deck_1297508 Flashcards
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
What % of the approximately 125mL/min of filtrate is reabsorbed from the renal tubules while the remainder is excreted as urine?
99%
26
Why does glucose get excreted in urine when past a certain concentration?
some substances like glucose have a maximum reabsorption value after which the remainder is excreted.
27
What factors can increase the GFR?
increased renal blood flow, dilation of the afferent arteriole, and increased resistance in the efferent arteriole increases GFR
28
Describe the activation and process of the RAA.
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
What is the short description for the proximal tubule?
"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
Describe the differences in permeability of the descending and ascending limb of the loop of Henle.
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
Describe the blood flow through the nephron.
afferent arteriole--> glomerulus--> unfiltered blood to efferent arterioles--> peritubular capillaries--> venous system
32
What happens to the ultrafiltrate once it leaves the glomerulus?
travels from the glomerulus through tubules for reabsorption/secretion; reabsorption--> goes into the interstitium and returns to systemic vasculature
33
Differentiate between the ECF effects of aldosterone and ADH.
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
Describe the "fine tuning" that occurs in the kidney.
(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
What is the end product when ADH is present vs not present?
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
What can prompt the activation of the RAA system?
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
What is angiotensin II and what countermeasures does it take?
it is a potent vasoconstrictor but also releases protective prostaglandins (vasodilate) to protect renal blood flow
38
What is the anhydrase equation?
acid-base balance via Na/H ion exchange; H + HCO3--> H2CO3--> H2O + CO2; Na is exchanged for H.... excess H requires for HCO3
39
What is the effect of hyperkalemia? Give common treatments.
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
What should you do for the hypoosmolar state?
free water overload or water intoxication: hyponatremia, so restrict free H20 and give hypertonic saline
41
What is the anion gap utilized for?
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
How do you calculate anion gap?
normal anion gap= Na-Cl-HCO3= 8-12 mM
43
Where is atrial natriuretic factor synthesized and what is its action on the kidneys?
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
What stimulates the release of ANF?
atrial distention, stretch, or pressure
45
Name two loop diuretics and their function.
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
What is the effect of thiazides and K+ sparing diuretics like spironolactone?
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
What is diamox and its function?
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
What is Mannitol and its effects?
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
What are some considerations for patients taking ACE inhibitors or ARBs?
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
How do you decide between 5% and 25% albumin?
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
What is refractory hypotension?
it is blocking action of angiotensin II, a powerful vasoconstrictor; blocks release of aldosterone and ADH
52
Name the normal values of Na, K, Ca, and Magnesium.
Na: 135-145, K: 3.5-4.5, Ca: 9.9-10.5, Magnesium: 1.7-2.5
53
What electrolytes control the following: 1) resting membrane potential (-90mV) and 2) threshold (-60mV)?
K+ controls the resting membrane potential; Ca+ controls the threshold
54
What is the most common electrolyte disturbance with renal failure?
hyperkalemia
55
How do you treat hyperkalemia and what are the effects?
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
The incidence of surgery related acute renal failure is ____ to _____ %.
18-47%
57
How do you calculate allowable blood loss?
EBVx (start Hct-target Hct)/ start Hct
58
What is the mL/kg to calculate obese patients estimated blood volume?
45-55mL/kg
59
Urine specific gravity > ______ shows that the kidneys are concentrating urine adequately.
> 1.018
60
What is the normal values for GFR?
125-140 mL/min; decreases 1% per year after the age of 20
61
What test is considered the NEST measure of renal function?
GFR
62
What is the normal range for serum creatinine?
0.6-1.0 mg/dL in women and 0.8-1.3 mg/dL in men
63
What is creatinine?
a waste product of muscle metabolism; not reabsorbed by the kidneys
64
What is the normal value for BUN?
5-20 mg/dL; increases can be seen in high protein diets
65
What are the normal values for specific gravity?
1.005-1.030; assesses renal tubular function by measuring the urine concentrating ability
66
What marker may turn out to be a better indicator of GFR than creatinine, but costs more money?
cystatin C; produced by all nucleated cells in the body and not influenced by muscle mass, gender, or age
67
What is the difference in acute kidney injury, nephritic disease, and renal tubular dysfunction?
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
Define oliguria and non-oliguric.
urine output 400cc/day
69
What are some causes of AKI?
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
What are 3 classifications of AKI?
pre-renal, intra-renal, post-renal
71
What is pre-renal azotemia?
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
What are some examples of pre-renal azotemia?
hemorrhage, GI fluid loss, trauma, surgery, burns, cardiogenic shock, sepsis, hepatic failure, aortic or renal clamping, thromboembolism
73
Among hospitalized patients, what are common causes of pre-renal azotemia?
CHF, liver dysfunction, septic shock
74
Where does intra-renal azotemia occur?
name implies that its cause lies within the parenchyma of the kidney itself
75
How is intra-renal azotemia categorized?
according to the primary site of injury: glomerulus, renal tubules, interstitium, renal vasculature
76
Why can injury to the kidneys occur during reperfusion?
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
What are some causes of intra-renal azotemia?
acute interstitial nephritis most often caused by allergic reactions to drugs, glomerulonephritis, renal artery emboli, renal vein thrombosis, and vasculitis
78
What is post-renal azotemia?
AKI when urinary outflow tracts are obstructed; can use renal ultrasonography
79
What are s\s of post-renal azotemia?
generalized malaise, fluid overload (dyspnea, edema, and HTN), lethargy, nausea, confusion, accumulation of protein and amino acid metabolites, encephalopathy
80
Oliguria is defined as < ______mL/day or < _______ cc/kg/hr.
<0.5cc/kg/hr
81
Anuria is defined as < _______cc/day.
100; complete anuria is very unusual
82
What are AKI complications seen in central nervous system, cardiovascular, hematologic, and GI systems?
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
What are some treatments for AKI?
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
What fluids are preferred in patients with renal impairment and why?
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
What is the role of dopamine in treatment of AKI?
useless and associated with a number of undesirable side effects.
86
What is the overall concern with the use of vasopressors with AKI?
vasoconstriction may exacerbate tubular injury
87
Regardless of the cause, a decrease in GFR < _____ mL/min generally requires dialysis or renal transplant.
<25
88
What are the two general patterns of glomerular disease?
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
What are some complications of nephrotic syndrome?
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
What is a renal problem characterized by inflammation of the renal pelvis (collecting ducts) and the kidney itself?
pyelonephritis; treated with antibiotics..... if infection ascends high enough, glomeruli are damaged
91
Are there any anesthetics we administer that have negative renal effects?
enflurane and sevoflurane, when in high doses, can potentially cause renal toxicity
92
What are ways to partially overcome renal impairment during anesthesia?
maintain adequate intravascular volume and normotension
93
Are renal effects more or less with regional vs. general anesthesia?
generally less
94
What are some indirect effects on the renal system during anesthesia caused by cardiac, neural, and endocrine effects?
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
Why is Ketorolac (Toradol) not a good choice in most patients with renal impairment?
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
What are some potential problems for the kidneys associated with ACE inhibitors?
these drugs block protective effects of angiotensin II and may result in additional reductions in GFR during surgery
97
What are some drugs that could cause renal artery vasospasm, direct cytotoxic injury, or renal tubular obstructions?
aminoglycosides, immunosuppressive agents (cyclosporins, tacrolimus), radiocontrast dyes
98
What are complications for the kidneys during aortic cross-clamping and CPB?
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
What lab values decrease in presence of renal failure?
calcium, albumin, red cell production/erythrpoietin/anemia
100
What lab values are increased in presence of renal failure?
potassium, phosphate, magnesium, uric acid
101
Why should cautionary use of PEEP be considered in renal patients?
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
What are the effects of pneumoperitoneum, CPB, and pelvic surgery on renal function?
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
Release of fluoride ions from VAA metabolic degradation with plasma concentrations > _____ micromol/L have been associated with renal toxicity.
>50 micromol/L; fluoride production is greatest with prolonged use of enflurane and sevoflurane (compound A).... but overall safe with impaired renal function
104
How does the body compensate to increase cardiac output?
Na retention and activation of renin-angiotensin system
105
What are considerations for induction of patients with renal disease?
slow and steady wins the race, RSI vs. standard d\t possible delayed gastric emptying, choice of agents
106
What are some considerations for intra-op maintenance of patients with renal disease?
focus on normotension, avoid hypoventilation (K, acidosis, etc) or hyperventilation (shift left)
107
Is morphine good for patients with renal disease?
not generally; morphine accumulation has been found to prolong respiratory depression in patients with renal failure; demerol has active metabolites associated with seizures
108
What is the NMB drug of choice for renal patients?
cisatricurium, atracurium, or mivacurium d\t ester hydrolysis and Hofmann elimination
109
What is the NMB drug of choice for renal patients?
cisatricurium, atracurium, or mivacurium d\t ester hydrolysis and Hofmann elimination
110
When can succinylcholine be safely administered to renal patients?
When serum K is <5meQ/L
111
When can succinylcholine be safely administered to renal patients?
When serum K is <5meQ/L
112
What are some renal considerations for vecuronium and rocuronium?
Vec is 20% eliminated in urine; prolongation of NMB with Rocuronium has been seen with severe renal disease
113
What are some renal considerations for vecuronium and rocuronium?
Vec is 20% eliminated in urine; prolongation of NMB with Rocuronium has been seen with severe renal disease
114
What is mannitol and its effects?
osmotic diuretic (6 carbon sugar); may activate intra-renal synthesis of vasodilating prostaglandins, increase, RBF, and act as a free radical scavenger
115
What is mannitol and its effects?
osmotic diuretic (6 carbon sugar); may activate intra-renal synthesis of vasodilating prostaglandins, increase, RBF, and act as a free radical scavenger
116
What is the danger in rapid correction of hyponatremia?
associated with demyelinating lesions in the pons resulting in serious permanent neurological conditions
117
What is the danger in rapid correction of hyponatremia?
associated with demyelinating lesions in the pons resulting in serious permanent neurological conditions
118
What is the effect of hypernatremia on anesthesia?
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
119
What is the effect of hypernatremia on anesthesia?
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
120
What is a cardiac consideration for patients with low calcium?
potentiation of negative inotropic effects of barbs and VAAs will be seen
121
What is a cardiac consideration for patients with low calcium?
potentiation of negative inotropic effects of barbs and VAAs will be seen
122
If a patient has magnesium imbalances, how does this effect anesthesia?
high: dosages of NDMBs should be decreased by 25-50%; low: cardiac arrythmias
123
If a patient has magnesium imbalances, how does this effect anesthesia?
high: dosages of NDMBs should be decreased by 25-50%; low: cardiac arrythmias
124
What are considerations during a TURP?
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
125
What are considerations during a TURP?
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
126
In coagulation.... what is the first line of defense?
The vessel wall
127
In coagulation.... what is the first line of defense?
The vessel wall
128
What are the 3 layers of the vessel wall?
Tunica---- adventitia, media, intima
129
What are the 3 layers of the vessel wall?
Tunica---- adventitia, media, intima
130
Which layer of the vessel wall is the endothelial layer?
tunica intima
131
Which layer of the vessel wall is the endothelial layer?
tunica intima
132
What happens during the initial phase of the coagulation process?
vascular constriction---- limits the flow of blood to the area of injury
133
What happens during the initial phase of the coagulation process?
vascular constriction---- limits the flow of blood to the area of injury
134
What are the vitamin K dependent factors?
II, VII, IX, X
135
What are the vitamin K dependent factors?
II, VII, IX, X
136
What factors are produced in the liver?
all but vWF, III (tissue factor), IV (calcium)
137
What factors are produced in the liver?
all but vWF, III (tissue factor), IV (calcium)
138
What are the extrinsic factors?
You can buy the extrinsic pathway for 0.37 cents..... III and VII
139
What are the extrinsic factors?
You can buy the extrinsic pathway for 0.37 cents..... III and VII
140
What are the intrinsic factors?
You can buy the intrinsic pathway for $12 or $11.98; XII or XI, IX, VIII
141
What are the intrinsic factors?
You can buy the intrinsic pathway for $12 or $11.98; XII or XI, IX, VIII
142
What is the common pathway?
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
143
What is the common pathway?
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
144
What is factor III?
tissue factor
145
What is factor III?
tissue factor
146
What is factor I?
fibrinogen; forms the clot (fibrin)
147
What factors are anti-coagulation?
C, S, plasminogen, urokinase (activates plasminogen), tissue plasminogen activator (tPA---activates plasminogen)
148
What is factor II?
prothrombin; its active form IIa activates I, V, VII, VIII, XI, XIII, protein C, platelets
149
What is factor II?
prothrombin; its active form IIa activates I, V, VII, VIII, XI, XIII, protein C, platelets
150
What is factor IV?
calcium; required for coagulation factors to bind to phospholipid
151
What is the difference between Type 1 and 2 HIT?
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
What is factor IX?
christmas factor; activates X and forms tenase complex with factor VIII
153
What is factor IX?
christmas factor; activates X and forms tenase complex with factor VIII
154
What is factor X?
Stuart-Prower factor; activates II
155
What is factor X?
Stuart-Prower factor; activates II
156
What factor is the Hageman factor?
XII
157
What are important pre-operative considerations for assessing coagulopathies?
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
What does factor XIII do?
crosslinks fibrin
159
What does factor XIII do?
crosslinks fibrin
160
What is the function of vWF?
binds to VIII, mediates platelet adhesion
161
What are the intra-operative considerations for the management of sickle cell disease?
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
162
What factors are pro-coagulation?
I-XIII
163
What factors are pro-coagulation?
I-XIII
164
What factors are anti-coagulation?
C, S, plasminogen, urokinase (activates plasminogen), tissue plasminogen activator (tPA---activates plasminogen)
165
What factors are anti-coagulation?
C, S, plasminogen, urokinase (activates plasminogen), tissue plasminogen activator (tPA---activates plasminogen)
166
Why are we concerned with "sickled" cells?
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
What is the normal value for PTT and what factors is it evaluating?
PTT: 30-40sec; common and intrinsic; 1,2,5,10,13,12,11,9,8
168
What is the target Hct for patients with sickle cell disease?
~30%
169
A fibrinogen level < ______ mg/dL is associated with spontaneous bleeding.
<100
170
What is the normal value for "bleeding time" and how accurate is this method?
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
171
What is a TEG test?
thromboelastography; wider encompassing test of clot formation, stability, and lysis
172
What is the most common coagulopathy seen in anesthesia and how is it defined?
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
173
The depletion of platelets secondary to markedly increased platelet consumption from coagulation pathway activation is called ____________.
thrombocytopenia; may lead to micro thrombi resulting in purpura (red/purple lesions on skin that do not blanch)
174
What are leukocytes and their function?
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
175
What platelet values are associated with mild, moderate, and severe DIC?
70,000-150,000= mild, 40-70= moderate, 20-40= severe
176
What are the two types of leukemia?
Acute and Chronic; many chemotherapy agents cause CNS toxicity, renal toxicity, and hepatic toxicity
177
What follows the same pathophysiology as DIC, combined with RBC hemolysis and elevated liver enzymes?
HELLP
178
What is the treatment of HELLP?
control of HTN and delivery of parasite
179
What is the only true treatment of DIC?
treatment of the underlying cause of DIC; platelet and plasma transfusions are only supportive therapies
180
What is the difference between Type 1 and 2 HIT?
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
181
What are the results of Type 2 HIT?
thrombocytopenia, venous and arterial thrombus formation, potentially severe end-organ damage
182
What are the results of Type 2 HIT?
thrombocytopenia, venous and arterial thrombus formation, potentially severe end-organ damage
183
At what level can bleeding be anticipated in patients with factor 1 deficiency?
50-100mg/dL
184
When does Type 2 HIT appear?
5-10 days after heparin use; can be seen if heparin therapy is restarted within 20 days of previous exposure
185
What is the main function of erythrocytes?
get oxygen delivered to the tissues; biconcave disk has the ability to change shape and increases surface area; contains large amounts of carbonic anhydrase
186
What are some anesthetic considerations for patients with HIT?
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
187
What is the cause of SIRS?
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
188
What is the average lifespan of the RBC?
120 days after leaving bone marrow
189
What are some management considerations with coagulopathy and SIRS?
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
190
What are some management considerations with coagulopathy and SIRS?
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
191
What are important pre-operative considerations for assessing coagulopathies?
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
192
What are important pre-operative considerations for assessing coagulopathies?
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
193
What can cause a sickle cell crisis?
decreased O2 sat, temperature, infections, dehydration, stasis and acidosis
194
What is the most important variable when considering a crisis in the sickle cell patient?
hypoxemia
195
What are the different types of sickle cell crisis?
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)
196
What are the intra-operative considerations for the management of sickle cell disease?
avoid all triggers, dehydration, acidosis, hypothermia, hypoxia, and hypotension.... know that pain can exacerbate complications
197
Sickle cell is a type of ______ characterized by the presence of hemoglobin ______ within the erythrocytes.
type of anemia, characterized by Hgb S; genetic mutation in which one amino acid (valine) replaces another (glutamic acid)
198
What are the names for the homozygous and heterozygous forms of sickle cell and which is more severe?
sickle cell hemolytic anemia is homozygous and is most severe; sickle cell thalassemia is heterozygous
199
When confronted with dehydration or deoxygenation how does Hgb S react?
Hgb S reacts by solidifying and stretching the erythrocyte into an elongated sickle shape
200
At what PaO2 will patients with sickle cell disease or trait begin to sickle?
30-40mm Hg for sickle cell disease; 20-30 mm Hg for sickle cell trait
201
Why are we concerned with "sickled" cells?
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
202
What is the "risk" of complications between sickle trait and sickle disease?
no increased mortality or morbidity with sickle cell trait; increased risk of peri-operative complications with sickle cell disease
203
What is the target Hct for patients with sickle cell disease?
~30%
204
What is the relationship of 2,3 DPG with the shifting of the oxygen-hemoglobin dissociation curve?
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
205
What are some anesthetic considerations for patients with leukemia?
lab assessment, correction of pancytopenia if necessary, evaluate antibiotic choice, aseptic technique at all times, possibility of thrush, review adverse effects associated with chemotherapy
206
What is 2,3 DPG?
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
207
Oxy-Hgb dissociation curve, when shifted to the left has what characteristics?
less release of oxygen to the tissues; P50 <26mmHg; alkalosis; hyperthermia; decreased 2,3 DPG
208
Oxy-Hgb dissociation curve, when shifted to the right has what characteristics?
more release of oxygen to the tissues; P50 >26mmHg; acidosis; hyperthermia; increased 2,3 DPG
209
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?
leukemia; excessive accumulation of leukemic cells results in an overcrowding of bone marrow which causes a decreased production and function of normal hematopoietic cells
210
What are the two types of leukemia?
Acute and Chronic; many chemotherapy agents cause CNS toxicity, renal toxicity, and hepatic toxicity
211
What happens during Factor I deficiency?
fibrinogen deficiency; caused by either decreased production or failure to work properly; clotting reaction is blocked prematurely and clot doesn't form
212
What is hemophilia A caused from?
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
213
What is the cause and effect of Von Willebrand factor deficiency?
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
214
What lab values would be normal and abnormal is patients with hemophilia 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
215
What lab values would be normal and abnormal is patients with vWF deficiency?
prolonged PTT; most common cause of prolonged PTT in those patients not taking heparin
216
What are the 3 types of factor 1 (fibrinogen) deficiency?
qualitative (dysfibrinogenemia---doesn't work how it should); quantitative (afibrinogenemia----complete lack of fibrinogen); combined (hypodysfibrinogenemia---combined defect involving low amounts and impaired function)
217
How is bilirubin produced?
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
218
What is the most abundant cell in the body?
erythrocytes (25 trillion cells)
219
What is the main function of erythrocytes?
get oxygen delivered to the tissues; biconcave disk has the ability to change shape and increases surface area
220
How are RBCs produced?
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
221
What vitamins are required for proper RBC function and production?
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
222
What is the average lifespan of the RBC?
120 days after leaving bone marrow
223
What are common causes of anemia?
impaired RBC production, blood loss (acute or chronic), increased RBC destruction
224
What is the difference between the "cytic" and "chromic" classifications of anemia?
-"cytic" refers to cell size; -"chromic" refers to Hgb content
225
What are the 3 main types of anemia?
microcytic/hypochromic; normocytic/normohromic; macrocytic/hypochromic
226
What type of anemia is associated with iron deficiency and thalassemia?
microcytic/hypochromic; small and decreases Hgb content
227
What anemia is associated with hemolytic, posthemorrhagic, aplastic, and anemia of chronic disease?
normocytic/normochromic
228
What anemia classification includes pernicious anemia and folate deficiency?
macrocytic/macrochromic
229
The loss of what factor leads to vitamin 12 deficiency?
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.
230
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
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)
231
What is the definition of hematocrit?
ratio of packed red blood cells to total blood volume (%); male 39-55%, female 36-48%
232
Describe the hepatic lobule.
liver is made up of 50,000-100,000 discrete anatomic units called lobules; each is composed of plates of hepatocytes
233
What two types of cells line the hepatic sinusoids?
endothelial cells and macrophages (Kupffer cells)
234
What is unique about hepatic blood flow?
dual afferent blood supply equal to 25% of CO; 70% supplied by portal vein and 30% supplied by hepatic artery
235
What are some anesthetic considerations when thinking about hepatic blood flow?
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
236
How many mL/min is normal hepatic blood flow?
1500 mL/min in adults
237
What is the normal hepatic blood volume?
450mL
238
Describe the blood-cleansing function of the liver.
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)
239
What are some metabolic functions of the liver?
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
240
What is the relation of serum albumin levels to liver function?
levels <2.5 are generally indicative of chronic liver disease, acute stress, or severe malnutrition
241
When is giving whole blood indicated?
in acute blood loss >30% EBV
242
When normal parenchyma in the liver is replaced with fibrous and nodular tissues it is called ______.
cirrhosis; hypoglycemia is common d\t inadequate gluconeogenesis
243
When does hepatic encephalopathy occur?
when the liver can no longer clear nitrogenous waste---- asterixis or flattened waves on the EEG
244
What is the Child-Pugh score?
used to predict surgical mortality in patients with cirrhosis; class C= greatly increased risk for peri-op morbidity and mortality
245
What are common anesthetic considerations for patients with decreased liver function?
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
246
What are the effects of inhaled and regional anesthetics on hepatic BF?
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
247
Describe anesthetic considerations for the acutely intoxicated patient.
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)
248
What is the function of the gallbladder?
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
249
What is the function of bile?
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
250
Where is bile formed?
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
251
How is bilirubin produced?
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
252
What is the definition of IBS?
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.
253
The coagulation cascade has 2 pathways called _______ and _______ that lead to the formation of ________.
intrinsic and extrinsic; fibrin
254
What are some common symptoms of IBS?
cramping, abdominal pain, bloating, constipation, and diarrhea
255
Tissue factor is factor # ______?
III
256
What is the long term health effects of IBS?
IBS has not been shown to lead to a serious disease
257
What are some anesthetic considerations of IBS?
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)
258
Define Crohns disease.
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
259
What is ulcerative colitis?
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
260
What are some anesthetic considerations for inflammatory bowel disease?
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)
261
What is the treatment for a drug induced hemorrhage for patients taking heparin or coumadin?
protamine reverses heparin; vitamin K or FFP can be given for coumadin
262
What is the definition of vomiting?
forceful expulsion of upper GI contents through mouth caused by powerful sustained contraction of abdominal muscles
263
What is the definition of retching?
labored rhythmic activity of the respiratory muscles, including the diaphargm and abdominal muscles, without expulsion of gastric content
264
What is the incidence of PONV?
general surgical population: 20-30%; high risk: 70-80%
265
Who is at high risk for PONV based on the 4 point scale?
females, nonsmoker, history of PONV, post-op opioids (1 point for each)
266
Based on the 4 point scale, what is the risk % associated with each point for PONV?
1:20%, 2:40%, 3:60%, 4:80%
267
Describe the brainstem emetic control center.
dorsal vagal complex: area postrema (chemoreceptor trigger zone), dorsal motor nucleus of vagus nerve
268
What 4 receptors are of concern when considering PONV?
5-HT3, H-1, A-Ch, D-2
269
What is the function of 5-HT3 blockers?
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
270
What is the function of histamine H-1 blockers?
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
271
What is the function of anticholinergics in PONV?
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
272
What is the function of the use of neuroleptics (dopaminergic D-2 receptor blockers) in PONV?
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
273
Is there a genetic link for patients with Crohns disease?
yes; 70-80% are type group A blood
274
When giving whole blood, what is the expected rise in Hct seen per unit in the 70kg non-bleeding adult?
3-4% per unit of WB
275
When is giving whole blood indicated?
in acute blood loss >30% EBV
276
What happens when whole blood is >24 hours old?
there is no viable platelets and factors V and VIII decrease
277
What are the 5 things that cryoprecipitate is rich in?
fibrinogen, factor VIII, vWF, fibrinectin, fibrin stabilizing factor (XIII)
278
Where is vWF and factor VIII made at?
NOT IN THE LIVER; made in endothelial cells
279
What is the shortest lived cell product?
platelets; shelf life of 7 days
280
Each unit of platelets will increase the count by how much?
5,000-10,000
281
When is FFP collected and how long is it good for?
FFP separated from EB and frozen within 6 hours and can go unused for 1 year
282
What are 3 types of immune hemolytic anemias?
alloimmune: pt makes antibody to foreign RBCautoimmune: pt makes auto antibody directed at their own RBCdrug induced: pt makes antibody to a particular drug---> damage to patients RBC
283
What is the role of platelets?
adhesion, aggregation, activation (VIII and vWF---platelet binding), platelet plug, platelet release (degranulation)
284
What are the primary 5 steps to achieve hemostasis?
vasocontriction-->platelet plug formation---> coagulation cascade activated---> blood clot formation----> fibrinolysis (clot retraction and dissolution)
285
What does TRALI stand for?
transfusion related acute lung injury; nausea, chills, dyspnea, decrease UOP and SaO2, bilateral pulmonary edema within 4 hours of tx, immune mediated
286
Describe clot formation.
fibrin--->fibrinogen; traumatized vessel wall releases activator substances and platelets--->clot forms in 15-20 seconds; fibroblasts later invade clot 7-10 days
287
The coagulation cascade has 2 pathways called _______ and _______ that lead to the formation of ________.
intrinsic and extrinsic; fibrin
288
What should be given for factor V deficiency?
FFP to increase range within 5-20% of normal
289
Tissue factor is factor # ______?
III
290
What can be seen in patients with a factor V deficiency?
prolonged bleeding time, PT, PTT; s\s of blood nose, bloody periods, severe bleeding
291
Heparin therapy is unable to be monitored by a PTT in patients with what factor deficiency?
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
292
Hemophilia A is associated with which factor deficiency?
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
293
What is the treatment for hemophilia A or Factor VIII deficiency?
give FFP or cryo
294
A fibrinogen level < ______ is associated with increased bleeding and may be indicative of _______.
<100; DIC
295
What is the treatment for a drug induced hemorrhage for patients taking heparin or coumadin?
protamine reverses heparin; vitamin K or FFP can be given for coumadin
296
For every ______ units of PRBC, give ______ units of FFP.
every 4 units PRBC give 1 unit of FFP
297
For every _______ units of PRBC, give ________ units of FFP and _________ of platelets.
8 units PRBC; give 2 units FFP and quad pack of platelets
298
What is the storage life and change in Hgb/Hct seen with PRBCs?
35 days; Hgb rises 1g/dL and Hct increases 3%
299
What is the progression of renal blood flow?
afferent arteriole--->glomerulus---> efferent arteriole----> peritubular capillaries---> renal vein
300
When Na levels are low, _______ is excreted and causes reabsorption in the _______ ________.
aldosterone; distal tubule
301
What are 3 factors in our body that defend against Na overload?
ANP (atria); BNP (brain); CNP (c-type)
302
What are some ways our body defends against Na depletion or hypovolemia?
RAAS; aldosterone; decreased stretch= increased sympathetic tone= increased renal perfusion= increased renin
303
H20 reabsorption in the collecting duct is mediated by _________.
ADH (vasopressin)
304
What are the 3 mechanisms for regulation of acid-base balance?
buffer system (secs), respiratory system (mins), renal system (hrs to days)
305
Where is HCO3 reabsorbed?
~85% in the PCT
306
Where is the daily H+ load excreted?
in the collecting duct
307
What is special in regards to the urinary system and acid base buffering?
it is the only system that can eliminate excess H+ permanently and restore bicarb buffering ions in the blood
308
When a patient is alkalotic, what is the response by the kidneys?
kidney excretes HCO3 to free up H+ in plasma
309
What is the response from the kidneys when a patient is acidotic?
kidney tubules produce HCO3; H+ is secreted
310
Where is the site of action for osmotic diuretics?
PCT and the thin descending limb
311
Where is the site of action for loop diuretics?
thick ascending limb
312
Where is the site of action for thiazides?
early DCT
313
Where is the site of action for spironolactone?
late DCT and CD---- competitively inhibits aldosterone
