Flashcards in Module 3-Path Deck (47):
what is edema?
Abnormal excess accumulation of fluid in intercellular spaces or body cavities
What are the most common places for edema to be?
SQ tissues of the lungs and brain
What are the most common causes of edema?
occur in heart or liver
What is anasarca?
extreme generalized edema
If a patient presents with acute edema will the levels of albumin be normal?
yep normal albumin levels because albumin lifespan is 120 days vs. chronic=abnormal
What are the different components of normal capillary filtration?
1. Colloid Osmotic Pressure in tissues (pressure for fluid to move out of vessel to the tissues)
2. Hydrostatic pressure in tissues (pressure for fluid to go back into vessel)
3. Hydrostatic pressure of vessel (pressure for fluid to leave vessel to tissue)
4. Oncotic pressure vascular (pressure for fluid to go into vessel)
5. Normally , 2ml of fluid empties into lymph
Clinical case 1: a forty year old male presents with complaints of swollen ankles and weakness.. what are the causes of swelling over the ankles?
Pitting or non-pitting
If non-pitting = myxedema: describes changes associated with hypothyoridism; excessive synthesis of GAGs= puffy features, enlarge tongue, hoarseness
if pitting: heart (SOB and chest pain) , liver (jaundice) , kidney (urine abnormalities) or GIT (nutrition). impaired wound healing, thickening, susceptible to infection
Explain what edema based on pleural space, pericardium and peritoneum
1. Pleural space: pleural effusion (hydrothorax)
2. Pericardium: pericardial effusion (hydropericardium)
3. Peritoneum: ascites (hydroperitoneum)
Edema is based on 4 different mechanisms, each card will go through one. 1)
1) Increased plasma hydrostatic pressure:
-Impaired venous return: congestive heart failure (if left sided: pul edema and if right sided: peripheral edema) and venous obstruction or compression: thrombosis or external pressure (neoplasm)
-hypervolemia: sodium retention (renal failure) = increased H20 = Increased Pressure (generalized)
2nd mechanism for edema
2) Decreased plasma oncotic pressure = hypoproteinemia
-Decreased albumin synthesis (leads to fluid leaking out) : malnutrition and liver disease
-Increased albumin loss: renal disease
-Decreased absorption: protein losing enteropathy
3rd mechanism for edema
3) Lymphatic obstruction (increased interstitial fluid colloid osmotic pressure):
-postsurgical/radiation -> exposed to radiation the rays kill all the tissues including blood vessels and this leads to fibrosis
-note the albumin level will be normal
-no other abnormalities in any other part of the body
4th mechanism for edema
4) Altered Membrane Permeability:
-inflammation (Acute or chronic) (localized except in anaphylaxis)
Clinicopathology of Edema includes 4 causes.. each card will go through one. 1)
1) Congestive heart failure
-Right heart failure: increased hydrostatic pressure-edema and dependent edema: legs, sacrum --> looks for bilateral pedal edema
-left heart failure: less blood to kidneys = Decreased GFR, RAS system = sodium retention to try and increase blood volume
-management: salt restriction, diuretics and aldosterone antagonists
2nd clinicopathology of edema
2) Renal Disease
-Damaged BM: excess albumin loss: hypoalbuminemia (nephrotic syndrome). Decreased albumin synthesis = decreased plasma oncotic pressure
-Glomerulonephritis (post streoptococcal): inflammatory damage w/clogging of glomerular capillaries --> reduced GFR. Secondary hyperaldosteronism: sodium and water retention. Generalized edema: initially periorbial edema
3rd clinicopathology of edema
3) Liver Disease:
-Cirrhosis of the liver: portal HTN --> increased hydrostatic pressure in splanchnic circulation --> ascites. Decreased albumin synthesis = decreased plasma oncotic pressure (so capillaries are gonna leak)
remember albumin is only low in chronic diseases
4th clinicopathology of edema
decreased serum albumin --> decreased plasma oncotic pressure --> decrease in effective plasma volume --> secondary hyperaldosteronism ---> sodium and water retention --> edema
Classification of edema is based on transudate and exudate. Explain Transudate
-Passive process (increased pressure)
-normal vascular permeability
-Plasma protein leak absent
- Protein content of fluid is low
---S.G. is low
What is exudate in edema
-Increased vascular permeability
-plasma protein leak present
-Protein content of fluid: High SG > 1.020 and proteins >1.5
Morphology of edema: describe it in aspects of the skin
Skin: some edema can be seen as swelling; affecting due to poor circulation (infection)
micro: cell swelling. clearing and separation of ECM
Morphology of edema: describe it in aspect of pulmonary edema
Interstitial: early phase
Alveolar: frothy fluid in alveolar lumen
Severely congested alveolar capillaries and alveolar filled with homogenous pink staining fluid
Clinical features: cough, dyspnea
Severe cases: frothy sputum, cyanosis --> fluid prevents gas exchange
Clinical Case: A 25 year old male complained of severe head ache. Opthalmic examination revealed features of papilledema. There was pupillary dilation and impaired ocular movements on one side. What does papilledema indicate?
Edema in the brain aka cerebral edema
-headache, papilledema--> blurred/swollen optic disk
-motor/sensory abnormalities; cingulate gyrus compression
-treated by IV mannitol and steriods
-Flattened gyri and narrowed sulci; midline shift of brain structures
-Compression of ventricular cavities
There are 2 categories of cerebral edema, each card will go through one. First one is Vasogenic edema
1. Vasogenic Edema:
-disruption of the BBB= allows intravascular proteins and fluid to penetrate brain= interstitial edema
-infections, trauma, neoplasms (damage to brain capillaries = more permeable)
2nd category of cerebral edema
2. Cytotoxic Edema (Gray matter)
-intracellular edema: due to cell injury --impaired function of Na/K pump; BBB intact
-hypoxic ischemic insult
-inadequate blood supply to neurons = not enough oxygen (Cell lysis)
There are three herniations addressed in this class. Each card will go through one. 1)
1) Transtentorial (uncal)--> displacement of the temporal lobe
-compression of CN3 and PSNS fibers; impaired ocular movements, pupillary dilation
-Duret hemorrhages in midbrain and pons
2nd herniation addressed
2) Tonsillar: through the foramen magnum
-brain stem compression of respiratory centers in medulla = cardio-respiratory arrest = death
3rd herniation addressed
3) Subfalcine: displacement of cingulate gyru under falx cerebri
-compression of branches of an anterior cerebral artery
=ischemic injury of primary motor and/or sensory cortex = weakness and/or sensory abnormalities in legs
What is hyperemia?
Active process with increased blood volume due to arteriolar dilation mediated by histamine
What are the physiological causes for hyperemia?
Blushing and exercise
What are the pathological causes for hyperemai?
Acute inflammation reaction of meningitis preceding formation of purulent exudate
What is the only time you see exudate in the lungs?
What is congestion?
Passive increase in the volume of blood in tissues (blue-red color) ; usually also accompained by edema
Acute/Chronic congestion of the lung is due to left heart failure, explain the mechanism
Hypertension/Aortic stenosis --> left heart failure --> pulmonary edema
-caused by impaired venous flow --> venules are predominantly affected
Before 2 weeks, what type of edema is seen?
Transudate (less protein, less inflammatory cells and lower specific gravity) due to increased hydrostatic pressure --> engorged capillaries --> dyspnea
Before 2 weeks what symptoms do you see in a patient with acute congestion of the lungs?
Coughing up frothy sputum
After 2 weeks, what is the key that you are gonna see on microscopic image?
Hemosiderin laden macrophages ( heart failure cells)
Fibrosis of alveolar walls
How is the patient going to present with a chronic congestion of the lungs?
SOB, orthopnea, paroxysmal nocturnal dyspnea, pink frothy sputum, pulmonary edema
On gross specimen of the acute pulmonary congestion, describe the what it looks like?
Boggy (wet) and red (due to all the RBCs)
Is acute congestion inflammation?
NOOOO! hence why you dont see any inflammatory cells or WBCs.
remember transudate for acute congestion
Chronic congestion is due to what?
Right heart failure
What are the cause of right heart failure?
Left Heart Failure
Pulmonary Valve Stenosis
Right Ventricular Hypertrophy
Recurrent Pulmonary Emboli
What are the classic symptoms of right heart failure?
Distended jugular veins
After 2 weeks of chronic congestion due to right heart failure, what is the liver referred to?
Nutmeg liver due to right heart failure (cardiac cirrhosis) or stenosis of hepatic vein (Budd Chiari)
Liver in chronic congestion will transform from heptaosplenomegaly to what?
In the gross specimen of the liver, what are the yellow and tan parts?
yellow/pale = fatty changes (steatosis)
Tan = coagulative necrosis and hemosiderian laden Kuppfer cells (macrophages)
Coagulative necrosis is referred to as red infarct. Describe zone 1 in nutmeg liver
-closest to the hepatic artery in the portal triad ( receives more O2) --> reversible fatty change in liver (Steatosis) (no oxygen for beta oxidation of FAs) -->pale areas
Use special fat stains for this
-more susceptible to toxins
Describe zone 3 in nutmeg liver
Zone 3: furthest from hepatic artery/closest to central vein in portal triad --> coagulative necrosis (centrilobular necrosis) with hemosiderin in Kuppfer cells because central portion is the last to receive blood