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medyokaloka-blog · 7 years
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THE BODY FLUID COMPARTMENTS: ECF AND ICF; EDEMA
Homeostasis – maintenance
 WATER IS ADDED TO THE BODY BY 2 MAJOR SOURCES:
·         Form of liquids or water in food (which add about 2100 ml/day)
·         Synthesized in the body by oxidation of CHO (which add about 200 ml/day)
 2300 ml/day – total water intake
 INTAKE OF WATER IS HIGHLY VARIABLE DEPENDING ON:
·         Climate
·         Habits
·         Level of physical activity
 Insensible water loss – not consciously aware of it
    700 ml/day – evaporation from the respiratory tract and diffusion through the skin
    300 to 400 ml/day – average water loss by diffusion through the skin (loss is minimized by the cholesterol-filled cornified layer of the skin) is also the same with diffusion through the respiratory tract
    3 to 5 L/day – rate of evaporation in those who have extensive burns
    As air enters the respiratory tract, it becomes saturated with moisture, to a vapor pressure of about 47 mmHg, before it is expelled.
    <47 mmHg – vapor pressure of inspired air
    Decreases to nearly 0 – in cold weather (this explains why there’s a dry feeling in the respiratory passages in cold weather)
 100 ml/day – fluid loss in sweat
  Increases to 1 to 2 L/hour – in very hot weather or during heavy exercise (this fluid loss would rapidly deplete the body fluids if intake were not also increased by activating the thirst mechanism)
 100 ml/day – water loss in feces
 The remaining water loss from the body occurs in the urine.
    0.5 L/day – urine volume in a dehydrated person
    20 L/day – in a person who has been drinking tremendous amounts of water
 20 mEq/day to 300 or 500 mEq/day – sodium intake
  If you’re a medical student or a doctor, and you’re reading this…you know what are the 2 body fluid compartments right?  ECF and ICF.  Yeah, right it’s written as the title.
    ECF IS DIVIDED INTO:
·         Interstitial fluid
·         Blood plasma
    Transcellular fluid – another small compartment of fluid that is usually considered to be a specialized type of ECF (it constitute about 1 to 2 L)
    In a 70-kg adult man, the total body water is about 60% or about 42 L of the body weight.
    PERCENTAGE DEPENDS ON:
·         Age
·         Gender
·         Degree of obesity
    50% of the body weight – women
    70 to 75% of the body weight – premature and newborn babies
   28 of the 42 L (40%) – ICF
 14 of the 42 L (20%) – ECF
    11 L (3/4) – interstitial fluid
  3 L (1/4) – plasma
    They both have the same composition except for proteins which have a higher concentration in the plasma.
 Blood – considered to be a separate fluid compartment because it is contained in a chamber of its own, the circulatory system (The average blood volume of adults is about 7% of body weight, or about 5 L.  60%of the blood is plasma and 40% is RBCs.)
 Hematocrit – packed RBC volume
    3 to 4% - plasma that is entrapped among the cells
    96% - true hematocrit
    0.40 – NV for men
  0.36 – women
  0.10 – severe anemia (barely sufficient to sustain life)
  0.65 – those who have polycythemia
  I honestly don’t know what’s the definition for the Donnan Effect.  I guess (based on my understanding) it just speaks of how opposite charges attract. :)  (Please correct me if I’m wrong.)
    The concentration of cations is slightly greater in the plasma than in the interstitial fluid.  The plasma proteins have a net negative charge and therefore tend to bind cations, thus holding extra amounts of these cations in the plasma along with the plasma proteins.  
    Conversely, anions tend to have a slightly higher concentration in the interstitial fluid compared with the plasma, because the negative charges of the plasma proteins repel the anions.  
  CATIONS FOUND IN THE ECF:
·         Na+
·         Ca++
    ANIONS FOUND IN THE ECF:
·         Cl-
·         HCO3
    CATIONS FOUND IN THE ICF:
·         K+
·         Mg++
    ANIONS FOUND IN THE ICF:
·         PO4 and organic ions
·         CHON
  MEASUREMENT OF TOTAL BODY WATER:
·         Radioactive water (tritium, 3H2O)
·         Heavy water (deuterium, 2H2O)
    Antipyrine – a very lipid soluble used also to measure total body water
 MEASUREMENT OF ECF VOLUME:
·         Radioactive sodium
·         Radioactive chloride
·         Radioactive iothalamate
·         Thiosulfate ion
·         Inulin
    Sodium space or the inulin space
 CALCULATION OF INTRACELLULAR VOLUME:  Total body water – Extracellular volume
 MEASUREMENT OF PLASMA VOLUME:
·         125I-albumin
·         Evans blue dye (T-1824)
 CALCULATION OF INTERSTITIAL FLUID VOLUME:  ECF volume – Plasma volume
  MEASUREMENT OF BLOOD VOLUME:  Plasma volume / (1 – Hematocrit)
   51Cr – a substance frequently used to label the RBCs
  Osmolality – osmoles per kg of water
 Osmolarity – osmoles per L of solution
 ISOTONIC SOLUTIONS:
·         0.9% NaCl
·         5% glucose
 HYPOTONIC SOLUTION:  <0.9% NaCl (swells)
 HYPERTONIC SOLUTION:  >0.9% NaCl (shrinks)
 Fluid usually enters the body through the gut.  It usually takes 30 minutes to achieve osmotic equilibrium everywhere in the body after drinking water.  
  DIFFERENT FACTORS THAT CAN CAUSE EXTRACELLULAR AND INTRACELLULAR VOLUMES TO CHANGE MARKEDLY:
·         Excess ingestion or renal retention of water
·         Dehydration
·         IV infusion of different types of solutions
·         Loss of large amounts of fluid from the GI tract
·         Loss of abnormal amounts of fluid by sweating or through the kidneys
  Glucose solutions – are widely used in administering nutritive purposes (5% is often used to treat dehydration…well except for dehydration which have other causes like bacterial diarrhea)
 Homogenized fat solutions – used to a lesser extent
Plasma sodium concentration – measurement that is readily available to the clinician for evaluating a patient’s fluid status (Why?  You should probably know the answer.  You’re a doctor after all!)
    Hyponatremia – mEq < 142
    Hypernatremia – otherwise
    CAUSES OF HYPONATREMIA:
·         Excess water (CONDITION THAT CAN CAUSE THIS:  excessive secretion of ADH which could lead to hyponatremia – overhydration)
·         Loss of sodium (CONDITIONS THAT CAN CAUSE THIS:  diarrhea, vomiting, overuse of diuretics, Addison’s disease from decreased secretion of aldosterone which impairs the kidney to reabsorb sodium)
    PRIMARY LOSS OF NaCl RESULTS IN:
·         Hyponatremia
·         Dehydration
    Cell swelling – consequence of hyponatremia (DUH!)
    RAPID REDUCTION IN PLASMA SODIUM CONCENTRATION:
·         Brain cell edema
·         Neurological symptoms (headache, nausea, lethargy, disorientation)
    FALLS BELOW 115 TO 120 mmol/L:
·         Seizures
·         Coma
·         Permanent brain damage
·         Death
    Glutamate (find out what is this for)
    Demyelination – loss of the myelin sheath from nerves when hypertonic solutions are added too rapidly to correct hyponatremia (AVOIDED BY LIMITING THE CORRECTION:  <10 to 12 mmol/L in 24 hours, <18mmol/L in 48 hours)
    Hyponatremia (oh boy, this came out in our Surgery exam) – most common electrolyte disorder encountered in clinical practice and may occur in up to 15% to 25% of hospitalized patients
  CAUSES OF HYPERNATREMIA:
·         Water loss
·         Excess sodium (hypernatremia-overhydration by excessive secretion of aldosterone)
    Increased aldosterone secretion – stimulates the secretion of ADH and the reason why hypernatremia is not more severe
    PRIMARY LOSS OF WATER:
·         Hypernatremia
·         Dehydration – more common cause of hypernatremia associated with decreased ECF volume
    “Central” diabetes insipidus – inability to secrete ADH so the kidneys excrete large amounts of dilute urine causing dehydration and increased concentration of NaCl in the ECF
    “Nephrogenic” diabetes insipidus – kidneys cannot respond to ADH
    Cell shrinkage – consequence of hypernatremia
    HYPERNATREMIA PROMOTES:
·         Intense thirst
·         Stimulates secretion of ADH
    SEVERE HYPERNATREMIA CAN OCCUR IN:
·         Hypothalamic lesions that impair the sense of thirst
·         Infants who may not have ready access to water
·         Elderly patients with altered mental status
·         Persons with diabetes insipidus
    CORRECTION OF HYPERNATREMIA:
·         Hypo-osmotic NaCl
·         Dextrose solutions
  Edema – presence of excess fluid in the body tissues;  occurs mainly in the ECF compartment
    CONDITIONS ESPECIALLY PRONE TO CAUSE INTRACELLULAR SWELLING:
·         Hyponatremia
·         Depression of the metabolic systems of the tissues
·         Lack of adequate nutrition to the cells
    Inflammation – usually increases cell membrane permeability
    CONDITIONS ESPECIALLY PRONE TO CAUSE EXTRACELLULAR EDEMA:
·         Abnormal leakage of fluid from the plasma to the interstitial spaces across the capillaries
·         Failure of the lymphatics to return fluid from the interstitium back into the blood (lymphedema)
    Excessive capillary fluid filtration – most common clinical cause of interstitial fluid accumulation
    FACTORS THAT CAN INCREASE CAPILLARY FILTRATION:
·         Increased capillary filtration coefficient
·         Increased capillary hydrostatic pressure
·         Decreased plasma colloid osmotic pressure
    Rise in CHON concentration – raises the colloid osmotic pressure of the interstitial fluid
  SUMMARY OF CAUSES OF EXTRACELLULAR EDEMA:
I          Increased capillary pressure
A.      Excessive kidney retention of salt and water (acute or chronic kidney failure, mineralocorticoid excess)
B.      High venous pressure and venous constriction (heart failure, venous obstruction, failure of venous pumps: paralysis of muscles, immobilization of parts of the body, failure of venous valves)
C.       Decreased arteriolar resistance (excessive body heat, insufficiency of sympathetic nervous system, vasodilator drugs)
 II       Decreased plasma proteins
A.      Loss of proteins in urine (nephrotic syndrome)
B.      Loss of protein from denuded skin areas (burns, wounds)
C.       Failure to produce proteins (liver disease, serious protein or caloric malnutrition)
 III     Increased capillary permeability
A.      Immune reactions that cause release of histamine and other immune products
B.      Toxins
C.       Bacterial infections
D.      Vitamin deficiency, especially vitamin C
E.      Prolonged ischemia
F.       Burns
 IV     Blockage of lymph return
A.      Cancer
B.      Infections
C.       Surgery
D.      Congenital absence or abnormality of lymphatic vessels
  Heart failure – one of the most serious and common causes of edema; arterial pressure tends to fall causing decreased excretion of salt and water; blood flow to the kidneys is reduced
    Renin – cause increased formation of angiotensin II and increased secretion of aldosterone, both of which cause additional salt and water retention by the kidneys
    Left-sided heart failure – blood is pumped into the lungs normally by the right side of the heart but cannot escape easily from the pulmonary veins to the left side of the heart; can cause death within a few hours
    MAIN EFFECTS OF LARGE AMOUNTS OF NaCl AND WATER ARE ADDED TO THE ECF:
·         Widespread increases in interstitial fluid volume
·         Hypertension
    Acute glomerulonephritis – renal glomeruli are injured by inflammation and therefore fail to filter adequate amounts of fluid, serious ECF fluid edema also develops; along with the edema, severe hypertension usually develops
    Cirrhosis – development of large amounts of fibrous tissue among the liver parenchymal cells
    Liver cirrhosis – sometimes compresses the abdominal portal venous drainage vessels as they pass through the liver before emptying back into the general circulation
    Ascites – a condition of transudation of large amounts of fluid and protein into the abdominal cavity
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medyokaloka-blog · 7 years
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HEPATITIS
The combination of episodic elevations in serum transaminase levels along with fattty change in hepatocytes is most suggestive of infection with
a.  Hepatitis A virus
b.  Hepatitis B virus
c.  Hepatitis C virus
d.  Hepatitis D virus
e.  Hepatitis E virus
ANSWER:  C.  Hepatitis C virus
The hepatitis viruses are responsible for most cases of chronic hepatitis, but the chance of developing chronic hepatitis varies considerably depending on which types of hepatitis virus is the infecting agent.  Neither hepatitis A nor E virus infection is associated with the development of chronic hepatitis.  About 5% of adults infected with hepatitis B develop chronic hepatitis, and about 1/2 of these patients progress to cirrhosis.  In contrast to hepatitis B, chronic hepatitis develops in about 50% of patients with hepatitis C.  Clinically, chronic hepatitis C is characterized by episodic elevations in serum transaminases, and also fatty change in liver biopsy specimens.  Hepatitis D infection occurs in 2 clinical settings.  There might be acute coinfection by hepatitis D and hepatitis B, which results in chronic hepatitis in less than 5%  of cases.  If, instead, hepatitis D is superinfected upon a chronic carrier of hepatitis B virus, then about 80% of cases progress to chronic hepatitis.
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medyokaloka-blog · 7 years
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HANSEN’S DISEASE
There are millions of cases of leprosy (Hansen’s disease) worldwide, but predominately in Asia and Africa.  The clinical spectrum of Hansen’s disease is best characterized by
a.  Immunologic anergy
b.  Chronic pneumonitis
c.  Peripheral neuritis
d.  Bacilli in lesions that digest tissues
e.  Erythematous lesions resembling concentric circles
ANSWER:  C.  Peripheral neuritis
Leprosy (Hansen’s disease) affects primarily skin, peripheral nerves, and mucous membranes.
The disease ranges from tuberculoid leprosy, which is characterized by few lesions containing small numbers of acid fast mycobacteria, to lepromatous leprosy, which is characterized by multiple lesions containing many microorganisms.  Chronic pulmonary infection is more characteristic of infection with M. tuberculosis than M. leprae.
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medyokaloka-blog · 7 years
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ANEMIA
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medyokaloka-blog · 7 years
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TUMORS
Which one of the following tumors is most likely to be associated with primary sclerosing cholangitis?
a.  Adenocarcinoma of the gallbladder
b.  Adenocarcinoma of the pancreas
c.  Cholangiocarcinoma
d.  Hepatoblastoma
e.  Hepatocellular carcinoma
ANSWER:  C.  Cholangiocarcinoma
Diseases of the biliary tract may lead to manifestations of jaundice, and, if prolonged and severe, may lead to cirrhosis.  These diseases can be classified as either primary or secondary.  Causes of secondary biliary cirrhosis include: biliary atresia, gallstones, and carcinoma of the head of the pancreas.  
Histologic examination of the liver may reveal bile stasis in the interlobular bile ducts and bile duct proliferation in the portal areas.  Two primary causes include: primary biliary cirrhosis and primary sclerosing cholangitis.  Primary sclerosing cholangitis (PSC) is characterized by fibrosing cholangitis that produces concentric “onion-skin” fibrosis in portal areas.  It is highly associated with chronic ulcerative colitits.
Abnormal development of the biliary tract may lead to several abnormalities, including von Meyenburg’s complex (small bile duct hamartomas near normal portal tracts) and Caroli’s disease (characterized by segmental dilation of the larger intrahepatic bile ducts).  There is an increase risk of developing cholangiocarcinoma, a malignancy of bile ducts, in pxs with PSC.  PBC is primarily a disease of middle-aged women and is characterized by pruritus, jaundice, and hypercholesterolemia.  More than 90% of pxs have antimitochondrial autoantibodies, particularly the M2 antibody to mitochondrial pyruvate dehydrogenase.  A characteristic lesion, called the florid duct lesion, is seen in portal areas and is composed of a marked lymphocytic infiltrate and occasional granulomas.  
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medyokaloka-blog · 7 years
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PULMONARY EMBOLISM
A 57-year-old man Ganni is admitted to the hospital because of acute shortness of breath shortly after a 12-hour automobile ride.  Findings on PE are normal except of tachypnea and tachycardia.  He does not have edema or popliteal tenderness.  An ECG  reveals sinus tachycardia but is otherwise normal.  Which of the following statements is correct?
a.  A normal D-dimer level excludes pulmonary embolus.
b.  If there is no contraindication to anticoagulation, full-dose heparin or enoxaparin should be started pending further testing.  
c.  Normal findings on examination of the lower extremities make pulmonary emoblism unlikely.
d.  Early treatment of pulmonary embolism has little effect on overall mortality.
e.  A normal lower extremity venous Doppler study will rule out a pulmonary embolus.
ANSWER:   B.  If there is no contraindication to anticoagulation, full-dose heparin or enoxaparin should be started pending further testing.  
The clinical situation strongly suggests pulmonary embolism.  In greater than 80% of cases, pulmonary emboli arise from thrombosis in the deep venous circulation (DVT) of the lower extremities, but a normal lower extremity Doppler does not exclude the diagnosis.  DVTs often begin in the calf, where they rarely if ever cause clinically significant pulmonary embolic disease.
However, thromboses that begin below the knee frequently “grow”, or propagate, above the knee; clots that dislodge from above the knee cause clinically significant pulmonary emboli.  Untreated pulmonary embolism is associated with a 30% mortality rate.  Interestingly, only about 50% of patients with DVT of the lower extremities have clinical findings of swelling, warmth, erythema, pain, or palpable “cord”.
When a clot does dislodge from the deep venous system and travels into the pulmonary vasculature, the most common clinical findings are tachypnea and tachycardia; chest pain is less likely and usually indicates pulmonary infarction.
The ABG (arterial blood gas) is usually abnormal, and a high percentage of patients exhibit low pCO2 with respiratory alkalosis, and a widening of the alveolar-arterial oxygen gradient.  The ECG usually shows sinus tachycardia, but atrial fibrillation, pseudoinfarction in the inferior leads, and acute right heart strain are also seen.  Initial treatment for suspected pulmonary embolic disease includes prompt hospitalization and institution of IV heparin or therapeutic dose SQ LMW-heparin.  It is particularly important to make an early diagnosis of pulmonary embolus, as intervention can decrease the mortality rate from 30% down to 5%.  A normal D-dimer level helps exclude pulmonary embolus in the low-risk setting.  This patient, however, has a high pretest probability of PE; further testing (CT pulmonary angiogram, V/Q lung scan) must be done to exclude this important diagnosis.
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