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Showing posts with label Organ. Show all posts
Showing posts with label Organ. Show all posts

Wednesday, April 14, 2021

Hypopituitarism and Non-Functioning Pituitary Adenomas

Hypopituitarism and Non-Functioning Pituitary Adenomas


Hypopituitarism and Non-Functioning Pituitary Adenomas
Non-functioning pituitary adenomas
Non-functioning pituitary adenomas (NFPAs) are bioc cally inert tumours. They usually present with the physical effects of a pituitary mass lesion (e.g. visual field loss, headache and hypopituitarism) or, increasingly, when discovered incidentally on routine brain MRI (‘pituitary incidentalomas’). Surgical decompression is indicated if there is a visual field defect or if the lesion is close to the optic chiasm.
The usual route for removal is trans-sphenoidally, although trans-cranial surgery is occasionally needed. NFPAs can cause hypopituitarism by compressing the normal gland, which requires endocrine replacement. Histologically, NFPAs can have positive immunostaining for inactive LH and FSH, but they do not secret bioactive hormones. Patients with significant postoperative residual tumour may require radiotherapy.

Hypopituitarism And Non-Functioning 5 Pituitary Adenomas

Hypopituitarism
Causes
Hypopituitarism has several causes, either congenital (from pituitary transcription factor defects) or acquired. Acquired hypopituitarism is most commonly caused by the presence of a pituitary tumour. Other acquired causes include inflammatory and infiltratitive disorders, traumatic brain injury and radiotherapy (Figure 5.1). In patients with hypopituitarism and a large empty pituitary fossa on MRI, it is important to enquire about a previous history of severe headache, as this may reflect missed pituitary apoplexy (Chapter 36).
3D NEURONAL STRUCTURE AND NEUROHISTOLOGY

3D NEURONAL STRUCTURE AND NEUROHISTOLOGY


3D NEURONAL STRUCTURE AND NEUROHISTOLOGY
3D NEURONAL STRUCTURE AND NEUROHISTOLOGY
        A. Spinal cord lower motor neuron. Nissl substance (rough endoplasmic reticulum) stains purple. The nucleolus is stained in the clear nucleus. Cresyl violet stain.
B.Cerebellar Purkinje neurons. Large dendrites branch from the cell body. Intraneuronal neurofibrils and background neural processes (neuropil) stain densely. Silver stain.
GLIAL CELL TYPES

GLIAL CELL TYPES


GLIAL CELL TYPES
Astrocytes provide structural isolation of neurons and their synapses and provide ionic (K+) sequestration, trophic support, and support for growth and signaling functions to neurons. Oligodendroglia (oligodendrocytes) provide myelination of axons in the CNS.
ASTROCYTE BIOLOGY

ASTROCYTE BIOLOGY


ASTROCYTE BIOLOGY
Astrocytes are the most abundant glial cells in the CNS. They arise from neuroectoderm and are intimately associated with neural processes, synapses, vasculature, and the pial-glial membrane investing the CNS. Astrocytes in gray matter are called protoplasmic astrocytes, and in white matter they are called fibrous astrocytes.
MICROGLIAL BIOLOGY

MICROGLIAL BIOLOGY


MICROGLIAL BIOLOGY
MICROGLIAL BIOLOGY
Microglial cells are mesenchymal cells derived from yolk sac that come to reside in the CNS. They are a unique resident population with the capacity for self-renewal. Microglia provide constant surveillance of the local microenvironment, moving back and forth up to 1.5 µm/min. Microglial processes can grow and shrink up to 2-3 µm/min. They have a territory 15-30 µm wide, with little overlap with each other. Resting microglia have soma of 5-6 µm diameter, and activated microglia are ameboid in appearance, with soma of approximately 10 µm diameter.
OLIGODENDROCYTE BIOLOGY

OLIGODENDROCYTE BIOLOGY


OLIGODENDROCYTE BIOLOGY
OLIGODENDROCYTE BIOLOGY
Oligodendrocytes are neuroectodermally derived glial cells that have the major role of myelinating central axons. The trigger for myelination may include associated axonal size and signal molecules (such as ATP, K+, glutamate, GABA, and some cell adhesion molecules). 

Tuesday, April 13, 2021

NEURONAL GROWTH FACTORS AND TROPHIC FACTORS

NEURONAL GROWTH FACTORS AND TROPHIC FACTORS


NEURONAL GROWTH FACTORS AND TROPHIC FACTORS

NEURONAL GROWTH FACTORS AND TROPHIC FACTORS
Neuronal growth factors and trophic factors are signal molecules produced by neurons, glia, and target tissues that can influence neuronal differentiation, growth of neurites, establishment of contacts for signaling, maintenance of neural contacts with their central or peripheral targets, and other functions. 
Central Nervous System

Central Nervous System


Central Nervous System
Time period: day 22 to postnatal development
Introduction
Ectoderm is induced by the notochord to form neuroectoderm during neurulation (see Chapter 17). This neuroectoderm in turn produces the neural tube and neural crest cells from which the central nervous system develops. The central nervous system comprises the brain and spinal cord.

Central Nervous System

Spinal cord
The caudal end of the neural tube continues to elongate and form the spinal cord. A lumen through the centre of the spinal cord, the neurocoel (or neural canal), forms by week 9 and will become the central canal. The neurocoel is lined with thickening layers of neuroepithelia known as the ventricular zone (Figure 44.1) or ependymal layer.
Peripheral Nervous System

Peripheral Nervous System


Peripheral Nervous System
Time period: day 27 to birth
Introduction
The peripheral nervous system develops in tandem with the brain and spinal cord. It connects the central nervous system to structures of the body as they form and includes the spinal nerves, cranial nerves and autonomic nervous system.
This process begins with neurulation (see Chapter 17), when ectoderm is induced by the notochord to form neuroectoderm. This neuroectoderm in turn produces neuroblasts (primitive neurons) and neural crest cells.
Spinal nerves

Spinal nerves
Neural crest cells migrate out from the neural tube, passing towards multiple targets throughout the embryo (see Chapter 18). Some neural crest cells only migrate a little way from the developing spinal cord, collect together and differentiate to form neurons of the dorsal root ganglia (Figure 45.1). Located bilaterally to the spinal cord, the dorsal root ganglia send afferent processes back towards the alar plate of the spinal cord (see Figure 44.1), eventually passing to the dorsal horn. The dorsal root ganglia also send processes out to run alongside processes of neurons of the ventral root. Their combined bundle of neuronal axons become the spinal nerve.
The Ear

The Ear


The Ear
Time period: 22 day to birth
Internal ear
The function of the internal ear is to receive sound waves and interpret them into nerve signals, and to identify changes in balance.

The Ear, Internal ear, Membranous labyrinth

Membranous labyrinth
At about 22 days, a thickening of ectoderm on either side of the hindbrain develops; this is the otic placode (Figure 46.1). The placode invaginates forming a pit that later becomes separated from the ectoderm, forming the otic vesicle (or otocyst) deep to the ectoderm. The otic vesicle is surrounded by mesoderm that will become the otic capsule, the cartilaginous precursor of the bony labyrinth.
The Eye

The Eye


The Eye
Time period: weeks 3–10
Introduction
The development of the eye begins around day 22 with bilateral invaginations of the neuroectoderm of the forebrain (Figure 47.1).
Optic cup and lens
As the neural tube closes these invaginations become the optic vesicles and remain continuous with the developing third ventricle (Figure 47.1). Contact of these optic vesicles with the surface ectoderm induces the formation of the lens placodes (Figures 47.1 and 47.2).
As the optic vesicle invaginates it forms a double‐walled structure, the optic cup (Figure 47.2). At the same time the lens placode invaginates and forms the lens vesicle which lies in the indent of the optic cup and is completely dissociated from the surface ectoderm. Epithelial cells on the posterior wall of the lens vesicle lengthen anteriorly and become long fibres that grow forwards. It takes about 2 weeks for these fibres to reach the anterior cell wall of the vesicle. These are primary lens fibres (Figure 47.3). Secondary lens fibres form from epithelial cells located at the equator of the lens and are continuously added throughout life along the scaffold made by the primary fibres from the centre of the lens. These cells elongate and eventually lose their nuclei to become mature lens fibres. This occurs in early adulthood.
The Eye, Optic cup and lens, Retina, Optic nerve, Meninges, Cornea, Extraocular muscles,

Retina
In the optic cup there is an outer layer that develops into the pigmented layer of the retina and an inner layer that becomes the neural layer.
Antenatal Screening

Antenatal Screening


Antenatal Screening
Introduction
Modern antenatal care is based on the assessment of risk and identification of the most appropriate care pathway for a pregnant woman. Obstetric ultrasound is a routine tool in antenatal screening for detecting foetal anomalies. Low risk women are offered ultrasound screening in the first and second trimesters, and as these are anomaly scans appropriate care and counselling should be immediately available.
Primary care practitioners will refer a pregnant woman to ante- natal care and aim for a first appointment with ultrasound scanning at approximately 10 weeks into the pregnancy from the date of the last menstrual period (8 weeks after fertilisation). A full obstetric history should be taken and it is good practice to take full gynaecological and medical histories. At the booking appointment the midwife will initiate a close relationship with the mother, and for primigravida women this is the opportunity to discuss the effects of early pregnancy and non‐specific symptoms. Tiredness, nausea and vomiting may be worrying, but hyperemesis gravidarum (excessive nausea and vomiting) should be identified and treated. The mother will be weighed at this meeting, but normally weight is not monitored throughout pregnancy.
Antenatal Screening

The first scan
The first‐trimester ultrasound scan, sometimes referred to as the ‘dating scan’, is performed at a minimum of 10 weeks’ gestation and usually before 14 weeks. Scanning at this stage will confirm foetal viability, give gestational dating information, identify multiple pregnancy, define chorionicity (see Chapter 11) and look for indicators of anomalous development (Figure 48.1). These indicators include nuchal translucency, abdominal wall defects (see Chapter 35) and brain anomalies (see Chapter 44). Nuchal translucency screening is not reliable in smaller foetuses and other anomalies may also be missed. Nuchal translucency measures the thickness of fluid between the cervical spine and skin, and is associated with a number of chromosomal anomalies such as Down syndrome, Turner syndrome, trisomy 18 and trisomy 13, and with cardiac anomalies (Figure 48.2). Skeletal dysplasias may be detectable by ultrasound in the first trimester, and in the near future cardiac defects may be screened for as the resolution of ultrasound scanning improves.
RENAL HANDLING OF POTASSIUM

RENAL HANDLING OF POTASSIUM


RENAL HANDLING OF POTASSIUM
Potassium is a primarily intracellular ion, with skeletal muscle alone containing more than 75% of the body’s total load. Less than 2% of this load is found in the extracellular fluid. The normal plasma concentration is between 3.5 and 5.0 mmol/L.
Extracellular potassium is freely filtered at the glomerulus. A large fraction of the filtered load is consistently reabsorbed along the proximal tubule (66%) and loop of Henle (25%). In the distal tubule, however, there is a variable degree of reabsorption or secretion that depends on input from homeostatic feedback mechanisms. In this manner, the kidneys make a crucial contribution to plasma potassium concentration.
RENAL HANDLING OF POTASSIUM

Transport Mechanisms
Proximal Tubule. In the proximal tubule, potassium is reabsorbed along a paracellular route. A chemical gradient is established as the reabsorption of sodium and water concentrates potassium in the tubular fluid. An electrical gradient is established as chloride is reabsorbed, which leaves a positive charge in the late part of the proximal tubule. There is some evidence that potassium also undergoes some transcellular reabsorption in this segment, but the details and relative importance of this pathway remain unknown.

Monday, April 12, 2021

RENAL HANDLING OF CALCIUM, PHOSPHATE, AND MAGNESIUM

RENAL HANDLING OF CALCIUM, PHOSPHATE, AND MAGNESIUM


RENAL HANDLING OF CALCIUM, PHOSPHATE, AND MAGNESIUM
Calcium
More than 98% of total body calcium is in bones, whereas the remainder is located in intracellular and extracellular fluid. Normal plasma concentrations, which range from 8.8 to 10.3 mg/dL, are maintained by the actions of PTH, 1,25-hydroxy vitamin D, and calcitonin on bones, the gastrointestinal tract, and the kidneys.
About half of the extracellular calcium load is in an active, ionized form, whereas the remainder complexes with albumin and other anions. The ionized calcium is freely filtered at the glomerulus, and normally almost all of it is reabsorbed.
In the proximal tubule, 50% to 60% of the filtered load is reabsorbed along a paracellular route. A chemical gradient is established as sodium and water are reabsorbed, concentrating calcium in the tubular fluid. Meanwhile, an electrical gradient is established by the paracellular reabsorption of chloride, which leaves a positive charge in the lumen. Specialized tight junction proteins, such as claudin-2, may form a cation-specific paracellular pathway.
In the thick ascending limb, 15% of the filtered load is reabsorbed along a paracellular route. An electrical gradient, formed secondary to K+ recycling, drives this process. Claudin-16, another tight junction protein, is an important component of this paracellular pathway, and mutations are associated with familial hypomagnesemia with hypocalciuria.
In the distal convoluted and connecting tubules, 10% to 15% of the filtered load is reabsorbed along a transcellular route. Calcium crosses the apical membrane through TRPV5 channels, binds to calbindin, then exits the basolateral membrane on the NCX1 Na+/Ca2+ exchanger and, to a lesser degree, a Ca2+ ATPase (PMCA).
The collecting duct makes an unknown, but likely minor, contribution to calcium reabsorption.
Hypocalcemia triggers release of PTH, which has numerous effects on renal function. In the proximal tubule, it inhibits the NHE-3 Na+/H+ exchanger, reducing the gradient for paracellular calcium reabsorption. (This seemingly paradoxical effect allows PTH to increase phosphate excretion, as discussed later.) In the distal nephron, however, it up-regulates the apical TRPV5 calcium channel, causing a net increase in calcium reabsorption. Meanwhile, hypercalcemia both suppresses PTH release and directly inhibits calcium reabsorption. In the thick ascending limb, for example, the increased load of reabsorbed calcium activates a basolateral calcium-sensing receptor (CaSR), which then inhibits NKCC2 transporters and ROM-K channels, reducing the electrical gradient for calcium reabsorption.
Finally, acidosis inhibits the TRPV5 calcium channel, whereas alkalosis has the opposite effect.
RENAL HANDLING OF CALCIUM AND PHOSPHATE
RENAL HANDLING OF CALCIUM AND PHOSPHATE

Phosphate
About 85% of total body phosphate is stored in bones, 14% in soft tissues, and 1% in extracellular fluid. Normal plasma concentrations, which range from 3 to 4.5 mg/dL, are maintained by the actions of PTH, 1,25-hydroxyvitamin D, and phosphatonins on the parathyroid glands, bones, gastrointestinal tract, and kidneys.
COUNTERCURRENT MULTIPLICATION

COUNTERCURRENT MULTIPLICATION


COUNTERCURRENT MULTIPLICATION
The countercurrent multiplier system is a sophisticated apparatus that evolved in mammals and birds to con-serve water. It forms a longitudinal concentration gradient in the medullary interstitium that increases in strength toward the papilla. This gradient is crucial for water reabsorption from the renal tubules, which is a passive process that depends on osmotic pressure from the interstitium.

MODEL OF THE COUNTERCURRENT MULTIPLIER: PART I
MODEL OF THE COUNTERCURRENT MULTIPLIER: PART I

The creation and maintenance of this gradient is best understood by first considering a simplified model of the loop of Henle. In this model, a tube of fluid is divided by a membrane in all but its most inferior aspect. The left side represents the entire descending limb, whereas the right side represents the entire ascending limb. Fluid enters at the top of the left-sided column, travels beneath the membrane, and then exits at the top of the right-sided column. The dividing membrane is impermeable to water but contains active transporters, which pump solute from the ascending limb to the descending limb. These transporters are powerful enough to establish a transmembrane gradient of about 200 milliosmoles (mOsm).
URINE CONCENTRATION AND DILUTION AND OVERVIEW OF WATER HANDLING

URINE CONCENTRATION AND DILUTION AND OVERVIEW OF WATER HANDLING


URINE CONCENTRATION AND DILUTION AND OVERVIEW OF WATER HANDLING
In normal kidneys more than 180 liters of fluid are filtered into the nephrons each day, but nearly all of it is reabsorbed into the peritubular circulation.
Tight junctions form a watertight seal between tubular epithelial cells throughout most of the nephron. Thus, water reabsorption occurs primarily through a transcellular route, requiring specialized channels known as aquaporins (AQPs) in both the apical and basolateral compartments of the plasma membrane.
URINE CONCENTRATION AND DILUTION AND OVERVIEW OF WATER HANDLING

Because aquaporins are channels, and not pumps, the reabsorption of water is a passive process, dependent on osmotic pressure from solutes concentrated in the sur-rounding interstitium.
ANTIDIURETIC HORMONE

ANTIDIURETIC HORMONE


ANTIDIURETIC HORMONE
ADH, also known as vasopressin, plays a crucial role in maintaining the normal osmolality of extracellular fluid, which depends primarily on the extracellular sodium concentration. ADH exerts its effect by altering the osmolality of excreted urine, which can range from 50 to 1200 mOsm/kg H2O.
When plasma osmolality increases, ADH release causes extensive water reabsorption in the distal nephron. As a result, the urine becomes highly concentrated, and the plasma consequently becomes more dilute. In contrast, when plasma osmolality decreases, inhibition of ADH release prevents water reabsorption in the distal nephron, leading to dilution of urine and concentration of plasma.
 
MECHANISM OF ANTIDIURETIC HORMONE IN REGULATING URINE VOLUME AND CONCENTRATION
MECHANISM OF ANTIDIURETIC HORMONE IN REGULATING URINE VOLUME AND CONCENTRATION
MECHANISMS OF RELEASE
ADH is produced in the supraoptic and paraventricular nuclei of the hypothalamus. It is then conveyed along axons to the posterior pituitary for storage and release. ADH release occurs primarily in response to activation of osmoreceptors in the anterior hypothalamus. These receptors, located outside of the blood-brain barrier, are extremely sensitive to changes in plasma osmolality. Their activation has been hypothesized to occur when there is a loss of intracellular fluid secondary to increased extracellular osmotic pressure. In support of this hypothesis, the osmoreceptors are not equally sensitive to all solutes. Sodium, for example, reliably activates osmoreceptors at high concentrations because, as a predominantly extracellular ion, it establishes a transmembrane osmotic gradient. In contrast, urea and glucose generally do not activate osmoreceptors even at high concentrations because they freely enter cells, thus failing to establish an osmotic gradient. When patients experience extreme insulin depletion, however, osmoreceptors may become sensitive to high concentrations of glucose, presumably because of its increased restriction to the extracellular space.
ACUTE FEBRILE NEUTROPHILIC DERMATOSIS (SWEET’S SYNDROME)

ACUTE FEBRILE NEUTROPHILIC DERMATOSIS (SWEET’S SYNDROME)


ACUTE FEBRILE NEUTROPHILIC DERMATOSIS (SWEET’S SYNDROME)
Acute febrile neutrophilic dermatosis is an uncommon rash that most often is secondary to an underlying infection or malignancy. The diagnosis is made by fulfilling a constellation of criteria. Both clinical findings and pathology results are required to make the diagnosis in a patient with a consistent history.

ACUTE FEBRILE NEUTROPHILIC DERMATOSIS (SWEET’S SYNDROME)

Clinical Findings: Acute febrile neutrophilic dermatosis is often associated with a preceding infection. The infection can be located anywhere but most commonly is in the upper respiratory system. Females appear to be more likely to be afflicted, and there is no race predilection. Patients present with fever and the rapid onset of juicy papules and plaques. Because the papules can look as if they are fluid filled, they are given the descriptive term juicy papules. They can occur anywhere on the body and can be mistaken for a varicella infection. Patients also have neutrophilia and possibly arthritis and arthralgias. If this condition is associated with a preceding infection, it is usually self-limited and heals without scarring, unless the papules and plaques are excoriated or ulcerated by scratching. Variable amounts of pruritus and pain are associated with this skin disease. When one is evaluating a patient with this condition, a thorough history is required. A skin biopsy must be performed. A chest radiograph, throat culture, and urinalysis should be performed to assess for the possibility of bacterial infection.
ALLERGIC CONTACT DERMATITIS

ALLERGIC CONTACT DERMATITIS


ALLERGIC CONTACT DERMATITIS
Allergic contact dermatitis is one of the rashes most frequently encountered in the clinician’s office. It is responsible for a large proportion of occupationally induced skin disease. Urushiol from the sap of poison ivy, oak, or sumac plants is the most common cause of allergic contact dermatitis in the United States. The clinical morphology, the distribution of the rash, and results from skin patch testing are used to make the diagnosis. Patch testing is performed when the causative agent is unknown. Nickel has been the most frequent cause of positive patch testing in the world for years. Urushiol is not tested clinically, because almost 100% of the population reacts to this chemical.

MORPHOLOGY OF ALLERGIC CONTACT DERMATITIS
MORPHOLOGY OF ALLERGIC CONTACT DERMATITIS

Clinical Findings: Allergic contact dermatitis can manifest in a multitude of ways. The acute form may show linear streaks of juicy papules and vesicles. Variable amounts of surrounding edema can be seen. Edema is much more common in the loose skin around the eyelids and facial region. Chronic allergic contact dermatitis can manifest with red-pink patches and plaques with various amounts of lichenification. There are localized forms and generalized forms. One of the unique forms of allergic contact dermatitis is the scattered generalized form. Pruritus is an almost universal finding, and it can be so severe as to cause excoriations and small ulcerations.
ATOPIC DERMATITIS

ATOPIC DERMATITIS


ATOPIC DERMATITIS
Atopic dermatitis is one of the most common dermatoses of childhood. It typically manifests in early life and can have varying degrees of expression. It is commonly associated with asthma and allergies. Most children eventually outgrow the condition. Atopic dermatitis has been estimated to affect up to 10% of all children and 1% of adults, and its prevalence has been steadily increasing. Patients frequently have a family history of atopic dermatitis, asthma, or skin sensitivity.

INFANTS AND CHILDREN WITH ATOPIC DERMATITIS
INFANTS AND CHILDREN WITH ATOPIC DERMATITIS

Clinical Findings: Atopic dermatitis typically begins early in life. There is no racial predilection. The clinical course is often chronic, with a waxing and waning nature. Infants a few months old may initially present with pruritic, red, eczematous patches on the cheeks and extremities as well as the trunk. The itching is typically severe and causes the child to excoriate the skin, which can lead to secondary skin infections. The skin of atopics is abnormally dry and is sensitive to heat and sweating. These children have difficulty sleeping because of the severe pruritus associated with the rash. During flares of the dermatitis, patients may develop weeping patches and plaques that are extremely pruritic and occasionally painful. With time, the patches begin to localize to flexural regions, particularly the antecubital and popliteal fossae. Severely afflicted children may have widespread disease. Patients with atopic dermatitis are more prone to react to contact and systemic allergens. Sensitivity to contact allergens is likely a consequence of the frequent use of topical medicaments and the broken skin barrier. This combination leads to increased exposure to foreign antigens that are capable of inducing allergic contact dermatitis. One should suspect a coexisting contact dermatitis if a patient who is doing well experiences a flare for no apparent reason or if a patient continues to get worse despite aggressive topical or oral therapy. Laboratory testing commonly shows an eosinophilia and an elevated immunoglobulin E (IgE) level.

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