STUDY GUIDE !!!

Question 1

• diabetes causes - What causes type 1 diabetes?

Answer 1

destruction of the beta cells of the pancreas.

Question 2

• diabetes causes - What causes type 2 diabetes

Answer 2

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.

Question 3

• Diabetes and regional - …kind of a vague study suggestion…

Answer 3

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)

Question 4

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

Answer 4

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…

Question 5

• 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?

Answer 5

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.

Question 6

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

Answer 6

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.

Question 7

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

Answer 7

octreotide (this is a somatostatin. somatostatins block hormones)

Question 8

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

Answer 8

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)

Question 9

• 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?

Answer 9

hypoxemia hypercarbia a light anesthetic plane

Question 10

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

Answer 10

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)

Question 11

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

Answer 11

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

Question 12

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

Answer 12

Rhabdo and MH

Question 13

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

Answer 13

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!)

Question 14

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

Answer 14

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

Question 15

• 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?

Answer 15

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

Question 16

• 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?

Answer 16

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

Question 17

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

Answer 17

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

Question 18

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

Answer 18

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

Question 19

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

Answer 19

dilated cardiomyopathy

Question 20

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

Answer 20

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

Question 21

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

Answer 21

-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

Question 22

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

Answer 22

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

Question 23

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

Answer 23

increased risk

Question 24

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

Answer 24

pleurisy, coughing, and/or dyspnea

Question 25

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

Answer 25

pleurisy pleural effusion pneumonitis interstitial lung disease pulmonary HTN alveolar hemorrhage

Question 26

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

Answer 26

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

Question 27

- 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?

Answer 27

restrictive

Question 28

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

Answer 28

15%

Question 29

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

Answer 29

1. Reduction of elastic tissue 2. Increased collagen

Question 30

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

Answer 30

It declines

Question 31

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

Answer 31

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

Question 32

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

Answer 32

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

Question 33

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

Answer 33

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

Question 34

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

Answer 34

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

Question 35

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

Answer 35

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

Question 36

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

Answer 36

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

Question 37

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

Answer 37

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

Question 38

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

Answer 38

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

Question 39

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

Answer 39

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

Question 40

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

Answer 40

Diminished ADLs Weight Loss CVA ETOH use Steroid use Lung disease

Question 41

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

Answer 41

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

Question 42

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

Answer 42

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

Question 43

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

Answer 43

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)

Question 44

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

Answer 44

Black Cohosh ....black hogwosh...depressing to my heart

Question 45

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

Answer 45

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...

Question 46

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

Answer 46

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

Question 47

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

Answer 47

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.

Question 48

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

Answer 48

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

Question 49

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

Answer 49

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

Question 50

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

Answer 50

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

Question 51

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?

Answer 51

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

Question 52

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

Answer 52

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

Question 53

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?

Answer 53

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

Question 54

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

Answer 54

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

Question 55

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

Answer 55

-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)

Question 56

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

Answer 56

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

Question 57

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

Answer 57

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

Question 58

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

Answer 58

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

Question 59

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

Answer 59

Medulla & Cortex

Question 60

Pheochromocytoma: What does the medulla secrete?

Answer 60

Catecholamines: -epi -NE -dopamine

Question 61

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

Answer 61

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

Question 62

Pheochromocytoma: What is a pheochromocytoma?

Answer 62

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

Question 63

Pheochromocytoma: What is the classic triad of pheo?

Answer 63

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

Question 64

Pheochromocytoma: Why is orthostatic hypotension common?

Answer 64

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

Question 65

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

Answer 65

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

Question 66

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

Answer 66

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

Question 67

Pheochromocytoma: Why are patients alpha blocked?

Answer 67

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

Question 68

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

Answer 68

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

Question 69

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

Answer 69

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

Question 70

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

Answer 70

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

Question 71

Pheochromocytoma: What are the postoperative concerns?

Answer 71

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

Question 72

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?

Answer 72

Nipride, Magnesium, Nicardipine, Phentolamine, Esmolol

Question 73

What can occur with long term steroid use?

Answer 73

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.

Question 74

What is pancreatitis and how does the pancreatic damage occur?

Answer 74

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

Question 75

What are the 2 types of pancreatitis?

Answer 75

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

Question 76

What is acute necrotizing pancreatitis?

Answer 76

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.

Question 77

What is the pathophysiology of acute pancreatitis?

Answer 77

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.

Question 78

What are the s/s of acute pancreatitis?

Answer 78

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).

Question 79

What is the diagnostic hallmark of acute pancreatitis?

Answer 79

Elevated serum amylase level

Question 80

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

Answer 80

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

Question 81

What are the causes of acute pancreatitis?

Answer 81

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

Question 82

What are the causes of chronic pancreatitis?

Answer 82

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

Question 83

What is the pathophysiology of chronic pancreatitis?

Answer 83

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.

Question 84

What are the s/s of chronic pancreatitis?

Answer 84

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

Question 85

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

Answer 85

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

Question 86

What are the anesthetic implications of pancreatitis in general?

Answer 86

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)

Question 87

What is hypothyroidism?

Answer 87

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

Question 88

What are the s/s of hypothyroidism?

Answer 88

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.

Question 89

How does myxedema coma occur?

Answer 89

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

Question 90

Pulmonary agent Phosgene, diphosgene, chloropicrin & chlorine treatment

Answer 90

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

Question 91

Cyanide Agents Hydrogen cyanide and cyanogen chloride treatment

Answer 91

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)

Question 92

Incapacitating agents BZ & Agent 15 treatment

Answer 92

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

Question 93

Vesicant Agents Mustard Gas, Lewisite, Phosgene Oxime treatment

Answer 93

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.

Question 94

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

Answer 94

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.

Question 95

-Cocaine Abuse and anesthesia- How does cocaine work?

Answer 95

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

Question 96

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

Answer 96

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

Question 97

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

Answer 97

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

Question 98

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

Answer 98

ranges from asthma -\> pulm hemorrhage

Question 99

-Cocaine Abuse and anesthesia- Misc side effects

Answer 99

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

Question 100

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

Answer 100

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

Question 101

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

Answer 101

peripheral vasoconstriction

Question 102

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

Answer 102

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

Question 103

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

Answer 103

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

Question 104

-Cocaine Abuse and anesthesia- Regional considerations Why do these patients have altered pain perception?

Answer 104

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

Question 105

-Parkinsons and Medications- Levodopa..... Do you continue it? Why or why not? What if your pt gets hypotensive from your descicion to stop levodopa?

Answer 105

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. **

Question 106

-Parkinsons and Medications- What may happen when you give alfentanil?

Answer 106

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

Question 107

-Parkinsons and Medications- Ketamine or not to ketamine..... or as josh says... ketaFUCKINmine

Answer 107

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.

Question 108

-Parkinsons and Medications- Complications of muscle relaxant

Answer 108

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

Question 109

-Parkinsons and Medications- What is Neurolepic Malignant Syndrome? (NMS)

Answer 109

NMS is characterized by autonomic instability, altered mental status, rigidity, and fever. Cn occur with abrupt stoppage of levodopa

Question 110

-Parkinsons and Medications- Unless the patient is having cardiac dysrhythmias or hypotension, why avoid Droperidol Haloperidol?

Answer 110

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)

Question 111

-Parkinsons and Medications- Synthetic dopamine agonists

Answer 111

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

Question 112

-Parkinsons and Medications- Anticholinergic treatment

Answer 112

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*

Question 113

-Common Nosocomial Infections- Can you name all 15 bugs?

Answer 113

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

Question 114

-Common Nosocomial Infections- What 4 medical equipment/ surgical sites relationship of infection do we care about?

Answer 114

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)

Question 115

-Common Nosocomial Infections- Organisms found on the anesthesia equipment

Answer 115

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

Question 116

-Sepsis and Flotrac- this is just a nice flochart to decide what you may need for anesthesia

Answer 116

Question 117

-Sepsis and Flotrac- Vigileo (aka flotrac) (SVV & SVI)

Answer 117

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

Question 118

-Sepsis and Flotrac- uno mas pictura

Answer 118

Question 119

-Sepsis and Flotrac- Just another good chart from last year.

Answer 119

Question 120

-Refractory Hypotension- Sepsis version.....

Answer 120

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%

Question 121

-Refractory Hypotension- Renal version

Answer 121

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

Question 122

-Immune Response- Anaphylaxis

Answer 122

type 1 hypersensitivity involves B cells, mast cells and basophils, rhinitis to anaphylaxis IgE is activated. Systemic reaction. Causes a massive histamine release.

Question 123

-Immune Response- Trauma

Answer 123

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