Br Pathology: Electrolyte, Acid-Base, And Hemodynamic Disorders

Front 1

TBW is what percent of body weight? ICF is how much? ECF is how much?

Back 1

1) 60%
2) 40%
3) 20%

Front 2

ECF volume has two components. What are they and which is greater?

Back 2

interstitial fluid(3/4) > vascular (1/4)

Front 3

What is the major intracellular anion?

Back 3

phosphate

Front 4

How is plasma osmolality calculated? What is the normal range?

Back 4

POsm = 2 (serum Na+) + serum glucose/18 + serum blood urea nitrogen (BUN)/2.8 = 275-295 mOsm/kg

Front 5

POsm roughly correlates with the serum which ion concentration?

Back 5

Na+

Front 6

Is urea restricted to one compartment in the body primarily? what formula do nephrologists use based on this to calculate POsm?

Back 6

1) no Urea diffuses freely between ECF and ICF
2) Effective Osm = 2 (serum Na+) + serum glucose/18

Front 7

Does water follow urea?

Back 7

no it is not osmotically active like Na+ and glucose because it freely diffuses

Front 8

How does hyponatremia effect water movement?

Back 8

(decreased POsm) causes water to shift from ECF to ICF

Front 9

How do hypernatremia and hyperglycemia effect water movement?

Back 9

(increased POsm) cause water to shift from ICF to ECF

Front 10

Fluid movement across a capillary/venule wall into the interstitial space is driven by what? What is an example?

Back 10

1) Starling pressures (not osmosis)
2) EX: An increase in plasma hydrostatic pressure or a decrease in plasma oncotic pressure (i.e., serum albumin) causes fluid to diffuse out of capillaries and venules and into the interstitial space, resulting in dependent pitting edema and body cavity effusions.

Front 11

Normal (isotonic) saline (0.9%) approximates plasma tonicity (POsm). When is it given?

Back 11

to patients to maintain the blood pressure when there is a significant loss of sodium-containing fluid (e.g., blood loss, diarrhea, sweat)

Front 12

Besides normal saline what solution can be used to increase plasma volume?

Back 12

Ringer's lactate and 5% albumin (remains in the vascular compartment)

Front 13

rapid infusion of saline into an alcoholic results in what?

Back 13

central pontine myelinolysis

Front 14

In pitting edema states what happens to the cardiac output? Which hormones are elevated?

Back 14

1) cardiac output is decreased
2) causes the release of catecholamines
3) activation of the renin-angiotensin-aldosterone system
4) stimulation of ADH release
5) increased renal retention of Na+

Front 15

In pitting edema states does the kidney reabsorb hyper or hypotonic water?

Back 15

The kidney reabsorbs a slightly hypotonic, Na+-containing fluid (↑TBNa+/↑↑TBW)

Front 16

Why in pitting edema states does the CO remain low even if the kidney is retaining water?

Back 16

1) the starling pressures are abnormal
2) fluid reabsorbed at kidney continues to move out of vascular space into interstital space
3) further increases edema and CO remains low

Front 17

What does serum Na+ reflect?

Back 17

the ratio of total body Na+ (TBNa+) to total body water (TBW)

Front 18

what are clinical signs of decreased TBNa+?

Back 18

signs of volume depletion:
(a) Dry mucous membranes
(b) Decreased skin turgor (i.e., skin tenting when the skin is pinched)
(c) Drop in blood pressure and increase in pulse when sitting up from a supine position (i.e., positive tilt test)

Front 19

what are signs of increased TBNa+? Which starling pressure is increased in TBNa+?

Back 19

1) body cavity effusions (e.g., ascites)
2) dependent pitting edema
3) plasma hydrostatic pressure.
a. Due to an increase in plasma volume

Front 20

The most common cause of an increase in weight in a hospitalized patient is an increase what?

Back 20

TBNa+

Front 21

What are examples of isotonic loss of fluid? What are clinical signs?

Back 21

1) adult diarrhea
2) loss of whole blood
Clinical:
3) equal loss of Na+ and H2O causes volume depletion signs of increased skin turgor, etc..

Front 22

With isotonic loss what happens to ICF concentration? what about with isotonic gain? which way does water flow in each?

Back 22

1) the intracellular concentration does not change
2) water does not move into or out of cells with isotonic gain or loss
3) water remains in ECF (gain) or water lost from ECF

Front 23

What are signs of an isotonic gain of water? what is an example?

Back 23

1) Pitting edema and body cavity effusions may be present.
2) Example is excessive infusion of isotonic saline

Front 24

What is always present in a hypotonic fluid disorder? Where does water shift?

Back 24

1) hyponatremia (decreased POsm)
2) Water shifts to the ICF compartment (expands)

Front 25

with a hypertonic loss of Na+ how does water shift? Are volume depletion signs present?

Back 25

1) ECF volume contracts and ICF volume expands
2) yes

Front 26

What are causes of a hypertonic loss of Na+?

Back 26

↓↓TBNa+/↓TBW
1) loop diuretic
2) Addison's disease
3) 21-hydroxylase deficiency

Front 27

What are causes of hyponatremia from water gain?

Back 27

1) [SIADH], e.g., small cell carcinoma of the lung)
2) compulsive water drinking

Front 28

What would happen to ECF and ICF if a hypotonic gain of Na+ occurred? What clinical signs would be present?

Back 28

1) both would expand
2) pitting edema states with Starling pressure alterations

Front 29

What can cause a hypotonic gain of Na+?

Back 29

a) Right-sided heart failure with increase in venous hydrostatic pressure
b) Cirrhosis and nephrotic syndrome with decrease in plasma oncotic pressure
Note: develop pitting edema

Front 30

When pitting edema is present what is your differential?

Back 30

1) right-side heart failure
2) cirrhosis
3) nephrotic syndrome
4) cardiac output decreased

Front 31

What happens to ICF and ECF in a hypertonic disorder?

Back 31

Water shifts from the ICF (contracts) to the ECF

Front 32

What are causes of a hypertonic loss of water? Are Signs of volume depletion present?

Back 32

1) sweating
2) osmotic diuresis (e.g., glucosuria)
3) yes

Front 33

How are ECF and ICF effected by a hypotonic loss of water? what about loss of pure water?

Back 33

1) Contraction of the ECF and ICF volumes
2) contraction of ECF and ICF but ECF contraction is mild, because there has been no loss of Na+

Front 34

With hypotonic loss of water are there volume depletion signs? what about pure water loss?

Back 34

1) yes
2) no because there has been no loss of Na+

Front 35

What are conditions that can cause pure water loss?

Back 35

a) Diabetes insipidus, due to loss of antidiuretic hormone (ADH) or refractoriness to ADH
b) Insensible water loss (e.g., fever)
a. Water evaporates from the warm skin surface

Front 36

How are ECF and ICF effected by a hypertonic gain of Na+? What clinical signs are present?

Back 36

1) ECF volume expands and ICF volume contracts.
2) Pitting edema and body cavity effusions may be present
3) both compartments have an increase in osmolarity

Front 37

How can a hypertonic gain of Na+ be caused?

Back 37

1) infusion of NaHCO3
2) Na+-containing antibiotics.

Front 38

What are causes of a hypertonic state due to hyperglycemia? How are the ICF and the ECF effected?

Back 38

1) diabetic ketoacidosis (DKA)
2) hyperosmolar nonketotic coma
3) Water shifts from the ICF to the ECF compartment

Front 39

When hyperglycemia is present what happens to Na+? How is water effected?

Back 39

a) Dilutional effect on serum Na+ causes hyponatremia.
b) Increased POsm (due to hyperglycemia) and hyponatremia (dilutional)
c) Water does not remain in the ECF, because glucose in urine acts as an osmotic diuretic causing loss of water and Na+

Front 40

Are there signs of volume depletion with hyperglycemia? why or why not?

Back 40

Glucosuria produces a hypotonic loss of water and Na+ (osmotic diuresis), causing signs of volume depletion

Front 41

How do carbonic anhydrase inhibitors effect HCO3- in kidney? What is an example of a drug?

Back 41

1) lower the renal threshold for reclaiming HCO3-
2) acetazolamide

Front 42

When acetazolamide is given what does HCO3- combine with? How is this observed on an ABG?

Back 42

1) HCO3- combines with Na+ to form NaHCO3, which is excreted, acting as a proximal tubule diuretic
2) Loss of HCO3- produces metabolic acidosis

Front 43

Which part of kidney is effected with lead and mercury poisoning? What results?

Back 43

1) the proximal tubule cells undergo coagulation necrosis
2) produces a nephrotoxic acute tubular necrosis
3) leads to fanconi syndrome

Front 44

what can cause fanconi syndrome? How are the electrolytes and other blood components effected?

Back 44

1) lead and mercury
The normal proximal renal tubule functions are destroyed resulting in:
2) loss of sodium (hyponatremia)
3) glucose (hypoglycemia)
4) uric acid (hypouricemia)
5) phosphorus (hypophosphatemia)
6) amino acids
7) bicarbonate (type II proximal renal tubular acidosis)
8) urea in the urine

Front 45

What are the main treatments of CHF and hypercalcemia?

Back 45

furosemide

Front 46

Which channel protein do loop diuretics act on? What is not reabsorbed

Back 46

1) attaches to the Cl- binding site of the cotransporter, which not only inhibits reabsorption of Na+, K+, and Cl- but also impairs the generation of fH2O
2) They decrease TBNa+ and TBW
3) decrease reabsorption of Ca2+ by the Na+-K+-2 Cl- cotransporter

Front 47

With a loop diuretic the electrolytes are lost in the urine as obligated water. What must patients be warned of consuming?

Back 47

the normal dilution process is impaired, patients must be warned against consuming excess amounts of water

Front 48

What electrolyte abnormalities can result from a loop diuretic? What is seen on an ABG?

Back 48

1) hypertonic loss of Na+ in the urine which, along with impaired dilution, may produce hyponatremia
2) electrolyte abnormalities include hypokalemia and metabolic alkalosis

Front 49

What is the main treatment of hypertension in blacks and the elderly? Why?

Back 49

1) thiazides
2) Both patient populations have renal retention of Na+ as the primary cause of the hypertension

Front 50

which diuretics can be used in the treatment of hypercalciuria in Ca2+ renal stone formers? What is the MOA of the drug?

Back 50

1) thiazides
2) attaches to the Cl- site and inhibits Na+ and Cl- reabsorption. 3) This leaves the Na+ channel open for Ca2+ reabsorption

Front 51

What electrolyte abnormalities can be seen in someone taking thiazides?

Back 51

1) Hyponatremia may occur due to a hypertonic loss of sodium in the urine.
2) hypokalemia and metabolic alkalosis
3) Hypercalcemia can occur

Front 52

What is the MOA of Amiloride? What is another drug with a similar mechanism?

Back 52

1) K+-sparer
2) bind to the luminal membrane Na+ channels, inhibiting Na+ reabsorption and K+ excretion
3) TRIAMTERENE

Front 53

What is the MOA of Spironolactone?

Back 53

1) K+-sparing effect
2) inhibits aldosterone, resulting in a loss of Na+ in the urine and retention of K+ in the blood .

Front 54

What electrolyte abnormalities occur with Spironolactone? What is seen on ABG?

Back 54

1) Hyperkalemia
2) H+ is retained, which produces metabolic acidosis in some cases

Front 55

How does ATII effect the cardiovascular system?

Back 55

1) ATII is normally a vasoconstrictor of peripheral resistance arterioles
2) increases afterload (resistance the heart must contract against)

Front 56

How does aldsoterone effect the cardiovascular system?

Back 56

1) normally reabsorbs sodium and increases preload (volume in the left ventricle)

Front 57

Do ACE inhibitors have an effect on preload or afterload?

Back 57

decreases both afterload (ATII) and preload (aldosterone)

Front 58

Na+ reabsorption is increased when cardiac output is decreased. What happens to EABV? FF? oncontic pressure and hydrostatic pressure?

Back 58

↓ EABV→ ↑ FF → Po > Ph

Front 59

How does congestive heart failure, cirrhosis, hypovolemia effect the EABV? FF? hydrostatic pressure and oncotic pressure?

Back 59

↑ EABV → ↓ FF → PH > PO

Front 60

Na+ reabsorption is decreased when cardiac output is increased. How are EABV, FF, hydrostatic pressure and oncotic pressure effected? What are causes?

Back 60

1) ↑EABV→↓ FF → PH > PO
2) mineralocorticoid excess, isotonic gain in fluid

Front 61

what is the mechanism by which HCO- is reabsorbed in PCT?

Back 61

(1) Hydrogen ions (H+) in tubular cells are exchanged for Na+ in the urine.
(2) H+ combines with filtered HCO3- to form H2CO3 in the brush border of the proximal tubules.
(3) Carbonic anhydrase (c.a.) dissociates H2CO3 to H2O and CO2
a. CO2 and H2O are reabsorbed into proximal renal tubular cells.
(4) H2CO3 is re-formed in the proximal renal tubular cells.
a. H2CO3 dissociates into H+ and HCO3-.
(5) HCO3- is reabsorbed into the blood.
(6) An Na+/K+-ATPase pump moves Na+ into the blood

Front 62

what is the Clinical effect of lowering renal threshold for reclaiming HCO3-?

Back 62

(1) Example-normal threshold is lowered from the normal of 24 mEq/L to 15 mEq/L.
(2) This results in loss of more of the filtered HCO3- than normal.
a. Urine pH > 5.5 (alkalinizing effect of increased HCO3-)
b. Urine loss of HCO3- occurs until serum HCO3- matches the renal threshold
c. Metabolic acidosis

Front 63

How does a carbonic anhydrase inhibitor effect urine pH?

Back 63

causes proximal renal tubular acidosis

Front 64

What is the Clinical effect of raising renal threshold for reclaiming HCO3-?

Back 64

(1) Example-volume depletion associated with vomiting
(2) Increased threshold means that proportionately more of the filtered HCO3- is reclaimed.
a. Increased reclamation of HCO3- is the most important factor contributing to the increase in serum HCO3- that defines metabolic alkalosis

Front 65

What is the primary function of TAL? what is secondary function?

Back 65

1) Primary function is to generate free water (fH2O)
2) Secondary function is to reabsorb calcium (Ca2+)

Front 66

How does TAL generate fH2O?

Back 66

the active Na+-K+-2 Cl- cotransporter

Front 67

Water proximal to which cotransporter is considered obligated (o)?

Back 67

TAL = Na+-K+-2 Cl- cotransporter

Front 68

How is fH2O generated?

Back 68

1) Water is normally bound to Na+ (oNa+), K+ (oK+), and Cl- (oCl-).
2) Obligated water must accompany every Na+, K+, or Cl- excreted in urine.
3) Cotransporter separates oH2O from Na+, K+, and Cl-.
4) Water left behind in the urine is fH2O.
a. fH2O is entirely free of electrolytes

Front 69

Can Obligated water be reabsorbed by ADH?

Back 69

1) no
2) only free water can be

Front 70

What is Urine Osm (UOsm) distal to the TAL medullary segment?

Back 70

∼150 mOsm/kg

Front 71

What channels are on the interstitial side of TAL that allow exchange?

Back 71

1) A Na+/K+-ATPase pump moves reabsorbed Na+ into the interstitium.
2) Reabsorbed Cl- and K+ diffuse through channels into the interstitium.
3) Ca2+ is also reabsorbed by the cotransporter

Front 72

Loop diuretics bind where? What do they cause in the body?

Back 72

1) Cl- binding site in Na+-K+-2 Cl- cotransporter
2) hyponatremia
3) hypokalemia
4) metabolic alkalosis

Front 73

The Na+-Cl- cotransporter in the early distal tubule can also take up what? What hormone enhances this channel?

Back 73

1) Na+ and Ca2+ share the same site for reabsorption
2) Parathyroid hormone (PTH)-enhanced Ca2+ reabsorption

Front 74

Where in the nephron do thiazides work? on what channel?

Back 74

1) inhibit Cl- site in Na+-Cl- cotransporter
2) early distal tubule

Front 75

How do thiazides effect the body?

Back 75

1) hyponatremia
2) hypokalemia
3) metabolic alkalosis
4) hypercalcemia

Front 76

What hormone enhances Na+ and K+ channels in the late distal tubule and collecting ducts?

Back 76

Aldosterone-enhanced pump functions to reabsorb Na+ and excrete K+

Front 77

Where is the primary site for K+ excretion?

Back 77

late distal tubule and collecting ducts

Front 78

What does hypokalemia lead to? what part of nephron is responsible?

Back 78

1) Hydrogen (H+) ions are excreted into the lumen in exchange for Na+ instead of K+.
2) HCO3- is reabsorbed into the ECF causing metabolic alkalosis.
3) late DCT and collecting duct

Front 79

What is the effect of increased distal delivery of Na+ from loop/thiazide diuretics to the Na+/K+ exchanger of late DCT and collecting ducts?

Back 79

1) Augmented Na+ reabsorption and K+ excretion
2) May produce hypokalemia, if K+ supplements are not taken
3) May produce metabolic alkalosis if H+ exchanges with Na+

Front 80

Where is the H+/K+-ATPase pump located? What is direction of flow?

Back 80

1) Located in the collecting tubule; primary site for excretion of H+ ions
2) H+ ions are secreted into the lumen and K+ is reabsorbed

Front 81

What does H+ combine with when it is excreted in the collecting tubule?

Back 81

1) H+ combines with HPO42- to produce NaH2PO4 (titratable acidity).
2) H+ also combines with NH3 and Cl- to produce NH4Cl

Front 82

What is the Most effective way of removing excess H+ ions?

Back 82

combining with NH3 and Cl- to produce NH4Cl in collecting ducts

Front 83

Where is the primary site for regenerating or synthesizing HCO3-?

Back 83

collecting ducts

Front 84

How is addisons usually caused? what is deficient?

Back 84

1) Most often due to autoimmune destruction of the adrenal cortex
2) Deficiency of aldosterone and other mineralocorticoids

Front 85

Why in addisons is there hyponatremia and hyperkalemia? Why metabolic acidosis?

Back 85

1) Due to inhibition of Na+ reabsorption and K+ excretion
2) Hypertonic loss of Na+ in the urine
a. Signs of volume depletion
3) Retention of H+ ions, which produces metabolic acidosis
a. Due to dysfunction of the H+/K+-ATPase pump

Front 86

What is Primary aldosteronism also called? What causes it?

Back 86

1) conns syndrome
2) Benign adenoma arising in the zona glomerulosa
3) produces aldosterone

Front 87

Clinically what does addisons disease result in?

Back 87

1) hyponatremia
2) hyperkalemia
3) metabolic acidosis

Front 88

Clinically what does conns disease result in?

Back 88

1) hypernatremia
2) hypokalemia - produces severe muscle weakness
3) metabolic alkalosis

Front 89

Explain the electrolyte abnormalities in Conns?

Back 89

(1) Enhanced activity of aldosterone channels and pumps
a. Increased Na+ reabsorption and H+ and K+ excretion
(2) Increased reabsorption of Na+ causes hypernatremia.
(3) Increased excretion of K+ causes hypokalemia.
a. Hypokalemia produces severe muscle weakness (see later).
(4) Increased excretion of H+
a. Causes increased synthesis and reabsorption of HCO3- (metabolic alkalosis)

Front 90

How does Conns syndrome effect stroke volume? capillary hydrostatic pressure? How does the capillary pressure in turn effect PCT reabsorption of Na+?

Back 90

(a) Increases stroke volume, which increases systolic blood pressure
(b) Increases peritubular capillary hydrostatic pressure (PH)
(c) Prevents the proximal tubule from reabsorbing Na+

Front 91

How does Conns syndrome effect renal blood flow? What enzyme is low?

Back 91

1) Increases renal blood flow
2) Inhibits the renin-angiotensin-aldosterone system causing a decrease in plasma renin activity (PRA)

Front 92

What type of HTN is primary aldosterone?

Back 92

low plasma renin type of hypertension

Front 93

How does Conn's syndrome effect peripheral smooth muscles?

Back 93

1) Excess Na+ enters smooth muscle cells of peripheral resistance arterioles.
a. Na+ opens up Ca2+ channels causing vasoconstriction of smooth muscle cells.
b. Increased total peripheral resistance increases the diastolic blood pressure.

Front 94

Clinically how does Conn's syndrome present?

Back 94

(1) Hypertension
(2) Polyuria and muscle weakness
a. Complication of hypokalemia
(3) Hypernatremia, hypokalemia, metabolic alkalosis
(4) Decreased PRA
(5) Absence of pitting edema and effusions

Front 95

Is there pitting edema in Conn's syndrome? Why or why not?

Back 95

1) Absence of pitting edema and effusions
a. Due to excessive loss of Na+ in the urine from inhibition of proximal reabsorption of Na+ (called the escape mechanism)
b. Although TBNa+ is increased, the amount of Na+-containing fluid in the interstitial space is not enough to produce pitting edema.

Front 96

Who does Barters syndrome occur in?

Back 96

Majority of cases occur in children

Front 97

What is defective in Barters syndrome? How are the electrolytes in turn messed up?

Back 97

(1) Renal defect in Cl- reabsorption in the Na+-K+-2 Cl- cotransporter
(2) Loss of Na+, K+, and Cl- ions in the urine
a. Hypertonic loss of Na+ causes hyponatremia.
(3) Augmented exchange of Na+ and excretion of K+ in distal/collecting tubules
a. Causes hypokalemia and metabolic alkalosis
(4) Hypokalemia stimulates increased prostaglandin synthesis in the kidneys
a. Stimulates hyperplasia of the juxtaglomerular apparatus
b. Increased renin causes hyperaldosteronism

Front 98

Barters syndrome is similar to taking what type of drug? Is there a hyper or hypotonic loss of Na+?

Back 98

1) Similar to the mechanism of a loop diuretic
2) Hypertonic loss of Na+ causes hyponatremia.

Front 99

Is there acidosis or alkalosis in Barters syndrome? Is there hyper or hypokalemia?

Back 99

1. Causes hypokalemia and metabolic alkalosis
2. Increased renin causes hyperaldosteronism

Front 100

Clinically how does someone with barters syndrome present?

Back 100

(1) Patients are normotensive (not hypertensive).
a. Due to vasodilation of peripheral resistance arterioles by prostaglandin
(2) Muscle weakness due to hypokalemia
(3) Increased PRA
Note: Decreased PRA in primary aldosteronism

Front 101

Is there hypo or hypertension in Barters?

Back 101

normotensive

Front 102

blood work in Barters shows what?

Back 102

1) hypokalemia
2) metabolic alkalosis
3) ↑ aldosterone and PRA

Front 103

How is Barters syndrome treated?

Back 103

(1) K+-sparing diuretic
a. Corrects K+ loss
(2) Nonsteroidal anti-inflammatory drug
a. Decreases prostaglandin synthesis

Front 104

When is demecloycline used? What is its MOA?

Back 104

1) patient has a small cell carcinoma of the lung
2) inhibits the effect of ADH on the collecting tubules causing loss of fH2O in the urine

Front 105

Taking demeclocycline is a form of what disease? Should water be restricted when taking this drug?

Back 105

1) acquired nephrogenic diabetes insipidus
2) not necessary to restrict water intake

Front 106

what is the normal UOsm in the late distal tubule/collecting ducts? Is most of the water free or obligate water?

Back 106

1) ∼150 mOsm/kg.
2) Most of the water is fH2O.
3) Small amount of water is obligated water (oH2O) accompanying solute

Front 107

How is positive free water clearance (CH2O) determined?

Back 107

CH2O = V - COsm
** V is the volume of urine in mL/min and COsm is obligated water

Front 108

How is obligated water excretion determined?

Back 108

COsm = UOsm × V/POsm
*where COsm is obligated water
**V is the volume of urine in mL/min
***UOsm is the urine osmolality

Front 109

what does a positive obligated water indicate?

Back 109

1) Positive CH2O indicates dilution.
a. Loss of fH2O is greater than obligated water

Front 110

If urine volume 10 mL, POsm 250 mOsm/kg, UOsm 150 mOsm/kg what is the obligated water excretion?

Back 110

1) COsm = UOsm × V/POsm
2) COsm = 150 × 10/250 = 6 mL
3) CH2O = 10 - 6 = 4 mL

Front 111

SIADH has multiple causes. What are they? List several drugs as well?

Back 111

1) Ectopic production of ADH
a. Small cell carcinoma of lung is the most common cause of SIADH.
2) Drugs that enhance ADH effect
a. Chlorpropamide
b. cyclophosphamide
c. phenothiazines
d. narcotics
3) CNS injury, lung infections (e.g., TB)

Front 112

What Accounts for nearly 50% of hyponatremia in hospitalized patients?

Back 112

SIADH from multiple causes

Front 113

What happens to free water clearance in SIADH? UOsm and POsm?

Back 113

1) Urine is always concentrated, because ADH is always present.
2) Negative CH2O
3) UOsm is greater than POsm

Front 114

What is the value of serum Na+ in SIADH? What happens to peritubular capillary hydrostatic pressure? What happens to PCT reabsorption of Na+?

Back 114

1) Serum Na+ is usually < 120 mEq/L (136-145 mEq/L)
2) Increased plasma volume increases peritubular capillary hydrostatic pressure (PH)
3) Decreased proximal tubular cell reabsorption of Na+ with random urine Na+ > 40 mEq/L

Front 115

Clinically what is seen in someone with SIADH? How is it treated?

Back 115

(a) Mental status abnormalities from cerebral edema
(b) Mild SIADH treated by restricting water.
(c) Acute SIADH treated by combination of slow intravenous drip of hypertonic saline and intravenous furosemide

Front 116

What stimulates ADH synthesis and release?

Back 116

Increased POsm... most important is volume depletion

Front 117

A negative water clearance indicates what?

Back 117

1) SIADH
2) fH2O is reabsorbed back into the blood.
3) Loss of obligated water is greater than fH2O

Front 118

The following values are obtained: urine volume 10 mL, POsm 300 mOsm/kg, UOsm 900 mOsm/kg. What does the person have?

Back 118

1) COsm = 900 × 10/300 = 30 mL
2) CH2O = 10 - 30 = -20 mL
3) SIADH with greater obligate than free water clearance
Note: COsm = UOsm × V/POsm and CH2O = V - COsm

Front 119

What are causes of central diabetes insipidus? what are causes of nephrogenic diabetes insipidus?

Back 119

1) Central diabetes insipidus (CDI) is absence of ADH.
a. Causes-CNS trauma and tumors
2) Nephrogenic diabetes insipidus (NDI) is refractoriness to ADH.
a. demeclocycline
b lithium
c. hypokalemia

Front 120

Is the free water clearance positive or negative in diabetes insipidus?

Back 120

1) Urine is always diluted and never concentrated.
a. Continual loss of fH2O
2) Positive CH2O

Front 121

What are clinical findings in diabetes insipidus? What plasma and urine osmolality levels?

Back 121

1) Increased thirst and polyuria
2) Hypernatremia due to a loss of water (TBNa+/↓↓TBW).
3) POsm > 295 mOsm/kg and UOsm < 500 mOsm/kg

Front 122

How is central diabetes insipidus treated? nephrogenic diabetes insipidus?

Back 122

1) CDI is treated with desmopressin acetate.
2) NDI is treated with thiazides.
a. Volume depletion decreases polyuria.

Front 123

What are 4 features of both central and nephrogenic diabetes insipidus?

Back 123

1) hypernatremia
2) polydipsia
3) polyuria
4) concentration disorder

Front 124

How does K+ effect insulin release?

Back 124

(1) Hypokalemia inhibits insulin secretion.
(2) Hyperkalemia stimulates insulin secretion.

Front 125

How and where does aldosterone effect and regulate K+ excretion/reabsorption?

Back 125

(1) Increases the excretion of K+ and H+ in the late distal and collecting tubules
(2) Increases reabsorption of K+ by the H+/K+-ATPase pump in the collecting tubules

Front 126

How does alkalosis in general effect K+? what can develop?

Back 126

1) alkalosis causes H+ to move out of cells and K+ into cells
2) Potential for hypokalemia

Front 127

How does acidosis in general effect K+? what can develop?

Back 127

1) acidosis causes H+ to move into cells (for buffering) and K+ out of cells
2) Potential for hyperkalemia

Front 128

What effect do insulin and beta-2 agonists like albuterol have on K+?

Back 128

1) may shift K+ into cell
2) hypokalemia

Front 129

Digitalis, β-blocker, succinylcholine have what effect on K+?

Back 129

1) may shift K+ out of the cell
2) hyperkalemia

Front 130

What are the most common causes of hypokalemia?

Back 130

1) thiazides
2) loop diuretics

Front 131

Diarrhea is the exception for K+ and pH change. Why?

Back 131

1) there is a loss of K+ and HCO3- in the stool, the former producing hypokalemia and the latter metabolic acidosis
2) Normally metabolic alkalosis produces hypokalemia
3) Normally metabolic acidosis produces hyperkalemia

Front 132

How does hypokalemia effect muscles?

Back 132

1) Muscle weakness
a. Due to changes in the intracellular/extracellular K+ membrane potential
2) Rhabdomyolysis
a. Hypokalemia inhibits insulin, which decreases muscle glycogenesis, leading to rhabdomyolysis

Front 133

Does oligouria or polyuria occur with hypokalemia? Why?

Back 133

1) polyuria
2) Collecting tubules are refractory to ADH (i.e., nephrogenic diabetes insipidus).
3) Tubule cells become distended with fluid (called vacuolar nephropathy).

Front 134

At what plasma level does hypokalemia result? what is seen on an EKG?

Back 134

1) serum K+ < 3.5 mEq/L
2) U wave

Front 135

What is the most common cause of hyperkalemia?

Back 135

renal failure

Front 136

How does hyperkalemia effect the heart? What is seen on an EKG?

Back 136

1) Ventricular arrhythmias
a. Severe hyperkalemia (e.g., 7-8 mEq/L) causes the heart to stop in diastole
2) Peaked T waves on an ECG
a. Due to accelerated repolarization of cardiac muscle

Front 137

How does hyperkalemia effect muscles?

Back 137

1) Muscle weakness
2) Hyperkalemia partially depolarizes the cell membrane which interferes with membrane excitability

Front 138

How does pseudohyperkalemia result?

Back 138

RBC hemolysis from difficult venipuncture

Front 139

clinically how does volume depletion present?

Back 139

1) hypotension
2) tachycardia
3) decreased skin turgor

Front 140

How do Adult diarrhea and Loss whole blood effect:
1) POsm to [Na+]
2) ECF VOLUME
3) ICF VOLUME

Back 140

1) Normal with ↓TBNa+/↓TBW
2) Contracted
3) Normal
Note: Isotonic net loss Na+ + H2O

Front 141

How do hypertonic saline effect:
1) POsm to [Na+]
2) ECF VOLUME
3) ICF VOLUME

Back 141

1) Normal with ↑ TBNa+/↑ TBW
2) Expanded
3) Normal

Front 142

How do Loop diuretics, Addison's disease, 21-Hydroxylase deficiency effect:
1) POsm to [Na+]
2) ECF VOLUME
3) ICF VOLUME

Back 142

1) Decreased ↓↓TBNa+/↓TBW
2) contracted
3) Expanded
Note: hypertonic loss of Na+

Front 143

How do SIADH and Compulsive water drinker effect:
1) POsm to [Na+]
2) ECF VOLUME
3) ICF VOLUME

Back 143

1) Decreased TBNa+/↑↑ TBW
2) Expanded
3) Expanded

Front 144

How do Right-sided heart failure,
Cirrhosis, Nephrotic syndrome effect:
1) POsm to [Na+]
2) ECF VOLUME
3) ICF VOLUME

Back 144

1) Decreased ↑ TBNa+/↑↑ TBW
2) Expanded
a. Starling pressure alteration
3) Expanded

Front 145

How does Osmotic diuresis with glucose Sweating effect:
1) POsm to [Na+]
2) ECF VOLUME
3) ICF VOLUME

Back 145

1) Increased ↓TBNa+/↓↓TBW
2) Contracted
3) Contracted
Note: hypotonic loss of Na+

Front 146

How does Insensible water loss from fever or Diabetes insipidus effect:
1) POsm to [Na+]
2) ECF VOLUME
3) ICF VOLUME

Back 146

1) Increased
2) TBNa+/↓↓TBW Contracted (mild) 3) Contracted

Front 147

How does Infusion of a Na+-containing antibiotic or Infusion of NaHCO3 effect:
1) POsm to [Na+]
2) ECF VOLUME
3) ICF VOLUME

Back 147

1) Increased ↑↑ TBNa+/↑ TBW
2) Expanded
3) Contracted

Front 148

How do Diabetic ketoacidosis and Hyperosmolar nonketotic coma (type 2 diabetes) effect:
1) POsm to [Na+]
2) ECF VOLUME
3) ICF VOLUME

Back 148

1) Increased ↑ Glucose ↓ Na+ (dilutional effect)
2) Contracted
3) Contracted

Front 149

How does EABV relate to ECF and Na+?

Back 149

1) ↓ EABV // ↓ ECF/↓ TBNa+
2) ↑ EABV // ↑ ECF/↑ TBNa+

Front 150

How does EABV change in edema states like right heart failure? Why?

Back 150

1) ↓ EABV // ↑ ECF/↑ TBNa+
2) Fluid shifts to interstitum

Front 151

Where are 3 places that EABV is monitored?

Back 151

1) arterial baroreceptors located in the aortic arch and carotid sinus
2) the flow of blood to the renal arteries

Front 152

How does the barorecptor response increase CO?

Back 152

1) vasoconstriction of peripheral resistance arterioles (increases diastolic blood pressure),
2) venoconstriction (increases venous return to the heart)
3) increases heart rate (chronotropic effect)
4) increases cardiac contractility (inotropic effect)

Front 153

The baroreceptor response also signals the hypothalamus. Which nuclei does it act on and what is released?

Back 153

1) supraoptic and paraventricular nuclei
2) release ADH

Front 154

What are 2 functions of ADH?

Back 154

1) reabsorption of free water from the collecting tubules in the kidneys
2) a potent vasoconstrictor of the peripheral resistance vessels

Front 155

Where are the JG cells located? what are 2 ways they are stimulated? what is released?

Back 155

1) afferent arteriole
2) reduced blood flow to the juxtaglomerular (JG) apparatus
3) direct sympathetic stimulation of the JG apparatus
4) enzyme renin

Front 156

What are the functions of ATII?

Back 156

1. Vasoconstriction of peripheral resistance arterioles
2. Stimulation of aldosterone synthesis and release from the zona glomerulosa (increases Na+ reabsorption in exchange for potassium ions [K+] and hydrogen ions [H+])
3. Direct stimulation of the thirst center in the brain

Front 157

When EABV is increased what are 3 mechanisms that are used to reduce it?

Back 157

1) atrial natriuretic peptide (ANP)
2) prostaglandin E2
3) brain natriuretic peptide (BNP)

Front 158

From where and when is ANP released?

Back 158

from the left and right atria in response to atrial distention (e.g., left- and/or right-sided heart failure)

Front 159

What are 5 effects of ANP?

Back 159

(1) suppression of ADH release
(2) inhibition of the effect of ATII on stimulating thirst and aldosterone secretion
(3) vasodilation of the peripheral resistance vessels
(4) direct inhibition of Na+ reabsorption in the kidneys (diuretic effect)
(5) suppression of renin release

Front 160

What are 3 functions of prostaglandin E2?

Back 160

(1) inhibits ADH
(2) blocks Na+ reabsorption in the kidneys
(3) is a potent intrarenal vasodilator that offsets the vasoconstrictive effects of ATII and the catecholamines

Front 161

From where and when in BNP released?

Back 161

increases in the blood when the right and/or left ventricles are volume overloaded (e.g., left- and/or right-sided heart failure).

Front 162

The reabsorption of solutes from the PCT is dependent on what?

Back 162

filtration fraction (FF) in the glomerulus in concert with Starling pressures that are operative in the peritubular capillaries

Front 163

What is the FF? How is it calculated?

Back 163

1) fraction of the renal plasma flow (RPF) that is filtered across the glomerular capillaries into the tubular lumen
2) (FF = GFR ÷ RPF)

Front 164

What percent of RPF is FF generally?

Back 164

FF is ∼20%, with the remaining 80% of the RPF entering the efferent arterioles, which divide to form the intricate peritubular capillary microcirculation

Front 165

How are PGE2 and ATII different?

Back 165

1) PGE2 isa vasodilator - controls the afferent arteriolar blood flow
2) ATII is a vasoconstrictor - monitors the efferent arteriolar blood flow leaving the glomerulus

Front 166

What is mainly responsible for the peritubular capillary reabsorbing solutes and water from PCT?

Back 166

1) A low peritubular capillary hydrostatic pressure coupled with a high oncotic pressure (PO)
2) moves solutes from the tubular lumen into the tubular cell out into the lateral intercellular space, and into the peritubular capillary

Front 167

What happens to FF, GFR and RPF with hypovolemia?

Back 167

↑FF = ↓GFR ÷ ↓↓RPF
Note: hence increasing the filtered load of Na+ and other solutes

Front 168

How is reabsorption in the PCT effected by hypovolemia? What pressures are involved?

Back 168

1) The hydrostatic pressure is decreased and the oncotic pressure is increased
2) leads to reabsorption of the filtered Na+ plus other solutes into the ECF compartment (e.g., urea) in isosmotic proportions

Front 169

How are FF, GFR, RPF, hydrostatic and oncotic pressure effected during hypervolemia?

Back 169

1) ↓FF = ↑GFR ÷ ↑↑RPF
2) the filtered load of Na+ and other solutes is decreased
3) capillary hydrostatic pressure is increased and the oncotic pressure is decreased
4) favoring loss of the filtered Na+ plus other solutes (e.g., urea, uric acid) in the urine (random UNa+ > 20 mEq/L)

Front 170

what age, pH, drugs can cause hypokalemia?

Back 170

1) Occurs in elderly patients, those with eating disorders
2) Alkalosis (intracellular shift of K+)
3) Drugs enhancing Na+/K+-ATPase pump: insulin, β2-agonists (e.g., albuterol)

Front 171

what GI problems can lead to hypokalemia?

Back 171

1) Diarrhea (∼30 mEq/L in stool)
2) Laxatives
3) Vomiting (∼5 mEq/L in gastric juice)

Front 172

List 7 renal conditions that lead to hypokalemia?

Back 172

1) Loop and thiazide diuretics (most common cause): excessive exchange of Na+ for K+ in late distal and collecting tubules
2) Osmotic diuresis: glucosuria
3) Mineralocorticoid excess: primary aldosteronism
4) 11-hydroxylase deficiency
5) Cushing syndrome (excessive exchange of Na+ for K+ in late distal and collecting tubules)
6) glycyrrhizic acid (licorice, chewing tobacco)
7) secondary aldosteronism (cirrhosis, congestive heart failure, nephrotic syndrome; decreased cardiac output decreases blood flow and activates renin-angiotensin-aldosterone system)

Front 173

What are 4 examples that cause secondary aldosteronism?

Back 173

1) cirrhosis
2) congestive heart failure
3) nephrotic syndrome
4) decreased cardiac output decreases blood flow and activates renin-angiotensin-aldosterone system

Front 174

What is the normal range for PaCO2 and pH?

Back 174

1) Paco2 = 33-45 mm Hg
2) pH=7.35-7.45

Front 175

What is a common cause of respiratory acidosis?

Back 175

Chronic bronchitis due to smoking

Front 176

When does respiratory acidosis occur?

Back 176

(1) Alveolar hypoventilation with retention of CO2
(2) Paco2 > 45 mm Hg
a. ↓ pH ∼ ↑ HCO3-/↑↑Pco2

Front 177

What should HCO3- be in acute and chronic respiratory acidosis?

Back 177

(1) Serum HCO3- ≤ 30 mEq/L in acute respiratory acidosis
(2) Serum HCO3- > 30 mEq/L (indicates renal compensation) in chronic respiratory acidosis
Note: Full compensation rarely occurs

Front 178

In an ACUTE respiratory acidosis what is the formula for determining if compensation has occurred?

Back 178

HCO3- compensation = 0.1 × ΔPco2 (difference from normal of 40 mm Hg)

Front 179

What is the formula for determining compensation for a CHRONIC respiratory acidosis?

Back 179

Expected HCO3- compensation = 0.4 × ΔPco2

Front 180

Clinically what are findings in respiratory acidosis?

Back 180

(1) Somnolence
(2) Cerebral edema (vasodilation of cerebral vessels)

Front 181

What is the most common cause of respiratory alkalosis?

Back 181

anxiety

Front 182

What is the pathogenesis of respiratory alkalosis?

Back 182

(1) Alveolar hyperventilation with elimination of CO2
(2) Paco2 < 33 mm Hg
a. ↑ pH ∼ ↓ HCO3-/↓↓ Pco2

Front 183

When are acute and chronic respiratory alkalosis compensated based on HCO3- conentration?

Back 183

(1) Serum HCO3- ≥ 18 mEq/L in acute respiratory alkalosis
(2) Serum HCO3- < 18 mEq/L but > 12 mEq/L (indicates renal compensation) in chronic respiratory alkalosis

Front 184

What is the formula for determining whether ACUTE respiratory alkalosis is compensated?

Back 184

Expected HCO3- compensation = 0.2 × ΔPaco2 (difference from normal of 40 mm Hg)

Front 185

What is the formula for determining if CHRONIC respiratory alkalosis is compensated?

Back 185

Expected HCO3- = 0.5 × ΔPaco2

Front 186

clinically how does respiratory alkalosis present?

Back 186

(1) Light-headedness and confusion
(2) Signs of tetany:
a. Thumb adduction into the palm (carpopedal spasm)
b. Perioral twitching when the facial nerve is tapped (Chvostek sign)
c. Perioral numbness and tingling

Front 187

What sign is commonly occurs in acute respiratory alkalosis?

Back 187

tetany

Front 188

How does alkalosis effect albumin and subsequently Ca2+?

Back 188

1) Alkalosis increases the number of negative charges on albumin (more COO- groups on acidic amino acids)
2) Ca2+ is displaced from the ionized calcium fraction and is bound to albumin, causing a decrease in ionized calcium levels and signs of tetany

Front 189

What is the normal concentration of HCO3-? How is Osmolal gap calculated?

Back 189

1) 22-28 mEq/L
2) POsm = 2 (serum Na+) + serum glucose/18 + serum blood urea nitrogen/2.8 + serum ethanol (mg/dL)/4.6 (if the patient is drinking ethanol) and is then subtracted from the measured POsm

Front 190

What is a normal Osmolal Gap? What is abnormal possibly indicative of?

Back 190

1) A difference of <10 mOsm/kg is normal.
2) A difference of >10 mOsm/kg is highly suspicious for methanol or ethylene glycol poisoning

Front 191

What is Osmolal gap used for?

Back 191

evaluating causes of an increased AG metabolic acidosis

Front 192

what is pathogenesis of metabolic acidosis?

Back 192

(1) Serum HCO3- < 22 mEq/L
a. ↓ pH ∼ ↓↓ HCO3-/↓ Pco2
(2) Addition of an acid (increased AG type)
(3) Loss of HCO3- or inability to synthesize HCO3- (normal AG type)

Front 193

How is compensation calculated for a metabolic acidosis?

Back 193

Expected Paco2 = 1.2 × ΔHCO3- +/- 2

Front 194

How is anion gap calculated?

Back 194

AG = serum Na+ - (serum Cl- + serum HCO3-) = 12 mEq ± 2, where the 12 mEq/L represent the anions that are not accounted for in the formula (e.g., phosphate, albumin, sulfate)

Front 195

If the AG is greater than 12 mEq/L ± 2 what is going on?

Back 195

additional anions present that should not be there (e.g., lactate, salicylate, acetoacetate, β-hydroxybutyrate anions).

Front 196

What is the most common cause of increased AG?

Back 196

1) lactic acidosis
2) from anaerobic glycolysis in shock

Front 197

In normal AG acidosis what blood ion increases?

Back 197

hyperchloremia

Front 198

How does metabolic acidosis effect respirations? blood vessels? bone?

Back 198

(1) Hyperventilation (Kussmaul breathing)
(2) Warm shock
a. Acidosis vasodilates peripheral resistance arterioles.
(3) Osteoporosis
a. Bone buffers excess H+ ions

Front 199

What is the most common cause of metabolic alkalosis?

Back 199

1) thiazides
2) loop diuretics

Front 200

What is the pathogenesis of metabolic alkalosis?

Back 200

(1) Due to a loss of H+ ions or a gain in HCO3-
(2) Serum HCO3- > 28 mEq/L
a. pH ∼ ↑↑ HCO3-/↑Pco2

Front 201

How can compensation be determined with a metabolic alkalosis?

Back 201

Expected Paco2 = 0.7 × ΔHCO3- ± 2

Front 202

How does metabolic alkalosis effect the heart? Hgb affinity for O2?

Back 202

(1) Increased risk for ventricular arrhythmias
(2) Metabolic alkalosis left-shifts the oxygen-binding curve and its compensation, respiratory acidosis, decreases arterial Po2 causing hypoxia in cardiac muscle, which precipitates ventricular arrhythmias

Front 203

How will ingestion of salicylates effect the pH? respiratory center?

Back 203

(a) Salicylic acid produces a primary metabolic acidosis.
(b) Salicylates overstimulate the respiratory center causing primary respiratory alkalosis
(c) pH will be NORMAL

Front 204

A patient with chronic bronchitis and also taking a loop diuretic will have what type of blood abnormality?

Back 204

(a) Chronic bronchitis produces a primary respiratory acidosis.
(b) Loop diuretics produce a primary metabolic alkalosis
(c) pH may be normal

Front 205

What is an example of Extreme acidemia due to a primary metabolic acidosis plus a primary respiratory acidosis?

Back 205

cardiorespiratory arrest with primary respiratory acidosis (no ventilation) and primary metabolic acidosis (lactic acidosis from hypoxia)

Front 206

What are several conditions that lead to tissue breakdown and subsequent hyperkalemia?

Back 206

1) Iatrogenic (e.g., venipuncture) = pseudohyperkalemia
2) Rhabdomyolysis (rupture of muscle)

Front 207

What drugs and pH conditions can lead to hyperkalemia?

Back 207

1) Acidosis
2) Drugs inhibiting Na+/K+-ATPase pump:
a. β-blocker (e.g., propranolol)
b. digitalis toxicity
c. succinylcholine

Front 208

What renal conditions can lead to hyperkalemia?

Back 208

1) Renal disease:
a. renal failure (most common cause)
b. interstitial nephritis (legionnaires' disease; lead poisoning)

Front 209

What hormonal conditions can predispose to hyperkalemia?

Back 209

1) Mineralocorticoid deficiency:
a. Addison's disease
b. 21-hydroxylase deficiency
c. hyporeninemic hypoaldosteronism (destruction of juxtaglomerular apparatus)

Front 210

Which drugs can lead to hyperkalemia?

Back 210

1) Drugs:
a. spironolactone (inhibits aldosterone)
b. triamterene
c. amiloride (inhibit Na+ channels)
d. K+-containing antibiotics

Front 211

What 2 conditions can effect the CNS respiratory center leading to respiratory acidosis?

Back 211

Depression of center:
1) trauma
2) barbiturates

Front 212

What 6 conditions can effect the CNS respiratory center leading to respiratory alkalosis?

Back 212

Overstimulation:
1) anxiety
2) high altitude
3) normal pregnancy (estrogen/progesterone effect)
4) salicylate poisoning
5) endotoxic (septic) shock
6) cirrhosis

Front 213

What are infections that can lead to upper airway respiratory acidosis?

Back 213

Obstruction:
1) acute epiglottitis (Haemophilus influenzae)
2) croup (parainfluenza virus)

Front 214

What are conditions that can cause respiratory muscle paralysis leading to respiratory acidosis?

Back 214

Paralysis:
1) ALS
2) phrenic nerve injury
3) Guillain-Barré syndrome
4) poliomyelitis
5) hypokalemia
6) hypophosphatemia (↓ ATP)

Front 215

How can trauma to thoracic cage produce respiratory alkalosis?

Back 215

Rib fracture: hyperventilation from pain

Front 216

What lung conditions lead to respiratory acidosis?

Back 216

Obstructive disease:
1) chronic bronchitis
2) cystic fibrosis
Other:
1) pulmonary edema
2) ARDS
3) RDS
4) severe bronchial asthma

Front 217

What lung conditions lead to respiratory alkalosis?

Back 217

Restrictive disease:
1) sarcoidosis
2) asbestosis
Others:
1) pulmonary embolus
2) mild bronchial asthma

Front 218

What is the most common type of increased anion gap metabolic acidosis?

Back 218

1) lactic acidosis
Examples:
2) shock
3) CN poisoning
4) CO poisoning
5) severe hypoxemia (Pao2 < 35 mm Hg)
6) CHF
7) severe anemia (Hb < 6 g/dL)
8) liver disease
9) alcoholism
10) phenformin

Front 219

How does alcoholism lead to lactic acidosis?

Back 219

1) Alcoholism: pyruvate is converted to lactate from the excess of NADH in alcohol metabolism.
2) Liver disease: liver normally converts lactate to pyruvate. Liver disease (e.g., hepatitis, cirrhosis) causes lactate to accumulate in the blood.

Front 220

What are 3 conditions that lead to ketoacidosis?

Back 220

1) Diabetic ketoacidosis (type 1 diabetes mellitus): accumulation of AcAc and β-OHB
2) Alcoholism: acetyl CoA in alcohol metabolism is converted to ketoacids. Increase in NADH causes AcAc to convert to β-OHB, which is not detected with standard tests for ketone bodies.
3) Starvation

Front 221

How does renal failure lead to increased anion gap metabolic acidosis?

Back 221

Retention of organic acids: e.g., sulfuric and phosphoric acids

Front 222

How does salicylate poisoning lead to increased anion gap metabolic acidosis?

Back 222

Salicylic acid is a mitochondrial toxin that uncouples oxidative phosphorylation leading to tissue hypoxia and lactic acidosis. In some cases, excess salicylate overstimulates the CNS respiratory center producing a primary respiratory alkalosis.

Front 223

How does ethylene glycol poisoning lead to increased anion gap metabolic acidosis?

Back 223

1) Ethylene glycol is in antifreeze
2) It is converted to glycolic and oxalic acid by alcohol dehydrogenase
3) Oxalate anions combine with calcium to produce calcium oxalate crystals that obstruct the renal tubules causing renal failure

Front 224

How is ethylene glycol poisoning treated?

Back 224

1) IV infusion of ethanol decreases the metabolism of ethylene glycol, because alcohol dehydrogenase is preferentially metabolizing alcohol.
2) flomepizole (4-methylpyrazole) - competitive inhibitor of alcohol dehydrogenase
3) Unmetabolized ethylene glycol is removed by hemodialysis.

Front 225

How does methanol poisoning lead to increased anion gap metabolic acidosis? what else can be damaged?

Back 225

1) Methyl alcohol is present in windshield washer fluid, Sterno, and solvents for paints.
2) It is converted into formic acid by alcohol dehydrogenase.
3) Formic acid damages the optic nerve causing optic neuritis and the potential for permanent blindness

Front 226

How can methanol poisoning be treated?

Back 226

1) IV infusion of ethanol decreases the metabolism of methyl alcohol, because alcohol dehydrogenase is preferentially metabolizing alcohol.
2) use of 4-methylpyrazole (fomepizole), which inhibits alcohol dehydrogenase.

Front 227

which two conditions have increased anion gap and Osmolal gap >10?

Back 227

1) ethylene glycol poisoning
2) methanol poisoning

Front 228

What is the most common cause of normal AG metabolic acidosis in children? what is pathogenesis?

Back 228

1) diarrhea
2) Loss of HCO3- in stool: HCO3- is secreted from the pancreas to alkalinize the gastric meal

Front 229

How does cholestyramine effect pH? does it increase AG?

Back 229

1) causes normal AG metabolic acidosis
2) Binds HCO3- as well as bile salts, vitamins, and some drugs

Front 230

massive secretion from gallbladder and pancreas will effect pH how? what will AG be?

Back 230

1) normal AG metabolic acidosis
2) Bile and pancreatic secretions contain large amounts of HCO3-

Front 231

What is the pathogenesis of Type I distal renal tubular acidosis? What ions are elevated/decreased in serum?

Back 231

1) Inability to regenerate HCO3- in the H+/K+-ATPase pump in the collecting tubules
2) Excess H+ ions in the blood combine with Cl- anions.
3) Hypokalemia is severe.

Front 232

What will the pH be in Type I distal renal tubular acidosis? Why? What are causes? How is it treated?

Back 232

1) Inability to secrete H+ ions decreases titratable acidity and NH4Cl causing the urine pH to be > 5.5.
2) Causes: amphotericin, light chains in multiple myeloma
3) Rx: oral administration of HCO3-

Front 233

How is Type II proximal renal tubular acidosis characterized? How does urine pH change? How is K+ effected?

Back 233

1) Renal threshold for reclaiming HCO3- is lowered from a normal of ∼ 24 mEq/L to ∼ 15 mEq/L
2) Urine pH is initially > 5.5 due to loss of filtered HCO3- in the urine.
3) When the serum HCO3- is equal to the renal threshold, the proximal tubules reclaim HCO3- causing the urine pH to drop to < 5.5.
4) Hypokalemia may occur due to K+ binding to HCO3-.

Front 234

What are causes of Type II proximal renal tubular acidosis?

Back 234

1) carbonic anhydrase inhibitors (most common cause)
2) primary hyperparathyroidism (PTH, ↓ proximal tubule HCO3- reclamation)
3) proximal tubule nephrotoxic drugs/chemicals (e.g., aminoglycosides, heavy metals).

Front 235

How is Type II proximal renal tubular acidosis treated? How does it work?

Back 235

thiazides to produce volume depletion, which increases the renal threshold for reclaiming HCO3-

Front 236

What are causes of Type IV renal tubular acidosis? how is K+ effected?

Back 236

1) destruction of the JG apparatus:
a. hyaline arteriolosclerosis of afferent arterioles in DM
b. acute or chronic tubulointerstitial inflammation (e.g., legionnaires' disease)
2) Produces hyporeninemic hypoaldosteronism which increases K+ in serum

Front 237

What is the only renal tubule acidosis that leads to hyperkalemia? why?

Back 237

1) type IV renal tubular acidosis
2) due to hypoaldosteronism from damaged JG cells

Front 238

How does vomiting cause metabolic alkalosis? What is role of kidney?

Back 238

1) Loss of hydrochloric acid
2) Each H+ ion lost in the vomitus there is addition of one HCO3- in the blood.
3) HCO3- is filtered by the kidney and must be reclaimed in order to maintain the increase in serum HCO3-.

Front 239

How does excessive vomiting effect renal reabsorption of HCO3-?

Back 239

1) Volume depletion from excessive vomiting increases proximal tubule reclamation of HCO3- (renal threshold for reclaiming HCO3- is increased).

Front 240

How is metabolic component of vomiting treated?

Back 240

1) Correction of volume depletion with 0.9% normal saline corrects the alkalosis (chloride-responsive), because the renal threshold returns to normal and the excess filtered HCO3- is lost in the urine.

Front 241

Does mineralcorticoid excess lead to metabolic alkalosis or acidosis? How?

Back 241

1) Gain in HCO3-
2) Enhanced function of aldosterone-mediated Na+-H+ channels in the late distal and collecting ducts increases the synthesis of HCO3- leading to metabolic alkalosis

Front 242

Can mineralcorticoid excess be treated the same as vomiting to correct alkalosis?

Back 242

infusion of 0.9% normal saline does not correct the metabolic alkalosis (chloride-resistant).

Front 243

What are causes of mineralcorticoid excess? does it lead to acidosis or alkalosis?

Back 243

Causes:
1) primary aldosteronism
2) 11-hydroxylase deficiency
3) Cushing syndrome

Front 244

How do thiazides and loop diuretics lead to metabolic alkalosis?

Back 244

1) Gain in HCO3-
2) Block in Na+ reabsorption leads to augmented late distal and collecting tubule reabsorption of Na+ and excretion of H+, the latter increasing synthesis of HCO3-, leading to metabolic alkalosis
2) volume depletion also increases the proximal tubule reclamation of HCO3-, which maintains the metabolic alkalosis.

Front 245

What are normal ranges of serum:
1) Na+
2) K+
3) Cl-
4) HCO3-

Back 245

1) 136-145
2) 3.5-5.0
3) 95-105
4) 22-28

Front 246

A blood chem shows the following electrolyte concentrations. What is the disorder?
1) Na+ = 118
2) K+ = 3.0
3) Cl- = 84
4) HCO3- = 22

Back 246

SIADH: dilutional effect of excess water on all electrolytes

Front 247

A blood chem shows the following electrolyte concentrations. What is the disorder?
1) Na+ = 128
2) K+ = 5.9
3) Cl- = 96
4) HCO3- = 20

Back 247

Addison's disease: lack of aldosterone causes loss of Na+ (hyponatremia), retention of K+ (hyperkalemia), and decreased synthesis of HCO3- (metabolic acidosis)

Front 248

A blood chem shows the following electrolyte concentrations. What is the disorder?
1) Na+ = 130
2) K+ = 2.9
3) Cl- = 80
4) HCO3- = 36

Back 248

1) Vomiting: loss of Na+ and K+ in vomitus (hyponatremia, hypokalemia); volume depletion causes increased reclamation of HCO3- in proximal tubule (metabolic alkalosis)
2) Loop and thiazide diuretics: hypertonic loss Na+ in urine (hypernatremia); augmented exchange of Na+ for K+ (hypokalemia) and increased regeneration of HCO3- (metabolic alkalosis)

Front 249

A blood chem shows the following electrolyte concentrations. What is the disorder?
1) Na+ = 152
2) K+ = 2.8
3) Cl- = 110
4) HCO3- = 33

Back 249

Mineralocorticoid excess: primary aldosteronism; augmented exchange of Na+ for K+ (hypernatremia, hypokalemia), and increased synthesis of HCO3- (metabolic alkalosis)

Front 250

How is a transudate characterized?

Back 250

1) Protein-poor (<3 g/dL) and cell-poor fluid
2) Produces dependent pitting edema and body cavity effusions
3) ↑ hydrostatic pressure and/or ↓ oncotic pressure in serum

Front 251

How is an exudate characterized?

Back 251

1. Protein-rich (>3 g/dL) and cell-rich (e.g., neutrophils) fluid
2. Produces swelling of tissue but no pitting edema

Front 252

How is lymphedema characterized?

Back 252

1. Protein-rich fluid
2. Nonpitting edema

Front 253

glycosaminoglycans can take on the form of edema. How is it characterized?

Back 253

1. Increase in hyaluronic acid and chondroitin sulfate
2. Nonpitting edema called myxedema

Front 254

Name 3 clinical examples of increased vascular hydrostatic pressure?

Back 254

(1) Pulmonary edema in left-sided heart failure
(2) Peripheral pitting edema in right-sided heart failure
(3) Portal hypertension in cirrhosis producing ascites

Front 255

Name 4 clinical examples of decreased vascular oncotic pressure?

Back 255

(1) Malnutrition with decreased protein intake
(2) Cirrhosis with decreased synthesis of albumin
(3) Nephrotic syndrome with increased loss of protein in urine (>3.5 g/24 hours)
(4) Malabsorption with decreased reabsorption of protein

Front 256

How do acute renal failure and glomerulonephritis effect serum hydrostatic and oncotic pressure?

Back 256

(1) Increases hydrostatic pressure (increased plasma volume)
(2) Decreases oncotic pressure (dilutional effect on albumin)

Front 257

List 4 causes of lymphedema?

Back 257

(1) Lymphedema following modified radical mastectomy and radiation
(2) Filariasis due to Wuchereria bancrofti
(3) Scrotal and vulvar lymphedema due to lymphogranuloma venereum
(4) Breast lymphedema (inflammatory carcinoma) due to blockage of subcutaneous lymphatics by malignant cells

Front 258

What are conditions that increase glycosaminoglycans? How?

Back 258

1) pretibial myxedema and exophthalmos in Graves' disease
2) T-cell cytokines stimulate fibroblasts to synthesize glycosaminoglycans

Front 259

What is a thrombus?

Back 259

an intravascular mass attached to the vessel wall and is composed of varying proportions of coagulation factors, RBCs, and platelets.

Front 260

Pathologically what occurs for a thrombus to form in the arterial system?

Back 260

1) Endothelial cell injury
a. Due to turbulent blood flow at arterial bifurcations or overlying atherosclerotic plaques; cigarette smoke
b. Platelets adhere to areas of injury.
(2) Hypercoagulable state

Front 261

Pathologically what occurs for a thrombus to form in the venous system?

Back 261

1) Stasis of blood flow
a. Procoagulants (e.g., tissue thromboplastin) released from damaged endothelium cause localized activation of the coagulation system.
b. Fibrin is produced, which forms a mesh around RBCs, platelets, and white blood cells in the stagnant blood within the vessel to produce a thrombus.
2) Hypercoagulable state

Front 262

what are a few causes of hypercoaguable states?

Back 262

(1) Hereditary or acquired factor deficiencies
a. Example-hereditary antithrombin III deficiency or acquired deficiency due to oral contraceptives
(2) Antiphospholipid syndrome
a. Due to lupus anticoagulant and/or anticardiolipin antibodies
(3) polycythemia vera

Front 263

What is most common site for venous thrombosis? What are other sites?

Back 263

(1) Deep vein in the lower extremity below the knee
2) Superficial saphenous, hepatic, and renal veins; dural sinuses

Front 264

What is a venous thrombus composed of? How do they look?

Back 264

1) Adherent, occlusive, dark red fibrin clot
2) Contains entrapped RBCs (primary component), white blood cells, and platelets

Front 265

How do anticoagulants help with venous thrombosis? What don't they do?

Back 265

1) Anticoagulants heparin and warfarin prevent formation of venous thrombi
2) Anticoagulants do not dissolve the thrombus; they only prevent further formation of a thrombus.
3) The fibrinolytic system (plasmin) is responsible for dissolution of the thrombus

Front 266

Where do arterial thrombi form? What do they tend to form over?

Back 266

(1) Elastic and muscular arteries
(2) Majority of thrombi overlie disrupted atherosclerotic plaques
a. Example-coronary artery thrombosis

Front 267

How do the thrombi in muscular arteries and in the aorta look? What helps inhibit their formation?

Back 267

1) Adherent, usually occlusive, gray-white fibrin clot composed of platelets
2) Aspirin and other inhibitors of platelet aggregation prevent formation of these thrombi

Front 268

How do thrombi appear in the heart and aorta? How is mixed thrombus prevented?

Back 268

1) Laminated thrombi with alternating pale and red areas (lines of Zahn)
a. Pale areas are composed of platelets held together by fibrin.
b. Red areas are composed predominantly of RBCs held together by fibrin.
c. Mixed type of thrombus is prevented by aspirin along with anticoagulant therapy

Front 269

What are example of thrombi that form in the heart?

Back 269

a) Thrombus in left ventricle due to a transmural myocardial infarction (mural thrombus)
b) Thrombus in left atrium in patients with mitral stenosis complicated by atrial fibrillation

Front 270

What does a postmortem clot look like? is it in the vessel wall?

Back 270

1. Fibrin clot of plasma (resembles chicken fat) without entrapped cells
2. It is not attached to the vessel wall.

Front 271

What is an embolism?

Back 271

Detached mass (e.g., clot, fat, gas) that is carried through the blood to a distant site

Front 272

Where do the majority of pulmonary embolisms originate?

Back 272

1) Majority originate from the femoral vein (extension of deep vein thrombus).
2) Others originate from the pelvic veins or vena cava

Front 273

Where is the location of a PE that causes sudden death?

Back 273

Due to a saddle embolus occluding the major pulmonary artery branches

Front 274

Why is it that Less than 10% of thromboemboli produce infarction in lungs?

Back 274

Due to dual blood supply of the lungs: pulmonary artery, bronchial artery

Front 275

What is a paradoxic embolism?

Back 275

Venous thromboembolus passes through an atrial septal defect into the systemic circulation

Front 276

what are the majority of systemic embolisms caused by?

Back 276

1. Thrombi from the left side of the heart (80% of cases)
a. Mural thrombus in left ventricle following acute myocardial infarction
b. Thrombus in the left atrium in mitral stenosis
c. Atrial fibrillation predisposes to atrial clot formation and embolization.
2. Atrial myxoma, vegetations from aortic or mitral valve

Front 277

Where are the most common sites for systemic artery emboli to lodge?

Back 277

1. Lower extremities (most common)
2. Brain (via the middle cerebral artery)
3. Small bowel (via the superior mesenteric artery)
4. Spleen and kidneys

Front 278

How do infarctions appear in digits, spleen, kidneys, GI and brain?

Back 278

1) Pale infarctions in the digits, spleen, and kidneys
2) Hemorrhagic infarctions in the brain and small bowel

Front 279

What are some causes of fat embolism?

Back 279

1) Most often due to traumatic fracture of the long bones (e.g., femur) or pelvis
2) Other causes include trauma to fat-laden tissues (liposuction), fatty liver

Front 280

Pathologically what occurs with a fat embolism?

Back 280

1) Microglobules of fat from the bone marrow gain access to the microvasculature.
2) Microglobules eventually obstruct the microvasculature in the brain, lungs, kidneys, and other sites.
a. Produces ischemia and hemorrhage
3) Fatty acids derived from breakdown of the microglobules damage vessel endothelium.
a. Platelet thrombi develop in areas of endothelial injury

Front 281

When do symptoms of fat embolism generally begin?

Back 281

Symptoms begin 24 to 72 hours after trauma

Front 282

What are common clinical findings with fat embolisms?

Back 282

1) Restlessness, delirium, coma
2) Dyspnea, tachypnea
a. Fat microglobules in pulmonary capillaries cause hypoxemia.
b. Massive perfusion defect
3) Petechiae commonly develop over the chest and upper extremities.
a. Due to thrombocytopenia from platelet adhesion to microglobules of fat
4) Death results in less than 10% of cases

Front 283

How is a fat embolism treated and diagnosed?

Back 283

1. Search for fat globules in urine, pulmonary alveolar lavage, spinal fluid
2. Treatment is supportive
a. Maintain good arterial oxygenatio

Front 284

When do amniotic fluid embolisms occur?

Back 284

Occurs during labor or immediately post-partum

Front 285

Pathologically how does an amniotic fluid embolism occur?

Back 285

1. Tears in placental membranes or uterine veins
2. Infusion of amniotic fluid into the maternal circulation
a. Leads to cardiorespiratory collapse (? anaphylactic reaction to fetal antigens) and disseminated intravascular coagulation (procoagulants in AF)

Front 286

How does an amniotic embolism clinically present?

Back 286

1) Abrupt onset of dyspnea, cyanosis, hypotension, and bleeding
a. Dyspnea is due to pulmonary edema or acute respiratory distress syndrome.
b. Bleeding is due to disseminated intravascular coagulation (DIC).

Front 287

When is diagnosis of an amniotic embolism made? What is seen?

Back 287

1) Usually at autopsy
2) Fetal squamous cells are present in the pulmonary vessels
3) Maternal mortality rate varies from 60% to 80%.
a. Most women who survive have permanent neurologic impairment.
4) Treatment is supportive

Front 288

What is decompression sickness? What is pathogenesis?

Back 288

1) form of gas embolism
2) Atmospheric pressure increases by 1 for every 33 feet of descent into water.
3) Nitrogen gas is forced out of the alveoli and dissolves in blood and tissues.
4) Rapid ascent causes nitrogen to expand and form gas bubbles in tissue and vessel lumens

Front 289

How does decompression sickness effect the extremities?

Back 289

1) Pain develops in joints, muscles, and bones.
a. Called "the bends"

Front 290

What can decompression sickness cause in the lungs? How?

Back 290

Pneumothorax:
(1) Complication of a sudden rise to the surface
(2) Due to rupture of a preexisting subpleural or intrapleural bleb
(3) Causes dyspnea and pleuritic chest pain

Pulmonary embolus:
(1) Pressure on the veins in the lower extremities produces stasis and thrombus formation.
(2) Pulmonary thromboembolism occurs
(3) Causes dyspnea and pleuritic chest pain

Front 291

What are chronic changes that occur with decompression sickness?

Back 291

Aseptic necrosis in bones (femur, tibia, humerus) from bone infarctions

Front 292

How is decompression sickness treated?

Back 292

Recompression (nitrogen forced back into tissue) followed by slow decompression

Front 293

When is someone considered to be hemorrhaging?

Back 293

Loss of greater than 20% of blood volume (∼1000 mL) results in shock.

Front 294

How are Hgb and Hct initially affected by hemorrhage? What is first hematologic sign? What happens when normal saline is infused?

Back 294

1) No initial effect on hemoglobin and hematocrit concentration
a. Absolute neutrophilic leukocytosis is the first hematologic sign.
b. Infusion of 0.9% saline immediately uncovers the RBC deficit.

Front 295

When is plasma replaced after a hemorrhage? When do RBCs start to be produced?

Back 295

1) Plasma is replaced first with fluid from the interstitial space.
a. Uncovers the RBC deficit within hours to days
2) RBC response in the bone marrow begins in 5 to 7 days.

Front 296

What is the pathophysiology behind hypovolemic shock?

Back 296

(1) Decreased cardiac output
a. Due to decreased volume of blood
(2) Decreased left ventricular end-diastolic pressure (LVEDP)
(3) Increased peripheral vascular resistance (PVR)
a. Due to vasoconstriction of arterioles from catecholamines, ADH, and angiotensin II, which are released in response to the decreased CO
(4) Decreased mixed venous oxygen content (MVO2)
a. Best indicator of tissue hypoxia

Front 297

what is the best indicator of tissue hypoxia?

Back 297

Decreased mixed venous oxygen content (MVO2)

Front 298

How and where is venous O2 content measured? why is it low in hypovolemic shock?

Back 298

1) Measured in the right side of the heart with a Swan-Ganz catheter
2) Indicates the degree of extraction of O2 from the blood delivered to tissue
3) In hypovolemic shock, decreased blood flow through the microcirculation leads to increased extraction of O2 from the blood and a decreased MVO2.
a. blood also more acidic shifting O2-RBC dissociation curve to right

Front 299

Clinically what is seen in someone with hypovolemic shock?

Back 299

(1) Cold, clammy skin due to vasoconstriction of skin vessels
(2) Hypotension; rapid, weak pulse (compensatory response to decreased CO)

Front 300

What is cardiogenic shock most commonly caused by?

Back 300

acute myocardial infarction

Front 301

What is the pathophysiolgy of cardiogenic shock?

Back 301

(1) Decreased CO
a. Due to decreased force of contraction in the left ventricle
(2) Increased LVEDP
a. Blood accumulates in the left ventricle.
(3) Increased PVR
a. Same mechanism as in hypovolemic shock
(4) Decreased MVO2
a. Same mechanism as in hypovolemic shock

Front 302

Clinically how does cardiogenic shock present?

Back 302

Chest pain followed by signs similar to hypovolemic shock such as:
1) Cold, clammy skin due to vasoconstriction of skin vessels
2) Hypotension; rapid, weak pulse (compensatory response to decreased CO)

Front 303

What is the most common cause of septic shock?

Back 303

E coli

Front 304

At the molecular level what is endotoxin doing to cause shock?

Back 304

(1) Endotoxins damage endothelial cells.
a. Causes the release of vasodilators such as nitric oxide and prostaglandin I2
(2) Endotoxins activate the alternative complement pathway.
a. Anaphylatoxins (C3a and C5a) are produced, which stimulate mast cell release of histamine (vasodilator)
(3) Interleukin 1 and tumor necrosis factor (TNF) are released from macrophages.
a. Activate neutrophil adhesion molecules, causing neutrophil adherence to pulmonary capillaries
b. Circulating neutrophil pool becomes part of the marginating neutrophil pool
c. High levels of TNF contribute to the vascular leakage syndrome.
Note: Important in the pathophysiology of acute respiratory distress syndrome

Front 305

What is the pathophysiology of septic shock?

Back 305

(1) Initial increase in CO
a. Due to rapid blood flow through dilated peripheral resistance arterioles, causing increased return of blood to the heart
(2) Decreased LVEDP
a. Due to neutrophil transmigration through the pulmonary capillaries into alveoli producing noncardiogenic pulmonary edema
(3) Decreased PVR
a. Due to vasodilation of peripheral resistance arterioles
(4) Increased MVO2
a. Tissues are unable to extract O2, because of the increased blood flow.

Front 306

Clinically how does someone with septic shock present?

Back 306

(1) Warm skin, due to vasodilation of skin vessels
(2) Bounding pulse, due to increased CO
(3) Acute respiratory distress syndrome
a. Due to neutrophil transmigration into alveoli
(4) Disseminated intravascular coagulation
a. Due to activation of the intrinsic and extrinsic coagulation system

Front 307

ischemic tubular necrosis can occur from shock. How are the kidneys effected?

Back 307

Coagulation necrosis of proximal tubule cells and cells in the thick ascending limb

Front 308

What is the most common cause of death in shock?

Back 308

multiorgan failure
Note: also develop Lactic acidosis due to tissue hypoxia

Front 309

How are CO, LVEDP, PVR and MVO2 effected by hypovolemic shock?

Back 309

1) ↓CO
2) ↓LVEDP
3) ↑PVR
4) ↓MVO2

Front 310

How are CO, LVEDP, PVR and MVO2 effected by cardiogenic shock?

Back 310

1) ↓CO
2) ↑LVEDP
3) ↑PVR
4) ↓MVO2

Front 311

How are CO, LVEDP, PVR and MVO2 effected in the initial phase of septic shock?

Back 311

1) ↑CO
2) ↓LVEDP
3) ↓PVR
4) ↑MVO2

Front 312

What is active hyperemia?

Back 312

localized arteriolar dilation like blushing or inflammation

Front 313

What causes acute passive congestion of the lung?

Back 313

1) shock
2) acute inflammation
3) sudden Lt heart failure

Front 314

Chronic passive congestion of the lung is caused mostly by? What does it lead to? How does lung appear on gross?

Back 314

1) left-sided heart failure
2) mitral stenosis
Leads to:
3) rupture of pulmonary capillaries
4) heart failure cells appear
5) longstanding congestion, fibrosis and hemosiderin deposition cause BROWN INDURATION

Front 315

Chronic passive congestion of the liver and lower extremities is primarily caused by? What changes occur in liver?

Back 315

1) right sided heart failure
2) Nutmeg liver - speckled liver
3) result of dilated and congested central veins and surrounding brownish-yellow sometimes fatty liver cells

Front 316

necrotic tissue is referred to as what?

Back 316

infarction

Front 317

Postmortem clots have a two layered appearance?

Back 317

1) currant jelly in red cell rich lower layer
2) chicken fat appearance in cell poor upper layer

Front 318

mural thrombi in left atrium are associated with what?

Back 318

1) mitral stenosis
2) atrial fib

Front 319

mural thrombi in the left ventricle are associated with what?

Back 319

MI

Front 320

What is the most common cerebral vessel infarcted?

Back 320

middle cerebral

Front 321

small infarcts in the CNS, bones and other tissues from decompression sickness are also known as what?

Back 321

caisson disease

Front 322

Who is at higher risk of decompression sickness? Why?

Back 322

obese people because nitrogen has affinity for adipose tissue

Front 323

What is anasarca?

Back 323

generalized edema

Front 324

What is the specific gravity of transudate? exudate?

Back 324

1) <1.012
2) >1.020

Front 325

LPS increases which cytokines?

Back 325

1) TNF = released from macrophages, leukocyte recruitment, vascular leakage, mediates septic shock
2) IL-1 = secreted by macrophages, acute inflammation, activates endothelium to express adhesion molecules, endogenous pyrogen
3) IL-6 = secreted by Th and macrophages, increases acute phase reactants and Igs
4) IL-8 = secreted by macrophages, chemotactic to neutrophils

Front 326

What are the stages of shock?

Back 326

1) nonprogressive - compensatory
2) progressive - hypoperfusion and metabolic acidosis
3) irreversible - survival is not possible

Front 327

What are morphologic changes with shock seen brain? liver? colon? adrenal cortex? pulmonary?

Back 327

1) areas of necrosis in brain
2) centrilobar necrosis of liver
3) fatty change of liver and heart
4) patchy mucosal hemorrhages in colon
5) depletion of lipid adrenal cortex
6) pulmonary edema

Front 328

with hemostasis what factor is involved in the neurogenic reflex? What activates the coagulation cascade?

Back 328

1) arteriolar vasonconstriction is mediated by endothelin
2) tissue factor

Front 329

What are steps in hemostatic response to blood vessel injury?

Back 329

1) neurogenic reflex causing arteriolar constriction
2) platelet adhesion and activation
3) activation of coagulation cascade
4) activation of counter-regulatory mechanisms like t-PA

Front 330

How do platelets contribute to endothelial repair?

Back 330

by releasing PDGF which has major effects on angiogenesis

Front 331

What are the proteins involved in platelets adhering to extracellular matrix? What factors do platelets release?

Back 331

1) vWF is a bridge between gIb on platelets and exposed collagen of endothelium
2) alpha granules: contain coagulation and growth factors
3) delta granules: ADP, Ca2+, histamine, serotonin
4) dense granules similar to delta granules

Front 332

What are important mediators of platelet aggregation? What platelet glycoprotein is needed to bind fibrinogen to allow aggregation?

Back 332

1) ADP and TxA2
2) GpIIb/GpIIIa

Front 333

What disease is it when vWF is deficient? When GpIb is deficient? when GpIIb/IIIa is deficient?

Back 333

1) von willebrand disease
2) Bernard soulier syndrome
3) glanzmann thrombasthenia

Front 334

Describe the extrinsic pathway?

Back 334

1) Tissue factor activates VII
2) tissue factor VIIa complex activates X
3) Xa with Ca2+ converts II to IIa
a. Va is a cofactor for conversion
4) IIa converts fibrinogen to fibrin

Front 335

The PT pathway measures which factors?

Back 335

extrinsic factors:
1) II
2) V
3) VII
4) X
5) fibrinogen

Front 336

What are some factors that endothelial cells produce to resist coagulation?

Back 336

1) heparin-like molecules that activate antithrombin III which deactivates thrombin, IXa and Xa
2) tPA activates plasmin
3) thrombomodulin is on endothelial cells and activates protein C which cleaves Va and VIIIa
4) protein S which is a cofactor for protein C
5) PGI2
6) NO

Front 337

which factors does protein C deactivate? Which factors does antithrombin III deactivate?

Back 337

1) Va and VIIIa
2) thrombin, IXa, Xa

Front 338

Which molecules activate the intrinsic pathway?

Back 338

1) factor XII (hageman factor)
2) prekallikrein
3) high-molecular weight kininogen
Note: this pathway is important in in vitro clotting in glass tubes

Front 339

List the steps of the intrinsic pathway?

Back 339

1) collagen and HMWK activate XII
2) XIIa:
a. cleaves pre-kallikrein to kallikrein
b. activates XI
3) XIa and Ca2+ activate IX
4) IXa, VIIIa, Ca2+ and PL activate X
5) Xa, Va, Ca2+ and PL activate prothrombin
6) thrombin activates fibrinogen
7) fibrinogen is cross-linked by XIIIa

Front 340

Factors VIII, V and XIII are all activated by what? Factor VIIa and tissue factor can activate which intrinsic pathway factor?

Back 340

1) thrombin = factor II
2) factor IX

Front 341

PTT checks which clotting factors?

Back 341

a) II
b) V
c) VIII
d) IX
e) X
f) XI
g) XII
h) fibrinogen

Front 342

Clotting is limited in blood vessels to sites that have exposed what? What cleaves fibrin? What activates the factor necessary to cleave fibrin?

Back 342

1) phospholipid
2) plasmin
3) t-PA generates plasmin from plasminogen

Front 343

What is the most frequent hereditary thrombophilia? What is pathogenesis?

Back 343

1) factor V leiden
2) mutation of V so that it can't be cleaved by protein C
3) Va is always on
4) known as hereditary resistance to protein C

Front 344

What is pathogenesis of prothrombin 20210A transition?

Back 344

1) G to A transition in 3' untranslated region of prothrombin gene
2) have increased levels of plasma thrombin and increased venous thrombosis

Front 345

Methylene tetrahydrofolate reductase mutation (MTHFR C677T) results in what?

Back 345

1) moderate increase in homocysteine
2) causes arterial and venous thrombosis
3) Can reduce symptoms with B12 and folate and B6

Front 346

How is antiphospholipid antibody syndrome characterized?

Back 346

1) autoantibodies to protein antigens complexed to phospholipids
2) recurrent arterial thromboembolism
3) fetal loss
4) thrombocytopenia
5) neurogenic manifestations

Front 347

How is antiphospholipid antibody syndrome diagnosed? What can it be associated with?

Back 347

1) incidentally from a prolonged PTT
2) SLE

Front 348

Heparin induced thrombocytopenia syndrome is the result of what? What is the MOA of heparin

Back 348

1) therapy with high molecular weight heparin
2) may be from antibodies that complex with heparin and platelet factor 4
3) Heparin binds to the enzyme inhibitor antithrombin III (AT) causing a conformational change that results in its activation
4) activated AT then inactivates thrombin and other proteases involved in blood clotting, most notably factor Xa
Note: heparin has no effect on clots that have already formed