Assessments Unit 3 Flashcards
1
Q
What fluid compartment is more immediately altered by the kidneys?
A
ECF
2
Q
What mediates osmolar homeostasis?
A
Osmolality sensors in anterior hypothalamus
3
Q
What does ANP do?
A
Increase diuresis
4
Q
What mediates volume homeostasis?
A
the JGA to alter water/Na reabsorption
5
Q
What can cause hypovolemic issues?
A
Na/water loss, diuretics, GI loss, burns, trauma
6
Q
What can cause euvolemic issues?
A
Salt restriction, endocrine related (hypothyroid, SIADH)
7
Q
What can cause hypervolemic issues?
A
ARF/CKD, CHF, vasopressin increase
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
9
Q
How would you treat hyponatremia?
A
Fix underlying cause. Replace Na (hypertonic saline, e-lyte drink, diuretics)
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
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
12
Q
Common causes of hypernatremia?
A
Excessive evaporation, poor PO intake, overcorrection of hyponatremia, DI, Gi loss, excessive NaBicarb
13
Q
What disease processes can cause hypervolemia?
A
Hyperaldosteronism, Cushings
14
Q
What disease processes can cause euvolemic hypernatremia?
A
DI or insensible losses via the respiratory tract/skin
15
Q
S/sx of hypernatremia?
A
Orthostasis, restlessness, lethargy, tremor/muscle twitching, seizure, death
16
Q
What is the treatment for hypo/hyper/euvolemic hypernatremia?
A
Hyper = diuretics
Eu = water replacement (PO or d5W)
Hypo = NS
17
Q
Goal Na reduction rate?
A
no more than 0.5 mmol per hour and less than 10 mmol per day
18
Q
Goal potassium range?
A
3.5 - 5 mmol/L
19
Q
What does aldosterone do to potassium?
A
Causes distal nephron to secrete K and reabsorb Na
20
Q
What are the 3 major categories of potassium loss?
A
Renal loss, GI loss and transcellular shift
21
Q
S/sx of hypokalemia?
A
U-wave, muscle cramp/weakness, ileus, dysrhythmias. Avoid excessive insulin, b-agonists, bicarb, hyperventilation and diuretics
22
Q
S/sx of hyperkalemia?
A
Tall peaked T-wave, prolonged QRS, sine waves, skeletal muscle paralysis.
23
Q
Common causes of hyperkalemia?
A
Renal failure, hypoaldosteronism, RASS inhibition, Sux, acidosis, cell death, massive blood transfusion
24
Q
1st initial treatment/fastest treatment for hyperkalemia?
A
Calcium - quickly stabilizes the cell membrane
25
What does PTH and calcitonin do?
PTH = stimulates the release of calcium from bones
Calcitonin = promotes calcium storage into the bone and out of the plasma
26
What can cause hypocalcemia?
Decreased PTH (common complication of thyroid surgery), Mg deficiency, low vitamin D, renal failure, massive blood transfusion
27
How does vitamin D affect calcium?
It promotes absorption of intestinal calcium
28
What can cause hypercalcemia?
Hyperparathyroidism, cancer. Less common = vitamin D intoxication, mlik-alkali syndrome and granulomatous diseases (sarcoidosis)
29
What is the major complication of a parathyroidectomy?
Hypocalcemia induced laryngospasm, a life threatening complication
30
Major concern with low Mg?
Torsades
31
What can cause hypermagnesemia?
Usually over treatment of eclampsia or pheochromocytoma
32
What s/x of hypermagnesemia occur at 4-5, 6 and 10 mEq/L?
4-5 = lethargy, N/V, flushing
6 = hypotension, decreased DTRs
10 = paralysis, apnea, heart blocks, cardiac arrest
33
Treatment for hypermagnesemia?
Diuresis, IV calcium, HD
34
How much CO do the kidneys receive?
20% or 1 - 1.25 L. Outer cortex gets the most blood flow
35
What 2 systems control volume/BP by acting on the kidneys?
RASS and ANP
36
What are some hormones the kidneys make?
Renin, Erythropoietin, Calcitriol, Prostaglandins
37
What lab value is particularly sensitive to fluid volume status?
GFR
38
Ideal range for GFR, creatinine clearance and serum creatinine?
GFR = 125 - 140 ml/min
CC = 110 - 140 ml/min
SC = 0.6 - 1.3 mg/dL
39
What does low/high BUN indicate?
High = high protein diet, dehydrated, GI bleed, trauma, muscle wasting
Low = malnourished or volume diluted
40
Normal BUN/Cr ratio?
10:1, a good measure of hydration status
41
Normal specific gravity?
1.001 - 1.035
42
Is drop in UOP an early or late sign of volume loss?
Late
43
What does a compressible IVC indicate?
Volume loss or dehydration at greater than 50% collapse of IVC. Can also test this via a PLR
44
What is azotemia?
Buildup of nitrogenous waste products like urea and creatinine - hallmark of AKI
45
Risk factors for AKI?
Adv age, CHF, PVD, DM, sepsis, Jaundice, major surgery, IV contrast
46
Diagnostic criteria for AKI?
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%
47
What are the basic differences of pre-renal, renal and post-renal azotemia?
Pre-renal = decreased renal perfusion
Renal = nephron injury
Post-renal = outflow obstruction and is easiest to treat
48
What lab value indicates pre-renal azotemia? Treatment?
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
49
Renal azotemia lab value?
BUN:Cr less than 20:1, generally indicates intrinsic renal disease
50
Treatment for post-renal azotemia?
Remove/relieve the obstruction, decrease nephron tubular hydrostatic pressure
51
What type of urine sediment would you find in pre/post and intrinsic renal injury?
Pre = bland or hyaline casts
Intrinsic = wide variety depending on disease process
Post = blood
52
What are some CV concerns with AKI?
Systemic HTN, LV hypertrophy, CHF, Pulmonary edema, uremic cardiomyopathy, arrhythmias
53
What is the order of incidence in cardiac insult due to AKI?
HTN→ LVH→ CHF → ischemic heart disease→ anemic heart failure→ rhythm disturbances → pericarditis with or without effusion→ cardiac tamponade, uremic cardiomyopathy
54
Hematological complications of an AKI?
Anemia (decreased EPO, RBC production and survival), platelet dysfunction, vWF disrupted by uremia (can treat with prophylactic DDAVP)
55
What constrictor is better at maintaining RBF?
Vasopressin
56
What are some anesthesia AKI implications/things you need to consider?
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
57
Leading causes of CKD?
DM (1st leading cause) and HTN (2nd leading cause)
58
How much does GFR decrease each decade starting at 20?
by 10 each decade
59
What would GFR be at each stage of CKD?
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
60
First line treatment for systemic HTN d/t CKD?
Thiazide diuretics followed by an ACE/ARB
61
Which populations are high risk to a silent MI?
Diabetics and women
62
Per lecture, best NMBD with kidney patients?
Nimbex
63
In general, what drugs do you want to avoid in renal patients?
Drugs with active metabolites or ones that are renally cleared
64
What lipid insoluble drugs need to be renally dosed based on GFR?
Thiazides, loop diuretics, digoxin and many Abx
65
What are the only coagulation factors that the liver does not synthesize?
Factors III, IV, VIII and vWF
66
How many segments of the liver are there? What separates L/R?
8 segments based on blood supply and bile drainage, and R/L are seperated by the falciform ligament
67
What 3 hepatic veins empty into the IVC?
Right, middle and left hepatic veins
68
What does bile drain into? How does bile enter the duodenum?
Drains through the hepatic duct into the gallbladder and common bile duct. Enters duodenum via Ampulla of Vater
69
How much CO does the liver receive?
25% or 1.25 - 1.5 L
70
What vessels provide the most blood flow to the liver?
Portal vein (75% of blood flow) and hepatic artery (25% of blood flow)
71
Blood from the portal vein contains deoxygenated blood from where?
Stomach, intestines, spleen and pancreas
72
How does portal HTN cause varices?
The increased pressure backs up blood into systemic circulation, causing increased pressure in the esophagus and stomach which can then cause varices
73
What is the normal, abnormal, and lethal hepatic vessel pressure gradients?
Normal: 1-5 mmHg
Clinically significant (can cause cirrhosis, varices): greater than 10 mmHg
Variceal rupture: greater than 12 mmHg
74
Why is liver disease hard to diagnose?
Because it is generally asymptomatic until late stage disease, and symptoms can be very vague
75
Physicals exam findings of liver disease?
Pruritis, Jaundice, Ascites, Asterixis (flapping tremor), Hepatomegaly, Splenomegaly, Spider nevi
76
What is the most specific liver enzyme test?
AST & ALT
77
What test can evaluate hepatic portal blood flow?
Doppler
78
What are the 3 groups of hepatobiliary injury?
Hepatocellular - increased AST/ALT
Reduced synthetic funciton: decreased albumin, increased PT/INR
Cholestasis: increased ALk phosphatase, increased GGT, increased bilirubin
79
Risk factors for cholelithiasis (gallstones)?
Obesity, increased cholesterol, DM, pregnancy, female, family history
80
S/sx of cholelithiasis (gallstones)? Tx?
RUQ pain, N/V, indigestion, fever
Tx: IVF, Abx, pain management, Lap Chole
81
Positioning for a lap chole?
Rev Trendelenburg with a left tilt
82
What is choledocholithiasis? Treatment? Positioning? Common complication?
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
83
What occurs with an increase in unconjugated vs conjugated bilirubin?
Un: imbalance between bilirubin synthesis and conjugation
Con: obstruction causing reflux of conjugated bilirubin into circulation
84
Causes of indirect and direct bilirubin?
85
What are the 5 types of viral hepatitis? More chronic ones?
A - E, B/C are the more chronic.
86
Which viral hepatitis most common reason for liver transplant?
HCV or type C, though modern treatment has reduced this with 12 week course of Sofosbuvir/Velpatasvir
87
Which viral hepatitis is blood borne?
B and C
88
What viral hepatitis is fecal-orally transmitted?
A and E
89
What viral hepatitis is percutaneously transmitted?
D
90
Most common cause of liver transplant?
ETOH related cirrhosis
91
What lab values may indicate alcoholic liver disease?
Increase in: Mean corpuscular volume, liver enzymes, y-glutamyl-transferase (GGT) and bilirubin
92
What can cause a fatty liver?
Obesity, insulin resistance, DM2, metabolic syndrome. Liver biopsy is gold standard to diagnose. Treat via diet and exercise
93
What is the progression of alcoholic vs non-alcoholic liver disease?
Alc: Alcoholic fatty liver -> Alcoholic hepatitis -> Alcoholic cirrhosis
Non-alc: Non-alcoholic fatty liver (NAFL) -> Non-alcoholic steatohepatitis (NASH) -> Liver fibrosis -> Cirrhosis
94
Who is most commonly affected by autoimmune hepatitis? Tx?
Women, AST/ALT may be 10-20x higher, treat with steroids and azathioprine. 60-80% achieve remission, though relapse is common
95
Most common modality of drug induced liver injury?
Tylenol OD
96
What are the 3 most common inborn errors of metabolism?
Wilsons disease, Alpha-1 Antitrypsin Deficiency and Hemochromatosis
97
What is Wilson's disease? Tx?
Autosomal recessive disease d/t impaired copper metabolism -> causes oxidative stress on the liver. Tx with copper-chelation therapy and oral zinc
98
What is Alpha-1 Antitrypsin Deficiency? Tx?
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
99
What is Hemochromatosis? Tx?
Excess Iron in the body leading to multi-organ dysfunction. Tx is weekly phlebotomy, iron-chelating drugs and liver transplant
100
What is Primary Biliary Cholangitis? Tx?
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
101
What is Primary Sclerosing Cholangitis (PSC)? Tx?
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
102
Most common cause of acute liver failure?
Drug induced d/t Tylenol OD
103
Common cirrhosis complications?
Portal HTN, Ascites, varices, hepatic encephalopathy and spontaneous bacterial peritonitis
104
What treatment can reduce portal HTN and help reduce ascites?
TIPS procedure (transjugular intrahepatic portosystemic shunt)
105
What is the cause of hepatic encephalopathy?
Build up of nitrogenous waste products. Treatment with lactulose and rifaximin to decrease the ammonia producing bacteria in the gut
106
What is platypnea?
Hypoxemia when upright due to R/L intrapulmonary shunt
107
What is hepatorenal syndrome? Tx?
Portal HTN eventually leading to decreased RBF. Excessive endogenous vasodilators (NO, PGs). Tx = midodrine, octreotide and albumin
108
What is hepatopulmonary syndrome?
Triad of chronic liver disease, hypoxemia, intrapulmonary vascular dilation. Characterized by hypoxemia when upright due to R/L intrapulmonary shunt (platypnea)
109
What can help treat portopulmonary HTN?
PD-I's, nitric oxide, prostacyclin analogs and endothelin receptor antagonists
110
What are 2 scoring systems to help determine severity of liver disease?
Child-Turcotte-Pugh (CTP): points based on bilirubin, albumin, PT, encephalopathy, ascites
Model for End Stage Liver Disease (MELD): score based on bilirubin, INR, creatinine, sodium
111
What MELD score or child class allows you to go to the OR?
MELD less than 10 or child class A
112
What MELD or child class score would require you to know if they have portal HTN before going to the OR?
MELD of 10 - 15 or child class B
113
What MELD or child class score would preclude you from going to the OR?
MELD greater than 16 or child class C
114
What are factors you need to be aware of prior to taking a liver disease patient to the OR?
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
Indications for TIPS? Contraindications?
Refractory variceal hemorrhage, refractory ascites.
Contra: heart failure, tricuspid regurg, severe pulmonary HTN
116
Why can a partial hepatectomy for cancer not necessarily impair liver function? Other considerations?
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
What can modulate CBF?
CRMO, cerebral perfusion pressure CPP (MAP - ICP), PaCO2, PaO2, drugs
118
What is the goal CBF rate with autoregulation?
50 ml/100g of brain tissue ~750 ml/min or 15% of CO
119
What is the Monro-Kellie hypothesis?
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
What are the meningeal barriers?
Falx cerebri: separates the cerebral hemispheres
Tentorium cerebelli: rostral to the cerebellum and separates the supratentorial and infratentorial spaces
121
Define subfalcine, transtentorial, cerebellar tonsil and uncal herniation
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 and respiratory compromise, and death
Un: a subtype of transtentorial herniation, where the uncus (medial portion of temporal lobe) herniates over the 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
What herniation compresses branches of the anterior cerebellar artery creating a midline shift?
Subfalcine
123
What herniation creates AMS, defects in gaze/ocular reflexes, hemodynamic and respiratory compromise, and death?
Transtentorial
124
What herniation results in ipsilateral oculomotor nerve dysfunction, pupillary dilatation, ptosis, lateral deviation of the affected eye, brainstem compression and death?
Uncal
125
What herniation causes cerebellar structures to herniate through the foramen magnum?
Herniation of the cerebellar tonsils
126
What herniation is indicated by the number 1?
Subfalcine
127
What herniation is indicated by the number 2?
Transtentorial
128
What herniation is indicated by the number 3?
Cerebellar contents are going into the foramen magnum
129
What herniation is indicated by the number 4?
Traumatic event causing herniation out of the cranial cavity
130
What are some common causes of ICP increase?
Tumors, hematomas, blood in the CSF and infections (meningitis/encephalitis). Any can cause either obstruction or decrease in ability to reabsorb CSF
131
Methods to reduce ICP?
Elevate head (promotes venous drainage), hyperventilation, externally drain (EVD), hyperosmotic drugs (mannitol), diuretics, steroids, cerebral vasoconstriction (propofol), surgical decompression
132
What are MS triggers?
Stress, elevated temperature, postpartum
133
Treatment of MS?
No cure; manage symptoms with steroids, immune modulators and targeted antibodies
134
What is MS?
Progressive, autoimmune demyelination of central nerve fibers
135
What common immunosuppressant may warrant an LFT?
Azathioprine
136
What paralytic must be avoided in MS? Why?
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
What is MG? What muscles are affected?
Autoimmune; Antibodies generated against N-Ach-R’s at skeletal motor endplate. Affects skeletal muscle (smooth and cardiac is spared)
138
MG treatment?
Acetylcholinesterase inhibitor (pyridostigmine), immunosuppressive's, steroids, plasmapheresis, IV-IG
139
What are some common themes in prep for anesthesia for MS and MG?
May need stress dose steroids, PFTs, reduce/avoid paralytics if possible
140
Why can certain drugs DOA be prolonged in MG?
They are commonly on pyridostigmine which can prolong the effect of Sux and Ester LA's
141
Describe Eaton-Lambert syndrome
Disorder causing the development of autoantibodies against VG Calcium channels. Reduced Ca influx reduces ACh release. S/sx are similar to MG
142
Eaton-Lambert syndrome treatment?
Potassium channel blocker (3-4 diaminopyridine), acetylcholinesterase inhibitors, immunologic agents (Azathioprine), steroids, plasmapheresis, IV-IG
143
What must be administered with extreme caution in ELS?
Paralytics; they are exceedingly sensitive to all paralytics
144
What lab value may be elevated in Duchennes?
Serum creatine kinase (CK)
145
What condition fairly common to Duchenne's dystrophy can mimic MH?
Hypermetabolic syndrome, also caused by Sux and volatiles -> rhabdomyolysis, hyperkalemia, Vfib, cardiac arrest
146
What is a common anesthesia strategy for Duchenne's dystrophy?
Low dose Roc and TIVA
147
What is myotonia?
Prolonged contraction after muscle stimulation
148
What are 3 examples of myotonia? Include appropriate diagnostic information/differences
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 the skeletal muscles (smooth and cardiac are spared)
Central Core disease: Rare. Core muscle cells lack mitochondrial enzymes. Proximal muscle weakness and scoliosis
149
What is common to all myotonia pathologies?
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
Anesthesia considerations in myotonia?
GI hypomotility (aspiration risk), endocrine abnormalities, keep them warm, avoid Sux and give opioids with caution
151
What are the most common types of dementia?
Alzheimer's (70%), Vascular dementia (25%), Parkinsons (5%)
152
What are some anesthesia considerations in dementia?
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
Treatment for parkinsons?
Levodopa (crosses BBB), anticholinergics, MAOIs (inhibit dopamine degradation), Deep brain stimulator
154
Parkinsons cause and #1 risk factor?
Degeneration of dopaminergic fibers of basal ganglia. RF = advancing age
155
Anesthesia concerns in parkinsons?
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
What are some common s/sx of brain tumors?
Increased ICP, Papilledema, HA, AMS, Mobility impairment, Vomiting, Autonomic dysfunction, Seizures
157
What is the most common glial cells?
Astrocytes
158
What is a common astrocytoma?
Glioma, least aggressive, common in young adults w/new onset seizures
159
What tumors occur in children/young adults and are benign with good outcomes?
Pilocytic astrocytomas
160
What is a poorly differentiated tumor that can evolved into a Glioblastoma Multiforme?
Anaplastic astrocytomas
161
Which brain tumor carries a very high mortality rate?
Glioblastoma Multiforme. Usually requires surgical debulking & chemo with very short life expectancy
162
What benign tumor arises from the dura or arachnoid tissue?
Meningiomas, usually good prognosis
163
What tumor is noncancerous with varying subtypes?
Pituitary adenomas, transsphenoidal or open craniotomy for removal is usually curative
164
What benign Schwannoma involves the vestibular component of CN VIII?
Acoustic neuromas, good prognosis with resection and radiation
165
What tumor can vary widely in origin and symptoms with less favorable outcomes?
Metastatic carcinomas
166
Anesthesia brain tumor concerns?
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
What stroke type is most common?
Ischemic (88%) then hemorrhagic (12%)
168
What is the global cause of death/disability?
Stroke
169
What are the 5 TOAST classification of ischemic strokes?
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
What is the gold standard for ischemic stroke treatment?
Revascularization; either via thrombolytics or intervention such as a thrombectomy device
171
What are 2 reliable predictors of outcomes in hemorrhagic strokes?
EBL and change in LOC
172
What are the 3 subtypes of hemorrhagic strokes?
1) Blood within the brain is 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
What are conservative treatment goals of ischemic strokes?
ICP/BP reduction, seizure precautions, and vigilant monitoring
174
What makes cerebral aneurysms so dangerous?
Only 1/3 have s/sx prior to rupture.
175
Cerebral aneurysm risk factors? When should an intervention be performed?
HTN, smoking, female, oral contraceptives, cocaine use. Within 72 hours
176
What surgeries may treat a cerebral aneurysm?
Coiling, stenting, trapping/bypass (very large aneurysms)
177
When do post-SAH vasospasms occur? What is the treatment?
3-15 days. HTN, hypervolemia and hemodilution. HTN is the preferred treatment. A surgeon can go in and directly inject a CCB
178
What is an AVM?
Arteriovenous malformation. This allows high flow arterial blood to shunt into low flow venous blood, usually congenital.
179
Where are most AVM's found?
Supratentorial
180
AVM treatment?
Radiation, angio-guided embolization, surgical resection (higher mortality)
181
What are 4 congenital brain abnormalities?
Chiari, Tuberous Sclerosis, Von Hippel-Lindau and Neurofibromatosis
182
What are the 4 types of Chiari?
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
What is tuberous sclerosis?
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
What is Von Hippel-Lindau disease?
Autosomal dominant condition where benign tumors of the CNS, eyes, adrenals, pancreas and kidneys develop. Common to have a pheochromocytoma.
185
Is neuraxial anesthesia a good choice in VHL (Von Hippel-Lindau)?
Generally no as it is common to have tumors of the spinal cord
186
What is neurofibromatosis? Anesthesia consideration?
Autosomal dominant with a wide variety of presentation, tumors everywhere. Avoid neuraxial d/t spinal tumors
187
What are the 2 types of neurofibromatosis?
Type I (most common) type II and Schwannomatosis (rare)
188
What is hydrocephalus?
A disorder of CSF accumulation, causing increased ICP, that results in ventricular dilatation.
189
Hydrocephalus treatment?
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
What is the biggest concern with a VP shunt?
Shunt malfunction; occurs most frequently in the first year of placement (high failure rate)
191
What are the 2 categories of a TBI?
Penetrating vs non-penetrating
192
What is the difference in primary vs secondary injuries in a TBI?
Primary = occurs at time of insult
Secondary = neuroinflammation, cerebral edema, hypoxia, anemia, electrolyte imbalances, and neurogenic shock
193
What anesthesia considerations are important with seizures?
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
What are the 3 main arterial pathologies?
aneurysms, dissections, occlusions
195
The aorta and its branches will more likely be affected by what pathologies? Peripheral arteries?
Aorta/branches = aneurysms and dissections
PAs = occlusions
196
When is surgery indicated on an aneurysm?
When it is at 5.5 cm or greater,10 mm growth over a year or family hx of dissection
197
What are the 2 types of aortic aneurysms? What causes their symptoms?
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
In suspected dissection, what is the fastest way to ascertain the severity of the dissection?
Doppler echo
199
What is a dissection?
Tear in the intimal layer of the vessel, causing blood to enter the medial layer
200
What is the difference in type A/B dissections? Treatment?
A = ascending aorta and should be an immediate surgery
B = descending aorta. Depends on stability, if stable medical management, if not, surgery
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What are some considerations to a type A aortic arch surgery?
Require cardiopulmonary bypass, profound hypothermia, and a period of circulatory arrest.
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What is the major complication of aortic arch surgery?
Neurologic deficits
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What are some s/sx of impending type B rupture?
persistent pain, hypotension, left-sided hemothorax); ischemia of the legs, abdominal viscera, spinal cord, and/or renal failure
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What are the DeBakey classifications of aortic dissections?
1 = tear in the ascending aorta that propagates to the arch
2 = tear confined to the ascending aorta
3 = tear in the descending aorta
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Match the DeBakey classifications to type A and B dissections
A = 1, 2
B = 3
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Risk factors for an aortic dissection?
HTN, atherosclerosis, aneurysms, family hx, cocaine use, & inflammatory diseases
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What inherited disease can place you at risk for a dissection? Iatrogenic causes?
Inherited = Marfans, Ehlers Danlos, Bicuspid Aortic Valve, non-syndrome familial hx
Iatrogenic = cardiac catheterization, aortic manipulation, cross-clamping & arterial incision
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What populations is dissection more common in?
Men and 3rd trimester pregnant women
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What is the triad of symptoms of aortic aneurysm rupture?
Hypotension, back pain and pulsatile abdominal mass
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What are the 4 major causes of mortality with thoracic aortic surgery?
MI, respiratory failure, renal failure, stroke
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What findings may be a contraindication to aortic surgery?
CAD, valve dysfunction, HF, ischemic heart disease, severely reduced FEV1, renal failure
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What is the most important indicator of post-aortic surgery renal failure?
Pre-op renal dysfunction (hydrate, avoid hypotension and nephrotoxins)
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What is the most common form of spinal cord ischemia?
Anterior spinal artery syndrome (this vessel has minimal to no collateral circulation)
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Ischemia of the anterior spinal artery can cause what?
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
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What is the 1st leading cause of disability and 3rd leading cause of death in the US?
Stroke
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Where does carotid stenosis commonly occur?
The internal/external carotid bifurcation
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Recommended timeframe to give TPA? Perform thrombectomy?
TPA = 4.5 hours
Thrombectomy = 8 hours
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What are 2 types of cerebral oximetry mentioned in lecture?
Foresight and INVOS
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What can affect cerebral oxygenation?
MAP, CO, SaO2, Hgb, PaCO2, temperature and anesthesia
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What is the definition of PAD?
An ABI (ankle brachial index) of < 0.9 which indicates hypo perfusion. Done by dividing the ankle MAP by the brachial MAP
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What is the relationship of PAD to MI and CVA?
3-5x increased risk of MI or CVA if you have PAD
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Risk factors for PAD?
Advanced age, Family hx, Smoking, DM, HTN, Obesity, ↑Cholesterol
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S/sx of PAD?
Intermittent claudication, Resting extremity pain, Decreased pulses, Subcutaneous atrophy, Hair loss, Coolness, Cyanosis, Relief w/hanging LE over side of bed (↑hydrostatic pressure)
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When is medical intervention warranted in PAD?
With disabling claudication or ischemia (surgical reconstruction or endovascular repair)
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Common causes of acute artery occlusion? Less common?
Common = LA or LV thrombus
Less common = valvular heart disease, endocarditis, PFO, atheroemboli, plaque rupture, hypercoagulability, trauma
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What is subclavian steal syndrome?
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
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Risk factors for subclavian steal syndrome? Treatment?
Atherosclerosis, Takayasu Arteritis, aortic surgery
Tx = endarterectomy
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Raynaud's treatment?
Avoid cold, CCBs, alpha-blockers, surgical sympathectomy is ischemia is severe
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What are common PVD processes that occur during surgery?
Superficial thrombophlebitis, DVT, chronic venous insufficiency
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What is Virchow's triad?
Venous stasis, hypercoagulability and disrupted vascular endothelium
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What is the most common surgery causing DVT and superficial thrombophlebitis?
Total hip replacements
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Risk factors for DVT?
Older than 40, surgery longer than 1 hour, cancer, ortho surgeries on pelvis & LEs, abdominal surgery
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How does regional anesthesia reduce DVT risk?
It allows for earlier ambulation
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What are some low and moderate risks for DVT? Treatment?
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)
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What are the pros/cons of LMWH?
Pros: longer half-life with predictable response, no serial PTTs, less bleeding risk
Cons: expensive, no reversal agent
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What is a treatment option for recurrent PEs in someone who can't tolerate anticoagulants?
IVC filter
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What are the large artery vasculitis pathologies?
Takayasu arteritis and temporal (giant cell) arteritis
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What are the medium artery vasculitis pathologies?
Kawasaki disease which mostly affects the coronaries
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What are the medium to small artery vasculitis pathologies?
Thromboangiitis obliterans, Wegener granulomatosis and polyarteritis nodosa
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What is temporal (giant cell) arteritis?
Inflammation of arteries of the head and neck
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S/sx of temporal (giant cell) arteritis?
unilateral in nature: headache, scalp tenderness, jaw claudication
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Temporal (giant cell) arteritis treatment and diagnosis?
Tx = corticosteroids
Dx = biopsy of temporal artery = shows arteritis in 90% of patients
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What is the only pathology that is an autoimmune occlusive response to nicotine?
Thromboangiitis Obliterans or “Buerger Disease
244
What population is most affected by buerger disease? Diagnostic critera?
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
Treatment of Buerger disease?
Stop smoking, surgical revascularization but there is no pharmacological treatment. Avoid invasive lines
246
What is an anti-neutrophil cytoplasmic antibody negative vasculitis?
Polyarteritis Nodosa
247
What is commonly associated with Polyarteritis Nodosa?
Hep B or C and hairy cell leukemia
248
Tx of Polyarteritis Nodosa?
Steroids, cyclophosphamide, treat underlying cause
249
What inflammatory vascular condition is generally secondary to another issue?
Polyarteritis Nodosa
250
Risk factors for lower extremity chronic venous disease?
Adv age, family hx, pregnancy, ligamentous laicity, prior venous thrombosis, lower extremity injuries, prolonged standing, smoking sedentary lifestyle, high estrogen
251
Diagnostic criteria of lower extremity chronic venous insufficiency?
S/sx of leg pain, heaviness, fatigue. Ultrasound showing venous reflux or retrograde blood flow of greater than 0.5 seconds
252
Lower extremity chronic venous disease treatment?
Diuretics, ASA, Abx, prostacyclin analogues, zinc and ablation if all else fails
253
What procedures may be used to treat lower extremity chronic venous disease?
Saphenous vein inversion, High saphenous ligation, Ambulatory Phlebectomy, Transilluminated-powered phlebectomy, Venous ligation, Perforator ligation
254
What complication is the leading cause of perioperative morbidity in non-cardiac surgery?
Cardiac complications
255
Carotid residual luminal diameter of what represents significant stenosis?
Residual luminal diameter of 1.5 mm or 70 - 75% stenosis
256
Increased AST/ALT indicated what type of hepatobiliary disease?
Hepatocellular injury
257
Decreased albumin and increased PT/INR indicates what type of hepatobiliary disease?
Reduced synthetic function
258
Increased Alkaline phosphatase, GGT and bilirubin indicate what type of hepatobiliary disease?
Cholestasis
259
An increase in unconjugated bilirubin indicates what?
An imbalance between bilirubin synthesis and conjugation
260
An increased in conjugated bilirubin indicates what?
An obstruction which causes reflux of conjugated bilirubin into circulation
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What liver condition creates fibrosis of the biliary tree creating strictures that have a beads on string appearance?
Primary sclerosing cholangitis (PSC)
262
What is the difference between primary sclerosing cholangitis and primary biliary cholangitis?
PSC = affects intra and extrahepatic ducts
PBC = intrahepatic ducts only
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What deficits would you expect with a anterior cerebral artery occlusion?
Contralateral leg weakness
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What deficits would you expect with a MCA occlusion?
Contralateral hemiparesis and hemisensory deficit, aphasia and contralateral visual field deficit
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What deficits would you expect with a PCA occlusion?
Contralateral visual field deficit and contralateral hemiparesis
266
What deficits would you expect with a posterior artery occlusion?
Contralateral hemiparesis and contralateral hemisensory deficits
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What deficits would you expect with a basilar artery occlusion?
Oculomotor deficits and/or ataxia with crossed sensory and motor deficits
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What deficits would you expect with a vertebral artery occlusion?
Lower cranial nerve deficits and/or ataxia with crossed sensory deficits
269
What is the timeframe for vasospasm post SAH? treatment?
3-15 days. Tx = triple H therapy (HTN, hypervolemia and hemodilution)
270
Where would you most likely find an AVM?
The supratentorial region of the brain
271
Why may fluid resuscitation be referred in aortic aneurysm rupture?
The tamponade effect in the left retroperitoneum may be slow exsanguination. Giving fluid to expand volume could make bleeding worse
