Definition
Von Hippel–Lindau disease (VHL) is an autosomal dominant disorder characterized by pheochromocytoma (frequently bilateral), paraganglioma (rarely), retinal angiomas, cerebellar hemangioblastoma, epididymal cystadenoma, renal and pancreatic cysts, and renal cell carcinoma.
Pheochromocytoma is reported to occur in about 10 to 20% of patients with VHL. Nearly 100% of patients with VHL have an identifiable gene mutation (VHL tumor suppressor gene).
Certain missense mutations appear to be associated with a “pheochromocytoma only” presentation of VHL
Sunday 28 August 2011
PHEOCHROMOCYTOMA IN PREGNANCY
Pheochromocytoma in pregnancy can cause the death of both the fetus and the mother.
The approach to the biochemical diagnosis is the same as for the nonpregnant patient. MRI is the preferred imaging modality, and 123I-MIBG is contraindicated.
The treatment of hypertensive crises is the same as for nonpregnant patients except that use of nitroprusside should be avoided.
Although the most appropriate management is debated, adrenal pheochromocytomas should be removed promptly if diagnosis is made during the first two trimesters of pregnancy. The preoperative preparation is the same as for a nonpregnant patient. If the pregnancy is in the third trimester, one operation is recommended for a cesarean delivery and removal of the adrenal pheochromocytoma at the same time. Spontaneous labor and delivery should be avoided. The management of catecholamine-secreting paragangliomas in pregnancy may require modification of these guidelines, depending on tumor location.
The approach to the biochemical diagnosis is the same as for the nonpregnant patient. MRI is the preferred imaging modality, and 123I-MIBG is contraindicated.
The treatment of hypertensive crises is the same as for nonpregnant patients except that use of nitroprusside should be avoided.
Although the most appropriate management is debated, adrenal pheochromocytomas should be removed promptly if diagnosis is made during the first two trimesters of pregnancy. The preoperative preparation is the same as for a nonpregnant patient. If the pregnancy is in the third trimester, one operation is recommended for a cesarean delivery and removal of the adrenal pheochromocytoma at the same time. Spontaneous labor and delivery should be avoided. The management of catecholamine-secreting paragangliomas in pregnancy may require modification of these guidelines, depending on tumor location.
Pheochromocytoma
Definition
Pheochromocytomas are autonomously functioning, catecholamine-secreting, chromaffin-cell neoplasms.
Etiology
About 90% are benign solitary nodules found within the adrenal medulla itself. However, because they can arise any
where neural crest tissue has migrated during the course of embryonic development, approximately 10% are located intra-abdominally in close proximity to the celiac or mesenteric sympathetic ganglia. Adrenal medullary pheochromocytomas are almost always (90%) unilateral. Bilateral lesions usually occur as familial neoplasms, as in type IIa (Sipple's syndrome) or type IIb multiple endocrine neoplasia syndrome (Table 69.5). The multiple endocrine neoplasia syndromes are transmitted as autosomal dominant diseases with incomplete penetrance and variable expression.
Sign And Symptoms
SPELL RELATED
Anxiety and fear of impending death
Diaphoresis
Dyspnea
Epigastric and chest pain
Headache
Hypertension
Nausea and vomiting
Pallor
Palpitation (forceful heartbeat)
Tremor
CHRONIC
Anxiety and fear of impending death
Cold hands and feet
Congestive heart failure—dilated or hypertrophic cardiomyopathy
Constipation
Diaphoresis
Dyspnea
Ectopic hormone secretion–dependent symptoms (e.g., CRH/ACTH, GHRH, PTH-RP, VIP)
Epigastric and chest pain
Fatigue
Fever
General increase in sweating
Grade II to IV retinopathy
Headache
Hyperglycemia
Hypertension
Nausea and vomiting
Orthostatic hypotension
Painless hematuria (associated with urinary bladder paraganglioma)
Pallor
Palpitation (forceful heartbeat)
Tremor
Weight loss
Diagnosis
The most commonly used screening test is a 24-hour urine measurement of catecholamines (norepinephrine and epinephrine) or their metabolites (metanephrine and vanillylmandelic acid).
Note:
(levodopa, tricyclic antidepressants, and decongestants) influence the test results, all medications should be withheld for a minimum of 1 to 2 days
Plasma norepinephrine, another useful screening test in pheochromocytomas, typically exceeds 2,000 pg/mL
Treatment
Surgical Therapy
Pheochromocytoma is almost always cured by surgical excision of the tumor
Medical Therapy
Combined α- and β-adrenergic blockade is one approach to control blood pressure and to prevent intraoperative hypertensive crises. α-Adrenergic blockade should be started 7 to 10 days preoperatively to normalize blood pressure and to expand the contracted blood volume.
Cushing's Syndrome
Definition
Cushing's syndrome is a condition caused by excess amounts of cortisol adenoma or cancer resulting from hypersecretion of the adrenal cortex which may result from a hypersecreting adrenal tumor, ectopic ACTH, or prolonged exposure to high therapeutic doses of glucocorticoids or prolonged exposure to high therapeutic doses of glucocorticoids.
Etiology
exogenous
the most common cause of Cushing's syndrome is iatrogenic or exogenous glucocorticoid use.
Endogenous
cases may be either
ACTH dependent (e.g., ACTH-secreting pituitary adenoma or ectopic ACTH-secreting neoplasm)
or
ACTH independent (e.g., adrenal adenoma, adrenal carcinoma)
Sign or Symptom
Decreased libido in men and women
Obesity or weight gain
Plethora
Round face
Menstrual changes
Hirsutism
Hypertension
Ecchymoses
Lethargy, depression
Striae
Weakness
Electrocardiographic changes or atherosclerosis
Dorsal fat pad
Edema
Abnormal glucose tolerance
Osteopenia or fracture
Headache
Backache
Recurrent infections
Abdominal pain
Acne
Female balding
Diagnosis
Urine free cortisol excretion during 24 hours is a good screening test
Dexamethasone Suppression Tests
It involves giving dexamethasone, 1 mg, orally between 2300 and midnight and measurement of plasma cortisol concentration between 0800 and 0900 the following morning.
Treatment
Surgical Therapy
The optimal treatment of Cushing's syndrome is surgical resection of the lesion that is producing excessive ACTH or cortisol
Radiation Therapy
Medical Therapy
Combination of Surgical and Medical Therapy is to be used
Medical therapy alone is rarely appropriate for Cushing's disease because it requires close monitoring and adjustment of dose and has low long-term efficacy.
Patients with ectopic ACTH secretion can be cured if the tumor can be removed and is not metastatic. Otherwise, adrenalectomy or medical therapy is chosen. Adrenalectomy is appropriate when the patient cannot tolerate the cost, medical toxicity, or adverse psychological effects of long-term medical therapy and monitoring or if the patient requires rapid correction of hypercortisolism. Adrenalectomy is appropriate when maximal daily doses of ketoconazole (1600 mg), aminoglutethimide (2 g), and metyrapone (2 g) given in combination do not render the patient eucortisolemic.
Cushing's syndrome is a condition caused by excess amounts of cortisol adenoma or cancer resulting from hypersecretion of the adrenal cortex which may result from a hypersecreting adrenal tumor, ectopic ACTH, or prolonged exposure to high therapeutic doses of glucocorticoids or prolonged exposure to high therapeutic doses of glucocorticoids.
Etiology
exogenous
the most common cause of Cushing's syndrome is iatrogenic or exogenous glucocorticoid use.
Endogenous
cases may be either
ACTH dependent (e.g., ACTH-secreting pituitary adenoma or ectopic ACTH-secreting neoplasm)
or
ACTH independent (e.g., adrenal adenoma, adrenal carcinoma)
Sign or Symptom
Decreased libido in men and women
Obesity or weight gain
Plethora
Round face
Menstrual changes
Hirsutism
Hypertension
Ecchymoses
Lethargy, depression
Striae
Weakness
Electrocardiographic changes or atherosclerosis
Dorsal fat pad
Edema
Abnormal glucose tolerance
Osteopenia or fracture
Headache
Backache
Recurrent infections
Abdominal pain
Acne
Female balding
Diagnosis
Urine free cortisol excretion during 24 hours is a good screening test
Dexamethasone Suppression Tests
It involves giving dexamethasone, 1 mg, orally between 2300 and midnight and measurement of plasma cortisol concentration between 0800 and 0900 the following morning.
Treatment
Surgical Therapy
The optimal treatment of Cushing's syndrome is surgical resection of the lesion that is producing excessive ACTH or cortisol
Radiation Therapy
Medical Therapy
Combination of Surgical and Medical Therapy is to be used
Medical therapy alone is rarely appropriate for Cushing's disease because it requires close monitoring and adjustment of dose and has low long-term efficacy.
Patients with ectopic ACTH secretion can be cured if the tumor can be removed and is not metastatic. Otherwise, adrenalectomy or medical therapy is chosen. Adrenalectomy is appropriate when the patient cannot tolerate the cost, medical toxicity, or adverse psychological effects of long-term medical therapy and monitoring or if the patient requires rapid correction of hypercortisolism. Adrenalectomy is appropriate when maximal daily doses of ketoconazole (1600 mg), aminoglutethimide (2 g), and metyrapone (2 g) given in combination do not render the patient eucortisolemic.
Saturday 27 August 2011
Atherosclerosis
Definition
Atherosclerosis is characterized by intimal lesions called atheromas (also called atheromatous or atherosclerotic plaques) that protrude into vessel lumens
atherosclerotic plaques mechanically obstructing blood flow, atherosclerotic plaques can rupture, leading to catastrophic vessel thrombosis; plaques also weaken the underlying media and thereby lead to aneurysm formation
Importance
Atherosclerosis causes far more morbidity and mortality (roughly half of all deaths) in the Western world than any other disorder
coronary artery disease is an important manifestation of the disease and therefore myocardial infarction is responsible for almost a quarter of all deaths in the United States.
Significant morbidity and mortality are also caused by aortic and carotid atherosclerotic disease and stroke.
SYMPTOMS:
Symptoms may develop
in any organ system with a blood supply
diminished by atherosclerosis. Commonly
these symptoms include angina
pectoris, intermittent claudication,
strokes, transient ischemic attacks, and
renal insufficiency.
EPIDEMIOLOGY
atherosclerosis is much less prevalent in Central and South America, Africa, and parts of Asia. It is more prevalent in United States so the mortality rate due to ischemic heart disease (IHD) in the United States is highest
Risk Factors
NONMODIFIABLE
Increasing age
Male gender
Family history
Genetic abnormalities
MODIFIABLE
Hyperlipidemia
Hypertension
Cigarette smoking
Diabetes
C-reactive protein
Other Risk Factors
Inflammation
Hyperhomocystinemia.
glucose intolerance,
elevated plasminogen activator inhibitor 1
lack of exercise;
competitive, stressful life style (“type A” personality)
obesity (which is often associated with hypertension, diabetes, hypertriglyceridemia, and decreased HDL).
Mechanism of Athrosclerosis
Endothelial injury, which causes (among other things) increased vascular permeability, leukocyte adhesion, and thrombosis
Endothelial injury, which causes (among other things) increased vascular permeability, leukocyte adhesion, and thrombosis
Accumulation of lipoproteins (mainly LDL and its oxidized forms) in the vessel wall
Monocyte adhesion to the endothelium, followed by migration into the intima and transformation into macrophages and foam cells
Platelet adhesion
Factor release from activated platelets, macrophages, and vascular wall cells, inducing smooth muscle cell recruitment, either from the media or from circulating precursors
Smooth muscle cell proliferation and ECM production
Lipid accumulation both extracellularly and within cells (macrophages and smooth muscle cells)
TREATMENT
Treatment includesregular exercise, smoking cessation,and a dietary regimen of low-cholesterol and low-fat foods. Medical treatment ofhypertension, lipid disorders, and diabetesmellitus is also helpful. Angioplasty,
atherectomy, or arterial bypass
graft operations are beneficial for selected
patients
If atherosclerosis is caused by hyperlipidemia then it is treated by Competitive Inhibitors of HMG-CoA Reductase which include Lovastatin, atorvastatin, fluvastatin, pravastatin, simvastatin, and rosuvastatin
Atherosclerosis is characterized by intimal lesions called atheromas (also called atheromatous or atherosclerotic plaques) that protrude into vessel lumens
atherosclerotic plaques mechanically obstructing blood flow, atherosclerotic plaques can rupture, leading to catastrophic vessel thrombosis; plaques also weaken the underlying media and thereby lead to aneurysm formation
Importance
Atherosclerosis causes far more morbidity and mortality (roughly half of all deaths) in the Western world than any other disorder
coronary artery disease is an important manifestation of the disease and therefore myocardial infarction is responsible for almost a quarter of all deaths in the United States.
Significant morbidity and mortality are also caused by aortic and carotid atherosclerotic disease and stroke.
SYMPTOMS:
Symptoms may develop
in any organ system with a blood supply
diminished by atherosclerosis. Commonly
these symptoms include angina
pectoris, intermittent claudication,
strokes, transient ischemic attacks, and
renal insufficiency.
EPIDEMIOLOGY
atherosclerosis is much less prevalent in Central and South America, Africa, and parts of Asia. It is more prevalent in United States so the mortality rate due to ischemic heart disease (IHD) in the United States is highest
Risk Factors
NONMODIFIABLE
Increasing age
Male gender
Family history
Genetic abnormalities
MODIFIABLE
Hyperlipidemia
Hypertension
Cigarette smoking
Diabetes
C-reactive protein
Other Risk Factors
Inflammation
Hyperhomocystinemia.
glucose intolerance,
elevated plasminogen activator inhibitor 1
lack of exercise;
competitive, stressful life style (“type A” personality)
obesity (which is often associated with hypertension, diabetes, hypertriglyceridemia, and decreased HDL).
Mechanism of Athrosclerosis
Endothelial injury, which causes (among other things) increased vascular permeability, leukocyte adhesion, and thrombosis
Endothelial injury, which causes (among other things) increased vascular permeability, leukocyte adhesion, and thrombosis
Accumulation of lipoproteins (mainly LDL and its oxidized forms) in the vessel wall
Monocyte adhesion to the endothelium, followed by migration into the intima and transformation into macrophages and foam cells
Platelet adhesion
Factor release from activated platelets, macrophages, and vascular wall cells, inducing smooth muscle cell recruitment, either from the media or from circulating precursors
Smooth muscle cell proliferation and ECM production
Lipid accumulation both extracellularly and within cells (macrophages and smooth muscle cells)
TREATMENT
Treatment includesregular exercise, smoking cessation,and a dietary regimen of low-cholesterol and low-fat foods. Medical treatment ofhypertension, lipid disorders, and diabetesmellitus is also helpful. Angioplasty,
atherectomy, or arterial bypass
graft operations are beneficial for selected
patients
If atherosclerosis is caused by hyperlipidemia then it is treated by Competitive Inhibitors of HMG-CoA Reductase which include Lovastatin, atorvastatin, fluvastatin, pravastatin, simvastatin, and rosuvastatin
Arteriosclerosis
Definition
A disease of the arterial vessels marked by thickening, hardening, and loss of elasticity in the arterial walls.
Arteriosclerosis literally means “hardening of the arteries”; it is a generic term reflecting arterial wall thickening and loss of elasticity.
It has three general patterns, with different clinical and pathologic consequences:
Arteriolosclerosis affects small arteries and arterioles, and may cause downstream ischemic injury.
Mönckeberg medial sclerosis is characterized by calcific deposits in muscular arteries in persons typically older than age 50.
The deposits may undergo metaplastic change into bone. the lesions do not encroach on the vessel lumen and are usually not clinically significant
Atherosclerosis, from Greek root words for “gruel” and “hardening,” is the most frequent and clinically important pattern
A disease of the arterial vessels marked by thickening, hardening, and loss of elasticity in the arterial walls.
Arteriosclerosis literally means “hardening of the arteries”; it is a generic term reflecting arterial wall thickening and loss of elasticity.
It has three general patterns, with different clinical and pathologic consequences:
Arteriolosclerosis affects small arteries and arterioles, and may cause downstream ischemic injury.
Mönckeberg medial sclerosis is characterized by calcific deposits in muscular arteries in persons typically older than age 50.
The deposits may undergo metaplastic change into bone. the lesions do not encroach on the vessel lumen and are usually not clinically significant
Atherosclerosis, from Greek root words for “gruel” and “hardening,” is the most frequent and clinically important pattern
Fibromuscular dysplasia
Definition
It is a focal irregular thickening of the walls of medium and large muscular arteries.
It include renal, carotid, splanchnic, and vertebral vessels
Causes
It is probably developmental, first-degree relatives of affected individuals have an increased incidence.
Complications
Segments of the vessel wall are focally thickened by a combination of irregular medial and intimal hyperplasia and fibrosis; this results in luminal stenosis, and in the renal arteries may be a cause of renovascular hypertension
Vascular outpouchings (aneurysms) may develop in the vessel segments with attenuated media and in some cases can rupture.
Fibromuscular dysplasia can manifest at any age, although it is seen most frequently in young women; there is no association with use of oral contraceptives or abnormalities of sex hormone expression
It is a focal irregular thickening of the walls of medium and large muscular arteries.
It include renal, carotid, splanchnic, and vertebral vessels
Causes
It is probably developmental, first-degree relatives of affected individuals have an increased incidence.
Complications
Segments of the vessel wall are focally thickened by a combination of irregular medial and intimal hyperplasia and fibrosis; this results in luminal stenosis, and in the renal arteries may be a cause of renovascular hypertension
Vascular outpouchings (aneurysms) may develop in the vessel segments with attenuated media and in some cases can rupture.
Fibromuscular dysplasia can manifest at any age, although it is seen most frequently in young women; there is no association with use of oral contraceptives or abnormalities of sex hormone expression
Muscles And Its Classifications
What is a Muscle?
Muscle is the basic structure for the movements. The cells of origin of all muscles are called myocytes and all muscle fibers contain contractile proteins i.e. myosin and actin.
Classification of Muscle
Divided in 3 groups on functional and histological bases:
A. SKELETAL, Striated, Voluntary
B. CARDIAC, Striated, Involuntary
C. SMOOTH, Non-striated, Involuntary
Skeletal Muscles
MAIN FEATURES:
Attached to bones
Voluntary i.e. these are under
our conscious control
Supplied by somatic nerves
Fatigue easily
Individual cells are large i.e. from few mm to many cm.
Main histological features:
Each cell is long tublar fiber
Longitudinal & cross striations
Multi nucleated
Nuclei arranged at the periphery
Physiology
MOTOR UNIT: Number of muscle fibers supplied by one motor neuron.
Ratio of fibers supplied depends upon functional demands.
For muscle performing precise & delicate movements ratio is 1:10
For large limb muscles meant for gross movements ratio is 1:1000
INTERNAL STRUCTURE:
Association with C.T:
1. Endomysium
2. Perimysium
3. Epimysium
PARTS:
Origin: Least mobile
Insertion: Most mobile
Belly: Fleshy part
Tendon: Non-cartilaginous part attached to bone
Aponeurosis: Tendons of some muscles form flat sheets
MORPHOLOGICAL CLASSIFICATION:
PARALLEL:
Quadrilateral e.g. Quadratus femoris, thyro-hyoid
Strap e.g. Sartorius, sternohyoid
Strap with tendinous intersections e.g Rectus abdominus
Fusiform- e.g Long head of biceps
B. OBLIQUE:
Triangular e.g. Adductor longus
Spiral e.g. Pectoralis major
Cruciate-two layers e.g. Sternocleidomastoid
Digastric-two bellies & intermediate tendon e.g. Omohyoid
PENNATE: tendon in center & direction of fibers at some angle
1. Unipennate e.g. Flexor pollicis longus
2. Bipennate e.g. Dorsal interossei
3. Multipennate e.g. Deltoid
4. Circumpennate e.g. Tibialis anterior
C. More than One Tendon of Origin:
Bicipital e.g Biceps femoris
Tricipital e.g Triceps
Quadricipital e.g Quadriceps femoris
FUNTIONAL CLASSIFICATION:
PRIME MOVER OR AGONIST: Muscle which initiates, maintains and completes a movement is prime mover for that particular movement e.g. Brachialis is agonist for flexion at elbow joint.
ANTAGONIST: Muscle that work opposite to agonist is called antagonist e.g. Brachialis is antagonist to triceps.
SYNERGISTS: Muscles of opposite group which prevent undesired movements.
FIXATORS: Simultaneous contraction of agonists and antagonists fixes a joint or a bone, so that movement can be carried out more distally e.g. Flexors and extensors of wrist contract simultaneously to fix the wrist thus permitting smooth movements at fingers.
ANTI GRAVITY: Muscles acting against gravity. Muscles which maintain the anatomical position, work against gravity. Maintenance of anatomical position is mainly function of extensors
Types of Muscle Contraction:
1. Isometric Contraction: Length not changed, tension increased & no movement produced. (Load is more than muscle power)
2. Isotonic Contraction: Length decreases, tone remains constant & movement take place. (Load less than muscle power)
3. Eccentric Action or Paradoxical Action: Initial isotonic contraction, followed by isotonic relaxation of same muscle & gravitational pull adds to the action.
Cardiac Muscle
Restricted to heart.
MAIN FEATURES:
No bony attachment
Involuntary
Supplied by autonomic nerves
Does not get fatigued
MAIN HISTOLOGICAL FEATURES:
Size: Individual cells are up to 100 um long
Longitudinal and cross striations
Each cell has single or at most
two nuclei located centrally
All cells branch and make a network
All cells connected to each other
by intercalated discs
Smooth Muscle
MAIN FEATURES:
No bony or tendinous attachment
Involuntary
Supplied by autonomic nerves
Slow but prolonged contraction
Can under go mitotic division throughout life (skeletal muscle fibers cannot divide after differentiation, cardiac muscle fibers can only divide till birth)
MAIN HISTOLOGICAL FEATURES:
Spindle shaped cell, thick in the middle and tapering ends
Single nucleus
No striations
FUNCTIONAL LOCATIONS:
To regulate diameter e.g in blood vessel walls
Propulsion of liquids or solids e.g in GIT or ureter
Expulsion of contents e.g in urinary bladder or uterus
Immunity
Definition
Ability of the body to resist all types of organisms or toxins that can damage tissues or organs.
TYPES
Specific or Acquired immunity
This develops after exposure to bacteria,viruses or toxins.
Innate or Non specific immunity
This type of immunity doesn’t require previous exposure to microorganisms or toxins.
COMPONENTS OF INNATE IMMUNITY
Neutrophils,Macrophages and Natural killer lymphocytes
Gastric acid
Intact skin and mucous membranes
Chemical compounds in blood and tissues
NEUTROPHILS
The neutrophils are mature cells that can attack and destroy bacteria even in the circulating blood.
MACROPHAGES
Begin life as monocytes in blood
Migrate to tissues to become tissue macrophages which can reach in size upto 80 microns.
Highly competant in combating infections
NATURAL KILLER CELLS
These are lymphocytes which can recognize and destroy foreign cells and even some infected cells.
GASTRIC ACID
HCL secreted in gastric juice by parietal cells destroy the microorganisms which are swallowed with food.
SKIN AND MUCOUS MEMBRANES
Intact healthy skin and mucous membrane act as efficient barriers against microorganisms.
PROTECTIVE CHEMICAL COMPOUNDS
These are
Lysozyme ,a mucolytic polysaccharide that attacks bacteria and destroy them.
Basic polypeptides, react with and inactivate certain types of Gram positive bacteria.
COMPLEMENT COMPLEX
A system of about 20 proteins that can be activated in various ways to destroy bacteria.
There are three complement pathways which the organism use as weapons to fight off pathogens,destroy tumors and kill viral infected cells .These are :
Lectin pathway
Alternative pathway
Classical pathway
Ability of the body to resist all types of organisms or toxins that can damage tissues or organs.
TYPES
Specific or Acquired immunity
This develops after exposure to bacteria,viruses or toxins.
Innate or Non specific immunity
This type of immunity doesn’t require previous exposure to microorganisms or toxins.
COMPONENTS OF INNATE IMMUNITY
Neutrophils,Macrophages and Natural killer lymphocytes
Gastric acid
Intact skin and mucous membranes
Chemical compounds in blood and tissues
NEUTROPHILS
The neutrophils are mature cells that can attack and destroy bacteria even in the circulating blood.
MACROPHAGES
Begin life as monocytes in blood
Migrate to tissues to become tissue macrophages which can reach in size upto 80 microns.
Highly competant in combating infections
NATURAL KILLER CELLS
These are lymphocytes which can recognize and destroy foreign cells and even some infected cells.
GASTRIC ACID
HCL secreted in gastric juice by parietal cells destroy the microorganisms which are swallowed with food.
SKIN AND MUCOUS MEMBRANES
Intact healthy skin and mucous membrane act as efficient barriers against microorganisms.
PROTECTIVE CHEMICAL COMPOUNDS
These are
Lysozyme ,a mucolytic polysaccharide that attacks bacteria and destroy them.
Basic polypeptides, react with and inactivate certain types of Gram positive bacteria.
COMPLEMENT COMPLEX
A system of about 20 proteins that can be activated in various ways to destroy bacteria.
There are three complement pathways which the organism use as weapons to fight off pathogens,destroy tumors and kill viral infected cells .These are :
Lectin pathway
Alternative pathway
Classical pathway
Fetal membranes
DEFINITION
ANY STRUCTURE THAT FUNCTIONS FOR THE PROTECTION, NOURISHMENT, RESPIRATION OR EXCRETION OF A DEVELOPING FETUS. THEY INCLUDE:
• Chorion
• Amnion
• Placenta
• Allantois
• Yolk sac
• Umbilical cord
Chorion Frondosum
In early weeks of development villi cover the entire surface of
chorion as it advances villi on embriyonic pole continue to grow
and expand give rise to the chorion frondosum
DECIDUA
A mucous membrane lining the uterus,modified during pregnancy
and shed at parturation or during menstruation
• Chorion frondosum (bushy or villous chorion)
• Chorion laeve (smooth chorion)
• Decidua basalis
• Decidua capsularis
• Decidua parietalis (decidua vera)
Structure of the Placenta
By the beginning of the 4th month, placenta has 2 components:
Fetal portion
Maternal portion
Chorionic & decidual plates
Junctional zone
Decidual septa & cotyledons
Circulation of the Placenta
• The intervillous spaces of a mature placenta contain approximately 150 ml of blood, which is replenished about 3 or 4 times per minute.
• Placental membrane / barrier (x)
Function of the Placenta
• Exchange of metabolic & gaseous products between maternal & fetal bloodstreams
Exchange of gases
Exchange of nutrients & electrolytes
Transmission of maternal antibodies
• Production of hormones
Fetal membranes in twins
Comparison of monozygotic and dizygotic twins
Monozygotic twins
Two babies developing
From similar zygote.
.Babies have one amnion , placenta and separate chorion.
.Babies have similar sex,
Habbits and blood group.
Dizygotic twins
Two ova fertilized by two Sperms.
.Each baby having its
Own amnion ,chorion and placenta.
.Babies may be males or female or may be one of
them is male and other
Is female.
ANY STRUCTURE THAT FUNCTIONS FOR THE PROTECTION, NOURISHMENT, RESPIRATION OR EXCRETION OF A DEVELOPING FETUS. THEY INCLUDE:
• Chorion
• Amnion
• Placenta
• Allantois
• Yolk sac
• Umbilical cord
Chorion Frondosum
In early weeks of development villi cover the entire surface of
chorion as it advances villi on embriyonic pole continue to grow
and expand give rise to the chorion frondosum
DECIDUA
A mucous membrane lining the uterus,modified during pregnancy
and shed at parturation or during menstruation
• Chorion frondosum (bushy or villous chorion)
• Chorion laeve (smooth chorion)
• Decidua basalis
• Decidua capsularis
• Decidua parietalis (decidua vera)
Structure of the Placenta
By the beginning of the 4th month, placenta has 2 components:
Fetal portion
Maternal portion
Chorionic & decidual plates
Junctional zone
Decidual septa & cotyledons
Circulation of the Placenta
• The intervillous spaces of a mature placenta contain approximately 150 ml of blood, which is replenished about 3 or 4 times per minute.
• Placental membrane / barrier (x)
Function of the Placenta
• Exchange of metabolic & gaseous products between maternal & fetal bloodstreams
Exchange of gases
Exchange of nutrients & electrolytes
Transmission of maternal antibodies
• Production of hormones
Fetal membranes in twins
Comparison of monozygotic and dizygotic twins
Monozygotic twins
Two babies developing
From similar zygote.
.Babies have one amnion , placenta and separate chorion.
.Babies have similar sex,
Habbits and blood group.
Dizygotic twins
Two ova fertilized by two Sperms.
.Each baby having its
Own amnion ,chorion and placenta.
.Babies may be males or female or may be one of
them is male and other
Is female.
Anion Gap and its Significance
The anion gap is the difference between unmeasured anions and unmeasured cations, and estimated as
plasma anion gap = (Na+) – (HCO3 ) – (Cl-)
Normal Values= 8-16mEq/L
• The most important cations are calcium, magnesium and potassium
• Major anions are albumin, phosphate, sulphate and other organic anions.
• The anion gap will increase if unmeasured anions increase or unmeasured cations fall
Use of Anion Gap
• In diagnosing different causes of metabolic acidosis
• Metabolic acidosis caused by excess nonvolatile acids (besides HCl), such as lactic acid or ketoacids, is associated with an increased plasma anion gap because the fall in [HCO3-] is not matched by equal increase in [Cl-].
• The metabolic acidosis associated with diarrhea or renal tubular acidosis has a normal anion gap because the decrease in [HCO3-] is matched by an increase in [Cl-].
Metabolic Acidosis Associated with Increased or Normal Anion Gap
Increased Anion Gap
• Diabetic Ketoacidosis
• Lactic Acidosis
• Chronic Renal Failure
• Aspirin Poisoning
• Methanol Poisoning
• Ethylene Glycol Poisoning
• Starvation
Normal Anion Gap (Hyperchloremia)
• Diarrhea
• Renal Tubular Acidosis
• Carbonic Anhydrase Inhibitors
• Addison Disease
• Acid Ingestion (HCl,NH4Cl)
• K+ -Sparing Diuretics
• Pancreatic fistula
Elevated Anion Gap
• Causes
• Ketoacid overproduction due to fat metabolism (diabetes, alcohol, starvation)
• Lactic Acid overproduction due to respiratory failure (the tissue has inadequate oxygen), genetic defects of enzymes of carbohydrate metabolism, nutritional deficiencies that impair the bodies ability to metabolize lactic acid (B vitamins, especially vitamin B1)
• Inability to excrete acids (sulfate and phosphate) due to renal disease (usually with an elevated BUN and creatinine).
• Dehydration.
• Medications such as salicylates causing a metabolic block.
• Toxins such as ethylene glycol, methanol, paraldehyde, propyl alcohol
Decreased Anion Gap
• Causes
• Alkalosis for any reason
• Hyperchloremic acidosis (excess chloride)
• Multiple Myeloma
• Hyponatremia (low blood sodium level;)
• Hypoalbuminemia (albumin can increase the amount of free blood calcium)
• Bromide Ingestion (displaces chloride)
• Uncalculated blood cations (calcium, magnesium)
• Lithium toxicity (can be due to effects on sodium)
• Primary hypothyroidism
• Kidney disease (due to the loss of the cations sodium and or potassium)
plasma anion gap = (Na+) – (HCO3 ) – (Cl-)
Normal Values= 8-16mEq/L
• The most important cations are calcium, magnesium and potassium
• Major anions are albumin, phosphate, sulphate and other organic anions.
• The anion gap will increase if unmeasured anions increase or unmeasured cations fall
Use of Anion Gap
• In diagnosing different causes of metabolic acidosis
• Metabolic acidosis caused by excess nonvolatile acids (besides HCl), such as lactic acid or ketoacids, is associated with an increased plasma anion gap because the fall in [HCO3-] is not matched by equal increase in [Cl-].
• The metabolic acidosis associated with diarrhea or renal tubular acidosis has a normal anion gap because the decrease in [HCO3-] is matched by an increase in [Cl-].
Metabolic Acidosis Associated with Increased or Normal Anion Gap
Increased Anion Gap
• Diabetic Ketoacidosis
• Lactic Acidosis
• Chronic Renal Failure
• Aspirin Poisoning
• Methanol Poisoning
• Ethylene Glycol Poisoning
• Starvation
Normal Anion Gap (Hyperchloremia)
• Diarrhea
• Renal Tubular Acidosis
• Carbonic Anhydrase Inhibitors
• Addison Disease
• Acid Ingestion (HCl,NH4Cl)
• K+ -Sparing Diuretics
• Pancreatic fistula
Elevated Anion Gap
• Causes
• Ketoacid overproduction due to fat metabolism (diabetes, alcohol, starvation)
• Lactic Acid overproduction due to respiratory failure (the tissue has inadequate oxygen), genetic defects of enzymes of carbohydrate metabolism, nutritional deficiencies that impair the bodies ability to metabolize lactic acid (B vitamins, especially vitamin B1)
• Inability to excrete acids (sulfate and phosphate) due to renal disease (usually with an elevated BUN and creatinine).
• Dehydration.
• Medications such as salicylates causing a metabolic block.
• Toxins such as ethylene glycol, methanol, paraldehyde, propyl alcohol
Decreased Anion Gap
• Causes
• Alkalosis for any reason
• Hyperchloremic acidosis (excess chloride)
• Multiple Myeloma
• Hyponatremia (low blood sodium level;)
• Hypoalbuminemia (albumin can increase the amount of free blood calcium)
• Bromide Ingestion (displaces chloride)
• Uncalculated blood cations (calcium, magnesium)
• Lithium toxicity (can be due to effects on sodium)
• Primary hypothyroidism
• Kidney disease (due to the loss of the cations sodium and or potassium)
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