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HemodynamicsHemodynamics
EDEMAEDEMA
Dr.CSBR.Prasad, M.D.
11:07 AM SDUMCpath-CSBRP 2
Normal tissue fluid circulationNormal tissue fluid circulation
• There is continuous interchange of fluid
between blood and tissues
• Fluid that leaks out of capillaries will be
returned to the blood stream thru
lymphatics
1 edema
1 edema
Constituents of Extracellular
and Intracellular Fluids
1 edema
1 edema
Body Fluid CompartmentsBody Fluid Compartments
The total body fluid is distributed mainly
between two compartments:
1- the extracellular fluid [1/3 rd] and
the interstitial fluid [¾ of ecf] and
the blood plasma [¼ of ecf]
2- the intracellular fluid [2/3rds]
3- transcellular fluid [1-2 ltrs]
Two forces act to maintain normal fluid balance between intravascular
and extravascular compartments
1- Hydrostatic pressure (HP):
drives the fluid out
~35mm of Hg
2- Protein osmotic pressure (Oncotic pressure - OP):
retains the fluid in the capillaries
~25mm of Hg
Arterial end: HP > OP = fluid forced out of capillary
Venous end: HP < OP = fluid is attracted into the vessel
Note: some fluid enters the lymphatic channels. This may be due to…
- partly due to tissue pressure
- partly due to OP of proteins in the lymphatics
Normal tissue fluid circulationNormal tissue fluid circulation
1 edema
Body water controlBody water control
In addition to those forces operating at
capillary level there are other
mechanisms which influence the
movement of fluid within the body in a
general manner:
1. Fluid intake
2. Integrity of the kidneys
3. Hormone activity (Aldosterone, ADH)
Definition:
The term edema signifies increased fluid in
the interstitial tissue and tissue spaces.
Depending on the site, fluid collections in the
different body cavities are variously designated
Hydrothorax,
Hydropericardium, &
Hydroperitoneum (Ascitis)
Anasarca is a severe and generalized edema with
profound subcutaneous tissue swelling.
EdemaEdema ((GrGr oidemaoidema==swellingswelling))
Increased Hydrostatic Pressure
Impaired venous return
Congestive heart failure
Constrictive pericarditis
Ascites (liver cirrhosis)
Venous obstruction or compression
Thrombosis
External pressure (e.g., mass)
Lower extremity inactivity with prolonged dependency
Arteriolar dilation
Heat
Neurohumoral dysregulation
Sodium Retention
Excessive salt intake with renal insufficiency
Increased tubular reabsorption of sodium
Renal hypoperfusion
Increased renin-angiotensin-aldosterone secretion
Inflammation
Acute inflammation
Chronic inflammation
Angiogenesis
Reduced Plasma Osmotic Pressure
(Hypoproteinemia)
Protein-losing glomerulopathies (nephrotic syndrome)
Liver cirrhosis (ascites)
Malnutrition
Protein-losing gastroenteropathy
Lymphatic Obstruction
Inflammatory
Neoplastic
Postsurgical
Postirradiation
List of pathophysiologicList of pathophysiologic
categories of edemacategories of edema
SitesSites
Although any organ or tissue in the body
may be involved, edema is most
commonly encountered in:
• subcutaneous tissues,
• the lungs, and
• the brain.
Note: Severe, generalized edema is called
anasarca.
Clinical importanceClinical importance
Effects of edema: may range from merely annoying to fatal
• Subcutaneous tissue edema in cardiac or renal failure is important
primarily because it signals underlying disease; however, when
significant, it can also impair wound healing or the clearance of
infection.
• Pulmonary edema can cause death by interfering with normal
ventilatory function. Not only does fluid collect in the alveolar septa
around capillaries and impede oxygen diffusion, but edema fluid in
the alveolar spaces also creates a favorable environment for
bacterial infection.
• Brain edema is serious and can be rapidly fatal; if severe, brain
substance can herniate (extrude) through, for example, the foramen
magnum, or the brain stem vascular supply can be compressed.
Either condition can injure the medullary centers and cause death.
EdemaEdema
Conditions which interfere with the pressure
gradients systems results in edema:
1- >HP (esp. in the venous end)
2- <OP (blood)
3- Alterations in capillary permeability
(ex: Inflammation)
4- Impeded lymphatic drainage
1-Increased HP
2-Decreased OP
3-Increased capillary permeability
4-Impaired lymphatic drainage
General Pathogenetic factors
1 edema
Hydrostatic edema
• Cardiac edema
• Portal edema
• Venous edema
• Osmotic edema
Oncotic edema
• Vascular edema
• Lymphedema
Hydrostatic edema
Portal edema:
Edema in the region drained by portal vein (esp.
in the intestines) or occuring in the setting of
portal HT
Ascites only occurs where the postsinusoidal
vessels are constricted, as can occur in
cirrhosis of the liver
1 edema
Budd-Chiari syndromeBudd-Chiari syndrome
Budd-Chiari syndromeBudd-Chiari syndrome
Ascites only occurs where the
postsinusoidal vessels are constricted
Cirrhosis
1 edema
AscitisAscitis
A special form of hydropsA special form of hydrops
Hydrops fetalisHydrops fetalis
Hydrostatic edema
Venous edema :
Edema occuring in the regions with impaired
venous drainage
Etiological factors:
1. Venous occlusion (thrombosis, compression)
2. Venous insufficiency (varicosities)
Varicose veinsVaricose veins
1 edema
1 edema
1 edema
1 edema
SuperiorSuperior
venacavalvenacaval
syndromesyndrome
Superior venacaval syndromeSuperior venacaval syndrome
Photographs of the patient showing the reduction in swelling of the face, neck and
upper extremities
(A) At initial presentation and (B) after treatment (hospital day 8)
Pleural effusion
Chylothorax
The chest
radiograph here
demonstrates a
large pleural
effusion nearly
filling the left chest
cavity.
Bilateral Pleural effusion
Osmotic edema
Edema resulting from an imbalance of
sodium chloride and water in the blood
Etiological factors:
1. Hypotonic hydration (excess water
intake, High ADH) - hyponatremia
2. Hypertonic hydration (increased intake
of Na+, Conn’s syn, Cushing’s
syndrome) - hypernatremia
Oncotic edema
Edema resulting from low colloidal osmotic
pressure due to protein deficiency
Etiological factors:
1. Proteinuria – Nephrotic syndrome
2. Protein losing enteropathy
3. Starvation (protein malnutrition)
4. Cirrhosis of liver (deficient albumin)
Vascular edema –
increased vascular permeability
Edema resulting from generation of inflammatory
mediators > increased vascular permeability
Etiological factors:
1. Pathogens and their toxins
2. Immune complexes
3. Chemical agents (mustard gas)
4. Toxic metabolites (uremia)
5. Release of chemical mediators of inflammation
6. Persistence of complement factors (inhibitor
deficiencies)
Lymphedema
Edema occuring as a result of functional and
/ or obstructive impairment of lymph
drainage from tissue
Etiological factors:
1. Primary lymphedema (congenital defects)
2. Secondary lymphedema (oblockage)
Normal lymph drainage
• Plasma along with the proteins passes in
to the interstitium (half of plasma proteins)
• They are taken by the lymphatics
• Returned to the blood by thoracic duct
Properties of lymphaticProperties of lymphatic
channelschannels
• Tube-like
• Numerous valves
• Drains fluid back to blood-stream – passes
through at least one lymph-node.
• Present in all tissues except
– CNS, Eyeballs, Internal Ear, Epidermis of the
skin, cartilage and bone.
Taken from Guyton & Hall – Human Physiology and
Mechanisms of Disease
Schematic of
lymphatic
channels
Taken from Colour Atlas of Anatomy –
Roden, Yokochi and Lutjen-Drecoll
Thoracic ductThoracic duct
1 edema
Lymphedema
Etiological factors:
Primary lymphedema (congenital defects)
• Milroy’s edema
• Obliterative lymphatic disease (sclerosis
of lymph vessels at the calf)
Lymphedema
Etiological factors:
Secondary lymphedema (oblockge)
• Lymphagiosis carcinomatosa
• Recurring lymphangiitis (erysipelas)
• Lymph vessel scarring after burns
• Sclerotherapy / LN block dissection
• Meigs’ syndrome
Lymphedema
Special forms of lymphedema:
1. Anasarca
2. Hydrops
Hydrops: is excessive accumulation of watery fluid in existing organ cavities.
Lymphedema - sequelae
1. Sclerosis
2. Dermatopathy
3. Stewart-Treves syndrome
Filariasis
Non-pitting edema
Dermatopathy
1 edema
1 edema
Peau d’ orange – Breast carcinoma
Breast carcinoma - lymphedema
Peau d‘ Orange (orange peel)
Inflammatory carcinoma – dermal lymphatic involvement
Lymphangitis carcinomatosa
1 edema
Stewart-Treves syndrome:
Lymphedema due to axillary
lymphnode dissection –
for breast cancer – and
she has developed
malignant tumor
(lymphangiosarcoma) of
upper arm
1 edema
Dilated lymphatics in instestinal wall
Milroy’s edemaMilroy’s edema
Milroy’sMilroy’s edemaedema
Milroy’sMilroy’s edemaedema
Milroy’s edemaMilroy’s edema
Chylothorax
Cerebral edema
Def: Diffuse / local accumulation of fluid in
the brain with a resulting increase in the
volume of the brain tissue
According to the magnitude: it may be
1. Generalized (involving entire brain)
2. Perifocal edema (inflammation, tumors)
Cerebral edema
Causes:
1. Vasogenic CE
2. Cytotoxic CE
3. Interstitial CE
4. Hyposmotic CE
Cerebral edema
Causes:
Vasogenic CE
Mechanism: disruption of BBB
Brain tumors
Cerebral infarcts
Injury
Massive cerebral hemorrhage
Cerebral abscess
Cerebral edema
Cytotoxic CE
Mechanism: disruption of BBB secondary
to collapse of energy metabolism
Loss of ATP-dependent ion pump >
passive inflow of water in to the cells
Ischemia
Liver failure
Cyanide poisoning
Cerebral edema
Interstitial CE
Mechanism: impaired drainage of CSF
Impaired drainage
Obstructive hydrocephalus
Cerebral edema
Hyposmotic CE
Mechanism: hypervolemia with
hyponatremia
Cerebral edema
Complications CE
Herniation of brain tissue (sub falcine,
transtentorial, tonsillar)
Clinical symptoms:
• Cardiac arrest
• Respiratory paralysis
Gross: The surface of the brain with cerebral edema
demonstrates widened gyri with a flattened surface.
The sulci are narrowed.
Herniation:
1-Sub falcine
2-Transtentorial
3-Tonsillar
• Acute brain swelling in the closed cranial cavity is
serious. Swelling of the left cerebral hemisphere has
produced a shift with herniation of the uncus of the
hippocampus through the tentorium, leading to the
groove seen at the white arrow.
• Acute cerebral swelling can also often produce
herniation of the cerebellar tonsils into the foramen
magnum.
• coronal view demonstrates a cysticercus cyst of the
brain which has a dark cystic center and distinct
bright border with gadolinium enhancement.
• This computed tomographic (CT) scan of the head
in transverse view demonstrates an abscess in the
brain in a patient who had septicemia
• This magnetic resonance imaging (MRI) scan of the
head in sagittal view reveals the presence of several
well-circumscribed metastatic tumor nodules of the
brain.
Hydrocephalus
Papilledema
Urticaria - Hives
• Crops of patches involving the skin which are
erythematous, edematous and itchy
• Secondary to mast cell degranulation mediated
by immune mechanisms
• Vasoactive substances are released resulting in
vasodilataion and increased vascular
permeability
• Factors: Histamine, PAF, LT-C4, D4, E4, PG-D2
Urticaria - Hives
1 edema
Coldurticaria: Ice cube test for cold urticaria
Angioneurotic edema
Deficiency of C3 convertase inhibitor
Result: unapposed activation of complement
with resultant vasoactive substances C3a,
C5a et.c. causing edema
Sites: Lips, Tongue, Larynx.
Classical complement pathway
1 edema
Angioneurotic edema
TermsTerms
• Ascites
• Hydrothorax
• Anasarca
• Lymphedema
• Pulmonary edema
• Cerebral edema
• Angioneurotic edema
Pulmonary edemaPulmonary edema
Pulmonary edemaPulmonary edema
The balance between these forces is relatively fine
and can be easily upset so that edema can
occur rapidly:
Cardiac failure & over transfusion / infusion
increased HP
Inhalation of irritant gases & inflammation
increased capillary permeability
Pulmonary edemaPulmonary edema
The smooth, glistening pleural surface of a lung is shown here. This patient had
marked pulmonary edema, which increased the fluid in the lymphatics that run
between lung lobules. Thus, the lung lobules are outlined in white.
Taken from Sternberg`s HISTOLOGY for PATHOLOGISTS
The alveoli in this lung are filled with a smooth to slightly floccular pink material
characteristic for pulmonary edema. Note also that the capillaries in the alveolar
walls are congested with many red blood cells.
Heart failure cells
Pulmonary
edema
Generalized edemaGeneralized edema
• Cardiac edema
• Renal edema
• Famine edema (Malnutrition)
Cardiac edemaCardiac edema
Generalized edema - CardiacGeneralized edema - Cardiac
Systemic
circulation
vs.
Pulmonary
circulation
Taken from
Robbins Pathologic Basis of Disease
↑↑ JVP
Acute nephritis
Nephrotic syndrome
Mechanism:
1. <OP due to protein loss thru the
kidneys
2. Na+ and H2O Retention
Generalized edema - RenalGeneralized edema - Renal
Renal edemaRenal edema
Acute NephritisAcute Nephritis NephrosisNephrosis
Degree of edema Slight Marked
Distribution Around eyes Generalized
Proteinuria Slight Marked
Plasma OP Normal Reduced
Mechanism Retention of fluid Low plasma OP
Two forms of renal diseases are associated with edema:
1- Acute nephritis & 2- Nephrotic syndrome
Malnutrition > [Food low in proteins] >
Protein deficiency > reduced OP >
generalized edema
Malnutrition > vitamin deficiency(B1) > Beri-
Beri > cardiac failure
Generalized edema - FamineGeneralized edema - Famine
1 edema
Pitting edemaPitting edema
Pitting edemaPitting edema
Pretibial myxedema
(Hyperthyroidism)
Taken from Guyton & Hall – Human
Physiology and Mechanisms of Disease
Oedema
• Water compartments
• Movement of water between the
compartments
• Causes of oedema
• Pulmonary oedema
• Cerebral oedema
Taken from Guyton & Hall – Human Physiology and Mechanisms
of Disease
Taken from Underwood – General and Systemic Pathology
Taken from
Guyton & Hall –
Human Physiology
and Mechanisms
of Disease
Taken from
Guyton & Hall
– Human
Physiology
and
Mechanisms
of Disease
Taken from Guyton & Hall – Human Physiology and
Mechanisms of Disease
Taken from Guyton & Hall – Human Physiology and
Mechanisms of Disease
Taken from Guyton & Hall – Human Physiology and
Mechanisms of Disease
Taken
from
Guyton &
Hall –
Human
Physiology
and
Mechanis
ms of
Disease
Taken from Underwood – General and Systemic Pathology
Taken from Underwood – General and Systemic Pathology
Taken from Underwood – General and Systemic Pathology
Taken from Sternberg`s HISTOLOGY for PATHOLOGISTS
Taken from Colour Atlas of
Anatomy – Roden, Yokochi
and Lutjen-Drecoll
Taken from Colour Atlas
of Anatomy – Roden,
Yokochi and Lutjen-
Taken from Colour
Atlas of Anatomy –
Roden, Yokochi
and Lutjen-Drecoll
E N DE N D

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1 edema

Editor's Notes

  • #4: Ref: Robbin’s Path Figure 4-1  Factors affecting fluid balance across capillary walls. Capillary hydrostatic and osmotic forces are normally balanced so that there is no net loss or gain of fluid across the capillary bed. However, increased hydrostatic pressure or diminished plasma osmotic pressure leads to a net accumulation of extravascular fluid (edema). As the interstitial fluid pressure increases, tissue lymphatics remove much of the excess volume, eventually returning it to the circulation via the thoracic duct. If the ability of the lymphatics to drain tissue is exceeded, persistent tissue edema results.
  • #9: Body Fluid Compartments: The total body fluid is distributed mainly between two compartments: the extracellular fluid and the intracellular fluid (Figure 25–1). The extracellular fluid is divided into the interstitial fluid and the blood plasma. There is another small compartment of fluid that is referred to as transcellular fluid. This compartment includes fluid in the synovial, peritoneal, pericardial, and intraocular spaces, as well as the cerebrospinal fluid; it is usually considered to be a specialized type of extracellular fluid, although in some cases, its composition may differ markedly from that of the plasma or interstitial fluid. All the transcellular fluids together constitute about 1 to 2 liters.
  • #12: 1-Fluid intake: intake via the gut or parenterally may exceed the ability of the kidneys to eliminate water. 2-Integrity of the kidneys: Damage to the renal parenchyma may diminish the elimination of fluid. 3-Hormone activity: Aldosterone (increases resorption of sodium by distal tubule which in turn results in retention of water). ADH (increases reabsorption of water by distal and collecting tubules).
  • #15: Subcutaneous edema may have different distributions depending on the cause. It can be diffuse, or it may be relatively more conspicuous at the sites of highest hydrostatic pressures. In the latter case, the edema distribution is typically influenced by gravity and is termed dependent. Edema of the dependent parts of the body (e.g., the legs when standing, the sacrum when recumbent) is a prominent feature of congestive heart failure, particularly of the right ventricle. Edema as a result of renal dysfunction or nephrotic syndrome is generally more severe than cardiac edema and affects all parts of the body equally. It may, however, initially manifest itself in tissues with a loose connective tissue matrix, such as the eyelids; thus, periorbital edema is a characteristic finding in severe renal disease. Finger pressure over substantially edematous subcutaneous tissue displaces the interstitial fluid and leaves a finger-shaped depression, so-called pitting edema. Pulmonary edema is a common clinical problem ( Chapter 15 ) most typically seen in the setting of left ventricular failure but also occurring in renal failure, acute respiratory distress syndrome ( Chapter 15 ), pulmonary infections, and hypersensitivity reactions. The lungs are two to three times their normal weight, and sectioning reveals frothy, blood-tinged fluid representing a mixture of air, edema fluid, and extravasated red blood cells. Edema of the brain may be localized (e.g., owing to abscess or neoplasm) or may be generalized, as in encephalitis, hypertensive crises, or obstruction to the brain&amp;apos;s venous outflow. Trauma may result in local or generalized edema depending on the nature and extent of the injury. With generalized edema, the brain is grossly swollen, with narrowed sulci and distended gyri, showing signs of flattening against the unyielding skull.
  • #16: Clinical Correlation. Effects of edema may range from merely annoying to fatal. Subcutaneous tissue edema in cardiac or renal failure is important primarily because it signals underlying disease; however, when significant, it can also impair wound healing or the clearance of infection. Pulmonary edema can cause death by interfering with normal ventilatory function. Not only does fluid collect in the alveolar septa around capillaries and impede oxygen diffusion, but edema fluid in the alveolar spaces also creates a favorable environment for bacterial infection. Brain edema is serious and can be rapidly fatal; if severe, brain substance can herniate (extrude) through, for example, the foramen magnum, or the brain stem vascular supply can be compressed. Either condition can injure the medullary centers and cause death.
  • #17: The term edema signifies increased fluid in the interstitial tissue spaces. In addition, depending on the site, fluid collections in the different body cavities are variously designated hydrothorax, hydropericardium, and hydroperitoneum (the last is more commonly called ascites). Anasarca is a severe and generalized edema with profound subcutaneous tissue swelling.
  • #19: Taken from Guyton &amp; Hall – Human Physiology and Mechanisms of Disease
  • #25: The Budd-Chiari Syndrome: syndrome hepatic venous obstruction. Note the grossly dilated veins in the abdominal wall, in which the flow of blood was upwards. The patient had continued to work as a builder&amp;apos;s labourer without symptoms, until he was admitted with coincidental appendicitis. The cause of his hepatic venous obstruction was unclear.
  • #32: varicosities-1 Varicose veins around the foot and medial leg varicosites-2 Varicose veins around the knee and thigh.
  • #36: Fig-1: A large amount of the thrombi extracted with a Fogarty catheter. Fig-2: The photograph on the left shows a massive thrombus in the femoral vein of the leg. This large thrombus dislodged, formed a thromboembolus, which traveled to the lung and resulted in pulmonary embolus. The photograph on the right shows the thromboembolus after removal from the pulmonary vessels. A large thromboembolus that completely occludes the entire pulmonary artery by lodging at the bifurcation of the pulmonary trunk is often fatal, as it was in this case. DVT = deep vein thrombosis; PE = pulmonary embolism. Sources: Cotran RS, Kumar V, Robbins SL. Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, Pa: WB Saunders; 1994:111; Yonkman FF, ed.
  • #37: Superior vena cacval syndrome: Superior vena cava obstruction causing dilated veins and plethora of the upper trunk and neck in a patient with bronchial carcinoma. Patients with SVC obstruction are occasionally referred to dermatologists with suspected contact allergy (eyelid swelling) or angioedema (facial or hand swelling).
  • #39: A pleural effusion occurs when fluid collects in the potential space between the parietal pleura on the lung and the visceral pleura on the chest wall. In this case, the fluid is red (serosanguinous), while the presence of clear fluid would be called a serous effusion--a transudate with few or no cells. However, an exudate would include cells and protein and have a cloudy appearance.
  • #40: -The right pleural cavity is filled with a cloudy yellowish-tan fluid, characteristic for a chylothorax, which is uncommon. In this case, malignant lymphoma involving the lymphatics of the chest and abdomen led to the collection of chylous fluid. The right lung is markedly atelectatic.
  • #41: The chest radiograph here demonstrates a large pleural effusion nearly filling the left chest cavity. This fluid collection occurred postoperatively following a left pneumonectomy.
  • #55: Hydrops: is excessive accumulation of watery fluid in existing organ cavities such as gall bladder. Special forms of hydrops include hydrocephalus and ascitis.
  • #56: Sclerosis: persistent lymphedema stimulates proliferation of stromal fibroblasts which form collagen. This leads to fibortic hardening of tissue that was formerly soft and edematous.
  • #61: peau d&amp;apos;orange (orange peel): Such a finely pitted appearance results from an accentuation of depressions in the skin at the site of hair follicles.
  • #63: There are prominent linear white markings outlining lung lobules as seen on the external surface of this lung. The metastases are following the lymphatics between the lobules. The cut surface of this lung reveals linear interstitial markings and nodules in a case of lymphangitic spread of metastatic carcinoma, one of the less common pattern of metastasis. Th chest CT scan above in lung window and below in bone window both demonstrate a diffuse reticular and nodular pattern of involvement by metastatic carcinoma spreading into the lymphatic channels of the lung. There is also a large malignant pleural effusion on the left.
  • #64: A nest of metastatic infiltrating ductal carcinoma from breast is seen in a dilated lymphatic channel in the lung. Carcinomas often metastasize via lymphatics. Prostatic adenocarcinoma is famous for metastasizing to the lungs in a &amp;quot;lymphangitic&amp;quot; pattern in which streaks of tumor appear between lung lobules and beneath the pleura in lymphatic spaces.
  • #72: The right pleural cavity is filled with a cloudy yellowish-tan fluid, characteristic for a chylothorax, which is uncommon. In this case, malignant lymphoma involving the lymphatics of the chest and abdomen led to the collection of chylous fluid. The right lung is markedly atelectatic.
  • #92: coldurticaria1: ice cube test for cold urticaria
  • #101: The smooth, glistening pleural surface of a lung is shown here. This patient had marked pulmonary edema, which increased the fluid in the lymphatics that run between lung lobules. Thus, the lung lobules are outlined in white.
  • #103: At high magnification, the alveoli in this lung are filled with a smooth to slightly floccular pink material characteristic for pulmonary edema. Note also that the capillaries in the alveolar walls are congested with many red blood cells. Congestion and edema of the lungs is common in patients with heart failure and in areas of inflammation of the lung.
  • #104: Pulmonary congestion with dilated capillaries and leakage of blood into alveolar spaces leads to an increase in hemosiderin-laden macrophages, as seen here. Brown granules of hemosiderin from break down of RBC&amp;apos;s appear in the macrophage cytoplasm. These macrophages are sometimes called &amp;quot;heart failure cells&amp;quot; because of their association with pulmonary congestion with congestive heart failure.
  • #107: Ref: Robbin’s Path Figure 4-2  Sequence of events leading to systemic edema due to primary heart failure, primary renal failure, or reduced plasma osmotic pressure (as in malnutrition, diminished hepatic protein synthesis, or loss of protein owing to the nephrotic syndrome). ADH, antidiuretic hormone; GFR, glomerular filtration rate.
  • #110: Distended Jugular Veins: This patient with severe mitral stenosis is sitting upright. Note the distention of the jugular veins almost to the mandible, reflecting elevated pressures in right heart pressure.
  • #112: OP=oncotic pressure.
  • #117: pretibialmyxedema2: Pretibial myxedema demonstrating the peau d’orange appearance which is typical of diffuse cutaneous mucin deposition. pretibialmyxedema1: Pretibial myxedema in thyrotoxicosis. Deposition of mucin in this condition is often variable in degree, leading to a cobblestoned appearance of the lower legs. Toes are also often affected.