STUDY GUIDE !!! Flashcards Preview

BioScience II > STUDY GUIDE !!! > Flashcards

Flashcards in STUDY GUIDE !!! Deck (123):

- diabetes causes - What causes type 1 diabetes?

destruction of the beta cells of the pancreas.


- diabetes causes - What causes type 2 diabetes

the body is unable to use insulin effectively. the beta cells of the pancreas produce insulin normally when the disease begins, but will eventually tire and not produce as much insulin.


- Diabetes and regional - ...kind of a vague study suggestion...

diabetics are more prone to infection. poorly controlled diabetics experience increased levels of post-op pain. diabetics are also typically dehydrated, so if you're doing a spinal, they may bottom out faster. (that's all i could find in the articles regarding regional and diabetes)


- diabetics and the reason they can become stiff - What is the reason diabetics become stiff?

i don't remember seeing this in the articles, but the reason is because the excess glucose floating around glycosylates with all of the cells of the body. this glycosylation or "activated glycosylated end-product" (AGE) thickens the cells and makes them stiff. that's why we check the HbA1C, because the RBCs have become glycosylated over the 3 month period prior. organs typically effected: kidneys, blood vessels, peripheral nerves, and lenses of the eye. (the way i learned it is that glycosylation is a non-enzymatic reaction that simply just occurs if there is too much glucose floating around for too long of a time. craziness.) wikipedia says it's an enzymatic reaction. whatever...


- carcinoid syndrome and the heart - Cardiac involvement has been reported in more than half of the patients with carcinoid syndrome. Cardiac lesions, if present, may result from the secretion of bioactive mediators and most often affect only the ______ side of the heart. What are the mediators and why only one side?

Right side of the heart is affected by fibrous thickenng of the endocardium and fixation of the tricuspid valve. The lungs have the ability to clear out the causative agents mediators: 5-HTP (serotonin) and substance P.


- carcinoid syndrome and the heart - Serotonin may cause vasoconstriction and vasodilation. Why?

At normal concentrations, serotonin does not affect cardiac function; however, the elevated levels seen in carcinoid syndrome may cause both inotropic and chronotropic responses. This action is due in part to an indirect effect from the release of norepinephrine.


- carcinoid tumors and medications to use and avoid - Medication used to treat the symptoms of any residual tumor remaining after surgery?

octreotide (this is a somatostatin. somatostatins block hormones)


- carcinoid tumors and medications to use and avoid - Release of _________ and _________ should be avoided when choosing which medications to use.

catecholamines and histamine (propofol and etomidate are good for induction; succs is debatable; don't use opioids that cause histamine release; only use NDNB that don't cause histamine release, vec is the best choice because of cardiac stability)


- carcinoid tumors and medications to use and avoid - Because these patients often have chronic right ventricular valvular lesions and heart failure, one should avoid anesthetic factors that increase RV work with potential precipitation of acute RV failure. What 3 factors does this include?

hypoxemia hypercarbia a light anesthetic plane


- carcinoid tumors and medications to use and avoid - What is the drug of choice for treating hypotension perioperatively in carcinoid tumor patients?

octreotide (IV boluses up to 1.0mg), along with fluids (hypotension can be a serious problem since the drugs usually used to treat hypotension may make it worse by further stimulating the release of peptides)


** For burn injury info, look at the other brainscape cards for burns **

.... no reason to rehash it since it was vague on the study guide ...


- anesthetics for the patient with muscular dystrophy - Duchenne muscular dystrophy and administration of Suc's, NDNMB and inhaled agents can trigger ?

Rhabdo and MH


- anesthetics for the patient with muscular dystrophy - Why can rhabdo or MH happen with muscular dystrophy patients? What is happening in the cell?

the absence of the dystrophin-glycoprotein complex results in instability and increased permeability of the sarcolemma and increased intracellular calcium levels. exposure of the sarcolemma to the potent inhalational agent (or succ's) stresses the muscle membrane and further increases the instability and permeability. consequently, intracellular calcium levels increase further and cell contents, such as potassium and CK, leak out. **a compensatory hypermetabolic response occurs in an attempt to reestablish membrane stability and prevent calcium fluxes. (this mechanism may explain the hyperkalemia, hyperthermia, tachycardia, and rhabdo observed in these patients. knowledge!)


- anesthetics for the patient with muscular dystrophy - Should you use inhalational agents or do a TIVA for these patients?

TIVA (a "trigger-free" anesthetic and a "clean" machine with the inhalational agents flushed out)


- anesthetics for the patient with muscular dystrophy - If anesthesia induced rhabdo is suspected, serial potassium levels should be measured and immediately treated if greater than ______ mmol/L. What is the treatment?

5.5 mmol/L treatment: IV sodium bicarb, insulin with 10% dextrose, and the patient hyperventilated to produce a respiratory alkalosis.


- anesthetics for the patient with muscular dystrophy - If anesthesia induced rhabdo is definitely happening, what additional steps need to be taken to protect the kidneys?

IV hydration and mannitol, to maintain the UOP > 1ml/kg/h


- anesthetics for the patient with muscular dystrophy - What is the treatment for perioperative hyperkalemic cardiac arrest?

IV calcium chloride (to antagonize the myocardial effects of hyperkalemia and help restore a spontaneous rhythm)


- Duchennes muscles issues, cardiac changes - Patients with Duchennes suffer from progressive degeneration of what types of muscle?

skeletal, cardiac, and smooth muscle (Lack of the dystrophin protein in muscle cells causes them to be fragile and easily damaged)


- Duchennes muscles issues, cardiac changes - _______ __________ occurs in over 50% of patients by 15 years of age.

dilated cardiomyopathy


- SLE confirmation and pulmonary issues/cardiac issues - What is the best diagnostic test for systemic lupus erythematous?

the antinuclear antibody (ANA) test (the ANA is positive in significant titer - usually 1:160 or higher)


- SLE confirmation and pulmonary issues/cardiac issues - SLE usually begins with one or several of the following features. (11)

-unexplained fever, fatigue, and weight loss -photosensitive rash (butterfly rash on face) -arthritis -raynaud phenomenon -serositis (pleuritis, pericarditis, peritonitis) -nephritis or nephrotic syndrome -neurologic symptoms, such as seizures, psychosis or stroke -alopecia -phlebitis -recurrent miscarriage -anemia


- SLE confirmation and pulmonary issues/cardiac issues - Which cardiac problem is relatively common with SLE?

pericarditis (side-note: verrucous [Libman-Sacks] endocarditis is usually clinically silent but can produce valvular insufficiency and serve as a source of emboli)


- SLE confirmation and pulmonary issues/cardiac issues - Do patients with SLE have an increased or decreased risk of coronary artery disease?

increased risk


- SLE confirmation and pulmonary issues/cardiac issues - What are often considered the first clues either to lung involvement or to SLE itself? (3)

pleurisy, coughing, and/or dyspnea


- SLE confirmation and pulmonary issues/cardiac issues - What are some lung issues that can occur in SLE? (6)

pleurisy pleural effusion pneumonitis interstitial lung disease pulmonary HTN alveolar hemorrhage


- SLE confirmation and pulmonary issues/cardiac issues - What issues would suggest shrinking lung syndrome? (4)

dyspnea episodic pleuritic chest pain progressive decrease in lung volume in the absence of interstitial fibrosis significant pleural disease


- SLE confirmation and pulmonary issues/cardiac issues - Pulmonary function tests are often significantly abnormal prior to complaints of dyspnea. Do they show obstructive or restrictive abnormalities?



Geriatric, pulmonary: By age 70, your alveolar surface available for gas exchange has decreased by how much?



Geriatric, pulmonary: Why does your alveolar surface available for gas exchange decrease by 15% by age 70? (2 reasons)

1. Reduction of elastic tissue 2. Increased collagen


Geriatric, pulmonary: What happens to PaO2 when the alveolocapillary membrane thickness increases in elderly patients?

It declines


Geriatric, pulmonary: What is the age-based formula for PaO2?

PaO2 = 100-(0.4 age [yrs]) mmHg


Geriatric, pulmonary: PaO2 on room air at age 20 is 90 mmHg; what is it in the 80 year old?

~70 mmHg (68, if you use the formula)


Geriatric, pulmonary: What are the causes for decreased alveolar compliance? (3)

1. V/Q mismatch 2. Increase in physiologic shunt 3. Decreased efficiency of oxygen exchange


Geriatric, pulmonary: Name 4 changes in respiratory functional efficiency in the elderly (think PFTs)

1. Decreased FEV1 & FVC 2. Increased closing volumes 3. 10% decrease in TLC by age 70 4. Diminished CNS response to hypoxia & hypercarbia


Geriatric, pulmonary: What are 4 airway changes in the elderly population?

1. diminished laryngeal & pharyngeal responses 2. narrowed airway passages 3. edentulous 4. cervical arthritis/OA


Geriatric, pulmonary: What are some of the consequences of having diminished laryngeal & pharyngeal responses?

- Decreased airway clearance (cough & swallowing) - Decreased gag reflex - Predisposition to aspiration


Geriatric, pulmonary: What are some of the consequences of having narrowed airway passages?

- More turbulent flow - Increased work of breathing - Difficult ventilation


Geriatric, pulmonary: What are some of the consequences of being edentulous?

Poor mask seal --> difficult mask ventilation Loss of upper airway muscle tone


Geriatric, pulmonary: What should you focus on during your preoperative assessment?

- Focused exam & history - Smoking hx - PFT for severe lung disease


Geriatric, pulmonary: What are some of the risk factors for postop PNA in the elderly?

Diminished ADLs Weight Loss CVA ETOH use Steroid use Lung disease


Geriatric, pulmonary: Name two post-op complications re: the pulmonary system, common in the elderly population

1. Post-op hypoxia (20-60%) 2. Post-op PNA (20-30% mortality)


Herbal med side effects: Name all of the herbal meds that can potentially cause increased bleeding

Alfalfa Capsicum Chamomile Dong quai Garlic Ginger Ginkgo Ginseng Guarana Echinacea Fish oil Feverfew Horse chestnut Vitamin E Willow bark ? Glucosamine mnemonic: ALF CAPped CHAMal DOwn, while 5 (possibly 6) G-nomes FEVERishly FISHed . wHORes' Vaginas WILL BARK ECHoes


Herbal med side effects: Name all of the herbal meds that cause increased CV stimulation

Ephedra (may also ↑ glucose) Ginseng Goldenseal Licorice Yohimbine Things that make me excited! Ephedra (duh), Gin, Gold, Licorice (yuck), YoHIMbine (that's just an exciting name right there)


Herbal med side effects: Name the herbal meds that causes decreased CV stimulation

Black Cohosh hogwosh...depressing to my heart


Herbal med side effects: Name all of the herbal meds that cause increased CNS stimulation

Ephedra ↑ Ginseng ↑ Goldenseal ↑ Yohimbine ↑ Feverfew ↑ Gotu kola ↑ Guarana ↑ St John’s Wort ↑ (first 4 - all of my hearts favorite things minus licorice PLUS: fevers, worts, guana & cola) my mnemonics are getting worse...


Herbal med side effects: Name all of the herbal meds that cause hepatotoxicity.

Aloe Chapparal Echinacea Germander Kava Kava Liferoot St. John’s Wort SCKAGLE (rock! - like fraggle rock...get it? but scanky? idk)


Herbal med side effects Name all the herbal meds that cause hypoglycemia

Alfafa Aloe Argimony Artichoke Chromium Coriander Dandelion root Devil’s claw Eucalyptus Fenugreek Garlic Ginseng Grape seed Hoodia Juniper Onions Periwinkle Yellow root Fuck - you're on your own with this one.


RA patient risks: Where can nerve entrapment occur? What is a common peripheral neuropathy in RA?

Nerve entrapment may occur at any site where peripheral nerves pass near the inflamed joint. Carpal tunnel syndrome is a common peripheral neuropathy.


RA patient risks: What problem can result from the TMJ synovitis experienced by RA patients?

Synovitis in TMJ occurs in 30-70% of RA patients; as the disease progresses, flexion contractures and soft-tissue swelling may lead to a marked limitation in the patient’s ability to open the jaw


RA patient risks: What problems does cervical spine involvement pose?

Cervical involvement may be extensive and can lead to limited movement or deformity of the neck and to severe laryngeal deviation. The most common spine synovitis is C1-C2; C1-C2 instability results from erosion and collapse of bone and from destruction of supporting cervical ligaments; symptoms occur when excessive motion between C1-C2 exerts pressure on the spinal cord. Additionally, separation of the atlanto-odontoid articulation may allow the odontoid process of the axis to impinge on the spinal cord, leading to neurologic damage. When this separation is severe, the odontoid process can protrude into the foramen magnum and exert pressure on the spinal cord or impair blood flow through the verterbral arteries.The atlantoaxial subluxation may also exert pressure and impair blood flow through vertebral arteries


RA patient risks: What sx does arthritis of the cricoarytenoid joint of the larynx occur? What will you see on DL? And what problems will it pose?

Occurs in 40% of pts w/severe RA. Sx: larynx tenderness, hoarseness, pain on swallowing w/radiation to ear, dypsnea or stridor, or asx May see red, swollen arytenoids on DL. Obstructs airflow & difficult intubation


RA patient risks: What problems will the medications for RA cause?

NSAIDs: platelet dyxfxn, liver/kidney Mild anemia: disease process or drug therapy Corticosteroids: HPA suppression, infection susceptibility


Thyroidectomy issues/concerns, monitoring: What are three post-op complications after a thyroidecomty? When do each occur? What are their causes? And how do you treat them?

1. Stridor (immediate) -b/l RLN injury -respiratory depression --> reintubation 2. Hematoma (early in postop period to 6hrs) -acute bleeding compromising airway -remove sutures, call surgeon 3. Hypoparathyroidism (24hrs post op) -unintentional removal of parathyroid glands -hypocalcemia - check calcium levels -s/s: neuromusc excitability, circumoral tingling, tetany, ventricular arrythmias, laryngospasm


Thyroidectomy issues/concerns, monitoring: What are some issues you should assess during preop in the hyperthyroid patient undergoing thyroidectomy?

Is patient euthyroid? If goiter present: inquire about duration (tracheomalacia) Positional dyspnea or stridor (CT to eval deviation or compression) Examine neck for tracheal deviation SVC obstruction (distended neck veins that don't change w/respiration) Neck ROM


Thyroidectomy issues/concerns, monitoring: What are some intraoperative issues/concerns for a thyroidectomy?

-Monitor CV fxn & temp -Protect eyes -Avoid SNS stimulating meds (Ketamine, ephedrine) -Chronic hypovolemia --> exaggerated hypoTN w/induction -Get adeq anes depth before DL/incision -NMB w/caution (increased incidence of myopathies & MG)


Thyroidectomy issues/concerns, monitoring: Describe thyroid storm (crisis): symptoms onset how it's different than MH in presentation treatment

Severe hypermetabolism Sx: altered LOC, hyperpyrexia, tachycardia, HTN or hTN Onset: 6-24 hr postop but may occur intraop MH-like sx but NO acidosis, muscle rigidity, elevated CK Tx: hydration & cooling; esmolol gtt for HR control, propylthiouracil 250-500 mg Q6H, correct underlying cause


Thyroidectomy issues/concerns, monitoring: What are the s/s of tracheomalacia?

stridor, hoarseness, sore throat, feeling of pressure in neck, coughing, dysphagia, dyspnea May need require prolonged intubation or trach Absence of leak around deflated cuff = alert you to possibility of tracheomalacia


Thyroidectomy issues/concerns, monitoring: Describe the use of a NIM tube for this procedure

NIM tube has 4 stainless steel wire electrodes (2 pairs) embedded in silicone shaft with short part exposed above cuff. Designed to make contact w/vocal cords for EMG monitoring of RLN. Should show consistent sound signal and action potential tracing. • Red wires for anterior & posterior portions of RIGHT true vocal cords • Blue for anterior & posterior portions of LEFT true vocal cords


Pheochromocytoma: What are the 2 portions of the adrenal gland?

Medulla & Cortex


Pheochromocytoma: What does the medulla secrete?

Catecholamines: -epi -NE -dopamine


Pheochromocytoma: What are the different zones of the cortex? What do they each produce/secrete?

Zona Glomerulosa: Aldosterone Zona Fasiculata: Cortisol (glucocorticoids/mineralocorticoids) Zona Reticularis: Testosterone (androgens), estrogens Valley Review: Remember (GFR-ACT) G - A F - C R - T


Pheochromocytoma: What is a pheochromocytoma?

tumor of the chromaffin cells secreting NE, epi, or dopamine


Pheochromocytoma: What is the classic triad of pheo?

Headache, sweating, tachycardia w/HTN (HTN = most frequent manifestation)


Pheochromocytoma: Why is orthostatic hypotension common?

D/t hypovolemia and impaired venous/arterial vasoconstrictor reflex response


Pheochromocytoma: Why must a pheo patient undergo alpha-blockade before beta-blockade?

bc blockade of vasodilatory peripheral beta receptors w/unopposed alpha receptor stimulation can lead to further elevation in BP


Pheochromocytoma: Roughly when should alpha and beta blockade be initiated.

10-14 days preop and 2-3 days preop, respectively


Pheochromocytoma: Why are patients alpha blocked?

To normalize BP and expand contracted blood volume Also: prevents paroxysmal hypertensive episodes, allows resensitization of adrenergic receptors, and decreases myocardial dysfunction. Alpha-blockade appears to protect myocardial performance and tissue oxygenation from adverse catecholamine effects


Pheochromocytoma: When is it recommended to stop alpha blockers and why?

Recommended to stop alpha blockers 24-48 hrs before surgery to avoid vascular unresponsiveness immediately following removal of the tumor; some say give a half dose morning of surgery


Pheochromocytoma: What kind of drugs should you avoid in these patients?

Avoid drugs that promote catecholamine release or potentiate catecholamine reactions -histamine releasing drugs: morphine, atracurium -vagolytic or sympathomimetic drugs (sux, atropine, pancuronium)


Pheochromocytoma: What should you anticipate once the tumor's blood supply is ligated?

Prepare for sudden decrease in BP after the tumor’s blood supply is ligated: -Volume support -Direct-acting vasopressor, i.e., Phenylephrine


Pheochromocytoma: What are the postoperative concerns?

Hypotension = most frequent cause of death in immediate postop period -Vasopressors, IV fluids Hypoglycemia: -Dextrose containing IV fluids -Monitor blood glucose for 24 hrs ICU for 24 hrs: Adequate pain control


Pheochromocytoma: What are some of the meds you would expect to have ready or will possibly use intraoperatively to maintain the patient's hemodynamics WNL?

Nipride, Magnesium, Nicardipine, Phentolamine, Esmolol


What can occur with long term steroid use?

Corticosteroid withdrawal Use of high-dose steroids for more than a week begins to produce suppression of the patient's adrenal glands because the exogenous glucocorticoids suppress hypothalamic corticotropin-releasing hormone (CRH) and pituitary adrenocorticotropic hormone (ACTH). With prolonged suppression, the adrenal glands atrophy (physically shrink), and can take months to recover full function after discontinuation of the exogenous glucocorticoid. During this recovery time, the patient is vulnerable to adrenal insufficiency during times of stress, such as illness.


What is pancreatitis and how does the pancreatic damage occur?

Inflammation of the pancreas. Pancreatic damage occurs when digestive enzymes are activated before they are secreted into the duodenum and begin attacking the pancreas.


What are the 2 types of pancreatitis?

Chronic: irreversible Acute: gland can return to normal if the underlying cause is removed


What is acute necrotizing pancreatitis?

Severe form of AP where necrosis and subsequent infection result. Inflammation leads to necrosis. Necrotic debris becomes infected, usually by gram-negative organisms from the alimentary tract. The acinar and ductal tissues and the Islets of Langerhans become infected. Vascular injury leads to massive hemorrhage within the pancreas.


What is the pathophysiology of acute pancreatitis?

Injury or disruption of pancreatic acinar cells permits leakage of pancreatic enzymes. Activated proteolases and lipases break down tissue and cell membranes causing inflammation, edema, vascular damage, hemorrhage, necrosis, and fibrosis.


What are the s/s of acute pancreatitis?

mid-epigastric pain that radiates to the back, n/v, fever, leukocytosis, hypermotility or paralytic ileus, abdominal distention/ascites, tetany (hypocalcemia) hypovolemia, shock, tachypnea, hypoxemia (atelectasis, pulmonary edema, effusions).


What is the diagnostic hallmark of acute pancreatitis?

Elevated serum amylase level


What is the goal of treatment and interventions for acute pancreatitis?

Goal: to stop process of autodigestion & prevent systemic complications. - Aggressive fluid administration: XL and colloid - Demerol instead of Morphine (< Sphincter of Oddi spasm) - Bowel rest: NG sxn, NPO - TPN - H2 blockers - Stone removal - Antibiotics if necrotizing - Surgery: ERCP, surgical debridement


What are the causes of acute pancreatitis?

GET SMASHED. Gallstones; Ethanol; Trauma; Steroids; Mumps; Autoimmune; Scorpion sting; Hypercalcaemia, hypertriglyceridaemia, hypothermia;


What are the causes of chronic pancreatitis?

Irreversible pancreatic damage caused by: -Chronic alcohol abuse -Obstruction from gallstones -Autoimmune disease -Genetic mutations -Smoking -Obesity


What is the pathophysiology of chronic pancreatitis?

toxic metabolites and chronic release of inflammatory cytokines contribute to the destruction of acinar cells and islets of Langerhans. Fibrosis, strictures, calcification, ductal obstruction, and pancreatic cysts result.


What are the s/s of chronic pancreatitis?

continuous or intermittent abdominal pain, weight loss, steatorrhea, DM.


What is the goal of treatment and interventions of chronic pancreatitis?

Prevent disease progression: -Lifestyle modification (abstain from smoking & drinking) -Fat-free diet -Enzyme replacement -Surgical drainage or partial resection


What are the anesthetic implications of pancreatitis in general?

Aspiration precautions, consider RSI Glucose monitoring Fluid and electrolyte disturbances Blood product administration Fluid resuscitation Coags Renal function (maintain UOP >0.5ml/kg/hr) Pulmonary assessment (CXR, ABG)


What is hypothyroidism?

Inadequate secretion of thyroid hormone caused by: autoimmune disease (Hashimoto’s thyroiditis), thyroidectomy, radioactive iodine, antithyroid medications, iodine deficiency.


What are the s/s of hypothyroidism?

weight gain, cold intolerance, muscle fatigue, lethargy, constipation, hypoactive reflexes, dull facial expression, depression, decreased CO, SV, HR, myocardial contractility. Pleural, abdominal, and pericardial effusions are common.


How does myxedema coma occur?

Results from extreme hypothyroidism: impaired mentation, hypoventilation, hypothermia, CHF.


Pulmonary agent Phosgene, diphosgene, chloropicrin & chlorine treatment

Steroids, antibiotics for pulmonary infection, theophylline and bronchodilators (albuterol) Latent period of 2-24 hours from initial exposure to possible pulmonary edema depending on exposure


Cyanide Agents Hydrogen cyanide and cyanogen chloride treatment

Mild: support circulation w/ crystalloids & vasopressors, correct m.acidosis w/ HCO3, benzo Sig: Na nitrate or amyl nitrate IV ( induces methemoglobin freeing up the Hgb from cyanide. Sodium thiosulfate is given to convert cyanide to thiocyanate (nontoxic)


Incapacitating agents BZ & Agent 15 treatment

Cholinesterase inhibitors. Tx hyperthermia and prevent injury from erratic behavior.


Vesicant Agents Mustard Gas, Lewisite, Phosgene Oxime treatment

Tx erythema w/ calamine, blisters <2cm leave alone. Irrigate lg blisters w/ sterile solution & cover w/ antibiotics. P irrigation of eyes, use anticholinergic eye drops w/ topical antibiotic.


Nerve Agents Sarin, Tabun, Soman, GF, VX treatment

Initial tx: remove clothing and wash skin . Atropine: comp antagonist @ muscarinic receptor & can blk stim both centrally & peripherally. 1-2 mg IV or up to 6 mg then 2 mg Q5-10 min until secretions have dissipated. Def tx: Pralidoxine cl interferes w/ covalent bond fromed by the NA & ach-esterase aka aging. Oximes wk by removing orangophosphoryl f(x)al group of the NA from ach-esterase= enzyme to regenerate.


-Cocaine Abuse and anesthesia- How does cocaine work?

Inhibits presynaptic uptake of sympathomimetic neurotransmitters (e.g. NE, serotonin and dopamine) Produces a powerful euphoria (lasting 5-30 min) as a result of free catecholamines stimulating the sympathoadrenal axis and the prolongation of dopaminergic activity in the limbic system and adrenal cortex


-Cocaine Abuse and anesthesia- what does it do to the blood flow?

Blood flow to arteries in areas like the heart and brain may be compromised as these vessels vasoconstrict or vasospasm temporarily, severely compromising oxygenation and supply; this may lead to irreversible brain damage, stroke and myocardial infarction or depression


-Cocaine Abuse and anesthesia- what does it do to the heart?

depressed ventricular function and slow electrical conduction. Can cause contract band necrosis and ventricular hypertrophy Rare: Aortic dissection, d/t severe and abrupt catecholamine release and HTN MI and Vent arrhythmia


-Cocaine Abuse and anesthesia- what does it do to the lungs?

ranges from asthma -> pulm hemorrhage


-Cocaine Abuse and anesthesia- Misc side effects

infection or perforation of the nasal septum, anxiety, restlessness, irritability, confusion, papillary dilatation, seizures, tachycardia, peripheral blood vessel constriction


-Cocaine Abuse and anesthesia- Regional considerations Can induce _________________, which is the result of platelet activation due to _________ __________ or part of the ___________ __________.

Cocaine-induced thrombocytopenia can occur, possibly the result of platelet activation due to arterial vasospasm or part of the autoimmune response


-Cocaine Abuse and anesthesia- Regional considerations HTN can result d/t what?

peripheral vasoconstriction


-Cocaine Abuse and anesthesia- Regional considerations If hypotension occurs what can happen?

Hypotension may occur, which may lead to cardiac dysrhythmias or myocardial dysfunction


-Cocaine Abuse and anesthesia- Regional considerations How do you treat hypotension in the coke head?


Ephedrine-resistant hypotension may be encountered – low doses of phenylephrine can usually restore BP 


-Cocaine Abuse and anesthesia- Regional considerations


Why do these patients have altered pain perception?

Patients may show combative behavior and altered pain perception, perhaps due to changes in m- and k-opioid receptor densities and abnormal endorphin levels


-Parkinsons and Medications-

Levodopa..... Do you continue it? Why or why not?

What if your pt gets hypotensive from your descicion to stop levodopa?

The elimination half-time of levodopa and the dopamine it produces is brief, so interruption of drug therapy for more than 6 to 12 hours can result in an abrupt loss of therapeutic effects.

Abrupt drug withdrawal can also lead to skeletal muscle rigidity, which can interfere with ventilation.

Therefore, levodopa therapy, including the usual morning dose on the day of surgery, must be continued throughout the perioperative period.

Oral levodopa can be administered approximately 20 minutes before induction of anesthesia, and the dose may be repeated intraoperatively and postoperatively via an orogastric or nasogastric tube as needed

The possibility of hypotension and cardiac dysrhythmias must be considered, and butyrophenones (e.g., droperidol, haloperidol) must be available to antagonize the effects of dopamine in the basal ganglia. 


-Parkinsons and Medications-

What may happen when you give alfentanil?

Acute dystonic reactions following administration of alfentanil might indicate an opioid-induced decrease in central dopaminergic transmission


-Parkinsons and Medications-

Ketamine or not to ketamine..... 


or as josh says... ketaFUCKINmine

The use of ketamine is controversial because of the possible provocation of exaggerated sympathetic nervous system responses, but ketamine has been administered safely to patients treated with levodopa. 


-Parkinsons and Medications-

Complications of muscle relaxant 

The choice of a muscle relaxant is not influenced by the presence of Parkinson's disease.


-Parkinsons and Medications-

What is Neurolepic Malignant Syndrome? (NMS)

NMS is characterized by autonomic instability, altered mental status, rigidity, and fever.


Cn occur with abrupt stoppage of levodopa


-Parkinsons and Medications-

Unless the patient is having cardiac dysrhythmias or hypotension, why avoid Droperidol

Antagonize the effects of dopamine in the basal ganglia. 

Remember parkinson pts have a loss of dopamine-secreting neurons, and the inequality of dopamine and acetylcholine are what cause the s/s. If the pt is hypotensive, and you antagonize the dopamine the acetylcholine can excite the brain/ body to increase the BP. (thats my understanding of this shit)


-Parkinsons and Medications-

Synthetic dopamine agonists

Act directly on the postsynaptic dopamine receptors. Side effects from these drugs include visual and auditory hallucinations, hypotension and dyskinesia


-Parkinsons and Medications-

Anticholinergic treatment

Blunt the effects of excitatory neurotransmitters acetylcholine, thus correcting the balance between dopamine and acetylcholine. Helps with tremor and salvation control, but does not effect skeletal muscle rigidity and bradykinesia


-Common Nosocomial Infections-

Can you name all 15 bugs?

  1. Acinetobacter
  2. Burkholderia cepacia
  3. Clostridium difficile
  4. Clostridium sordelli
  5. Enterobacteriaceae
  6. HIV
  7. Influenza
  8. Klebsiella
  9. MRSA
  10. Mycobacterium abscessus
  11. Norovirus
  12. Pseudomonas aeruginosa
  13. Staphylococcus aureus
  14. Tuberculosis
  15. VRE


-Common Nosocomial Infections-

What 4 medical equipment/ surgical sites relationship of infection do we care about?

Related to medical devices:

  1. Central Line-Associated Blood Stream Infections (CLABSI)
  2. Ventilator-Associated Pneumonia (VAP)
  3. Catheter-Associated Urinary Tract Infections (CAUTI)

Related to surgical site:

  1. Surgical Site Infections (SSI)


-Common Nosocomial Infections-

Organisms found on the anesthesia equipment

(A. Streptococcus, Acinetobacter, Staphylococcus aureas, and gram-negative rods)


-Sepsis and Flotrac- 

this is just a nice flochart to decide what you may need for anesthesia


-Sepsis and Flotrac-

Vigileo (aka flotrac) (SVV & SVI)

For use on control ventilated patients
Variation in arterial pulsations caused by volume changes during positive pressure inspiration
>15% may indicate hypovolemia


-Sepsis and Flotrac-

uno mas pictura


-Sepsis and Flotrac-

Just another good chart from last year. 



-Refractory Hypotension-

Sepsis version.....

Sepsis with refractory hypotension despite fluid administration. Septic Shock

refractory hTN defined as SBP < 90 mm Hg or MAP < 60 mm Hg (or drop of ≥ 40 mm Hg from baseline)

Later, septic shock, is marked by a decline in peripheral vascular resistance and an increase in cardiac output in response to the fall in PVR. This response is the body’s mechanism to maintain adequate perfusion, despite the presence of myocardial depressant activity exerted by TNF-alpha, PAF, IFN-gamma, arachidonic acid metabolites and other endogenous factors. Their effect may decrease ejection fraction to as little as 20%


-Refractory Hypotension-

Renal version

Blocking action of angiotension II, a powerful vasoconstrictor
Blocks release of aldosterone and ADH (endogenous vasopressin)
Give fluids: crystalloid or colloid


-Immune Response-


type 1 hypersensitivity

involves B cells, mast cells and basophils, rhinitis to anaphylaxis

IgE is activated. Systemic reaction. Causes a massive histamine release. 


-Immune Response-


alright.... in his presentation (i watched it AGAIN), all it says is trauma reduces your immunity. But it rebounds.... It maybe related to the triad (Hemodilution, hypothermia and acidosis) just a stab in the dark, stab stab stab