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Special Populations > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Liver accounts for ____% body mass in adults.

A

2%

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2
Q

Liver receives _____% CO.

A

25%

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3
Q

Liver receives blood flow from:

A

oxygenated blood from hepatic artery
nutrient rick blood from portal vein

each vessel provides 50% of hepatic oxygen supply

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4
Q

What controls resistance in hepatic venules?

A

sympathetic innervation from T3-T11

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5
Q

In presence of reduced portal venous flow, the hepatic artery can increase flow by as much as ____% to maintain hepatic oxygen delivery.

A

100%

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6
Q

what is the reciprocal relationship between flow in 2 afferent vessels?

A

hepatic arterial buffer response

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7
Q

portal vein supplies ____% blood oxygen and hepatic artery supplies ______%

A

75% portal vein
25% hepatic artery

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8
Q

How many segments of the liver are there?

A

8

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9
Q

liver removes ammonia through

A

formation of urea

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10
Q

liver is capable of deamination of amino acids, which is required for energy production or conversion of amino acids to carbs or fats. Deamination produces _____.

A

ammonia

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11
Q

liver stores important nutrients like:

A

-vitamin A, D, E, K, B12, iron and minterals
-stores glycogen which can be converted to glucose
-in patients with altered liver function, BG concentration can rise several fold higher than postprandial levels found in patients with normal hepatic function

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12
Q

What cells in the liver destroy bacteria and remove foreign particles from the blood. It produces immune factors and proteins that combat infections.

A

kupffer cells

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13
Q

liver filters about ____ of blood per minute, removing toxins, waste products, bacteria and old RBCs

A

1.4L

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14
Q

liver produces bile which is stored in the gallbladder. Bile contains bile salts and phospholipids that emulsify fats and aid in their digestion and absorption.

A
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15
Q

all blood clotting facters with exception of what factors are synthesized in the liver

A

3, 4, 8

tissue thromboplastin
calcium
von Willebrand

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16
Q

Vitamin K is required for the synthesis of:

A

-prothrombin (factor II)
7
9
10

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17
Q

Albumin

A

-most abundant plasma protein made by liver
maintains oncotic pressure
-transports lipids and hormones
antioxidant properties
-serum albumin levels reflect liver function and nutritional status

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18
Q

C-reactive protein

A

acute phase reactant produced by liver increases dramatically during inflammation and infection
-activates complement and phagocytosis

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19
Q

Ceruloplasmin

A

copper-binding glycoprotein made in liver carries 90% of plasma copper and has ferroxidase activity

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20
Q

lipoproteins

A

liver produces VLDL aand HDL which transport lipids through circulation

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21
Q

protease inhibitors

A

alpha-1 antitrypsin made by liver protects tissues from proteases like elastase
low levels increase risk of emphysema

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22
Q

fibrinogen

A

soluble plasma glycoprotein synthesized by liver and magkaryocytes (bone marrow cells)
-during coagulation, thrombin converts fibrinogen into fibrin forming the fibrin meshwork of a blood clot
10-15% is produced by megakaryocytes which helps maintain adequate fibrinogen level even in severe liver disease

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23
Q

Phase 1 liver metabolism

A

-modifies drug with functionalization actions resulting in loss of pharmacologic acitvity

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24
Q

Phase II metabolism

A

conjugates the metabolite with a second molecule (glucuronic acid, sulfate, glutathione, amino acid, or acetate) forming a covalent link

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25
Q

_______indicated unconjugated bili levels and indicated excess production of bilirubin

A

unconjugated

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26
Q

what is a more sensitive indicator of hepatic disease because of shorter half life of factor 7

A

PT/INR

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27
Q

albumin is______ in chronic liver disesae

A

decreased

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28
Q

Which liver cells have the greatest quantity of cytochrome P450 enzymes and are the site of anaerobic metabolism?

A

pericentral hepatocytes

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29
Q

Which zone is affected most by hypoxia and reactive intermediates from biotransformation?

A

zone 3

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30
Q

Positive pressure ventilation effects on liver blood flow

A

Mechanical ventilation with positive pressure can impair venous return and CO, reducing perfusion to the liver.

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31
Q

effects of drugs used during anesthesia like inhaled anesthetics on liver

A

vasodilation decreasing hepatic vascular resistance and flood flow

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32
Q

What effect does hypotension have on the liver

A

low blood pressure reduces perfusion pressure to the liver. Causes include hypovolemia, blood loss, effects of anesthetic drugs.

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33
Q

Spinal anesthesia effects on liver blood flow

A

-induces sympathetic blockade and vasodilation, esp if high spinal
-redistributes blood flow to splanchnic vascular bed, helps sustain vascular perfusion
-vascular resistance reduced in hepatic arterial and portal circulation
-vasodilation mediated by decreased vasoconstrictor hormones

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34
Q

Anesthetic agents reduce hepatic blood flow by _____after induction.

A

30-50%

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35
Q

which IA increases hepatic blood flow via direct vasodilation properties?

A

isoflurane

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36
Q

treatment of opioid induced spasm of oddi sphincer

A

Nalbuphine or naloxone
-atropine
-glyco
-glucagon
-nitro

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37
Q

in liver disease, Reduced response to endogenous vasocontrictors (AGII, AVP, adn norepi) may be related to what

A

release of nitric oxide, prostacyclin and other endothelial-derived factors in response to humoral and mechanical stimuli

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38
Q

3 major indications for albumin treatment of cirrhotic liver disease:

A
  • after large volume paracentesis
    -to prevent renal impairment (bili >4mg/dL or creat >1mg/dL
    -presence of HRS-SKI-use in conjunction with splanchnic vasoconstrictors
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39
Q

portal hypertension

A

abnormally high BP in portal vein system, which carries blood from intestines, spleen, pancreas, GB to liver

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40
Q

cirrhosis

A

histological development of regenerative nodules surrounded by fibrous bands in response to chronic liver injury

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41
Q

most common reason for liver transplantation in developing countries is

A

both HBV and HCV

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42
Q

_____has acute symptomology

A

HAV

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43
Q

_____ and _____associated with significant chronic sequelae

A

HBV and HCV

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44
Q

current treatment regimens for liver disease

A

2 direct acting antiviral drugs that target specific steps within the HCV replication cycle with or without interferon for a duration of 8-12 weeks

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45
Q

antiviral drug choice and treatment duration for liver disease are based on:

A

-genotype of HCV
-stage of liver disease
-presence of cirrhosis
-previous response to interferon

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46
Q

_________is most common form in US (70%) and is treated with sofosbuvir/velpatasvir drug combo.

A

genotype 1A

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47
Q

Hyperemesis gravidarum

A

1st trimester, risk factors:
-hyperthyroidism
-molar pregnancy
-multiple pregnancies
-up to 20-fold elevation of all liver enzymes but not bilirubin

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48
Q

HELLP

A

-most common of later pregnancy liver disease
-microangiopathic hemolytic anemia (MAHA)
elevated liver enzymes
-low PLT count in the preeclamptic patient compromises the HELLP syndrome and occurs in 20% of severely preeclamptic patients up to 25% maternal mortality

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49
Q

AFLP

A

-result of rapid microvesicular fatty infiltration of the liver resulting in acute portal htn and encephalopathy
-association between it and abnormalities in enzymes involved in Beta oxidation of fatty acids
-smytpoms similar to severe preeclampsia and HELLP syndrome but AFLP may have additional clinical findings more unique to liver failure: hypoglycemia, elevated ammonia, asterixis and encephalopathy

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50
Q

Normal portal venous pressure

A

HVPG=1-5mmHg

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51
Q

Clinically significant portal HTN (cirrhosis, esophageal varices)

A

HVPG>10

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52
Q

variceal rupture HVPG

A

> 12

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53
Q

Key complications of portal HTN include:

A
  1. variceal bleeding-ruptured varices are leading cause of death
  2. ascites-fluid accumulating in the abdominal cavity
  3. hepatic encephalopathy-confusion, altered mental state
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54
Q

cirrhotic leads to have a bleeding diathesis vs DIC which is a thrombotic diasthesis

A
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55
Q

portopulmonary syndrome

A

pulmonary arterial HTN in setting of hortal HTN with or without liver disease
-systemic vasodilation with local pulmonary production of vasoconstrictor
-mean PAP >25mmHG
-curative tx is liver transplant

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56
Q

Hepatopulmonary syndrome

A

-arterial hypoxemia caused by intrapulmonary vascular dilatations
-triad of portal hypertension, hypoxemia and pulmonary vascular dilatations
-PaO2 <80 mmHg or A:a gradient >15mmHg
-poor tolerance of gravitational effects on pulmonary blood flow leading to platypnea-orthodeoxia: standing worsens hypoxemia, supine improves oxygenation

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57
Q

hepatorenal syndrome defined as

A

acute, reversible kidney failure due to end-stage liver disease
-impaired renal blood flow and intense vasoconstriction

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58
Q

causes of hepatorenal syndrome

A

-splanchnic vasodilation and reduced systemic resistance in liver failure
-decreased effective arterial blood volume
-activation of renin-angiotensin and sns
-intense renal vasoconstriction

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59
Q

patho of hepatorenal syndrome

A

reduced GFR but structurally intact kidneys
-diminished natriuresis, sodium retention, ascites

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60
Q

management hepatorenal syndrome

A

fluid restriction vs intravascular volume depletion, ablumin, avoid nephrotoxins
-vasocontrictors, midodrine, octreotide, norepi
-liver transplantation (without: mortality> 50%)

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61
Q

hepatic encephalopathy

A

-neurotoxins (ammonia) acumulate and alter neurotransmission via glutamate or altered cerebral energy homeostasis
-mild apraxia <behavioral>decerebrate posturing<coma
-poor metabolism of gut-produced ammonia vs intracranial bleeding
-failure to metabolize vs failure to synthesize substances; shunting
trx: nonabsorbable disaccharides</behavioral>

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62
Q

absolute contraindications for TIPS

A

-heart failure
-severe tricuspid regurgitation
-severe pulmonary hypertension

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63
Q

TIPS increases

A

-venous return which can unmask undiagnosed cardiac dysfunction or pulmonary HTN, two conditions with increased prevalence in patients with CLD

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64
Q

Complications of TIPS

A

-pneumo
-vascular injury
-dysrythmias
hemmorhage

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65
Q

MELD score

A

Model for End-Stage Liver Disease (MELD) is a validated system that UNOS uses for prioritizing patients on a liver transplant waiting list
-uses serum total bili, serum creatinine and INR values to mathematically rank adult patients according to their expected survival rate without transplantation

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66
Q

Which meld score is associated with 100% mortality rate?

A

> /- 40

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67
Q

s/s of liver transplantation

A

-anorexia
-weakness
-n/v/
-abdominal pain
-hepatosplenomegaly
-ascites
-jaundice
-metabolic encephalopathy
spider nevi
-ascites: aspiration of fluid may see big hemodynamic shifts

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68
Q

what is the gold standard for hemodynamic monitoring in liver transplantation

A

PAC

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69
Q

intraop managment during liver transplantation

A

-normovolemia
-coagulopathy: hyper/or hypocoagulable
-temp: keep warm
-limited sensation
-no contraindications to induction agents
-muscle relaxants
-opioid of choice
-post-induction hypotension
-altered pharmacokinetic and pharmacodynamic response
-ICP monitoring

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70
Q

wilson disease

A

an autosomal recessive disease characterized by impaired copper metabolism

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71
Q

Alpha-1 antitrypsin deficiency

A

-genetic disorder that results in defective production of alpha-1 antitrypsin protein
-this protein protects the liver and lungs from enutrophil elastase, an enzyme that can disrupt connective tissue leading to inflammation, cirrhosis and HCC
-in the lungs, patients with alpha-1 antitrypsin deficiency can develop early -onset panlobar emphysema and symptoms of chronic obstructive pulmonary disease

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72
Q

hemochromatosis

A

-disorder associated with excess iron in the body that can lead to multiorgan dysfunction

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73
Q

cholecystitis

A

-caused by obstruction, infection or both
-acute cholecystitis usually related to gallstones 90-95% of the time
-ss include right upper quadrant tenderness, fever and leukocytosis
-inspiratory efforts worsen pain-Murphy Sign
-jaundice-complete obstruction of cytic duct

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74
Q

Charcot’s triad

A

-fever/chills
-jaundice
-RUQ pain

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75
Q

contraindications to cholecystitis

A

-coagulopathy
-severe COPD
-ESLD
-CHF

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76
Q

insufflation during cholecystitis

A

-decreased FRC, CC and increased PIP hypotension
-15mmHG routine, higher decreases CO, preload
-increased risk of gastric reflux

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77
Q

Achalasia

A

-impaired relaxation of LES
-chronic achalasia results in dilation of esophagus, more food and fluids retained -aspiration risk

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78
Q

Peptic ulcer diseae

A

-gastric ulcer is loss of mucosa due to inflammation
-approx 98% of peptic ulcer in the stomach and duodenum
-H.pylori infection is associated with development of 90% of duadenal ulcers and roughly 75% gastric ulcers

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79
Q

common complications of

A

-hemorrhage
-perforation
-obstruction

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80
Q

gastritis

A

-inflammatory disorder of gastric mucosa
-stress ulceration, stress erosive gastritis and hemorrhagic gastritis

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81
Q

gastric ulcer disease

A

-develop from degeneration of stomach’s mucosal barrier against gastric acid
-pain and anorexia predispose pt to wt loss and metabolic changes
-most common complication is perforation
-most occur in anterior aspect of lesser curvature

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82
Q

Gastric neoplastic disease

A

-gastric cancer 2nd most common cancer worldwide
-7th most in US
-s/s include pain (constant, non-radiating and not relieved by food), wt loss, anorexia, fatigue, and vomiting
-gastrectomy and partial gastrecrtomy remains the primary curative tx

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83
Q

mesenteric traction syndrome

A

-tachycardia and hypotension
-antihistamine and NSAIDS

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84
Q

postoperative ileus risk factors

A

-pain
-anesthesia
-manipulation of bowel contents
-unbalanced electrolytes
-immobility
-intestinal wall swelling from IV fluids

prevention:
start PO feeds ASAP
-early ambulation
minimize bowel manipulation

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85
Q

Anastamotic leakage risk factors

A

-anemias
-co-morbidities
-diabetics
-vascular disease
-decreased perfusion

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86
Q

splanchnic blood flow

A

ANS and the stress response

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87
Q

Zollinger-ellison snydrome

A

-gastroduodenal and intestinal uleration together with gastrin hypersecretion and a non-beta islet cell tumor of the pancreas (gastrinoma)
-gastrin stimulates acid secretion through gastrin receptors on parietal cells and via histamine release
-also excerts a trophic effect on gastric epithelial cells
-gastrinomas can develop in the presence of multiple endocrine neoplasia (MEN) type 1, a disorder involving three primarily 3 organ sites:
-parathyroid glands
-pancreas
-pituitary gland

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88
Q

abominal compartment snydrome

A

-greater than 20mmHG intrabdominal pressure
-normal pressure <10mmHg
-measured with bladder manometer
-organ dysfunction develops if longer than six hours can lead to death
–abdominal trauma, hemoperitoneum, mesentric arterial thrombosis, acute pancreatitis, intestinal obstruction, visceral edema and massive fluid volume replacement
-resuscitative efforts and exposure of the abdomen induce mesenteric edema formation and bowel dilation; delay closure until tension is resolved

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89
Q

carcinoid tumors

A

benign, slow growing
-syptoms related to space occupying
-usually originates in the GIT
-usually asymptomatic
-can be metastatic
-hormones released are metabolized by the liver
-serotonin, histamine, kinin peptides

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90
Q

systemic effects of carcinoid syndrome

A

-flushing
-bronchoconstriction
-hypotension
-HTN
-diarrhea
-life-threatening perioperative hemodynamic instability

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91
Q

Treatment of carcinoid syndrome

A

octreotide

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92
Q

carcinoid heart disease

A

-right sided cardiac involvement
-tricuspid and pulmonary valves
-tumors along valves
-bronchoconstriction
-metastazised by lungs

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93
Q

anesthetic plan for carcinoid syndrome

A

-treat hypoTN with fluids and octreotide, no ephedrine, zofran

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94
Q

carcinoid syndrome avoid

A

-avoid meds that increase release of hormones and mediators from tumor cells
-carcinoid crisis can noecrose and release massive amounts of substances into circulations
-avoid meds that will release hsistamine

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95
Q

insulin secretion is enhanced by

A

-parasympathetic vagal stimulation
-beta adrenergic sympathetic activation
-cholinergic drug administration

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96
Q

insulin suppression from

A

-arterial hypoxemia
-hypothermia
-traumatic stress
-surgical stress

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97
Q

alpha adrenergic sympathetic stimulation _____insulin secretion

A

inhibits

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98
Q

beta adrenergic sympathetic and cholinergic blockade also inhibit insulin secretion

A
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99
Q

endocraine functional cells reside in the islets of langerhands

A

alpha cells secrete glucagon
beta cells secrete insulin

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100
Q

acute pancreatitis

A

causes include:
-alcohol abuse
-trauma
-ulcerative penetration
-infection
-vascular
-metabolic disorders
-autoimmune
-80% pancreatic disorder fromalcohol and gallstones

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101
Q

s/s of acute pancreatitis

A

-abdominal distension
-n/v/
pain
-hypotension
-hypovolemia

102
Q

severe acute pancreatitis

A

-associated with organ failure, local complications, prolonged ICU and 25% mortality rate
-multiple organ dysfunction main cause of death
-pain radiates from midepigastric to periumbilical can be worse with supine position

103
Q

anesthetic considerations o pancreatic disease

A

-fluids and electrolytes resuscitation is imperative
-monitor labs: CRP>150mg/L correlates with severity
-ASA standard monitors, large IVs, consider CVP, and A-line
-caution with meds that undergo hepatic biotransformationc

104
Q

chronic pancreatitis

A

-permanent and irreversible damage to the pancreas
-chronic inflammation, fibrosis, destruction of exocrine and endocrine tissue
-most common etiology is alcohol -70% of cases

105
Q

s/s chronic pancreatitis

A

abdominal pain
-weight loss
-malnutrition
-hepatic disease
-predisposed to pericardial and pleural effusions
-hypoalbuminemia
-hypomagnesemia

106
Q

pancreatic tumors

A

pancreatic cancer 80-90% ductal adenocarcinomas
-can grow extensively before they can produce symptoms
-generally resected by pancreaticoduodenectomy (Wipple)

107
Q

pancreatic disease

A

-painless jaundice
-dull aching midepigastric or back pain
-anorexia
-fatigue
-new-onset DM1 occasionally 1st symptoms

108
Q

diagnostic hallmark-Wipple triad

A

-hypoglycemia (catecholamine release)
-low blood glucose (40-50mg/do)
-relief after IV administration of glucose

109
Q

what is the most common functioning tumor of the pancreas

A

insulinoma
-hypoglycemia
-seizures
-coma (syptoms of catecholamine release)

110
Q

Splenic blood flow

A

300ml/min arises from splenic artery

111
Q

functions of spleen

A

-blood filtering
-maintenane of normal erythrocytes and immune processing of blood-borne foreign antigens
–abnormal blood cells from disease such as sickle cell disease, thalassemia and spherocytosis removed by macrophages
-can lead to worsening anemia and symptomatic splenomegaly
-pt undergoing splenectomy are at greater risk for post op infection
-spleen not essential for life

112
Q

spleen is the most frequently injured organ

A

25-60^ of adults intrabd trauma

113
Q

how much CO does spleen receive

A

5%

114
Q

AST found primarily where

A

non-hepatic tissues so elevations not specific for hepatic disease
-heart
-skeletal muscle
-kidney
-brain

115
Q

what is the most sensitive laboratory indicator of biliary tract disease

A

serum GGT

116
Q

what is a sensitive indicator of hepatic disease?

A

PT/INR because of short 1/2 life of factor 7

117
Q

is serum albumin a reliable indicator of acute liver disease

A

no, because of 3 week 1/2 life

118
Q

insufflation of CO2 into the peritoneal cavity raises intra-abdominal pressure _______mmHg

A

12-15

119
Q

Increases In IAO compresses Inferior vena cava, reducing_______ and _______

A

venous return and decreasing preload

120
Q

Ratio of thyroid hormones

A

T3:T4=1:10 raitio of secretion

80% deiodination of T4 by body tissues

121
Q

elimination half time T3

A

24-30 hours

122
Q

elimination half time T4

A

7 days

123
Q

how much T 3 is free and biologically active

A

0.3% total T3

124
Q

how much T4 is free and biologically active

A

0.03% of T4

125
Q

Role of T3 and T4

A

promote gene transcription and basal cell metabolism
-intestinal absorption of glucose and insulin transport of glucose into cells
-enhance hepatic gluconeogenesis and glycogenolysis
-increase lipid utilization from adipose tissue
-increases the number of Beta-adrenergic receptors and sensitivity to catecholamines–>increases myocardial contractility, decreases SVR, and increases systemic volume
-promote in utero-brain development
-thermogenesis
-heat from body’s vital processes
-adaptive thermogenesis

126
Q

Thyroid function is regulated by:

A

-TSH
-TRH
-T3, T4 and circulating levels of iodine

127
Q

TSH

A

produced in the pituitary gland and enhances and regulates iodine uptake, T3/T3 production/ secretion by thyroid gland

128
Q

TRH

A

produced in the hypothalamus and promotes TSH secretion

129
Q

High iodine level effect

A

down regulate T3/T4 production

130
Q

Calcitonin role

A

inhibits:
-osteoclast activity
-inhibit renal reabsorption of calcium and phosphorus

131
Q

parathyroid glands

A

4
-secrete calcitonin in response to high Ca levels which decreases levels of calcium and phosphorus
-negative feedback loop

132
Q

Calcium present in 3 forms

A
  1. 50% protein bound
  2. 45% ionized fraction (physiologically active and homeostatically regulated)
  3. 5% non-ionized fraction bound with phosphate, bicarbonate and citrate
133
Q

normal calcium level

A

8.8-10.4mg/dL

134
Q

calcium important for:

A

-muscle contraction
-coagulation
-NT release
-endocrine secretion

135
Q

for every ____g/dl change in albumin=_____mg/dl change in ca level

A

1g/dl
0.8g/dl

136
Q

albumin binds ____% protein bound calcium, so albumin levels affect Ca++ levels.

A

90

137
Q

acidosis and calcium

A

acidosis:
decreases protein binding of Ca++
-increases ionized ca++ levels in blood

138
Q

alkalosis and calcium

A

increases protein binding of Ca++
-decreases ionized ca++ levels in blood

139
Q

first sign of hypocalcemic tetany

A

-laryngeal stridor
-laryngospasm

140
Q

serum thyroxine (T4) levels

A

evaluated thyroid function
-90% hyperthyroid pt have elevated levels
-85% hypothyroid have low levels

141
Q

serum triiodothyronine

A

measures T3 levels
-detect disease in patients with clinical s/s of hyerthyroidism

142
Q

Normal range TSH

A

0.4-4.5

143
Q

radioactive iodine uptake test

A

measures amount of thyroid uptake of iodine and thyroid activity
-scan after p.o ingestion and measure amount of thyroid activity

144
Q

Graves disease

A

-most common cause of hyperthyroidism
-autoimmune multinodular (goiter) disease
-thyroid gland hypertrophy
-commonly seen in females (20-40 years)
-due to IgG antibodies attacking the TSH receptor
-commonly seen with Myasthenia Gravis
-exopthalmos (bulging eyes)

145
Q

thyroid adenoma

A

2nd most common cause of hyperthyroidism
-autonomic functioning thyroid tissue that is not downregulated by increased TSH

146
Q

thyroiditis

A

hyperthyroidism
-inflammatory process after acite URI with flu like symptoms and treated with NSAIDs

147
Q

Which iodine rich drug can produce thyrotoxicosis (hyperthyroid disease)

A

amiodarone

148
Q

treatment of hyper thyroidism

A

antithyroid agents: tapazole (methimazole), PTU-propylthiouracil
-beta-blockers-propanolol (decreases conversion of T4 to T3 but takes up to 2-weeks for this response), metoprolol
-recommended for children and females who are pregnant or breastfeeding
-glucocorticoids (dexamethasone, hydrocortisone) inhibits peripheral conversion of T4 to T3

Surgical resection
-thyroidectomy-large symptomatic goiter or refractory to pharmacologic
thyroid cancer
-obstructive symptoms

149
Q

Anesthetic preop considerations thyroid

A

primary goal=euthyroid prior to sx
-pharmacologic tx:
-minimum time 10-14 days but up to 8 weeks preop tx
-PTU inhibits conversion of T4 to T3
-methimazole inhibit organification of iodide and blocks T3/T4 synthesis
-beta blockers-decrease SNS activity
-steroids continued through day of surgery, may need stress dose

150
Q

Intra op considerations hyperthyroid

A

maintain adequate anesthetic depth to block SNS response from surgical stimulation (prevent exaggerated highs/lows in hemodynamics) and avoid the use of SNS -stimulating drugs (ketamine or pancuronium)

Potential complications and risks:
-airway compression or compromise from goiter (continuously evalulaate high airway pressure during surgery)-consider awake fiberoptic intubation with a very large thyroid gland
-cardiac arrhythmias
-potential hyperthermia
-myasthenia gravis incidence increased- initial dose of paralytic should be lowered and TOF twitch monitor required

151
Q

intraop pharm tx

A

hypotension-use direct acting vasoconstrictors-phenylephrine
tachycardia-esmolol, diltiazam if SVT

152
Q

RLN 1 sided

A

voice hoarseness (vocal cord paralysis_

153
Q

bilateral RLN injury

A

vocal cord paralysis -reintubation necessary
-stridor
-aphonia
-respiratory distress from closed vocal cords

154
Q

thyroid storm

A

acute and life threatening
-acute exacerbation of hyperthyroidism
-most commonly seen in undiagnosed disease or undertreated hyperthyroidism pts because of surgical stress or non-thyroid illness
-can be provoked by surgery on an acutely hyperthyroid gland
-hyperthermia
-tachycardia/dysrhthmias
-myocardial ischemia/CHF
-agitation
-confusion
-HTN

155
Q

Treatment of thyroid storm

A

=CV and ventilatory support
-immediate cooling
-keep HR <100/min
-high fio2
-stop precipitating factor
-B blockers (esmolol drip or propanolol)
-corticosteroids : hydrocortisone (50-100mg IV Q 6)
-antithyroid meds (PTU)
-sodium iodide 250mg IV Q 6

156
Q

what do you want to avoid in thyroid storm?

A

salicylates and lasix-both can increase thyroid hormone levels

mortality rate 10-75%

157
Q

Primary hypothyroidism

A

95% of cases
-decreased production of thyroid hormone despite normal levels of TSH
-surgical section
-iodine (or I-131) or amio tx
-lithium use-blocks thyroid hormone synthesis and release
-hashimoto disease-autimmune thyroid gland destruction

158
Q

secondary hypothyroidism

A

-cause by hypothalamic or pititary disease
-often associated with other pituitary pathology (post-partum pituitary necrosis, pituitary mass, surgical resection, intracranial radiation therapy)
consider hydrocortisone stress dose esp if they have adrenal insufficiency

159
Q

s/s hypothyroidism

A

-lethargy
-slow mental functioning
-cold intolerance/hypothermia
-slow movements
-depression
-obesity
-HLD
-reduced metabolic activity

160
Q

if mild to moderate hypothyroid dz is it safe for elective surgery?

A

yes

161
Q

if severe hypothyroidism

A

patients neeed to be euthyroid before sx

162
Q

goals for hypothryoid patient:

A

-respiratory depression
-hypovolemia
-hypoglycemia
-hyponatremia
-hypothermia

163
Q

hypothyroid with CAD

A

increased risk of MI during euthyroid tx due to increased HR and myocardial O2 demands

164
Q

continue levothyroxine preop has 1/2 life of ____ but needs to be continued in op period

A

5-7 days

165
Q

hypothyroidism intraoperative tx

A

-potential difficlt airway if large goter
-exaggerated response to cardio-depressant drugs
-prolonged NMBD relaxation
-hypocarbia
-hyponatremia
-hypoglycemia
-CHF
-refractory hypotension-may have adrenal insuff (steroid dose)
-severe disease invasive monitoring
-keep warm, increase room temp

166
Q

hypothyroid postop care

A

-recovery may be delayed
-TOF recovery may be delayed
=use quantitative monitoring if available, ensure full muscle recovery/strength before extubation
-ensure normothermic prior to extubation
-toradol (NSAIDS) and peripheral neuraxial anesthesia are preferred for pain control over excess narcotics
-may have prolonged PACU Stage 1 recovery

167
Q

myxedema Coma

A

medical emergency-severe hypothyroidism
-low MAP
-need for mechanical ventilation
-concurrent sepsis
-only life-saving surgery should be performed
-IV thyroid replacement T4
diagnosed by very low levels of T3/T4

168
Q

myxedema s/s

A

-impaired LOC/ seizures
-loss of DTRs
-hypoventilation
hypothermia
hyponatremia
-hypoglycemia
-bradycardia
low EKG voltage
non-specific ST/T wave changes
CHF

169
Q

myxedema Tx

A

-mechanical ventilation
-CV support (inotropes pressors)
IV thyroid hormone replacement
-steroids (tx adrenal insufficiency)
0.9NaCL IVF
-glucose
-gradual correction of both:
hypothermia-too fast can cause CV collapse
hyponatremia-central pontine demyelination

170
Q

primary hyperparathyrodism causes____

A

hypercalcemia

171
Q

symptoms of hyperparathyroidism (primary)

A

-nephrolithiasis most common 60-70%
-depression
-confusion
-memory loss
-HTN
-Ekg changes
-heart block with very high Ca levels

172
Q

other causes of primary hyperparathyroidism

A

-parathyroid ademona (90%)
-hyperplasia (9%)-usually affects all 4 glands
-rarely parathyroid carcinoma
-can exist as part of MEN-multiple endocrine neoplasia
-symtpoms-mainly caused by hypercalcemia
-in pregnancy 50% maternal//fetal mortality-can cause spontaneous abortion

173
Q

primary hyperparathyroidism may result from ectopic production of PTH or analog-like substances from malignancies in:

A

-lungs
-genitourinary
-breast
GI
-lymphatic system
-tumors can produce hypercalcemia through direct bone reabsorption mechanisms

174
Q

secondary hyperparathyroidism

A

-increase in parathyroid function that is the result of disease processes that cause:
-hypocalcemia
-decreased vit D metabolism-GI disorders that disrupt absorption
-low Ca_+levels leads to increased PTH secretion
-hyperphosphatemia (ESRD)
-due to decreased renal phosphate excretion

175
Q

Emergency tx for hypercalcemia before surgery

A

-ca exceeding 15mg/dl
-expand intravascular volume with 0.9 saline IVF
-promote sodium diuresis with lasix promotes Na and Ca excretion
correct hypophosphatemia if prevent
-hemodialysis or peritoneal dialysis when other methods c/i

176
Q

chronic hypercalemia patients need:

A

EKG /cardiac clearance
-cNS eval
-renal system eval

177
Q

Parathyroidectomy anesthetic management

A

-GETA commonly used
-TIVA with remi/propofol
-there must be 2nd free back flowing IV for intraop Ca__ and PTH levels, serial draws will typically be 5 apart
-may use NIMS ETT for RLN monitoring-
-sx tx is chosen over any other type of tx modality of hyperparathyroidism because it is curative

178
Q

hypoparathyroidism

A

-Ca levels <8mg/dl
-most common cause-surgical removal with thyroidectomy
-other causes:neck trauma, malignancy, granulomatous disease

symptoms: neuronal irritability, skeletal muscle spasms, twitching, tetany, seizures

clinical dx: chvostek sign and trousseau

179
Q

treatment of hypoparathyroidism/hypocalcemia

A

severe symptomatic tx: IV calcium gluconate followed by elemental Ca via IV infusion

180
Q

Calcium gluconate is how much elemental Ca

A

9% (90mg)

181
Q

Calcium carbonateis how much elemental Ca

A

40% (500mg)

182
Q

Calcium chloride is how much elemental Ca

A

27% (270 mg)

183
Q

Calcium citrate is how much elemental Ca

A

21% (210mg)

184
Q

Adrenal cortex function

A

to secrete 3 types of hormones:
1. Glucocorticoids (cortisol)
2. mineralocorticoids (aldosterone)
3. androgens

185
Q

Zona glomerulosa

A

mineralocorticoids=aldosterone and corticosterone

186
Q

zona fasciculata

A

glucocorticoids–cortisol and cortisone

187
Q

zona reticularis

A

androgens-estrogen and testosterone

188
Q

what is the most potent glucocorticoid?

A

cortisol

189
Q

cortisol

A

-produced in inner portion of adrenal cortex
-has immediate effects on metabolism of carbs, proteins, FA
-responsible for maintenance of immune and circulatory functions
-inactivated by liver and excreted in urine

190
Q

aldosterone

A

-produced by adrenal gland
-major function is to regulate extracellular fluid volume and potassium homeostasis through the reabsorption of Na+ and secretion of K+ by tissues

191
Q

androgens

A

responsible for sex organ development and changes that manifest during puberty

192
Q

cushings snydrome

A

-overproduction of cortisol by adrenal cortex and overdosing of exogenous glucocorticoid therapy
-can also be caused by neoplasm

193
Q

symptoms of cushings

A

-truncal obestiy
-HTN
-hyperglycemia
-intravascular volume increase
-decreased K
-fatiguability
-abdominal striae
-osteoporosis
-muscle weakness

194
Q

management of cushings

A

=preop tx of DM, fluid management, HTN and correct electrolyte imbalance
-spirinolactone diuresis-mobilizes excess fluid
-if b/l adrenalectomy is planned the patient will need glucocorticoid replacement tx

195
Q

anesthesia and cushings

A

-no specific plan but if pt has severe cushings do not use etomidate it will inhibit steroid synthesis (adrenal suppression)

196
Q

mineralocorticoid excess

A

-too much aldosterone causes HTN, hypokalemic alkalosis, skeletal muscle weakness and fatigue

Anesthetic considerations:
-restore IV fluid volume, electrolyte balance
-HTN and hypokalemia can be controlled by Na intake restriction

197
Q

addisson’s disease

A

-undersecretion of adrenal steroid hormones (decrease of ACTH)
-not apparent until 90% adrenal cortex has been destroyed
-previously due to TB
-now mainly due to autoimmune destruction of the gland
-Hashimoto’s thyroiditis is associated with Addisons
-other causes: bacterial, fungal, advanced HIV, sepsis, hemorrhage
s/s: weight loss, n/v,d. chronic fatigue hypotension

198
Q

acute addisions crisis

A

-abdominal pain
-severe vomiting
-diarrhea
-low BP
-decreased LOC
-shock symtpoms
-severe hyperkalemia

199
Q

management of acute adrenal insufficienc

A

hydrocortisone 100mg IV bolus followed by hydrocortisone 100mg Q6H for 24 hours
-fluid and electrolyte replacement as indicated by vital signs, serum electrolytes and serum glucose

200
Q

catecholamines are derived from

A

tyrosine

201
Q

pheochromocytoma arise from

A

chromaffin cells of adrenal medulla

202
Q

75% of pheochromocytoma are solidary and found where

A

right adrenal gland
-secrete epinephrine and norepinephrine

203
Q

paragangliomas

A

extra-adrenal pheochromocytomsa==as

204
Q

s/s pheochromocytoma

A

-headache
-HTN
-palpitations
-tremors
-sweating
-anxiety
-hyperglycemia
-catecholamine-induced ccardiomyopathy

205
Q

diagnosis of pheochromocytoma

A

-excess catecholamine or metabolite level

Metanephrine
-normetanephrine
-vanillymandelic acid

206
Q

anesthetic considerations pheochromocytoma

A

-can masquerade as mh minus increase in etco2
-excision mortality decreased from 50% to 0-3% with preop use of:
-alpha antagonism (must be blocked first):
prevents HTN effects of catecholamines
-started 10-14 days preop along with IVF replacement to mitigate orthostatic hypotension
-long acting irreversible drugs: phenoxybenzamine
-short acting competitive: doxazosin, prazosin, terazosin

beta antagonism-blocked 2nd
-propanolol, atenolol, metoprolol

-should only be started after several days of alpha blockade to avoid unopposed alpha constriction insevere HTN, MI , HF, and other end organ hypertensivefailure

207
Q

post tumor excision of pheochromocytoma

A

expect precipitous drop in BP (have all pressor agents in line)

208
Q

diabetic fasting glucose levels

A

> 126mg/dL (HBA1C>/6.5%

209
Q

pre-diabetic fasting glucose

A

100-125mg/dL
HBA1C>/5.7-6.4%

210
Q

type 1 DM

A

-autoimmune pancreatic B cell destruction causing absolute insuline deficiency and insulin dependence
-hard to maintain blood glucose within normal limits
onset usually <20 years old
risk for DKA and HHNC
=frequently have complications over their life span, retinopathy/blindness, limb infections/amputations, CV disease, neuropathies

211
Q

poorly controlled or long term diabetics

A

higher risk for heart failure (2-3x higher risk for CAD)

212
Q

autonomic dysfunction and DM

A

-neuropathy of the autonomic nerves which control vascular tone responses, GI and bladder emptying
-severe bradycardia post-induction and hypotension
-hypothermia

213
Q

insulin day of surgery

A

-decrease long-acting insulin dose
-skip short acting dose
-ask patient how they manage their insulin especially type 1 DM
-insuline pumps-know how to manage and show how to give insuline dose if necessary during surgery

214
Q

would we prefer a patients glucose level to be low or high during surgery?

A

=higher sugar better under anesthsia-patient typically used to running with high BG level, low will put the in a stressful state

check glucose hourly if rapidly changing or dose insulin check 30 min

215
Q

hyperosmolar, hyperglycemia non-ketotic coma

A

BG>600mg/dL
-they are not in ketoaacidosis
-profoudn dehydration (need 1-2 L of NS bolus over 1 hour)
insulin infusion follows above rehydration
-giving insulin infusion before rehydration will cause CV collapse

216
Q

diabetic ketoacidosis

A

-ketonemia
-hyperglycemia
-acidemia
-bg 250-500mg/dL
-always dehaydrated due to hyperglycemia osmotic diuresis n/v
TX: fluids, insulin, electrolyte replacement

217
Q

Whipple triad

A

-symptomes of neuroglycopenia (lack of glucose to the brain/CNS symptoms)
-BG <40mg/dL
-relief of symptoms with glucose administration

218
Q

where is the pituitary gland located

A

-base of brain in sella turcica

219
Q

anterior pituitary (hyposecretion_

A

-hyposecretion of anterior pituitary tx with hormone replacement therapy and stress doses of corticosteroids
-caused by decrease in ACTH secretion

220
Q

Anterior pituitary (hypersecretion)

A

-caused by adenoma secondary to cushings secondary to increase in ACTH
-giantism or acromegaly due to excess growth hormone

221
Q

posterior pituitary

A

secretes vasopressin (ADH)
-oxytocin (uterine contractions and breast milk secretion)

222
Q

diabetes insipidus

A

-inadequate secretion of ADH or renal tubular resistance to ADH

223
Q

s/s DI

A

-polydypsia
–hypernatremia
-high output of poorly concentrated urine
-hypovolemia

224
Q

treatment of DI

A

DDAVP or vasopressin infusion
-isotonic crystalloid
-frequent Na serum level meaasurements

225
Q

causes of DI

A

destruction of pituitary gland by trauma (head, subarachnoid hemm, brain death) or surgical iinjury

226
Q

siadh causes

A

-caused bhy excessive ADH production
-head injuries
-intracranial tumors
-pulmonary infections
-lung small cell carcinoma
-hypothyroidism

227
Q

s.s SIADH

A

-hyponatremia
-very low urine OP
-skeletal muscle weakness
-confusion/seizures

228
Q

treatment of SIADH

A

-fluid restriction (as low as 800ml/day)
–hypertonic saline infusion (3% NS)
-lasix

229
Q

dont correct serum sodium levels more than:

A

9meq/L in 24 hours

230
Q

location of kidneys

A

-behind peritoneum
-right lower than left
-held in place by inferior mesenteric artery
-renal artery enters at hilum

231
Q

bladder pns innervation from

A

T11-L2
S2-S4 segments

-retropubic space

232
Q

kidneys receive____% CO

A

25

233
Q

plasma filtration rates:

A

125-140ml/min

234
Q

2 major determinants of glomerular filtration pressure

A
  1. glomerular capillary pressure
  2. glomerular oncotic pressure
235
Q

renal autoregulation of blood flow is controlled by

A

primarily local feedback signals that regulate glomerular arteriolar tone to protect glomeruli from excessive pressure

236
Q

proximal tubule reabsorbs 2/3rd of NA+ filtrate
ATP drives NA+ into tubular cells and H20 passively follows

A
237
Q

most common cause of AKI

A

ATN
tubular necrosis
surgical cause

seen in critically ill patients that have high morbidity rates
-causes high levels of creatine and urea in the blood
-prerenal causes: low MAP and hypoperfusion states
-mortality rate up to 80% : 20-30 min prolonged period of hypotension can precipitate an aKI

238
Q

prerenal azotemia

A

increased BUN from renal hypoperfusion or ischemia

239
Q

intrinsic acute kidney injury

A

AKI due to ischemia, nephrotoxins, renal parencyhmal disease

240
Q

post-renal AKI (obstructive)

A

some type of downstream obstruction tin urinary flow caused by high back pressure into kidney

241
Q

nephrotoxin drugs

A

-aminoglycosides
-amphotericin B
-cyclosporin A
-ACE inhibitors increase risk of AKI
-loop diuretics linked to postop kidney injury

heavy meatls
-contrast media
nsaids
-antimicrobial and chemo

242
Q

uremic syndrome

A

extreme form of renal failure in which GFR decreases below 10% of normal
-kidney cant regulate volume and composition of ECF
-excretion of waste products
-pt has low K clearance and need continuous dialysis
-high risk of life-threatening hyperkalemia, metabolic acidosis, CV complications from fluid overload, HTN, autonomic system hyperactivity, electrolyte disturbances

243
Q

anesthetic agents in renal failure

A

prolonged half life in drugs that are eliminated unchanged:
nmbd
anticholinesterase inhibitors
antibiotics
digoxin

244
Q

which anesthetic agents are ok in renal failure

A

ketamine
propofol
etomidate

245
Q

s/s of acute hyponatremia in TURP NA 120

A

CNS changes: confusion restlessness
EKG: possible widening of QRS

246
Q

s/s of acute hyponatremia in TURP NA 115

A

somnolence
nausea

widened QRS
elevated ST

247
Q

s/s of acute hyponatremia in TURP NA 110

A

seizures
coma
ventricular tachycardia or fibrillation

248
Q

treatment of Transurethral resection syndrome

A

-ensure oxygenation and circulatory support
–notify surgeon and terminate procedure asap
-consider insertion of invasive monitors if CV instability occurs
-send blood to lab
-12 lead ECG
-treat mild symptoms > 120 with fluid restriction and loop diuretic
severe <120 with 3% ns at rate of <100ml/hr
d/c 3% when NA >120

249
Q

absolute contraindications to ESQL-shock wave therapy

A

bleeding disorders/anticoag
pregnancy

250
Q

relative contraindications to ESWL

A

-large calcified aortic/renal aneurysms
-untreated UTI
-obstruction distal to calculi
-pacemaker, AICD
neurostimulator
morbid obesity

251
Q
A

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