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Semester 2 TxWes > Assessments Unit 3 > Flashcards

Assessments Unit 3 Flashcards

1
Q

What fluid compartment is more immediately altered by the kidneys?

A

ECF

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2
Q

What mediates osmolar homeostasis?

A

Osmolality sensors in anterior hypothalamus

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3
Q

What does ANP do?

A

Increase diuresis

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4
Q

What mediates volume homeostasis?

A

the JGA to alter water/Na reabsorption

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5
Q

What can cause hypovolemic issues?

A

Na/water loss, diuretics, GI loss, burns, trauma

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6
Q

What can cause euvolemic issues?

A

Salt restriction, endocrine related (hypothyroid, SIADH)

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7
Q

What can cause hypervolemic issues?

A

ARF/CKD, CHF, vasopressin increase

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8
Q

What level would mild, moderate and severe s/sx of hyponatremia manifest?

A

Mild = 130 - 135 mEq/L
Moderate = 120 - 130
Severe = less than 120

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9
Q

How would you treat hyponatremia?

A

Fix underlying cause. Replace Na (hypertonic saline, e-lyte drink, diuretics)

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10
Q

Why do you slowly treat hyponatremia? What’s the safe rate?

A

Too much can cause osmotic demyelination syndrome which can cause permanent neuro damage. No more than 6 mEq/L per 24 hours should be replaced

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11
Q

What is the dose of hypertonic saline in hyponatremic seizures?

A

3-5 ml/kg of 3% saline over 20 minutes or until seizure resolve

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12
Q

Common causes of hypernatremia?

A

Excessive evaporation, poor PO intake, overcorrection of hyponatremia, DI, Gi loss, excessive NaBicarb

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13
Q

What disease processes can cause hypervolemia?

A

Hyperaldosteronism, Cushings

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14
Q

What disease processes can cause euvolemic hypernatremia?

A

DI or insensible losses via the respiratory tract/skin

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15
Q

S/sx of hypernatremia?

A

Orthostasis, restlessness, lethargy, tremor/muscle twitching, seizure, death

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16
Q

What is the treatment for hypo/hyper/euvolemic hypernatremia?

A

Hyper = diuretics
Eu = water replacement (PO or d5W)
Hypo = NS

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17
Q

Goal Na reduction rate?

A

no more than 0.5 mmol per hour and less than 10 mmol per day

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18
Q

Goal potassium range?

A

3.5 - 5 mmol/L

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19
Q

What does aldosterone do to potassium?

A

Causes distal nephron to secrete K and reabsorb Na

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20
Q

What are the 3 major categories of potassium loss?

A

Renal loss, GI loss and transcellular shift

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21
Q

S/sx of hypokalemia?

A

U-wave, muscle cramp/weakness, ileus, dysrhythmias. Avoid excessive insulin, b-agonists, bicarb, hyperventilation and diuretics

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22
Q

S/sx of hyperkalemia?

A

Tall peaked T-wave, prolonged QRS, sine waves, skeletal muscle paralysis.

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23
Q

Common causes of hyperkalemia?

A

Renal failure, hypoaldosteronism, RASS inhibition, Sux, acidosis, cell death, massive blood transfusion

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24
Q

1st initial treatment/fastest treatment for hyperkalemia?

A

Calcium - quickly stabilizes the cell membrane

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25
Q

What does PTH and calcitonin do?

A

PTH = stimulates the release of calcium from bones
Calcitonin = promotes calcium storage into the bone and out of the plasma

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26
Q

What can cause hypocalcemia?

A

Decreased PTH (common complication of thyroid surgery), Mg deficiency, low vitamin D, renal failure, massive blood transfusion

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27
Q

How does vitamin D affect calcium?

A

It promotes absorption of intestinal calcium

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28
Q

What can cause hypercalcemia?

A

Hyperparathyroidism, cancer. Less common = vitamin D intoxication, mlik-alkali syndrome and granulomatous diseases (sarcoidosis)

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29
Q

What is the major complication of a parathyroidectomy?

A

Hypocalcemia induced laryngospasm, a life threatening complication

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30
Q

Major concern with low Mg?

A

Torsades

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31
Q

What can cause hypermagnesemia?

A

Usually over treatment of eclampsia or pheochromocytoma

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32
Q

What s/x of hypermagnesemia occur at 4-5, 6 and 10 mEq/L?

A

4-5 = lethargy, N/V, flushing
6 = hypotension, decreased DTRs
10 = paralysis, apnea, heart blocks, cardiac arrest

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33
Q

Treatment for hypermagnesemia?

A

Diuresis, IV calcium, HD

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34
Q

How much CO do the kidneys receive?

A

20% or 1 - 1.25 L. Outer cortex gets the most blood flow

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35
Q

What 2 systems control volume/BP by acting on the kidneys?

A

RASS and ANP

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36
Q

What are some hormones the kidneys make?

A

Renin, Erythropoietin, Calcitriol, Prostaglandins

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37
Q

What lab value is particularly sensitive to fluid volume status?

A

GFR

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38
Q

Ideal range for GFR, creatinine clearance and serum creatinine?

A

GFR = 125 - 140 ml/min
CC = 110 - 140 ml/min
SC = 0.6 - 1.3 mg/dL

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39
Q

What does low/high BUN indicate?

A

High = high protein diet, dehydrated, GI bleed, trauma, muscle wasting
Low = malnourished or volume diluted

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40
Q

Normal BUN/Cr ratio?

A

10:1, a good measure of hydration status

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41
Q

Normal specific gravity?

A

1.001 - 1.035

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42
Q

Is drop in UOP an early or late sign of volume loss?

A

Late

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43
Q

What does a compressible IVC indicate?

A

Volume loss or dehydration at greater than 50% collapse of IVC. Can also test this via a PLR

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44
Q

What is azotemia?

A

Buildup of nitrogenous waste products like urea and creatinine - hallmark of AKI

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45
Q

Risk factors for AKI?

A

Adv age, CHF, PVD, DM, sepsis, Jaundice, major surgery, IV contrast

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46
Q

Diagnostic criteria for AKI?

A

Increase in SCr by 0.3 mg/dL in 48 hours, increase in SCr by 50% in 7 days, decrease in creatinine clearance by 50%

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47
Q

What are the basic differences of pre-renal, renal and post-renal azotemia?

A

Pre-renal = decreased renal perfusion
Renal = nephron injury
Post-renal = outflow obstruction and is easiest to treat

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48
Q

What lab value indicates pre-renal azotemia? Treatment?

A

BUN:Cr ratio is greater than 20:1 and is the most common source of AKI, usually a reversible volume issue

Tx = fluids, mannitol, diuretics, maintain MAP, pressors

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49
Q

Renal azotemia lab value?

A

BUN:Cr less than 20:1, generally indicates intrinsic renal disease

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50
Q

Treatment for post-renal azotemia?

A

Remove/relieve the obstruction, decrease nephron tubular hydrostatic pressure

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51
Q

What type of urine sediment would you find in pre/post and intrinsic renal injury?

A

Pre = bland or hyaline casts
Intrinsic = wide variety depending on disease process
Post = blood

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52
Q

What are some CV concerns with AKI?

A

Systemic HTN, LV hypertrophy, CHF, Pulmonary edema, uremic cardiomyopathy, arrhythmias

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53
Q

What is the order of incidence in cardiac insult due to AKI?

A

HTN→ LVH→ CHF → ischemicheartdisease→ anemicheartfailure→ rhythm disturbances → pericarditis with or without effusion→cardiactamponade, uremic cardiomyopathy

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54
Q

Hematological complications of an AKI?

A

Anemia (decreased EPO, RBC production and survival), platelet dysfunction, vWF disrupted by uremia (can treat with prophylactic DDAVP)

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55
Q

What constrictor is better at maintaining RBF?

A

Vasopressin

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56
Q

What are some anesthesia AKI implications/things you need to consider?

A

Correct fluid/e-lyte imbalances, NS preferred to hydrate in renal issues, use colloids carefully, maintain MAP, first constrictor choice is either A-agonists or vasopressin, low threshold for invasive monitoring, ensure pre-op HD has been done

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57
Q

Leading causes of CKD?

A

DM (1st leading cause) and HTN (2nd leading cause)

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58
Q

How much does GFR decrease each decade starting at 20?

A

by 10 each decade

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59
Q

What would GFR be at each stage of CKD?

A

Stage 1 (normal) = GFR greater than 90
Stage 2 (kidney damage, mild drop in GFR) = 60 - 89
Stage 3 (moderate drop in GFR) = 30 - 59
Stage 4 (severely decreased GFR) = 15 - 29
Kidney failure = GFR less than 15

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60
Q

First line treatment for systemic HTN d/t CKD?

A

Thiazide diuretics followed by an ACE/ARB

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61
Q

Which populations are high risk to a silent MI?

A

Diabetics and women

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62
Q

Per lecture, best NMBD with kidney patients?

A

Nimbex

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63
Q

In general, what drugs do you want to avoid in renal patients?

A

Drugs with active metabolites or ones that are renally cleared

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64
Q

What lipid insoluble drugs need to be renally dosed based on GFR?

A

Thiazides, loop diuretics, digoxin and many Abx

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65
Q

What are the only coagulation factors that the liver does not synthesize?

A

Factors III, IV, VIII and vWF

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66
Q

How many segments of the liver are there? What separates L/R?

A

8 segments based on blood supply and bile drainage, and R/L are seperated by the falciform ligament

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67
Q

What 3 hepatic veins empty into the IVC?

A

Right, middle and left hepatic veins

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68
Q

What does bile drain into? How does bile enter the duodenum?

A

Drains through the hepatic duct into the gallbladder and common bile duct. Enters duodenum via Ampulla of Vater

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69
Q

How much CO does the liver receive?

A

25% or 1.25 - 1.5 L

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70
Q

What vessels provide the most blood flow to the liver?

A

Portal vein (75% of blood flow) and hepatic artery (25% of blood flow)

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71
Q

Blood from the portal vein contains deoxygenated blood from where?

A

Stomach, intestines, spleen and pancreas

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72
Q

How does portal HTN cause varices?

A

The increased pressure backs up blood into systemic circulation, causing increased pressure in the esophagus and stomach which can then cause varices

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73
Q

What is the normal, abnormal, and lethal hepatic vessel pressure gradients?

A

Normal: 1-5 mmHg
Clinically significant (can cause cirrhosis, varices): greater than 10 mmHg
Variceal rupture: greater than 12 mmHg

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74
Q

Why is liver disease hard to diagnose?

A

Because it is generally asymptomatic until late stage disease, and symptoms can be very vague

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75
Q

Physicals exam findings of liver disease?

A

Pruritis, Jaundice, Ascites, Asterixis (flapping tremor), Hepatomegaly, Splenomegaly, Spider nevi

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76
Q

What is the most specific liver enzyme test?

A

AST & ALT

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77
Q

What test can evaluate hepatic portal blood flow?

A

Doppler

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78
Q

What are the 3 groups of hepatobiliary injury?

A

Hepatocellular - increased AST/ALT
Reduced synthetic funciton: decreased albumin, increased PT/INR
Cholestasis: increased ALk phosphatase, increased GGT, increased bilirubin

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79
Q

Risk factors for cholelithiasis (gallstones)?

A

Obesity, increased cholesterol, DM, pregnancy, female, family history

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80
Q

S/sx of cholelithiasis (gallstones)? Tx?

A

RUQ pain, N/V, indigestion, fever
Tx: IVF, Abx, pain management, Lap Chole

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81
Q

Positioning for a lap chole?

A

Rev Trendelenburg with a left tilt

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82
Q

What is choledocholithiasis? Treatment? Positioning? Common complication?

A

Stone obstructing the common bile duct.
Tx: ERCP -> guidewire into the Ampulla of Vater to retrieve stone.
Pos: GA, prone with left tilt (tape ETT to the left)
Comp: Oddi spasm, give glucagon

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83
Q

What occurs with an increase in unconjugated vs conjugated bilirubin?

A

Un: imbalance between bilirubin synthesis and conjugation
Con: obstruction causing reflux of conjugated bilirubin into circulation

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84
Q

Causes of indirect and direct bilirubin?

A
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85
Q

What are the 5 types of viral hepatitis? More chronic ones?

A

A - E, B/C are the more chronic.

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86
Q

Which viral hepatitis most common reason for liver transplant?

A

HCV or type C, though modern treatment has reduced this with 12 week course of Sofosbuvir/Velpatasvir

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87
Q

Which viral hepatitis is blood borne?

A

B and C

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88
Q

What viral hepatitis is fecal-orally transmitted?

A

A and E

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89
Q

What viral hepatitis is percutaneously transmitted?

A

D

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90
Q

Most common cause of liver transplant?

A

ETOH related cirrhosis

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91
Q

What lab values may indicate alcoholic liver disease?

A

Increase in: Mean corpuscular volume, liver enzymes, y-glutamyl-transferase (GGT) and bilirubin

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92
Q

What can cause a fatty liver?

A

Obesity, insulin resistance, DM2, metabolic syndrome. Liver biopsy is gold standard to diagnose. Treat via diet and exercise

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93
Q

What is the progression of alcoholic vs non-alcoholic liver disease?

A

Alc: Alcoholic fatty liver -> Alcoholic hepatitis -> Alcoholic cirrhosis
Non-alc: Non-alcoholic fatty liver (NAFL) -> Non-alcoholic steatohepatitis (NASH) -> Liver fibrosis -> Cirrhosis

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94
Q

Who is most commonly affected by autoimmune hepatitis? Tx?

A

Women, AST/ALT may be 10-20x higher, treat with steroids and azathioprine. 60-80% achieve remission, though relapse is common

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95
Q

Most common modality of drug induced liver injury?

A

Tylenol OD

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96
Q

What are the 3 most common inborn errors of metabolism?

A

Wilsons disease, Alpha-1 Antitrypsin Deficiency and Hemochromatosis

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97
Q

What is Wilson’s disease? Tx?

A

Autosomal recessive disease d/t impaired copper metabolism -> causes oxidative stress on the liver. Tx with copper-chelation therapy and oral zinc

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98
Q

What is Alpha-1 Antitrypsin Deficiency? Tx?

A

Lack of anti-trypsin = neutrophil elastase breaks down connective tissue all over the body. Pooled A-1 antitrypsin can treat pulmonary s/sx, but doesn’t fix the liver disease. Liver transplant is the only thing that can fix the disease

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99
Q

What is Hemochromatosis? Tx?

A

Excess Iron in the body leading to multi-organ dysfunction. Tx is weekly phlebotomy, iron-chelating drugs and liver transplant

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100
Q

What is Primary Biliary Cholangitis? Tx?

A

Autoimmune progressive destruction of bile ducts with periportal inflammation & cholestasis. Can lead to liver cirrhosis. More common in females than men. No cure, exogenous bile acid can slow progression

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101
Q

What is Primary Sclerosing Cholangitis (PSC)? Tx?

A

Autoimmune, chronic inflammation of the larger bile ducts that can progress to cirrhosis and ESLD. More common in males than females. Liver transplant is the only treatment.

Characterized by deficiency of fat-soluble vitamins A, D, E and K

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102
Q

Most common cause of acute liver failure?

A

Drug induced d/t Tylenol OD

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103
Q

Common cirrhosis complications?

A

Portal HTN, Ascites, varices, hepatic encephalopathy and spontaneous bacterial peritonitis

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104
Q

What treatment can reduce portal HTN and help reduce ascites?

A

TIPS procedure (transjugular intrahepatic portosystemic shunt)

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105
Q

What is the cause of hepatic encephalopathy?

A

Build up of nitrogenous waste products. Treatment with lactulose and rifaximin to decrease the ammonia producing bacteria in the gut

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106
Q

What is platypnea?

A

Hypoxemia when upright due to R/L intrapulmonary shunt

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107
Q

What is hepatorenal syndrome? Tx?

A

Portal HTN eventually leading to decreased RBF. Excessive endogenous vasodilators (NO, PGs). Tx = midodrine, octreotide and albumin

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108
Q

What is hepatopulmonary syndrome?

A

Triad of chronic liver disease, hypoxemia, intrapulmonary vascular dilation. Characterized by hypoxemia when upright due to R/L intrapulmonary shunt (platypnea)

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109
Q

What can help treat portopulmonary HTN?

A

PD-I’s, nitric oxide, prostacyclin analogs and endothelin receptor antagonists

110
Q

What are 2 scoring systems to help determine severity of liver disease?

A

Child-Turcotte-Pugh (CTP):points based on bilirubin, albumin, PT, encephalopathy, ascites

Model for End Stage Liver Disease (MELD): scorebased on bilirubin, INR, creatinine, sodium

111
Q

What MELD score or child class allows you to go to the OR?

A

MELD less than 10 or child class A

112
Q

What MELD or child class score would require you to know if they have portal HTN before going to the OR?

A

MELD of 10 - 15 or child class B

113
Q

What MELD or child class score would preclude you from going to the OR?

A

MELD greater than 16 or child class C

114
Q

What are factors you need to be aware of prior to taking a liver disease patient to the OR?

A

CBC, BMP, PT/INR, low threshold for invasive monitoring, give colloids over crystalloid, drugs may have a prolonged effect, avoid Sux and cisatracurium, bleeding is a big concern, plasma cholinesterase may be decreased

115
Q

Indications for TIPS? Contraindications?

A

Refractory variceal hemorrhage, refractory ascites.

Contra: heart failure, tricuspid regurg, severe pulmonary HTN

116
Q

Why can a partial hepatectomy for cancer not necessarily impair liver function? Other considerations?

A

The liver can regenerate itself to a certain degree, you can remove up to 75% of the liver and it can be tolerated. Be aware the surgeon may clamp the IVC or hepatic artery. Coagulation disturbances are common.

117
Q

What can modulate CBF?

A

CRMO, cerebral perfusion pressure CPP (MAP - ICP), PaCO2, PaO2, drugs

118
Q

What is the goal CBF rate with autoregulation?

A

50 ml/100g of brain tissue ~750 ml/min or 15% of CO

119
Q

What is the Monro-Kellie hypothesis?

A

That an increase in one component of intracranial volume must be offset by a decrease in another compartment, if the other compartments cannot offset, then ICP can elevate

120
Q

What are the meningeal barriers?

A

Falx cerebri: separates the cerebral hemispheres
Tentorium cerebelli: rostral to the cerebellum and separates the supratentorial and infratentorial spaces

121
Q

Define subfalcine, transtentorial, cerebellar tonsil and uncal herniation

A

SF: Herniation of hemispheric contents under the falx cerebri; typically, compressing branches of the anterior cerebral artery, creating a midline shift

TT: Herniation of the supratentorial contents past the tentorium cerebelli, causing brainstem compression in a rostral to caudal direction. This leads to AMS, defects in gaze and ocular reflexes, hemodynamic andrespiratory compromise, and death

Un: a subtype of transtentorial herniation, where the uncus (medial portion of temporal lobe)herniatesoverthe tentorium cerebelli. This results in ipsilateral oculomotor nerve dysfunction

CT: occurs due to elevated infratentorial pressure causing the cerebellar structures to herniate through the foramen mangum

122
Q

What herniation compresses branches of the anterior cerebellar artery creating a midline shift?

A

Subfalcine

123
Q

What herniation creates AMS, defects in gaze/ocular reflexes, hemodynamic andrespiratory compromise, and death?

A

Transtentorial

124
Q

What herniation results in ipsilateral oculomotor nerve dysfunction, pupillary dilatation, ptosis, lateral deviation of the affected eye, brainstem compression and death?

A

Uncal

125
Q

What herniation causes cerebellar structures to herniate through the foramen magnum?

A

Herniation of the cerebellar tonsils

126
Q

What herniation is indicated by the number 1?

A

Subfalcine

127
Q

What herniation is indicated by the number 2?

A

Transtentorial

128
Q

What herniation is indicated by the number 3?

A

Cerebellar contents are going into the foramen magnum

129
Q

What herniation is indicated by the number 4?

A

Traumatic event causing herniation out of the cranial cavity

130
Q

What are some common causes of ICP increase?

A

Tumors, hematomas, blood in the CSF and infections (meningitis/encephalitis). Any can cause either obstruction or decrease in ability to reabsorb CSF

131
Q

Methods to reduce ICP?

A

Elevate head (promotes venous drainage), hyperventilation, externally drain (EVD), hyperosmotic drugs (mannitol), diuretics, steroids, cerebral vasoconstriction (propofol), surgical decompression

132
Q

What are MS triggers?

A

Stress, elevated temperature, postpartum

133
Q

Treatment of MS?

A

No cure; manage symptoms with steroids, immune modulators and targeted antibodies

134
Q

What is MS?

A

Progressive, autoimmune demyelination of central nerve fibers

135
Q

What common immunosuppressant may warrant an LFT?

A

Azathioprine

136
Q

What paralytic must be avoided in MS? Why?

A

Sux; an effect of this disease process is an upregulation of N-ACh receptors. With all these receptors, Sux can have a profound effect

137
Q

What is MG? What muscles are affected?

A

Autoimmune; Antibodies generated against N-Ach-R’s at skeletal motor endplate. Affects skeletal muscle (smooth and cardiac is spared)

138
Q

MG treatment?

A

Acetylcholinesterase inhibitor (pyridostigmine), immunosuppressive’s, steroids, plasmapheresis, IV-IG

139
Q

What are some common themes in prep for anesthesia for MS and MG?

A

May need stress dose steroids, PFTs, reduce/avoid paralytics if possible

140
Q

Why can certain drugs DOA be prolonged in MG?

A

They are commonly on pyridostigmine which can prolong the effect of Sux and Ester LA’s

141
Q

Describe Eaton-Lambert syndrome

A

Disorder causing the development of autoantibodiesagainst VG Calcium channels. Reduced Ca influx reduces ACh release. S/sx are similar to MG

142
Q

Eaton-Lambert syndrome treatment?

A

Potassium channel blocker (3-4 diaminopyridine), acetylcholinesterase inhibitors, immunologic agents (Azathioprine), steroids, plasmapheresis, IV-IG

143
Q

What must be administered with extreme caution in ELS?

A

Paralytics; they are exceedingly sensitive to all paralytics

144
Q

What lab value may be elevated in Duchennes?

A

Serum creatine kinase (CK)

145
Q

What condition fairly common to Duchenne’s dystrophy can mimic MH?

A

Hypermetabolic syndrome, also caused by Sux and volatiles -> rhabdomyolysis, hyperkalemia, Vfib, cardiac arrest

146
Q

What is a common anesthesia strategy for Duchenne’s dystrophy?

A

Low dose Roc and TIVA

147
Q

What is myotonia?

A

Prolonged contraction after muscle stimulation

148
Q

What are 3 examples of myotonia? Include appropriate diagnostic information/differences

A

Myotonic Dystrophy: most common myotonia. Muscle wasting in face, masseter, hand, pre-tibial muscles, can affect pharyngeal/laryngeal and diaphragmatic muscles. 20% have mitral valve prolapse and cardiac conduction may be affected

Myotonia Congenita: Milder form, involving theskeletal muscles (smooth and cardiac are spared)

Central Core disease: Rare. Core muscle cells lack mitochondrial enzymes. Proximal muscle weakness and scoliosis

149
Q

What is common to all myotonia pathologies?

A

All are triggered by stress and cold temperature. No cure, symptom management with Quinine, Procainamide (class IA Na channel blocker, throwback to the man, the myth, the legend, Dr. T) and steroids

150
Q

Anesthesia considerations in myotonia?

A

GI hypomotility (aspiration risk), endocrine abnormalities, keep them warm, avoid Sux and give opioids with caution

151
Q

What are the most common types of dementia?

A

Alzheimer’s (70%), Vascular dementia (25%), Parkinsons (5%)

152
Q

What are some anesthesia considerations in dementia?

A

Review meds as many can interact with anesthetics (ACh-E inhibitors, MAOIs, pysch meds, many are enzyme inducers), increased risk of post-op delirium, increased aspiration risk RA preferred to reduce opioid use

153
Q

Treatment for parkinsons?

A

Levodopa (crosses BBB), anticholinergics, MAOIs (inhibit dopamine degradation), Deep brain stimulator

154
Q

Parkinsons cause and #1 risk factor?

A

Degeneration of dopaminergic fibers of basal ganglia. RF = advancing age

155
Q

Anesthesia concerns in parkinsons?

A

Increased aspiration risk, Levodopa must be continued to avoid unstable extreme extrapyramidal effects like chest wall rigidity, Avoid Reglan, Phenothiazines, Butyrophenones avoid Demerol if on MAOI

156
Q

What are some common s/sx of brain tumors?

A

Increased ICP, Papilledema, HA, AMS, Mobilityimpairment, Vomiting, Autonomic dysfunction, Seizures​

157
Q

What is the most common glial cells?

A

Astrocytes

158
Q

What is a common astrocytoma?

A

Glioma, least aggressive, common in young adults w/new onset seizures

159
Q

What tumors occur in children/young adults and are benign with good outcomes?

A

Pilocytic astrocytomas

160
Q

What is a poorly differentiated tumor that can evolved into a Glioblastoma Multiforme?

A

Anaplastic astrocytomas

161
Q

Which brain tumor carries a very high mortality rate?

A

Glioblastoma Multiforme. Usually requires surgical debulking & chemo with very short life expectancy

162
Q

What benign tumor arises from the dura or arachnoid tissue?

A

Meningiomas, usually good prognosis

163
Q

What tumor is noncancerous with varying subtypes?

A

Pituitary adenomas, transsphenoidalor open craniotomy for removal is usually curative

164
Q

What benign Schwannoma involves the vestibular component of CN VIII?

A

Acoustic neuromas, good prognosis with resection and radiation

165
Q

What tumor can vary widely in origin and symptoms with less favorable outcomes?

A

Metastatic carcinomas

166
Q

Anesthesia brain tumor concerns?

A

Often on steroids, know prior cancer treatment (chemo, radiation), usually on anti-convulsant therapy (can affect anesthetic drugs), check imaging, keep seizure meds going if possible

167
Q

What stroke type is most common?

A

Ischemic (88%) then hemorrhagic (12%)

168
Q

What is the global cause of death/disability?

A

Stroke

169
Q

What are the 5 TOAST classification of ischemic strokes?

A
  1. Large artery atherosclerosis (e.g., carotid stenosis)
  2. Small vessel occlusion (e.g., lacunar stroke)
  3. Cardioaortic embolic (e.g., emboli from atrial fibrillation)
  4. Other etiology (e.g., stroke due to hypercoagulable states or vasculopathies)
  5. Undetermined etiology
170
Q

What is the gold standard for ischemic stroke treatment?

A

Revascularization; either via thrombolytics or intervention such as a thrombectomy device

171
Q

What are 2 reliable predictors of outcomes in hemorrhagic strokes?

A

EBL and change in LOC

172
Q

What are the 3 subtypes of hemorrhagic strokes?

A

1) Bloodwithin the brainis called an intraparenchymal hemorrhage

2) Blood in the epidural, subdural, or subarachnoid spaces are referred to as epidural hematoma, subdural hematoma, and subarachnoid hemorrhages, respectively.

3)Blood located in the ventricular system is an intraventricular hemorrhage, and usually occurs in conjunction with other types of hemorrhagic stroke

173
Q

What are conservative treatment goals of ischemic strokes?

A

ICP/BP reduction, seizure precautions, and vigilant monitoring

174
Q

What makes cerebral aneurysms so dangerous?

A

Only 1/3 have s/sx prior to rupture.

175
Q

Cerebral aneurysm risk factors? When should an intervention be performed?

A

HTN, smoking, female, oral contraceptives, cocaine use. Within 72 hours

176
Q

What surgeries may treat a cerebral aneurysm?

A

Coiling, stenting, trapping/bypass (very large aneurysms)

177
Q

When do post-SAH vasospasms occur? What is the treatment?

A

3-15 days. HTN, hypervolemia and hemodilution. HTN is the preferred treatment. A surgeon can go in and directly inject a CCB

178
Q

What is an AVM?

A

Arteriovenous malformation. This allows high flow arterial blood to shunt into low flow venous blood, usually congenital.

179
Q

Where are most AVM’s found?

A

Supratentorial

180
Q

AVM treatment?

A

Radiation, angio-guided embolization, surgical resection (higher mortality)

181
Q

What are 4 congenital brain abnormalities?

A

Chiari, Tuberous Sclerosis, Von Hippel-Lindau and Neurofibromatosis

182
Q

What are the 4 types of Chiari?

A

Type 1: downward displacement of cerebellum
Type 2 (Arnold Chiari):downward displacement of cerebellar vermis, often assoc w/myelomeningocele
Type 3: Rare; occipital encephalocele w/downward cerebellar displacement
Type 4: cerebellar hypoplasia w/o displacement of posterior fossa contents (life threatening)

183
Q

What is tuberous sclerosis?

A

Bourneville Disease, Autosomal dominant disease causing benign hemartomas, angiofibromas and other malformations that can occur anywhere in the body. Common for patient to present with mental retardation and seizure.

184
Q

What is Von Hippel-Lindau disease?

A

Autosomal dominant condition where benign tumors of the CNS, eyes, adrenals, pancreas and kidneys develop. Common to have a pheochromocytoma.

185
Q

Is neuraxial anesthesia a good choice in VHL (Von Hippel-Lindau)?

A

Generally no as it is common to have tumors of the spinal cord

186
Q

What is neurofibromatosis? Anesthesia consideration?

A

Autosomal dominant with a wide variety of presentation, tumors everywhere. Avoid neuraxial d/t spinal tumors

187
Q

What are the 2 types of neurofibromatosis?

A

Type I (most common) type II and Schwannomatosis (rare)

188
Q

What is hydrocephalus?

A

A disorder of CSF accumulation, causing increased ICP, that results in ventricular dilatation.

189
Q

Hydrocephalus treatment?

A

Diuretics (lasix, acetazolamide decreases CSF production). Most get a VP shunt or endoscopic third ventriculostomy (catheter placed into the lateral ventricle that drains into the peritoneal space, right atrium, or more rarely the pleural space)

190
Q

What is the biggest concern with a VP shunt?

A

Shunt malfunction; occurs most frequently in the first year of placement (high failure rate)

191
Q

What are the 2 categories of a TBI?

A

Penetrating vs non-penetrating

192
Q

What is the difference in primary vs secondary injuries in a TBI?

A

Primary = occurs at time of insult
Secondary = neuroinflammation, cerebral edema, hypoxia, anemia, electrolyte imbalances, and neurogenic shock

193
Q

What anesthesia considerations are important with seizures?

A

Determine source of seizures (if known) and how well they are controlled. Want anti-seizure drugs on board before incision. Review drugs; Phenytoin, Tegretol, Barbiturates are enzyme-inducers

194
Q

What are the 3 main arterial pathologies?

A

aneurysms, dissections, occlusions

195
Q

The aorta and its branches will more likely be affected by what pathologies? Peripheral arteries?

A

Aorta/branches = aneurysms and dissections
PAs = occlusions

196
Q

When is surgery indicated on an aneurysm?

A

When it is at 5.5 cm or greater,10 mm growth over a year or family hx of dissection

197
Q

What are the 2 types of aortic aneurysms? What causes their symptoms?

A

Fusiform: Uniform dilation along entire circumference of arterial wall
Saccular: berry-shaped bulge to one side
Sx: Asymptomatic or pain d/t surrounding compression

198
Q

In suspected dissection, what is the fastest way to ascertain the severity of the dissection?

A

Doppler echo

199
Q

What is a dissection?

A

Tear in the intimal layer of the vessel, causingblood to enter the medial layer

200
Q

What is the difference in type A/B dissections? Treatment?

A

A = ascending aorta and should be an immediate surgery
B = descending aorta. Depends on stability, if stable medical management, if not, surgery

201
Q

What are some considerations to a type A aortic arch surgery?

A

Require cardiopulmonary bypass, profound hypothermia, and a period of circulatory arrest.

202
Q

What is the major complication of aortic arch surgery?

A

Neurologic deficits

203
Q

What are some s/sx of impending type B rupture?

A

persistent pain, hypotension, left-sided hemothorax); ischemia of the legs, abdominal viscera, spinal cord, and/or renal failure

204
Q

What are the DeBakey classifications of aortic dissections?

A

1 = tear in the ascending aorta that propagates to the arch
2 = tear confined to the ascending aorta
3 = tear in the descending aorta

205
Q

Match the DeBakey classifications to type A and B dissections

A

A = 1, 2
B = 3

206
Q

Risk factors for an aortic dissection?

A

HTN, atherosclerosis, aneurysms, family hx, cocaine use, & inflammatory diseases

207
Q

What inherited disease can place you at risk for a dissection? Iatrogenic causes?

A

Inherited = Marfans, Ehlers Danlos, Bicuspid Aortic Valve, non-syndrome familial hx
Iatrogenic = cardiac catheterization, aortic manipulation, cross-clamping & arterial incision

208
Q

What populations is dissection more common in?

A

Men and 3rd trimester pregnant women

209
Q

What is the triad of symptoms of aortic aneurysm rupture?

A

Hypotension, back pain and pulsatile abdominal mass

210
Q

What are the 4 major causes of mortality with thoracic aortic surgery?

A

MI, respiratory failure, renal failure, stroke

211
Q

What findings may be a contraindication to aortic surgery?

A

CAD, valve dysfunction, HF, ischemic heart disease, severely reduced FEV1, renal failure

212
Q

What is the most important indicator of post-aortic surgery renal failure?

A

Pre-op renal dysfunction (hydrate, avoid hypotension and nephrotoxins)

213
Q

What is the most common form of spinal cord ischemia?

A

Anterior spinal artery syndrome (this vessel has minimal to no collateral circulation)

214
Q

Ischemia of the anterior spinal artery can cause what?

A

Loss of motor function below the infarct, diminished pain and temperature sensation below the infarct and autonomic dysfunction leading to hypotension and loss of bowel & bladder function

215
Q

What is the 1st leading cause of disability and 3rd leading cause of death in the US?

A

Stroke

216
Q

Where does carotid stenosis commonly occur?

A

The internal/external carotid bifurcation

217
Q

Recommended timeframe to give TPA? Perform thrombectomy?

A

TPA = 4.5 hours
Thrombectomy = 8 hours

218
Q

What are 2 types of cerebral oximetry mentioned in lecture?

A

Foresight and INVOS

219
Q

What can affect cerebral oxygenation?

A

MAP, CO, SaO2, Hgb, PaCO2, temperature and anesthesia

220
Q

What is the definition of PAD?

A

An ABI (ankle brachial index) of < 0.9 which indicates hypo perfusion. Done by dividing the ankle MAP by the brachial MAP

221
Q

What is the relationship of PAD to MI and CVA?

A

3-5x increased risk of MI or CVA if you have PAD

222
Q

Risk factors for PAD?

A

Advanced age, Family hx, Smoking, DM, HTN, Obesity, ↑Cholesterol

223
Q

S/sx of PAD?

A

Intermittent claudication, Resting extremity pain, Decreased pulses, Subcutaneous atrophy, Hair loss, Coolness, Cyanosis, Relief w/hanging LE over side of bed (↑hydrostatic pressure)

224
Q

When is medical intervention warranted in PAD?

A

With disabling claudication or ischemia (surgical reconstruction or endovascular repair)

225
Q

Common causes of acute artery occlusion? Less common?

A

Common = LA or LV thrombus
Less common = valvular heart disease, endocarditis, PFO, atheroemboli, plaque rupture, hypercoagulability, trauma

226
Q

What is subclavian steal syndrome?

A

An occluded SCA proximal to the vertebral artery, this causes vertebral artery blood to be diverted away from the brainstem by reversing flow in the ipsilateral artery

227
Q

Risk factors for subclavian steal syndrome? Treatment?

A

Atherosclerosis, Takayasu Arteritis, aortic surgery
Tx = endarterectomy

228
Q

Raynaud’s treatment?

A

Avoid cold, CCBs, alpha-blockers, surgical sympathectomy is ischemia is severe

229
Q

What are common PVD processes that occur during surgery?

A

Superficial thrombophlebitis, DVT, chronic venous insufficiency

230
Q

What is Virchow’s triad?

A

Venous stasis, hypercoagulability and disrupted vascular endothelium

231
Q

What is the most common surgery causing DVT and superficial thrombophlebitis?

A

Total hip replacements

232
Q

Risk factors for DVT?

A

Older than 40, surgery longer than 1 hour, cancer, ortho surgeries on pelvis & LEs, abdominal surgery

233
Q

How does regional anesthesia reduce DVT risk?

A

It allows for earlier ambulation

234
Q

What are some low and moderate risks for DVT? Treatment?

A

Low = less than 40, pregnant (SCDs, ambulation)
Mod = Postpartum period, MI, CHF (SCDs, SubQ heparin or IV dextran)
High = everything else (SCDs, SubQ heparin, Dextran, vena cava filter, warfarin)

235
Q

What are the pros/cons of LMWH?

A

Pros: longer half-life with predictable response, no serial PTTs, less bleeding risk
Cons: expensive, no reversal agent

236
Q

What is a treatment option for recurrent PEs in someone who can’t tolerate anticoagulants?

A

IVC filter

237
Q

What are the large artery vasculitis pathologies?

A

Takayasu arteritis and temporal (giant cell) arteritis

238
Q

What are the medium artery vasculitis pathologies?

A

Kawasaki disease which mostly affects the coronaries

239
Q

What are the medium to small artery vasculitis pathologies?

A

Thromboangiitis obliterans, Wegener granulomatosis and polyarteritis nodosa

240
Q

What is temporal (giant cell) arteritis?

A

Inflammation of arteries of the head and neck

241
Q

S/sx of temporal (giant cell) arteritis?

A

unilateral in nature: headache, scalp tenderness, jaw claudication

242
Q

Temporal (giant cell) arteritis treatment and diagnosis?

A

Tx = corticosteroids
Dx = biopsy of temporal artery = shows arteritis in 90% of patients

243
Q

What is the only pathology that is an autoimmune occlusive response to nicotine?

A

Thromboangiitis Obliterans or “Buerger Disease

244
Q

What population is most affected by buerger disease? Diagnostic critera?

A

Men under 45. Differential criteria of 5 factors: history of smoking, onset before 50, infrapopliteal arterial occlusive disease, upper limb involvement, absence of other risk factors

245
Q

Treatment of Buerger disease?

A

Stop smoking, surgical revascularization but there is no pharmacological treatment. Avoid invasive lines

246
Q

What is an anti-neutrophil cytoplasmic antibody negative vasculitis?

A

Polyarteritis Nodosa

247
Q

What is commonly associated with Polyarteritis Nodosa?

A

Hep B or C and hairy cell leukemia

248
Q

Tx of Polyarteritis Nodosa?

A

Steroids, cyclophosphamide, treat underlying cause

249
Q

What inflammatory vascular condition is generally secondary to another issue?

A

Polyarteritis Nodosa

250
Q

Risk factors for lower extremity chronic venous disease?

A

Adv age, family hx, pregnancy, ligamentous laicity, prior venous thrombosis, lower extremity injuries, prolonged standing, smoking sedentary lifestyle, high estrogen

251
Q

Diagnostic criteria of lower extremity chronic venous insufficiency?

A

S/sx of leg pain, heaviness, fatigue. Ultrasound showing venous reflux or retrograde blood flow of greater than 0.5 seconds

252
Q

Lower extremity chronic venous disease treatment?

A

Diuretics, ASA, Abx, prostacyclin analogues, zinc and ablation if all else fails

253
Q

What procedures may be used to treat lower extremity chronic venous disease?

A

Saphenous vein inversion, High saphenous ligation, Ambulatory Phlebectomy, Transilluminated-powered phlebectomy, Venous ligation, Perforator ligation

254
Q

What complication is the leading cause of perioperative morbidity in non-cardiac surgery?

A

Cardiac complications

255
Q

Carotid residual luminal diameter of what represents significant stenosis?

A

Residual luminal diameter of 1.5 mm or 70 - 75% stenosis

256
Q

Increased AST/ALT indicated what type of hepatobiliary disease?

A

Hepatocellular injury

257
Q

Decreased albumin and increased PT/INR indicates what type of hepatobiliary disease?

A

Reduced synthetic function

258
Q

Increased Alkaline phosphatase, GGT and bilirubin indicate what type of hepatobiliary disease?

A

Cholestasis

259
Q

An increase in unconjugated bilirubin indicates what?

A

An imbalance between bilirubin synthesis and conjugation

260
Q

An increased in conjugated bilirubin indicates what?

A

An obstruction which causes reflux of conjugated bilirubin into circulation

261
Q

What liver condition creates fibrosis of the biliary tree creating strictures that have a beads on string appearance?

A

Primary sclerosing cholangitis (PSC)

262
Q

What is the difference between primary sclerosing cholangitis and primary biliary cholangitis?

A

PSC = affects intra and extrahepatic ducts
PBC = intrahepatic ducts only

263
Q

What deficits would you expect with a anterior cerebral artery occlusion?

A

Contralateral leg weakness

264
Q

What deficits would you expect with a MCA occlusion?

A

Contralateral hemiparesis and hemisensory deficit, aphasia and contralateral visual field deficit

265
Q

What deficits would you expect with a PCA occlusion?

A

Contralateral visual field deficit and contralateral hemiparesis

266
Q

What deficits would you expect with a posterior artery occlusion?

A

Contralateral hemiparesis and contralateral hemisensory deficits

267
Q

What deficits would you expect with a basilar artery occlusion?

A

Oculomotor deficits and/or ataxia with crossed sensory and motor deficits

268
Q

What deficits would you expect with a vertebral artery occlusion?

A

Lower cranial nerve deficits and/or ataxia with crossed sensory deficits

269
Q

What is the timeframe for vasospasm post SAH? treatment?

A

3-15 days. Tx = triple H therapy (HTN, hypervolemia and hemodilution)

270
Q

Where would you most likely find an AVM?

A

The supratentorial region of the brain

271
Q

Why may fluid resuscitation be referred in aortic aneurysm rupture?

A

The tamponade effect in the left retroperitoneum may be slow exsanguination. Giving fluid to expand volume could make bleeding worse

Semester 2 TxWes (16 decks)

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