Test 1 (Renal, Obesity, Coags, hepatic, gallbladder...) Flashcards Preview

Bioscience II > Test 1 (Renal, Obesity, Coags, hepatic, gallbladder...) > Flashcards

Flashcards in Test 1 (Renal, Obesity, Coags, hepatic, gallbladder...) Deck (313)
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1
Q

What is the % of CO that is partitioned to renal blood flow?

A

20-25% via the renal artery

2
Q

The renal cortex gets what % of the RBF?

A

80% (extracts very little O2)

3
Q

The renal juxtamedullary gets what % of the RBF?

A

10-15%

4
Q

What area of the renal system is most sensitive to ischemia?

A

The medulla: which uses high metabolic activity for solute absorption and requires low blood flow to maintain osmotic gradients.

5
Q

What MAP is appropriate to maintain autoregulation in the kidneys?

A

MAP of 75-160mmHg

6
Q

A MAP below _____ % can be associated with impaired filtration.

A

<70

7
Q

Filtration ceases at a MAP less than ______%.

A

<40-50

8
Q

Your 2 kidneys are comprised of 2 regions called the _______ and the ________.

A

cortex and medulla

9
Q

What is the functional unit of the kidney? How many are there?

A

nephron; approx. 1.25 million per kidney

10
Q

What is the function of the nephron?

A

functional unit of the kidney; it holds filtrate that is filtered by blood, excretes waste, and absorbs important substances such as water and bicarbonate

11
Q

What does renal fraction mean?

A

renal fraction is the portion of the blood that passes through the kidney

12
Q

What is the renal fraction of the CO? and in mL?

A

20-25%; 1100-1200mL per minute

13
Q

What is the glomerulus?

A

It is a high pressure capillary bed formed by the afferent arterioles.

14
Q

In what two ways is RBF regulated?

A

intrinsic autoregulation and neural regulation

15
Q

What is neural regulation and the effect of SNS stimulation on the RBF?

A

afferent and efferent arterioles are innervated by the sympathetic nervous system, stimulation of the SNS causes vasoconstriction….. and thus a decrease in RBF

16
Q

What are the main functions of the kidney?

A

maintenance of ECF composition and volume, endocrine functions (erythropoietin, RAA system, vitamin D), regulation of arterial BP

17
Q

What is the significance of erythropoietin, the RAA, and vitamin D?

A

erythropoietin stimulates the production of RBCs; RAA regulates BP, K, and Na excretion; kidney converts vitamin D into its active form to absorb Ca from the intestine… so a deficiency in vitamin D results in hypocalcemia

18
Q

What does one nephron consist of and what are its 4 main functions?

A

consists of the glomerulus (bowmans capsule), proximal and distal convoluted tubule (in the cortex), and the loop of henle and collecting tubule (in the medulla); functions include glomerular filtration, tubular reabsorption, tubular secretion, and excretion (byproduct of the previous 3 functions)

19
Q

What are the 2 types of nephrons? Describe.

A

cortical nephrons (extend only partially into the medulla) and juxtamedullary (lie deep in the cortex and extend deep into the medulla); 1/5 to 1/3 are juxtamedullary—> play an important role in the concentration of urine.

20
Q

What is the name of the peritubular capillaries of the loop of Henle?

A

vasa recta

21
Q

What is the difference between reabsorption and secretion?

A

reabsorption is when a substance is transported from the tubule to the capillary….. secretion is when a substance is transported from the capillary to the tubule

22
Q

What part of the medulla is most vulnerable to ischemia?

A

outer medulla (top of the loop of Henle)

23
Q

What is the % and mL/min value for GFR?

A

20% RBF (125mL/min)

24
Q

The release of what substance causes RAA activation?

A

renin

25
Q

What % of the approximately 125mL/min of filtrate is reabsorbed from the renal tubules while the remainder is excreted as urine?

A

99%

26
Q

Why does glucose get excreted in urine when past a certain concentration?

A

some substances like glucose have a maximum reabsorption value after which the remainder is excreted.

27
Q

What factors can increase the GFR?

A

increased renal blood flow, dilation of the afferent arteriole, and increased resistance in the efferent arteriole increases GFR

28
Q

Describe the activation and process of the RAA.

A

SNS stimulation and decreased delivery of sodium and chloride to the macula densa cause the juxtaglomerular cells to release renin—> renin clears angiotensinogen from the liver to form angiotensin I—> in the lung, angiotensin I is changed into angiotensin II under the influence of a converting enzyme—> in addition to having a generalized vasoconstriction effect, angiotensin II causes constriction of the efferent arteriole—> this causes pressure in the glomerulus to increase and the GFR to return to normal

29
Q

What is the short description for the proximal tubule?

A

“coarse control”: reabsorbs the bulk of glomerular filtrate (65-75%); NaCl, water, bicarb, glucose, protein, amino acids, potassium, magnesium, calcium, phosphates, uric acid, urea; also produces ammonia; has active (at the cost of metabolic energy d\t electrochemical gradient) and passive (movement of substances across concentration gradients) transport

30
Q

Describe the differences in permeability of the descending and ascending limb of the loop of Henle.

A

descending is highly permeable to water but not actively transport sodium and chloride–> this leaves the remaining fluid in the descending limb concentrated; ascending retains water within the tubule, while the countercurrent exchange begins in the thick ascending limb with the active transport of sodium and chloride out of the tubular lumen and into the medullary interstitium—> since it is impermeable to water the tubular fluid becomes hypoosmotic (dilute) and the intertitium hyperosmotic

31
Q

Describe the blood flow through the nephron.

A

afferent arteriole–> glomerulus–> unfiltered blood to efferent arterioles–> peritubular capillaries–> venous system

32
Q

What happens to the ultrafiltrate once it leaves the glomerulus?

A

travels from the glomerulus through tubules for reabsorption/secretion; reabsorption–> goes into the interstitium and returns to systemic vasculature

33
Q

Differentiate between the ECF effects of aldosterone and ADH.

A

aldosterone: ECF volume via sodium reabsorption (water follows NaCl) and controls K+ secretion.; ADH: ECF osmolality via H2) reabsorption/secretion (to dilute osmolality, conserve H20)

34
Q

Describe the “fine tuning” that occurs in the kidney.

A

(actions via hormones): distal tubule: aldosterone (Na reabsorption/K+ secretion; Na reabsorption/H secretion—- acid base buffering); collecting tubule: ADH (adjusts permeability to H20 dependent on osmolality)

35
Q

What is the end product when ADH is present vs not present?

A

ADH present—– water is reabsorbed so there is a small volume of concentrated urine; ADH not present—– water stays in tubules so there is a large volume of dilute urine

36
Q

What can prompt the activation of the RAA system?

A

low glomerular flow, SNS stimulation (vasoconstriction=decreased renal blood flow), decreased NaCl concentration at the site of macula densa (part of the JGA which is next to the glomerulus)

37
Q

What is angiotensin II and what countermeasures does it take?

A

it is a potent vasoconstrictor but also releases protective prostaglandins (vasodilate) to protect renal blood flow

38
Q

What is the anhydrase equation?

A

acid-base balance via Na/H ion exchange; H + HCO3–> H2CO3–> H2O + CO2; Na is exchanged for H…. excess H requires for HCO3

39
Q

What is the effect of hyperkalemia? Give common treatments.

A

hyperexcitability b\c the resting membrane potential is closer to threshold potential; Ca++ will help stabilize the membrane potential (decrease excitability by spreading potentials further from each other), HCO3, insulin, albuterol (to shift K+ back into the cell)

40
Q

What should you do for the hypoosmolar state?

A

free water overload or water intoxication: hyponatremia, so restrict free H20 and give hypertonic saline

41
Q

What is the anion gap utilized for?

A

for differential diagnosis of metabolic acidosis; it is the difference between the primary measured cations (Na and K+) and the primary measured anions (Cl- and HCO3-) in serum

42
Q

How do you calculate anion gap?

A

normal anion gap= Na-Cl-HCO3= 8-12 mM

43
Q

Where is atrial natriuretic factor synthesized and what is its action on the kidneys?

A

it is a peptide hormone synthesized, stored, and secreted in the cardiac atria; acts on the kidney to increase urine flow and sodium excretion, and it may enhance renal blood flow and GFR; it enhances both the release and end-organ effects of renin, aldosterone, and ADH; the stimulus for ANF is atrial distention, stretch, or pressure; one of the most potent diuretics known

44
Q

What stimulates the release of ANF?

A

atrial distention, stretch, or pressure

45
Q

Name two loop diuretics and their function.

A

lasix and bumex; stops reabsorption of ions in ascending loop of Henle–> decreases osmololity and increases water excretion—> fluid volume deficit; they act by binding with the Na-K-Cl symporter to inhibit the reabsorption of these ions from the asc loop…. water will follow the Na…. so since ion reabsorption is inhibited….. often results in hypokalemia…. also triggers release of prostaglandins from the kidneys which cause venodilation and decrease in BP d\t decrease preload.

46
Q

What is the effect of thiazides and K+ sparing diuretics like spironolactone?

A

work on distal tubule of the nephron to inhibit sodium reabsorption, thereby again decreasing water reabsorption… spironolactone competitively inhibits aldosterone increasing sodium excretion and promotes sodium retention; aldosterone is an important regulator of K+

47
Q

What is diamox and its function?

A

it is a carboxic-anhydrase inhibitor; inhibits the action of carbonic anhydrase in the proximal tubule of the kidney—> inhibits bicarb reabsorption (more bicarb is left in the interstitium to bind with H); sodium reabsorption also decreases–> diuresis and hyperchloremic metabolic acidosis results

48
Q

What is Mannitol and its effects?

A

it is an osmotic diuretic; agent that is impermeable to the renal tubule exerts an osmotic pulling force decreasing the reabsorption of water leading to increased water excretion; hypokalemia can result (secondary to increased distal tubule flow)

49
Q

What are some considerations for patients taking ACE inhibitors or ARBs?

A

these drugs block protective effects of RAA system leading to hypotension that is often refractory to our commonly used adrenergic agonists (neo and ephedrine); often more responsive to fluid resuscitation and vasopressin administration (bolus dose of 0.2-0.4 units/kg of vasopressin may be effective….2-4 units of vasopressin usually given); can also consider albumin (do not exceed 250g in 48hr)

50
Q

How do you decide between 5% and 25% albumin?

A

depends if patient requires primarily volume (5%) or primarily protein/oncotic pressure (25%); 5%= hypovolemic shock, burns, hypoproteinemia, cardiopulmonary bypass, acute liver disease; 25%: acute nephrosis, acute liver failure, ARDS, burns, cardiopulmonary bypass, hypoproteinemia, renal dialysis, hypovolemic shock, hemolytic disease of newborn, hepatic surgery/transplant

51
Q

What is refractory hypotension?

A

it is blocking action of angiotensin II, a powerful vasoconstrictor; blocks release of aldosterone and ADH

52
Q

Name the normal values of Na, K, Ca, and Magnesium.

A

Na: 135-145, K: 3.5-4.5, Ca: 9.9-10.5, Magnesium: 1.7-2.5

53
Q

What electrolytes control the following: 1) resting membrane potential (-90mV) and 2) threshold (-60mV)?

A

K+ controls the resting membrane potential; Ca+ controls the threshold

54
Q

What is the most common electrolyte disturbance with renal failure?

A

hyperkalemia

55
Q

How do you treat hyperkalemia and what are the effects?

A

calcium: move threshold away from resting membrane potential (stabilizes); Na HCO3 and hyperventilation: decrease concentration of H+ in plasma….. H+ from ICF to ECF, K back inside; beta-2 agonist (albuterol) and insulin: stimulate Na-K pump, drives K back into cells, give dextrose to prevent hypoglycemia

56
Q

The incidence of surgery related acute renal failure is ____ to _____ %.

A

18-47%

57
Q

How do you calculate allowable blood loss?

A

EBVx (start Hct-target Hct)/ start Hct

58
Q

What is the mL/kg to calculate obese patients estimated blood volume?

A

45-55mL/kg

59
Q

Urine specific gravity > ______ shows that the kidneys are concentrating urine adequately.

A

> 1.018

60
Q

What is the normal values for GFR?

A

125-140 mL/min; decreases 1% per year after the age of 20

61
Q

What test is considered the NEST measure of renal function?

A

GFR

62
Q

What is the normal range for serum creatinine?

A

0.6-1.0 mg/dL in women and 0.8-1.3 mg/dL in men

63
Q

What is creatinine?

A

a waste product of muscle metabolism; not reabsorbed by the kidneys

64
Q

What is the normal value for BUN?

A

5-20 mg/dL; increases can be seen in high protein diets

65
Q

What are the normal values for specific gravity?

A

1.005-1.030; assesses renal tubular function by measuring the urine concentrating ability

66
Q

What marker may turn out to be a better indicator of GFR than creatinine, but costs more money?

A

cystatin C; produced by all nucleated cells in the body and not influenced by muscle mass, gender, or age

67
Q

What is the difference in acute kidney injury, nephritic disease, and renal tubular dysfunction?

A

AKI is a blanket term that can be applied to most any acute renal disease; nephritic disease covers diseases involving inflammation of the nephrons; renal tubular dysfunction is established by demonstrating the kidneys do not produce appropriately concentrated urine in the presence of physiologic stimulus for release of ADH

68
Q

Define oliguria and non-oliguric.

A

urine output 400cc/day

69
Q

What are some causes of AKI?

A

systemic diseases (cardiogenic shock, sepsis, hepatic failure, vasculitis), drugs (aminoglycosides, NSAIDS, ACE inhibitors, solvents such as ethylene glycol, heavy metals such as mercury), interventional therapies (radiographic contrast dyes, aortic or renal artery clamping)

70
Q

What are 3 classifications of AKI?

A

pre-renal, intra-renal, post-renal

71
Q

What is pre-renal azotemia?

A

azotemia is characterized by abnormally high levels of nitrogen-containing compounds, such as urea, creatinine, various body waste compounds, and other nitrogen-rich compounds in the blood; pre-renal azotemia implies the problem lies somewhere proximal to the kidney itself, so there is nothing structurally wrong with the kidney. rapidly reversible if the underlying cause is treated—– if not treated—> ischemia induced acute tubular nephrosis—> intrarenal problem

72
Q

What are some examples of pre-renal azotemia?

A

hemorrhage, GI fluid loss, trauma, surgery, burns, cardiogenic shock, sepsis, hepatic failure, aortic or renal clamping, thromboembolism

73
Q

Among hospitalized patients, what are common causes of pre-renal azotemia?

A

CHF, liver dysfunction, septic shock

74
Q

Where does intra-renal azotemia occur?

A

name implies that its cause lies within the parenchyma of the kidney itself

75
Q

How is intra-renal azotemia categorized?

A

according to the primary site of injury: glomerulus, renal tubules, interstitium, renal vasculature

76
Q

Why can injury to the kidneys occur during reperfusion?

A

d\t an influx of inflammatory cells, cytokines, and oxygen-free radicals; ischemia and toxins combine to cause AKI in severely ill patients with conditions such as sepsis or AIDS.

77
Q

What are some causes of intra-renal azotemia?

A

acute interstitial nephritis most often caused by allergic reactions to drugs, glomerulonephritis, renal artery emboli, renal vein thrombosis, and vasculitis

78
Q

What is post-renal azotemia?

A

AKI when urinary outflow tracts are obstructed; can use renal ultrasonography

79
Q

What are s\s of post-renal azotemia?

A

generalized malaise, fluid overload (dyspnea, edema, and HTN), lethargy, nausea, confusion, accumulation of protein and amino acid metabolites, encephalopathy

80
Q

Oliguria is defined as < ______mL/day or < _______ cc/kg/hr.

A

<0.5cc/kg/hr

81
Q

Anuria is defined as < _______cc/day.

A

100; complete anuria is very unusual

82
Q

What are AKI complications seen in central nervous system, cardiovascular, hematologic, and GI systems?

A

CNS: confusion, asterixis, somnolence, seizures, polyneuropathy—all are ameliorated by dialysis; CARDIO: systemic HTN, CHF, pulmonary edema, uremic pericarditis, peaked T waves and widened QRS (hyperkalemia), dysrhythmias—-ameliorated by dialysis; HEMAT: anemia (Hct as low as 20-30% d\t hemodilution and decreased erythropoietin production), coagulopathy (uremia induced platelet dysfunction; also give DDAVP–1-desamino-8-D-arginine vasopressin– to temporarily increase concentrations of vWF and factor VIII to improve circulation); GI: anorexia, N/V, paralytic ileus, GI bleed, gastroparesis

83
Q

What are some treatments for AKI?

A

no specific treatments; limit further renal injury and correct fluid, electrolyte, and acid-base derangement; treat underlying cause; maintain MAP 65— no evidence that higher MAP and CO is better outcome

84
Q

What fluids are preferred in patients with renal impairment and why?

A

0.9% Saline d\t lack of K+, but too much can cause hyperchloremic metabolic acidosis which secondarily causes hyperkalemia; no evidence to support use of colloids over crystalloids

85
Q

What is the role of dopamine in treatment of AKI?

A

useless and associated with a number of undesirable side effects.

86
Q

What is the overall concern with the use of vasopressors with AKI?

A

vasoconstriction may exacerbate tubular injury

87
Q

Regardless of the cause, a decrease in GFR < _____ mL/min generally requires dialysis or renal transplant.

A

<25

88
Q

What are the two general patterns of glomerular disease?

A

nephritic (inflammation and an active urine sediment containing red and white blood cells) and nephrotic (marked by proteinuria and relatively inactive urine sediment) patterns

89
Q

What are some complications of nephrotic syndrome?

A

less circulating protein d\t proteinuria; result in higher circulation of highly protein-bound drugs d\t hypoalbuminemia—> need diuretics to offset kidneys propensity to retain sodium—> diruese slowly because abrupt natriuresis can cause hypovolemia and AKI

90
Q

What is a renal problem characterized by inflammation of the renal pelvis (collecting ducts) and the kidney itself?

A

pyelonephritis; treated with antibiotics….. if infection ascends high enough, glomeruli are damaged

91
Q

Are there any anesthetics we administer that have negative renal effects?

A

enflurane and sevoflurane, when in high doses, can potentially cause renal toxicity

92
Q

What are ways to partially overcome renal impairment during anesthesia?

A

maintain adequate intravascular volume and normotension

93
Q

Are renal effects more or less with regional vs. general anesthesia?

A

generally less

94
Q

What are some indirect effects on the renal system during anesthesia caused by cardiac, neural, and endocrine effects?

A

most inhalation and IV anesthetics cause some degree of cardiac depression or vasodilation and can decrease arterial BP; sympathectomy caused by regional; decreases in BP below autoregulation can decrease RBF, GFR, urinary flow, and sodium excretion; neural effects such as sympathetic activation (DL, light anesthesia, tissue trauma) can cause increases in renal vascular resistance and activate hormonal systems— both tend to decrease GFR, RBF, and UO; endocrine effects: stress response to surgical stimulation, CV depression, hypoxia, or acidosis…. increases in catecholamines, ADH, and angiotensin II all reeice RBF by inducing renal arterial constriction….aldosterone enhances Na+ reabsorption

95
Q

Why is Ketorolac (Toradol) not a good choice in most patients with renal impairment?

A

NSAID inhibits prostaglandin synthesis preventing renal production of vasodilatory prostaglandins in patient with high levels of angiotensin II and norepinephrine….. this attenuation of normal protective response can decrease GFR and produce renal dysfunction in some patients

96
Q

What are some potential problems for the kidneys associated with ACE inhibitors?

A

these drugs block protective effects of angiotensin II and may result in additional reductions in GFR during surgery

97
Q

What are some drugs that could cause renal artery vasospasm, direct cytotoxic injury, or renal tubular obstructions?

A

aminoglycosides, immunosuppressive agents (cyclosporins, tacrolimus), radiocontrast dyes

98
Q

What are complications for the kidneys during aortic cross-clamping and CPB?

A

regardless of clamp position the RBF is decreased by 50%, clamp release causes increase RBF but GFR is impaired to only 2/3 normal for up to 24h, tubular functions (concentrating ability, sodium, and water conservation), mannitol—dopamine—-fenoldopam for renal protection

99
Q

What lab values decrease in presence of renal failure?

A

calcium, albumin, red cell production/erythrpoietin/anemia

100
Q

What lab values are increased in presence of renal failure?

A

potassium, phosphate, magnesium, uric acid

101
Q

Why should cautionary use of PEEP be considered in renal patients?

A

studies found that 15cmH2O PEEP depressed CO, RBF, GFR, and urine volume by 20-30% and was associated with increases in renin and aldosterone

102
Q

What are the effects of pneumoperitoneum, CPB, and pelvic surgery on renal function?

A

Pneumoperitoneum-(or even PEEP) abdominal compartment syndrome-like- state d/t renal vein and vena cava compression. Leads to increases in renin, aldosterone, and ADH.

Cardiopulmonary bypass- non pulsatile flow, production of free radicals, and decreased renal perfusion at cross clamp time.

Pelvic surgery- compression of the bladder by retractors, ligation of ureters, trendelenberg position impeding emptying of the bladder

103
Q

Release of fluoride ions from VAA metabolic degradation with plasma concentrations > _____ micromol/L have been associated with renal toxicity.

A

> 50 micromol/L; fluoride production is greatest with prolonged use of enflurane and sevoflurane (compound A)…. but overall safe with impaired renal function

104
Q

How does the body compensate to increase cardiac output?

A

Na retention and activation of renin-angiotensin system

105
Q

What are considerations for induction of patients with renal disease?

A

slow and steady wins the race, RSI vs. standard d\t possible delayed gastric emptying, choice of agents

106
Q

What are some considerations for intra-op maintenance of patients with renal disease?

A

focus on normotension, avoid hypoventilation (K, acidosis, etc) or hyperventilation (shift left)

107
Q

Is morphine good for patients with renal disease?

A

not generally; morphine accumulation has been found to prolong respiratory depression in patients with renal failure; demerol has active metabolites associated with seizures

108
Q

What is the NMB drug of choice for renal patients?

A

cisatricurium, atracurium, or mivacurium d\t ester hydrolysis and Hofmann elimination

108
Q

What is the NMB drug of choice for renal patients?

A

cisatricurium, atracurium, or mivacurium d\t ester hydrolysis and Hofmann elimination

109
Q

When can succinylcholine be safely administered to renal patients?

A

When serum K is <5meQ/L

109
Q

When can succinylcholine be safely administered to renal patients?

A

When serum K is <5meQ/L

110
Q

What are some renal considerations for vecuronium and rocuronium?

A

Vec is 20% eliminated in urine; prolongation of NMB with Rocuronium has been seen with severe renal disease

110
Q

What are some renal considerations for vecuronium and rocuronium?

A

Vec is 20% eliminated in urine; prolongation of NMB with Rocuronium has been seen with severe renal disease

111
Q

What is mannitol and its effects?

A

osmotic diuretic (6 carbon sugar); may activate intra-renal synthesis of vasodilating prostaglandins, increase, RBF, and act as a free radical scavenger

111
Q

What is mannitol and its effects?

A

osmotic diuretic (6 carbon sugar); may activate intra-renal synthesis of vasodilating prostaglandins, increase, RBF, and act as a free radical scavenger

112
Q

What is the danger in rapid correction of hyponatremia?

A

associated with demyelinating lesions in the pons resulting in serious permanent neurological conditions

112
Q

What is the danger in rapid correction of hyponatremia?

A

associated with demyelinating lesions in the pons resulting in serious permanent neurological conditions

113
Q

What is the effect of hypernatremia on anesthesia?

A

increases MAC for inhaled anesthetics in animal studies….. if related to hypovolemia, cardiac depressant and vasodilatory effects of these drugs will be enhanced leading to hypotension and hypoperfusion of tissues; less volume of distribution of IV medications and more rapid uptake of VAA because of decreased CO

113
Q

What is the effect of hypernatremia on anesthesia?

A

increases MAC for inhaled anesthetics in animal studies….. if related to hypovolemia, cardiac depressant and vasodilatory effects of these drugs will be enhanced leading to hypotension and hypoperfusion of tissues; less volume of distribution of IV medications and more rapid uptake of VAA because of decreased CO

114
Q

What is a cardiac consideration for patients with low calcium?

A

potentiation of negative inotropic effects of barbs and VAAs will be seen

114
Q

What is a cardiac consideration for patients with low calcium?

A

potentiation of negative inotropic effects of barbs and VAAs will be seen

115
Q

If a patient has magnesium imbalances, how does this effect anesthesia?

A

high: dosages of NDMBs should be decreased by 25-50%; low: cardiac arrythmias

115
Q

If a patient has magnesium imbalances, how does this effect anesthesia?

A

high: dosages of NDMBs should be decreased by 25-50%; low: cardiac arrythmias

116
Q

What are considerations during a TURP?

A

prostate is resected and large amounts of irrigation fluid are used; slightly hypotonic/non-electrolyte solutions are used d\t cautery; open venous sinuses in prostate and pressure of irrigation fluid allow systemic absorption of this irrigation fluid (2L or more); intra-op: arrthymias/hypotension; post-op: confusion, dyspnea, seizures; height of irrigation and length of procedure is KEY

116
Q

What are considerations during a TURP?

A

prostate is resected and large amounts of irrigation fluid are used; slightly hypotonic/non-electrolyte solutions are used d\t cautery; open venous sinuses in prostate and pressure of irrigation fluid allow systemic absorption of this irrigation fluid (2L or more); intra-op: arrthymias/hypotension; post-op: confusion, dyspnea, seizures; height of irrigation and length of procedure is KEY

117
Q

In coagulation…. what is the first line of defense?

A

The vessel wall

117
Q

In coagulation…. what is the first line of defense?

A

The vessel wall

118
Q

What are the 3 layers of the vessel wall?

A

Tunica—- adventitia, media, intima

118
Q

What are the 3 layers of the vessel wall?

A

Tunica—- adventitia, media, intima

119
Q

Which layer of the vessel wall is the endothelial layer?

A

tunica intima

119
Q

Which layer of the vessel wall is the endothelial layer?

A

tunica intima

120
Q

What happens during the initial phase of the coagulation process?

A

vascular constriction—- limits the flow of blood to the area of injury

120
Q

What happens during the initial phase of the coagulation process?

A

vascular constriction—- limits the flow of blood to the area of injury

121
Q

What are the vitamin K dependent factors?

A

II, VII, IX, X

121
Q

What are the vitamin K dependent factors?

A

II, VII, IX, X

122
Q

What factors are produced in the liver?

A

all but vWF, III (tissue factor), IV (calcium)

122
Q

What factors are produced in the liver?

A

all but vWF, III (tissue factor), IV (calcium)

123
Q

What are the extrinsic factors?

A

You can buy the extrinsic pathway for 0.37 cents….. III and VII

123
Q

What are the extrinsic factors?

A

You can buy the extrinsic pathway for 0.37 cents….. III and VII

124
Q

What are the intrinsic factors?

A

You can buy the intrinsic pathway for $12 or $11.98; XII or XI, IX, VIII

124
Q

What are the intrinsic factors?

A

You can buy the intrinsic pathway for $12 or $11.98; XII or XI, IX, VIII

125
Q

What is the common pathway?

A

The common pathway can be purchased at the 5 (V) and dime (X) for $1 (I) or $2 (II) on the 13th (XIII) of each month

125
Q

What is the common pathway?

A

The common pathway can be purchased at the 5 (V) and dime (X) for $1 (I) or $2 (II) on the 13th (XIII) of each month

126
Q

What is factor III?

A

tissue factor

126
Q

What is factor III?

A

tissue factor

127
Q

What is factor I?

A

fibrinogen; forms the clot (fibrin)

127
Q

What factors are anti-coagulation?

A

C, S, plasminogen, urokinase (activates plasminogen), tissue plasminogen activator (tPA—activates plasminogen)

128
Q

What is factor II?

A

prothrombin; its active form IIa activates I, V, VII, VIII, XI, XIII, protein C, platelets

128
Q

What is factor II?

A

prothrombin; its active form IIa activates I, V, VII, VIII, XI, XIII, protein C, platelets

129
Q

What is factor IV?

A

calcium; required for coagulation factors to bind to phospholipid

129
Q

What is the difference between Type 1 and 2 HIT?

A

heparin induced thrombocytopenia; 1: is non-immune HIT, seen on 1st day of heparin therapy and is transient and clinically insignificant; 2: is immune mediated HIT, formation of antibodies to heparin platelet factor 4 complex—> these antibodies can induce platelet activation and aggregation…… further release of heparin platelet factor 4 upon platelet activation…..heparin platelet factor 4 complex may bind to endothelial cells, stimulating thrombin production

130
Q

What is factor IX?

A

christmas factor; activates X and forms tenase complex with factor VIII

130
Q

What is factor IX?

A

christmas factor; activates X and forms tenase complex with factor VIII

131
Q

What is factor X?

A

Stuart-Prower factor; activates II

131
Q

What is factor X?

A

Stuart-Prower factor; activates II

132
Q

What factor is the Hageman factor?

A

XII

132
Q

What are important pre-operative considerations for assessing coagulopathies?

A

history of bleeding issues (gums, epistaxis, mucous membrane bleeding, nose bleeds), bleeding with dental procedures, liver insufficiency or malnutrition, coag workup prior to surgery if there is a history of bleeding disorders, discuss transfusion possibility

133
Q

What does factor XIII do?

A

crosslinks fibrin

133
Q

What does factor XIII do?

A

crosslinks fibrin

134
Q

What is the function of vWF?

A

binds to VIII, mediates platelet adhesion

134
Q

What are the intra-operative considerations for the management of sickle cell disease?

A

avoid all triggers, dehydration, acidosis, hypothermia, hypoxia, and hypotension…. know that pain can exacerbate complications; anesthetic technique does not affect complications; orthopedic tourniquets can be used but increase incidence of peri-operative complications; aggressively treat post-op pain

135
Q

What factors are pro-coagulation?

A

I-XIII

135
Q

What factors are pro-coagulation?

A

I-XIII

136
Q

What factors are anti-coagulation?

A

C, S, plasminogen, urokinase (activates plasminogen), tissue plasminogen activator (tPA—activates plasminogen)

136
Q

What factors are anti-coagulation?

A

C, S, plasminogen, urokinase (activates plasminogen), tissue plasminogen activator (tPA—activates plasminogen)

137
Q

Why are we concerned with “sickled” cells?

A

they tend to plug the blood vessels causing vascular occlusion, pain, and organ infarction; sickled cells undergo hemolysis in the spleen or become sequestered there causing blood pooling and infarction of splenic vessels

138
Q

What is the normal value for PTT and what factors is it evaluating?

A

PTT: 30-40sec; common and intrinsic; 1,2,5,10,13,12,11,9,8

139
Q

What is the target Hct for patients with sickle cell disease?

A

~30%

140
Q

A fibrinogen level < ______ mg/dL is associated with spontaneous bleeding.

A

<100

141
Q

What is the normal value for “bleeding time” and how accurate is this method?

A

1-9min; evaluates platelet function and vascular constriction capability but does NOT provide accurate platelet count and does NOT prove with certainty of an abnormality with a single test

142
Q

What is a TEG test?

A

thromboelastography; wider encompassing test of clot formation, stability, and lysis

143
Q

What is the most common coagulopathy seen in anesthesia and how is it defined?

A

dilutional coagulopathy; 1 fluid volume/24hr or 1/2 fluid volume/3hours—-> coagulation factors and platelets become significantly diluted; the use of blood products to replace this volume will help mitigate these effects but will still contribute to hemodilution

144
Q

The depletion of platelets secondary to markedly increased platelet consumption from coagulation pathway activation is called ____________.

A

thrombocytopenia; may lead to micro thrombi resulting in purpura (red/purple lesions on skin that do not blanch)

145
Q

What are leukocytes and their function?

A

WBCs; defend the body against organisms that cause infection; remove debris including dead or injured host cells transported in circulation but act primarily at tissues

146
Q

What platelet values are associated with mild, moderate, and severe DIC?

A

70,000-150,000= mild, 40-70= moderate, 20-40= severe

147
Q

What are the two types of leukemia?

A

Acute and Chronic; many chemotherapy agents cause CNS toxicity, renal toxicity, and hepatic toxicity

148
Q

What follows the same pathophysiology as DIC, combined with RBC hemolysis and elevated liver enzymes?

A

HELLP

149
Q

What is the treatment of HELLP?

A

control of HTN and delivery of parasite

150
Q

What is the only true treatment of DIC?

A

treatment of the underlying cause of DIC; platelet and plasma transfusions are only supportive therapies

151
Q

What is the difference between Type 1 and 2 HIT?

A

heparin induced thrombocytopenia; 1: is non-immune HIT, seen on 1st day of heparin therapy and is transient and clinically insignificant; 2: is immune mediated HIT, formation of antibodies to heparin platelet factor 4 complex—> these antibodies can induce platelet activation and aggregation…… further release of heparin platelet factor 4 upon platelet activation…..heparin platelet factor 4 complex may bind to endothelial cells, stimulating thrombin production

152
Q

What are the results of Type 2 HIT?

A

thrombocytopenia, venous and arterial thrombus formation, potentially severe end-organ damage

152
Q

What are the results of Type 2 HIT?

A

thrombocytopenia, venous and arterial thrombus formation, potentially severe end-organ damage

153
Q

At what level can bleeding be anticipated in patients with factor 1 deficiency?

A

50-100mg/dL

153
Q

When does Type 2 HIT appear?

A

5-10 days after heparin use; can be seen if heparin therapy is restarted within 20 days of previous exposure

154
Q

What is the main function of erythrocytes?

A

get oxygen delivered to the tissues; biconcave disk has the ability to change shape and increases surface area; contains large amounts of carbonic anhydrase

154
Q

What are some anesthetic considerations for patients with HIT?

A

platelet transfusion is life threatening; discontinue drug; in thrombic event administer direct thrombin inhibitor (argatroban, bivalirudin); hold warfarin and oral contraceptives; delay cardiac surgery if possible

155
Q

What is the cause of SIRS?

A

systemic inflammatory response syndrome; so with infection you get an initiation of the inflammatory response and decreased blood flow d\t vasodilation…… the coagulation cascade is activated

155
Q

What is the average lifespan of the RBC?

A

120 days after leaving bone marrow

156
Q

What are some management considerations with coagulopathy and SIRS?

A

maintain Hgb 7-9; FFP to cover surgery; platelet transfusion to maintain >50,000; recombinant protein C—- septic shock with multiple organ dysfunction, IV infusion of 24 mcg/kg/hr for 96hrs

156
Q

What are some management considerations with coagulopathy and SIRS?

A

maintain Hgb 7-9; FFP to cover surgery; platelet transfusion to maintain >50,000; recombinant protein C—- septic shock with multiple organ dysfunction, IV infusion of 24 mcg/kg/hr for 96hrs

157
Q

What are important pre-operative considerations for assessing coagulopathies?

A

history of bleeding issues (gums, epistaxis, mucous membrane bleeding, nose bleeds), bleeding with dental procedures, liver insufficiency or malnutrition, coag workup prior to surgery if there is a history of bleeding disorders, discuss transfusion possibility

157
Q

What are important pre-operative considerations for assessing coagulopathies?

A

history of bleeding issues (gums, epistaxis, mucous membrane bleeding, nose bleeds), bleeding with dental procedures, liver insufficiency or malnutrition, coag workup prior to surgery if there is a history of bleeding disorders, discuss transfusion possibility

158
Q

What can cause a sickle cell crisis?

A

decreased O2 sat, temperature, infections, dehydration, stasis and acidosis

159
Q

What is the most important variable when considering a crisis in the sickle cell patient?

A

hypoxemia

160
Q

What are the different types of sickle cell crisis?

A

vasoocclusive (sickling in the microcirculation, as blood flow is obstructed thrombosis and infarction of local tissue can occur), aplastic (transient cessation in RBC production), sequestrian (large amounts of blood become acutely pooled in the liver and spleen), hyperhemolytic (accelerated rate of RBC destruction)

161
Q

What are the intra-operative considerations for the management of sickle cell disease?

A

avoid all triggers, dehydration, acidosis, hypothermia, hypoxia, and hypotension…. know that pain can exacerbate complications

162
Q

Sickle cell is a type of ______ characterized by the presence of hemoglobin ______ within the erythrocytes.

A

type of anemia, characterized by Hgb S; genetic mutation in which one amino acid (valine) replaces another (glutamic acid)

163
Q

What are the names for the homozygous and heterozygous forms of sickle cell and which is more severe?

A

sickle cell hemolytic anemia is homozygous and is most severe; sickle cell thalassemia is heterozygous

164
Q

When confronted with dehydration or deoxygenation how does Hgb S react?

A

Hgb S reacts by solidifying and stretching the erythrocyte into an elongated sickle shape

165
Q

At what PaO2 will patients with sickle cell disease or trait begin to sickle?

A

30-40mm Hg for sickle cell disease; 20-30 mm Hg for sickle cell trait

166
Q

Why are we concerned with “sickled” cells?

A

they tend to plug the blood vessels causing vascular occlusion, pain, and organ infarction; sickled cells undergo hemolysis in the spleen or become sequestered there causing blood pooling and infarction of splenic vessels

167
Q

What is the “risk” of complications between sickle trait and sickle disease?

A

no increased mortality or morbidity with sickle cell trait; increased risk of peri-operative complications with sickle cell disease

168
Q

What is the target Hct for patients with sickle cell disease?

A

~30%

169
Q

What is the relationship of 2,3 DPG with the shifting of the oxygen-hemoglobin dissociation curve?

A

shift to left: occurs when 2,3 DPG decreases which increases the affinity of Hgb for oxygen; shift to right: occurs when 2,3 DPG is increased and results in more release of oxygen to the tissues

170
Q

What are some anesthetic considerations for patients with leukemia?

A

lab assessment, correction of pancytopenia if necessary, evaluate antibiotic choice, aseptic technique at all times, possibility of thrush, review adverse effects associated with chemotherapy

171
Q

What is 2,3 DPG?

A

an organic phosphate which is present in RBCs; binds to Hgb, diminishing the oxygen affinity of Hgb; amount of 2,3 DPG in RBCs determines how readily Hgb gives up O2; results in increased release of O2 to the tissues; increases at higher altitudes

172
Q

Oxy-Hgb dissociation curve, when shifted to the left has what characteristics?

A

less release of oxygen to the tissues; P50 <26mmHg; alkalosis; hyperthermia; decreased 2,3 DPG

173
Q

Oxy-Hgb dissociation curve, when shifted to the right has what characteristics?

A

more release of oxygen to the tissues; P50 >26mmHg; acidosis; hyperthermia; increased 2,3 DPG

174
Q

What is a clonal malignant disorder of the blood and blood forming organs causing an accumulation of dysfunctional cells and loss of cell division regulation?

A

leukemia; excessive accumulation of leukemic cells results in an overcrowding of bone marrow which causes a decreased production and function of normal hematopoietic cells

175
Q

What are the two types of leukemia?

A

Acute and Chronic; many chemotherapy agents cause CNS toxicity, renal toxicity, and hepatic toxicity

176
Q

What happens during Factor I deficiency?

A

fibrinogen deficiency; caused by either decreased production or failure to work properly; clotting reaction is blocked prematurely and clot doesn’t form

177
Q

What is hemophilia A caused from?

A

most common factor deficiency; caused by a factor VIII deficiency treated with cryoprecipitate or recombinant factor VIII; factor VIII is a procoagulant protein— component of the intrinsic pathway required for activation of factor X; vWF prevents degredation of factor VIII in free plasma

178
Q

What is the cause and effect of Von Willebrand factor deficiency?

A

caused by quantitative or qualitative defects involving factor VIII (most important function is to promote adhesion of platelets); secreted by endothelial cells and released into circulation

179
Q

What lab values would be normal and abnormal is patients with hemophilia A?

A

normal bleeding time, normal platelet count, normal PT and prolonged PTT—-factor VIII specific assays are required for diagnosis; thromboplastin generation test is the most sensitive and can ID deficiencies of factors VIII and IX

180
Q

What lab values would be normal and abnormal is patients with vWF deficiency?

A

prolonged PTT; most common cause of prolonged PTT in those patients not taking heparin

181
Q

What are the 3 types of factor 1 (fibrinogen) deficiency?

A

qualitative (dysfibrinogenemia—doesn’t work how it should); quantitative (afibrinogenemia—-complete lack of fibrinogen); combined (hypodysfibrinogenemia—combined defect involving low amounts and impaired function)

182
Q

How is bilirubin produced?

A

primarily the end product of hemoglobin metabolism and formed from degradation of the heme ring in Kupffer cells (liver); heme oxygenase breaks down Hgb into biliverdin, carbon monoxide, and iron—-> biliverdin reductase then converts the former into bilirubin…. bilirubin is then released into blood where it binds to albumin…. hepatic uptake of bilirubin…. excreted into bile canalculi…. 1/2 bilirubin secreted into the intestine is converted by colonic bacteria into urobilinogen

183
Q

What is the most abundant cell in the body?

A

erythrocytes (25 trillion cells)

184
Q

What is the main function of erythrocytes?

A

get oxygen delivered to the tissues; biconcave disk has the ability to change shape and increases surface area

185
Q

How are RBCs produced?

A

bone marrow-vertebrae, sternum, ribs, pelvis, promixal ends of humerus and femur; controlled by ability to transport oxygen to the tissues; erythropoietin; erythrpoietin is a glycoprotein synthesized in response to arterial hypoxemia (kidneys release erythropoetic factor into circulation)….. stimulates bone marrow to produce RBCs with peak effect in 5 days; hypoxemia corrected production drops to zero almost immediately

186
Q

What vitamins are required for proper RBC function and production?

A

B12 (cyanobalamin) ad folic aci— synthesis of DNA; liver stores 1000x this much (takes months for anemia to present); folic acid contributes to maturation of RBCs

187
Q

What is the average lifespan of the RBC?

A

120 days after leaving bone marrow

188
Q

What are common causes of anemia?

A

impaired RBC production, blood loss (acute or chronic), increased RBC destruction

189
Q

What is the difference between the “cytic” and “chromic” classifications of anemia?

A

-“cytic” refers to cell size; -“chromic” refers to Hgb content

190
Q

What are the 3 main types of anemia?

A

microcytic/hypochromic; normocytic/normohromic; macrocytic/hypochromic

191
Q

What type of anemia is associated with iron deficiency and thalassemia?

A

microcytic/hypochromic; small and decreases Hgb content

192
Q

What anemia is associated with hemolytic, posthemorrhagic, aplastic, and anemia of chronic disease?

A

normocytic/normochromic

193
Q

What anemia classification includes pernicious anemia and folate deficiency?

A

macrocytic/macrochromic

194
Q

The loss of what factor leads to vitamin 12 deficiency?

A
Pernicious anemia (also known as Biermer's anemia, Addison's anemia, or Addison–Biermer anemia) is one of many types of the larger family of megaloblastic anemias. It is caused by loss of gastric parietal cells, which are responsible, in part, for the secretion of intrinsic factor, a protein essential for subsequent absorption of vitamin B12 in the ileum.
Usually seated in an atrophic gastritis, the autoimmune destruction of gastric parietal cells (and autoantibody inactivation of intrinsic factor) leads to a lack of intrinsic factor.[1] Since the absorption from the gut of normal dietary amounts of vitamin B12[2] is dependent on intrinsic factor, the loss of intrinsic factor leads to vitamin B12 deficiency. While the term 'pernicious anemia' is sometimes also incorrectly used to indicate megaloblastic anemia due to any cause of B12 deficiency, its proper usage refers to that caused by atrophic gastritis, parietal cell loss, and lack of intrinsic factor only.
195
Q

Anemia related to blood loss is related to % of TBV lost. What is the mL value and clinical manifestations associated with 10, 20, 30, 40, and 50 % TBV blood loss? Post - hemorrhagic anemia

A

10: 500mL (no manifestations; 20: 1000mL (tachycardia with increased exercise); 30: 1500mL (postural hypotension, tachycardia); 40: 2000mL (CVP, CO, BP low, air hungry, cold/clammy skin); 50: 2500mL (severe shock, lactic acidosis, death)

196
Q

What is the definition of hematocrit?

A

ratio of packed red blood cells to total blood volume (%); male 39-55%, female 36-48%

197
Q

Describe the hepatic lobule.

A

liver is made up of 50,000-100,000 discrete anatomic units called lobules; each is composed of plates of hepatocytes

198
Q

What two types of cells line the hepatic sinusoids?

A

endothelial cells and macrophages (Kupffer cells)

199
Q

What is unique about hepatic blood flow?

A

dual afferent blood supply equal to 25% of CO; 70% supplied by portal vein and 30% supplied by hepatic artery

200
Q

What are some anesthetic considerations when thinking about hepatic blood flow?

A

SNS stimulation can increase splanchic vascular resistance and decrease hepatic blood flow; beta blockers are associated with decreases in hepatic blood flow; positive pressure ventilation, CHF, and fluid overload can decrease hepatic blood flow; cirrhosis of liver increases resistance to blood flow through the portal vein and decreases hepatic blood flow; total hepatic blood flow is directly proportional to perfusion pressure across the liver and inversely related to splanchic vascular resistance

201
Q

How many mL/min is normal hepatic blood flow?

A

1500 mL/min in adults

202
Q

What is the normal hepatic blood volume?

A

450mL

203
Q

Describe the blood-cleansing function of the liver.

A

blood from the gut contains large quantities of colonic bacilli—> cleansing by Kupffer cells (macrophages) that line the hepatic sinuses–> endothelial cells line the hepatic sinuses and allow diffusion of large plasma proteins and other substances into extravascular spaces in the liver resulting in large lymph quanity—> produces 1/2 lymph needed by body (in space of disse)

204
Q

What are some metabolic functions of the liver?

A

carbohydrate, fat, protein, and drug (phase 1 and 2 biotransformation) metabolism; storage of vitamins (ADEK and anti-pernicious anemia factor and B12); bilirubin formation and excretion (conjugation of free bilirubin and secretion into bile); synthesis of coagulation factors and inhibitors (most except factor VIII); phagocytosis (filtration and destruction of bacteria and debris in blood—Kupffer cells); iron hemostasis; copper regulation; produces albumin

205
Q

What is the relation of serum albumin levels to liver function?

A

levels <2.5 are generally indicative of chronic liver disease, acute stress, or severe malnutrition

206
Q

When is giving whole blood indicated?

A

in acute blood loss >30% EBV

207
Q

When normal parenchyma in the liver is replaced with fibrous and nodular tissues it is called ______.

A

cirrhosis; hypoglycemia is common d\t inadequate gluconeogenesis

208
Q

When does hepatic encephalopathy occur?

A

when the liver can no longer clear nitrogenous waste—- asterixis or flattened waves on the EEG

209
Q

What is the Child-Pugh score?

A

used to predict surgical mortality in patients with cirrhosis; class C= greatly increased risk for peri-op morbidity and mortality

210
Q

What are common anesthetic considerations for patients with decreased liver function?

A

RSI or modified RSI; hypotension (low SVR and hypovolemia); blood glucose monitoring (decreased gluconeogenesis); no halothane; potential exagerrated effects with given doses of drugs (important with drugs that are highly protein bound); plasma cholinesterase is also produced in the liver and may be low (prolonged Sux effects and enhance the potential toxicity of ester local anesthetics); postop evaluate for jaundice

211
Q

What are the effects of inhaled and regional anesthetics on hepatic BF?

A

decrease HBF 20-30% in absence of stimulation; iso, des, and sevo undergo minimal hepatic metabolism= “safe”; des is probably most ideal; greatest decrease when operation site is near liver…. up to 60% decrease

212
Q

Describe anesthetic considerations for the acutely intoxicated patient.

A

require less anesthesia (additive depressant effect), aspiration precautions (slowed gastric emptying and decreased LES tone), increased surgical bleeding (interferrence with PLT aggregation); brain is less tolerant of hypoxia; circulating catecholamines are increased (labile vitals and exagerrated stimulus responses)

213
Q

What is the function of the gallbladder?

A

holds 30-50mL fluid; pear shaped; bile ducts from hepatic lobules join, eventually forming the right and left hepatic ducts, which then combine to form the hepatic duct, which together with the cystic duct from the gallbladder becomes the common bile duct; at termination, these ducts are enveloped in smooth muscle, the sphincter of Oddi (provides a barrier to intestinal bacteria); both biliary and pancreatic tracts empty into the duodenum via the ampulla of Vater; blood supply is the cystic artery… a branch of the right hepatic artery

214
Q

What is the function of bile?

A

emulsify and enhance absorption of ingested fats and fat soluble vitamins; provide excretory pathway for bilirubin, drugs and toxins, and immunoglobulin A (IgA); maintain duodenal alkalization

215
Q

Where is bile formed?

A

hepatocytes in each lobule continuously secrete bile into bile canaliculi at rate of ~1L/day…. the gallbladder then concentrates biliary fluid between meals and stores it; biliary flow into the duodenum is controlled by the Sphincter of Oddi

216
Q

How is bilirubin produced?

A

primarily the end product of hemoglobin metabolism and formed from degradation of the heme ring in Kupffer cells (liver); heme oxygenase breaks down Hgb into biliverdin, carbon monoxide, and iron—-> biliverdin reductase then converts the former into bilirubin…. bilirubin is then released into blood where it binds to albumin…. hepatic uptake of bilirubin…. excreted into bile canalculi…. 1/2 bilirubin secreted into the intestine is converted by colonic bacteria into urobilinogen

217
Q

What is the definition of IBS?

A

long-term or recurrent disorder of GI functioning; usually involves disturbances in the large intestine (colon) and small intestine; the disturbances involve motor function (motility), sensation, and secretion.

218
Q

The coagulation cascade has 2 pathways called _______ and _______ that lead to the formation of ________.

A

intrinsic and extrinsic; fibrin

219
Q

What are some common symptoms of IBS?

A

cramping, abdominal pain, bloating, constipation, and diarrhea

220
Q

Tissue factor is factor # ______?

A

III

221
Q

What is the long term health effects of IBS?

A

IBS has not been shown to lead to a serious disease

222
Q

What are some anesthetic considerations of IBS?

A

consider RSI if GERD present; bowel distention could result in limited diaphragmatic excursion; use cuffed tube; ensure proper fluid volumes; metabolic alkalosis (normal saline is superior)

223
Q

Define Crohns disease.

A

chronic inflammatory condition of the GI tract most often found at end of small bowel (the ileum) and beginning of colon, but may affect any part from mouth to anus; can also affect entire thickness of bowel wall, while ulcerative colitis only involves innermost lining of colon

224
Q

What is ulcerative colitis?

A

affects only the innermost lining of large intestine and rectum; occurs on continuous stretches of colon (does not “skip” like crohns); abdominal pain, fever, bloody diarrhea

225
Q

What are some anesthetic considerations for inflammatory bowel disease?

A

fluid and electrolyte status; possible extracolonic complications (liver, sepsis, anemia, arthritis, hypoalbumin,…); prophylactic steroid coverage is likely indicated particularly with patients on long term steroid use; avoid N2O if distended bowel; TPN may be needed (continue at prescribed rate)

226
Q

What is the treatment for a drug induced hemorrhage for patients taking heparin or coumadin?

A

protamine reverses heparin; vitamin K or FFP can be given for coumadin

227
Q

What is the definition of vomiting?

A

forceful expulsion of upper GI contents through mouth caused by powerful sustained contraction of abdominal muscles

228
Q

What is the definition of retching?

A

labored rhythmic activity of the respiratory muscles, including the diaphargm and abdominal muscles, without expulsion of gastric content

229
Q

What is the incidence of PONV?

A

general surgical population: 20-30%; high risk: 70-80%

230
Q

Who is at high risk for PONV based on the 4 point scale?

A

females, nonsmoker, history of PONV, post-op opioids (1 point for each)

231
Q

Based on the 4 point scale, what is the risk % associated with each point for PONV?

A

1:20%, 2:40%, 3:60%, 4:80%

232
Q

Describe the brainstem emetic control center.

A

dorsal vagal complex: area postrema (chemoreceptor trigger zone), dorsal motor nucleus of vagus nerve

233
Q

What 4 receptors are of concern when considering PONV?

A

5-HT3, H-1, A-Ch, D-2

234
Q

What is the function of 5-HT3 blockers?

A

ondansetron, dolasetron, tropisetron; blocks serotonin receptors centrally in chemoreceptor trigger zone and peripherally at vagal nerve terminals in the intestine; reduces n/v by preventing serotonin release in the small intestine and by blocking signals to the CNS

235
Q

What is the function of histamine H-1 blockers?

A

ranitidine, cimetidine, famotidine, promethezine; does not inhibit histamine release, rather attaches to the receptors and prevent responses mediated by histamine such as the secretion of hydrogen ions from parietal cells and CNS stimulation

236
Q

What is the function of anticholinergics in PONV?

A

blocks muscarinic cholinergic CNS emetic receptors in cerebral cortex and pons; scopolamine—- apply evening prior to surgery or four hours before end because of its limitations…. 2-4hr onset of effect

237
Q

What is the function of the use of neuroleptics (dopaminergic D-2 receptor blockers) in PONV?

A

phenothiazines, chloropromazine, butryophenones, droperidol; extrapyrimidal effects are induced by neuroleptics causing hypotension, possible prolonged QT; do NOT administer to patients with parkinsons; these drugs are antagonists at the dopaminergic receptors in the chemoreceptor trigger zone of the medulla and are most effective in treating opioid induced n/v

238
Q

Is there a genetic link for patients with Crohns disease?

A

yes; 70-80% are type group A blood

239
Q

When giving whole blood, what is the expected rise in Hct seen per unit in the 70kg non-bleeding adult?

A

3-4% per unit of WB

240
Q

When is giving whole blood indicated?

A

in acute blood loss >30% EBV

241
Q

What happens when whole blood is >24 hours old?

A

there is no viable platelets and factors V and VIII decrease

242
Q

What are the 5 things that cryoprecipitate is rich in?

A

fibrinogen, factor VIII, vWF, fibrinectin, fibrin stabilizing factor (XIII)

243
Q

Where is vWF and factor VIII made at?

A

NOT IN THE LIVER; made in endothelial cells

244
Q

What is the shortest lived cell product?

A

platelets; shelf life of 7 days

245
Q

Each unit of platelets will increase the count by how much?

A

5,000-10,000

246
Q

When is FFP collected and how long is it good for?

A

FFP separated from EB and frozen within 6 hours and can go unused for 1 year

247
Q

What are 3 types of immune hemolytic anemias?

A

alloimmune: pt makes antibody to foreign RBC
autoimmune: pt makes auto antibody directed at their own RBC
drug induced: pt makes antibody to a particular drug—> damage to patients RBC

248
Q

What is the role of platelets?

A

adhesion, aggregation, activation (VIII and vWF—platelet binding), platelet plug, platelet release (degranulation)

249
Q

What are the primary 5 steps to achieve hemostasis?

A

vasocontriction–>platelet plug formation—> coagulation cascade activated—> blood clot formation—-> fibrinolysis (clot retraction and dissolution)

250
Q

What does TRALI stand for?

A

transfusion related acute lung injury; nausea, chills, dyspnea, decrease UOP and SaO2, bilateral pulmonary edema within 4 hours of tx, immune mediated

251
Q

Describe clot formation.

A

fibrin—>fibrinogen; traumatized vessel wall releases activator substances and platelets—>clot forms in 15-20 seconds; fibroblasts later invade clot 7-10 days

252
Q

The coagulation cascade has 2 pathways called _______ and _______ that lead to the formation of ________.

A

intrinsic and extrinsic; fibrin

253
Q

What should be given for factor V deficiency?

A

FFP to increase range within 5-20% of normal

254
Q

Tissue factor is factor # ______?

A

III

255
Q

What can be seen in patients with a factor V deficiency?

A

prolonged bleeding time, PT, PTT; s\s of blood nose, bloody periods, severe bleeding

256
Q

Heparin therapy is unable to be monitored by a PTT in patients with what factor deficiency?

A

Factor VII; no association with excessive bleeding despite increase PTT; these patients are vulnerable to thromboembolic events; cannot monitor heparin dosing because heparin activity monitoring relies on F 7 activation in the body

257
Q

Hemophilia A is associated with which factor deficiency?

A

Factor VIII (anti-hemophilic A); inability to form; no fibrin; persistent umbilical cord bleeding; CNS hemorrhage common d\t bleeding time increase; all coags are WNL d\t position of factor VIII in the coagulation cascade

258
Q

What is the treatment for hemophilia A or Factor VIII deficiency?

A

give FFP or cryo

259
Q

A fibrinogen level < ______ is associated with increased bleeding and may be indicative of _______.

A

<100; DIC

260
Q

What is the treatment for a drug induced hemorrhage for patients taking heparin or coumadin?

A

protamine reverses heparin; vitamin K or FFP can be given for coumadin

261
Q

For every ______ units of PRBC, give ______ units of FFP.

A

every 4 units PRBC give 1 unit of FFP

262
Q

For every _______ units of PRBC, give ________ units of FFP and _________ of platelets.

A

8 units PRBC; give 2 units FFP and quad pack of platelets

263
Q

What is the storage life and change in Hgb/Hct seen with PRBCs?

A

35 days; Hgb rises 1g/dL and Hct increases 3%

264
Q

What is the progression of renal blood flow?

A

afferent arteriole—>glomerulus—> efferent arteriole—-> peritubular capillaries—> renal vein

265
Q

When Na levels are low, _______ is excreted and causes reabsorption in the _______ ________.

A

aldosterone; distal tubule

266
Q

What are 3 factors in our body that defend against Na overload?

A

ANP (atria); BNP (brain); CNP (c-type)

267
Q

What are some ways our body defends against Na depletion or hypovolemia?

A

RAAS; aldosterone; decreased stretch= increased sympathetic tone= increased renal perfusion= increased renin

268
Q

H20 reabsorption in the collecting duct is mediated by _________.

A

ADH (vasopressin)

269
Q

What are the 3 mechanisms for regulation of acid-base balance?

A

buffer system (secs), respiratory system (mins), renal system (hrs to days)

270
Q

Where is HCO3 reabsorbed?

A

~85% in the PCT

271
Q

Where is the daily H+ load excreted?

A

in the collecting duct

272
Q

What is special in regards to the urinary system and acid base buffering?

A

it is the only system that can eliminate excess H+ permanently and restore bicarb buffering ions in the blood

273
Q

When a patient is alkalotic, what is the response by the kidneys?

A

kidney excretes HCO3 to free up H+ in plasma

274
Q

What is the response from the kidneys when a patient is acidotic?

A

kidney tubules produce HCO3; H+ is secreted

275
Q

Where is the site of action for osmotic diuretics?

A

PCT and the thin descending limb

276
Q

Where is the site of action for loop diuretics?

A

thick ascending limb

277
Q

Where is the site of action for thiazides?

A

early DCT

278
Q

Where is the site of action for spironolactone?

A

late DCT and CD—- competitively inhibits aldosterone