical history is particularly important as the source of the haemorrhage leading to iron deficiency or the presence of a chronic disease may be revealed. The country of origin and the family history may suggest a possible diagnosis of thalassaemia or other genetic defect of haemoglobin. Physical examination may also be helpful in determining a site of haemorrhage, features of a chronic inflammatory or malignant disease, koilonychia or, in some haemoglobinopathies, an enlarged spleen or bony deformities.

Friday, November 15, 2019

Anaemia Of Chronic Disorders

Anaemia Of Chronic Disorders


Anaemia Of Chronic Disorders
One of the most common anaemias occurs in patients with a variety of chronic inflammatory and malignant diseases (Table 3.6). The characteristic features are:

1.    Normochromic, normocytic or mildly hypochromic (MCV rarely <75 fL) indices and red cell morphology.
2.    Mild and non‐progressive anaemia (haemoglobin rarely <90 g/L) – the severity being related to the severity of the disease.
3.    Both the serum iron and TIBC are reduced.
4.    The serum ferritin is normal or raised.
5.  Bone marrow storage (reticuloendothelial) iron is normal but erythroblast iron is reduced (Table 3.7).

Tuesday, September 3, 2019

Iron Deficiency

Iron Deficiency


Iron Deficiency
Clinical features
When iron deficiency is developing, the reticuloendothelial stores (haemosiderin and ferritin) become completely depleted before anaemia occurs (Fig. 3.6). As the condition develops, the patient may show the general symptoms and signs of anaemia (see p. 20) and also a painless glossitis, angular stomatitis, brittle, ridged or spoon nails (koilonychia) (Fig. 3.7) and unusual dietary cravings (pica). The cause of the epithelial cell changes is not clear but may be related to reduction of iron‐containing enzymes. In children, iron deficiency is particularly significant as it can cause irritability, poor cognitive function and a decline in psychomotor development. There is also evidence that oral or parenteral iron may reduce fatigue in iron‐deficient (low serum ferritin) non‐anaemic women.

Thursday, August 22, 2019

Neural Plasticity And Neurotrophic Factors I: The Peripheral Nervous System

Neural Plasticity And Neurotrophic Factors I: The Peripheral Nervous System


Neural Plasticity And Neurotrophic Factors I: The Peripheral Nervous System
The peripheral nervous system (PNS) is capable of significant repair, to some extent independent of the age at which damage occurs. In contrast, the central nervous system (CNS) has always been thought of as being unable to repair itself, although there is now mounting evidence for considerable plasticity within it even in the adult state and that most, if not all areas of the CNS, are capable of some degree of reorganization (see Chapter 49).
Emotion, Motivation And Drug Addiction

Emotion, Motivation And Drug Addiction


Emotion, Motivation And Drug Addiction
Emotion
Initial attempts to understand the brain bases of emotions focused on the limbic system (see Chapter 45), with the amygdala as the key component in the system thought to be central to emotional processing. The evidence to support such an association has already been discussed in part (in Chapter 45), but it is also worth mentioning the Klüver–Bucy syndrome. This condition is seen with bilateral amygdala damage and is characterized by, among other phenomena, an apparent absence of the normal fear response and by marked placidity.

Wednesday, August 7, 2019

Oogenesis

Oogenesis


Oogenesis
Time period: week 12 to menopause
Overview
Female germ cells proliferate by mitosis in the ovaries to form a large number of oogonia. These cells are diploid, contain two X sex chromosomes, and will become haploid mature oocytes via the process of oogenesis. This process is similar to spermatogene- sis but has some significant differences.
The germ cells that will form the female gametes (oocytes) are derived from germ cells that migrate from the yolk sac into the site of early gonad formation (see Chapter 38).
Spermatogenesis

Spermatogenesis


Spermatogenesis
Time period: puberty to death
Meiosis continued
In the last chapter we talked about the importance of meiosis in sexual reproduction and diversity, and saw how haploid cells are formed. In males, meiosis occurs during spermatogenesis, in which spermatogonia in the testes become spermatozoa.
The germ cells that will form the male gametes (spermatozoa) are derived from germ cells that migrate from the yolk sac into the site of early gonad formation (see Chapter 38).
Meiosis

Meiosis


Meiosis
Time period: day 0 to adult
Diversity
Cell division by mitosis gives no opportunity for change or diversity, which is ideal for processes like growth and repair. In humans, sex- ual reproduction allows random mingling of maternal and paternal DNA to produce a new, unique individual. This is able to occur because of a different type of cell division called meiosis.

Sunday, August 4, 2019

Lung Cancer

Lung Cancer


Lung Cancer
More people die in the USA and Europe from lung cancer than from breast, prostate and colon cancer combined. Furthermore, the number of cases is likely to increase in the next 25 years due to continued use of cigarettes, particularly in women. Lung cancer has a worse prognosis than other common cancers, with an overall 5-year survival of 13%.
The Immunocompromised Host

The Immunocompromised Host


The Immunocompromised Host
The immune system is most frequently impaired after chemotherapy and in patients with human immunodeficien y virus (HIV) infection. Immunodeficien y also occurs in patients with malignancies of the lym- phoproliferative system (e.g. leukaemia), immediately following bone marrow transplants (BMT) and in those on immunosuppressive drugs (e.g. steroids and azothioprine) particularly after transplant surgery (e.g. renal). Malnutrition or chronic illness (e.g. diabetes) may also impair immunity. Respiratory disease is particularly common in the immunocompromised host.

Friday, July 26, 2019

Memory

Memory


Memory
The term memory is commonly used to refer to the ability to remember information but it is important to understand that there are several different types of memory that subserve different functions. In the first instance, there is a distinction between motor and non-motor memories – the former is a form of implicit memory and typically involves the cerebellum, motor cortical areas and basal ganglia (see Chapters 38–42) and will not be discussed further in this chapter. The other forms of memory are more involved with the taking in, manipulating and storing of information for problem solving (working memory), events and factual knowledge (explicit memory).
Limbic System And Long-Term Potentiation

Limbic System And Long-Term Potentiation


Limbic System And Long-Term Potentiation
Anatomy of the limbic system
Many different definitions of the limbic system exist, and in this chapter we will be restricting our definition to structures that lie primarily along the medial aspect of the temporal lobe: cingulate gyrus, parahippocampal structures (postsubiculum, parasubiculum, presubiculum and perirhinal cortex), entorhinal cortex, hippocampal complex (dentate gyrus, CA1–CA4 subfields and subiculum), septal nuclei and the amygdala. Additional structures closely associated with the limbic system include the mammillary bodies of the hypothalamus, the olfactory cortex and the nucleus accumbens (see Chapters 11, 30, 42 and 47, respectively).
Consciousness And Theory Of Mind

Consciousness And Theory Of Mind


Consciousness And Theory Of Mind
In this chapter we discuss what is meant by consciousness, and how this can be altered in certain pathological conditions. This ability to be aware of what we are doing, namely consciousness, is then discussed further in terms of how we can understand the thought processes of others, so-called theory of mind, disorders of which may underlie a range of conditions, especially autism.

Tuesday, July 16, 2019

Male Reproduction Pathophysiology

Male Reproduction Pathophysiology


Male Reproduction Pathophysiology
Clinical background
Male infertility has a large number of causes, both endocrine and non-endocrine in origin and few are specifically treatable. In the majority of cases an exact diagnosis is not reached despite investigation and the condition may result from previous testicular damage, varicocoele or non-specific inflammation. All patients should be assessed with their partner in a specialist fertility unit and in the undiagnosed group the use of intracytoplasmic sperm injection may offer the best chance of fertility. The clinical features of male infertility are shown in Table 33.1.
Male Reproduction Actions of Androgens

Male Reproduction Actions of Androgens


Male Reproduction Actions of Androgens
Clinical scenario
Effects of the failure of androgen action may be best seen in patients with hypogonadotrophic hypogonadism (Fig. 32a). This is caused by a failure of hypothalamic GnRH secretion or by pituitary disease resulting in impaired gonadotrophin release and hence low androgen concentrations (Table 32.1). The clinical features of hypogonadotrophic hypogonadism depend on the timing of its onset, such that males developing the condition after puberty present with features of secondary testicular failure (poor libido, loss of secondary sexual characteristics and subfertility). Prior to puberty, boys present with delayed or failed puberty or, less commonly, the condition presents in the neonatal period with cryptorchidism and micropenis Idiopathic hypogonadotrophic hypogonadism describes those patients in whom there are no anatomical abnormalities of the hypothalamus and pituitary and no associated endocrine disorders.
Male Reproduction The Testis

Male Reproduction The Testis


Male Reproduction The Testis
Clinical background
Normal fertility in the male is produced by a complex interac- tion between genetic, autocrine, paracrine and endocrine function. The endocrine control of reproductive function in the male depends upon an intact hypothalamo–pituitary–testicular axis. The testis has a dual role – the production of spermatozoa and the synthesis and secretion of testosterone needed for the development and maintenance of secondary sexual characteristics and essential for maintaining spermatogenesis. These functions in turn depend upon the pituitary gonadotrophin hormones: luteinizing hormone (LH; required to stimulate testicular Leydig cells to produce testosterone); and follicle stimulating hormone (FSH; required for the development of the immature testis and a possible role in adult spermatogenesis). Gonadotrophin production occurs in response to stimulation by hypothalamic GnRH. Testosterone exerts a negative feedback on the secretion of LH and FSH and the hormone inhibin-β, also synthesized by the testis, has a specific regulatory role for FSH. Thus in primary seminiferous tubular failure, low testosterone concentrations are associated with elevated gonadotrophins whereas in the presence of hypothalamic pituitary disease the gonadotrophin concentrations are low (secondary testicular failure).

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