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Semester 2 TxWes > Assessments Unit 4 > Flashcards

Assessments Unit 4 Flashcards

1
Q

What layer of the smooth membrane secretes serous fluid to enclose the cavity and reduce friction?

A

Serosa

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2
Q

List the GI layers from outer to inner

A

The serosa, longitudinal muscle layer, circular muscle layer, submucosa, and mucosa

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3
Q

List the layers of the mucosa from outer to inner

A

muscularis mucosae, lamina propria, and epithelium

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4
Q

What 2 muscle layers work together to propagate gut motiliy?

A

The longitudinal and circular muscle layers

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5
Q

What innervates GI organs up to the proximal transverse colon?

A

The celiac plexus

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6
Q

What innervates the descending colon and distal GI tract?

A

Inferior hypogastric plexus

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7
Q

What does the myenteric plexus do? The submucosal plexus?

A

Myenteric = lies in between smooth muscle layers and regulates the smooth muscle

Submucosal = transmits information from the epithelium to the enteric and CNS

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8
Q

In the mucosa layer, what contains blood vessels/nerve endings? Where are GI contents sensed, enzymes are secreted, nutrients are absorbed, and waste is excreted?

A

Vessels/nerves = Lamina Propria

GI content = epithelium

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9
Q

What 2 systems make up the GI ANS?

A

The extrinsic nervous system and enteric nervous system (this system is independent of the CNS and controls motility, secretion and blood flow)

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10
Q

Describe the effects of the SNS and PNS on the GI system

A

SNS = inhibitory and decrease GI motility
PNS = excitatory and increases/activates GI motility

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11
Q

What cells of the enteric nervous system help carry out motiliy?

A

the interstitial cells of Cajal (ICC cells), GI pacemakers and smooth muscle cells

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12
Q

What is the primary anesthesia concern with an upper GI endoscopy (EGD)?

A

We have to share the airway with the endoscopist

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13
Q

What is the primary anesthesia concern with a colonoscopy?

A

Dehydration -> potential BP problems

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14
Q

What does High Resolution Manometry (HRM) measure?

A

Pressures along the esophagus; diagnoses motility disorders

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15
Q

What does a barium GI series measure?

A

Swallowing function and GI transit

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16
Q

What does small intestine manometry measure

A

Contraction pressure and motility of the small intestine. Evaluatescontractions during three periods: fasting, during a meal, and post-prandial.Normally the recording time consists of 4 hrs fasting, followed by ingestion of a meal, and 2 hrs post-meal

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17
Q

What does a lower GI series evaluate?

A

Using a barium enema, it outlines the intestines and allows for detection of colorectal anatomical abnormalities

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18
Q

What categories are the diseases of the esophagus grouped into?

A

Anatomical, mechanical and neurologic

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19
Q

What are anatomical causes of esophageal disease?

A

Diverticula, hiatal hernia, and changes assoc w/ chronic acid reflux. These abnormalities interrupt the normal pathway of food,which changes the pressure zones of the esophagus

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20
Q

What are mechanical causes of esophageal disease?

A

Achalasia (esophagus doesn’t contract properly), esophageal spasms, and ahypertensive LES

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21
Q

What are neurologic causes of esophageal disease?

A

Stroke, vagotomy or hormone deficiences

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22
Q

What are the most common s/sx of esophageal disease?

A

Dysphagia, heartburn, GERD

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23
Q

What are the 3 types of Achalasia?

A

Type I: minimal esophageal pressure, responds well to myotomy
Type II: entire esophagus pressurized; responds well to treatment, has best outcomes
Type III: esophageal spasms w/premature contractions; has worst outcomes

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24
Q

What is Achalasia?

A

Outflow obstruction of neurotransmitters causing inadequate LES tone and a dilated hypomobile esophagus (such as unopposed cholinergic stimulation = LES can’t relax)

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25
Q

What are some treatments for Achalasia?

A

All are palliative: nitrates, CCBs to relax LES Endoscopic botox injections
Pneumatic dilation * most effective nonsurgicaltx
Laparoscopic Hellar Myotomy *best surgical tx
Peri-oral endoscopic myotomy (POEM)- endoscopic division of LES muscle layers (40% develop pneumothorax or pneumoperitoneum)
Esophagectomy- only considered in the most advanced dz states

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26
Q

What is the best surgical treatment of Achalasia?

A

Laparoscopic Hellar myotomy

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27
Q

Treatment for diffuse esophageal spasms?

A

Nitroglycerin, antidepressants and PD-Is (phospho-diesterase inhibitors)

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28
Q

List the types of Esophageal Diverticula

A

Pharyngoesophageal (Zenker diverticulum): bad breath d/t food retention

Midesophageal: may be caused by old adhesions or inflamed lymph nodes

Epiphrenic (supradiaphragmatic): pts may experience achalasia

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29
Q

Describe a hiatal hernia

A

Herniation of stomach into thoracic cavity, occurs through the esophageal hiatus in the diaphragm (could be related to weakening in anchors of GE junction to the diaphragm)

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30
Q

What is the mortality rate of esophageal cancer?

A

Very high because of the abundance of lymph nodes for the cancer to metastasize to

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31
Q

What are the most common esophageal cancers?

A

Adenocarcinomas are the most common, squamous cell carcinoma comprise the rest

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32
Q

What are some risk factors for esophageal adenocarcinoma?

A

GERD, Barrets esophagus (esophageal changes with repeated exposure to stomach acid) and obesity

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33
Q

What is the definition of GERD?

A

Incompetence of the gastro-esophageal junction, leading to reflux

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34
Q

What are the reflux contents from GERD?

A

HCL, pepsin, pancreatic enzymes and bile

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35
Q

What are the 3 mechanisms of GE incompetence?

A

Transient LES relaxation, elicited by gastric distention
LES hypotension (normal LES pressure-29mmHg, avg GERD pressure-13 mmHg)
Autonomic dysfunction of GE junction

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36
Q

What are some pre-op interventions for GERD?

A

H2 blockers, PPIs prior to surgery, sodium citrate, reglan (good for DM, obese and pregnancy)

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37
Q

During induction/intubation, what has become a controversial intervention?

A

Cricoid pressure

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38
Q

What can increase intraop aspiration risk (a lot of things are listed)?

A

Emergent surgery, Full Stomach, Difficult airway, Inadequate anesthesia depth,, Lithotomy, Autonomic Neuropathy, Gastroparesis, DM, Pregnancy, ↑ Intraabdominal pressure, Severe Illness, Morbid Obesity

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39
Q

What hormones increase strength/frequency of GI contractions? Inhibit?

A

Increase = gastrin and motilin
Decrease = gastric inhibitory peptide

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40
Q

What is the most common cause of non-variceal upper GI bleeding? More common in men or women?

A

PUD, men, has 10% risk of perforation without treatment

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41
Q

What are the s/sx of gastric outlet obstruction? Treatment?

A

Recurrent vomiting, dehydration & hyperchloremic alkalosis,
Tx = NGT, IV hydration; Normally resolves in 72h

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42
Q

What is a potential outcome of chronic gastric outlet obstruction?

A

Repetitive ulceration & scarring may lead to fixed-stenosis and chronic obstruction

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43
Q

What are the 5 types of gastric ulcers?

A

Type I: Along the lesser curvature close to incisura; no acid hypersecretion
Type II: Two ulcers, first on gastric body, second duodenal; usually acid hypersecretion
Type III: Pre-pyloric with acid hypersecretion
Type IV: At lesser curvature near gastroesophageal junction; no acid hypersecretion
Type V: anywhere in stomach, usually seen with NSAID use

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44
Q

What types of gastric ulcers have hypersecretion of acid?

A

Type II and III

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45
Q

What type(s) of gastric ulcers are related to NSAID use?

A

Type V

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46
Q

Tx of gastric ulcers?

A

Antacids, H2 blockers, PPIs, prostaglandin analogues, cytoprotective agents

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47
Q

H. Pylori treatment?

A

Tripple therapy (2 abx and a PPI) for 14 days

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48
Q

What is Zollinger Ellison syndrome?

A

Non B cell islet tumor of the pancreas, causing gastrin hypersecretion (gastrin stimulates gastric acid secretion). Normally, gastric acid suppresses further gastrin release (negative feedback), this loop is not present in ZE syndrome. More common in men ages 30 - 50

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49
Q

What is the cancer concern with Zollinger Ellison syndrome?

A

up to 50% of patients have gastrinomas that are metastatic

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50
Q

Tx and Pre-op of Zollinger Ellison?

A

PPIs and surgical resection of gastrinoma.
Pre-op = correct lytes and increase gastric pH with meds, RSI

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51
Q

What are reversible vs irreversible causes of small bowel dysmotility?

A

Reversible: mechanical obstructions (hernia, adhesions), bacterial overgrowth, ileus, e-lyte abnormalities and critical illness
Irreversible: structural or neuropathic.
Structural = scleroderma, connective tissue disorders, IBD
Neuropathic = pseudo-obstruction in which the intrinsic and extrinsic nervous systems are altered and the intestines can only produce weak, uncoordinated contractions

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52
Q

How frequent are giant migrating complexes in the intestine?

A

6-10x a day

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53
Q

What are the 2 primary s/sx of colonic dysmotility?

A

altered bowel habits and intermittent cramping

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54
Q

What are the clinical diagnostic criteria of IBS (ROME II criteria)?

A

abdominal discomfort along with 2 of the following features:
defecation relieves discomfort
pain is associated w/abnormal frequency (> 3x per day or < 3xper week)
pain is associated with a change in the form of the stool

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55
Q

What are the 2 most common inflammatory disorders?

A

RA is first, IBD is 2nd

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56
Q

What labs reflect ulcerative colitis?

A

Increased platelets and erythrocyte sedimentation rate, decreased H/H and albumin

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57
Q

What GI complication is triggered by e-lyte disturbances?

A

Toxic megacolon. 1/2 resolve, the other 1/2 require colectomy (perforation is a dangerous complication with 15% mortality)

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58
Q

What is Crohn’s disease?

A

Acute or chronic inflammatory process that may affect any/all of the bowel.
S/sx = weight loss, fear of eating, anorexia and diarrhea (patients are afraid to eat d/t pain)

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59
Q

What differentiates early vs late stage Crohn’s?

A

Early = diarrhea
Late = chronic bowel obstruction

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60
Q

What are common secondary s/sx of Crohn’s?

A

1/3 Crohn’s pts have an additional symptoms s/a arthritis, dermatitis, kidney stones

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61
Q

IBD treatment?

A

Medical: 5-Acetylsalicylic acid (5-ASA)- mainstay for IBD *antibacterial & anti-inflammatory, PO/IV Glucorticoids during flares, Antibiotics (Rifaximin, Flagyl, Cipro), Purine analogues

Surgery = last resort, removal of more than 1/2 the small intestine can cause short bowel syndrome which requires TPN permanently

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62
Q

Where do most carcinoid tumors originate?

A

The GI tract, any portion

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63
Q

What is carcinoid syndrome?

A

Massive release of serotonin and vasoactives = flushing, diarrhea and HTN or hypotension. Puts a lot of strain on the right heart (left is spared)

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64
Q

Pre-op treatment for carcinoid syndrome?

A

Octreotide to attenuate volatile hemodynamic changes

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65
Q

How much serotonin is secreted from carcinoid tumors in the foregut, midgut and hindgut?

A

Fore = low
Mid = high
Hind = rare

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66
Q

What carcinoid tumors are most likely to cause carcinoid syndrome?

A

Midgut carcinoid tumors -> release tachykinins

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67
Q

ETOH and gallstones are the most common causes of acute pancreatitis, what are some lesser known causes?

A

Immunodeficiency syndrome and hyperparathyroidism

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68
Q

Hallmark labs of acute pancreatitis?

A

Increased serum amylase and lipase

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69
Q

Tx of acute pancreatitis?

A

Pain control, rehydrate, NPO to rest pancreas, tube feed

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70
Q

Is upper or lower GI bleed more common?

A

Upper

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71
Q

How much blood loss creates hypotension/tachycardia in a GI bleed?

A

25% loss

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72
Q

Orthostatic hypotension indicates a HCT of what?

A

Less than 30%

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73
Q

Most common population for lower GI bleed? Causes?

A

Elderly, diverticulosis, tumors, colitis

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74
Q

Treatment of an ileus?

A

Fix e-lytes, hydrate, mobilize, NGT suction, enemas. Can give 2 - 2.5 mg of neostigmine but this requires cardiac monitoring

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75
Q

Describe the trend of the GI tract recovering from anesthesia

A

Small intestine recovers first, followed by the stomach within 24 hours, then the colon 30-40 hours after

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76
Q

Do NMBDs affect the GI tract?

A

No, NMBDs only affect skeletal muscle

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77
Q

What hormone stimulates glycogenolysis and gluconeogenesis, and inhibits glycolysis?

A

Glucagon

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78
Q

List the 3 types of DM

A

DM IA = 1a diabetes is caused by a T-cell–mediated autoimmune destruction of β cells within pancreatic islets, leading to minimal or absentcirculating insulin levels

DM IB = diabetes is a rare disease of absolute insulin deficiency, which is not immune mediated

DM II = diabetes is also not immune mediated and results from defects in insulin receptors and post-receptor intracellular signaling pathways

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79
Q

When does hyperglycemia with DM I generally start to occur?

A

When 80-90% of B cell function is lost

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80
Q

What are the 3 main abnormalities with DM II?

A

↑hepatic glucose release cause by a reduction in insulin’s inhibitory effect on liver

Impaired insulin secretion

Insufficient glucose uptake in peripheral tissues

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81
Q

What are 3 causes of insulin resistance?

A

Abnormal insulin molecules
Circulating insulin antagonists
Insulin receptor defects

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82
Q

With HgbA1c, what are the values for normal, prediabetic and diabetic?

A

Normal = less than 5.7
Pre = 5.7-6.4
DM = 6.5 or greater

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83
Q

What DM II treatment has significant cardiac concerns?

A

Sulfonylureas

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84
Q

Per the DM lecture there is a chart that lists what can decrease A1C, what are the 2 initial therapy’s listed?

A

Lifestyle modifications and metform

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85
Q

How often is Insulin needed in DM I and II?

A

DM I = 100% of the time
DM II = 30%

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86
Q

What can repetitive hypoglycemic episodes lead to?

A

Hypoglycemia awareness - dangerous as the patient become desensitized to hypoglycemia

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87
Q

What types of insulin are lente and ultralente?

A

Lente = intermediate
Ultralente = long acting

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88
Q

What type of DM is DKA more common in ?

A

DM I

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89
Q

What lab values are consistent with DKA?

A

BG greater than 300, pH less than 7.3, bicarb less than 18, serum osmolarity less than 320 (pt is very dehydrated) and moderate to high ketone levels

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90
Q

DKA treatment?

A

Fluids, Insulin: Loading dose 0.1u/kg Regular + low dose infusion @ 0.1u/kg/hr, bicarb and fix e-lytes

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91
Q

HHNK or hyperglycemic hyperosmolar syndrome is fairly similar to DKA, what can differentiate the two?

A

HHNK generally has MUCH higher sugar levels and the level of acidosis is generally not as severe as DKA. HHNK generally has fewer or no ketones

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92
Q

What type of DM is more likely to cause ESRD? What can slow the progression of proteinuria?

A

DM I and an ACE/ARB can slow disease progression

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93
Q

Treatment of DM related peripheral neuropathy?

A

BG control, NSAIDs, antidepressants and anticonvulsants

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94
Q

Prevention of DM related retinopathy?

A

Glycemic control and control BP

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95
Q

What are some GI complications of DM? Treatment/management?

A

GI: ↓gastric secretions & motility, eventually causing gastroparesis
S/sx: N/V, early satiety, bloating, epigastric pain
Tx: glucose control, small meals, prokinetics

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96
Q

What is an insulinoma? Diagnosis? Preop treatment?

A

Rare, benign insulin-secreting pancreatic islet tumor
Diagnosis = Whipple triad (Hypoglycemia w/fasting, Glucose <50 w/sx and S/sx relief w/glucose)
Pre-op: Diazoxide can inhibit insulin release from B cells (other drugs: verapamil, phenytoin, propranolol, glucorticoids, octreotide)

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97
Q

What nerves are in close proximity to the thyroid gland and prone to injury with thyroid surgery?

A

The recurrent laryngeal nerves

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98
Q

What is the T4/3 ratio, and the primary proteins they bind to?

A

10:1, and bind to thyroxine-binding globulin (80%), pre-albumin (10–15%), and albumin (5–10%).

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99
Q

Describe the basic process of hormonal control of the thyroid starting from the hypothalamus

A

TRH is released -> TSH is now released form the anterior pituitary -> TSH promotes synthesis/secretion of T3/4

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100
Q

How does TSH affect thyroid gland size?

A

Increased TSH = larger gland
Less TSH = smaller or atrophied gland

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101
Q

What is the normal TSH level?

A

0.4 - 5.0 milliunits/L

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102
Q

What do thermal thyroid scans of warm vs hot vs cold indicate?

A

Warm = gland is normal
Hot = hyperfunctioning
Cold = hypofunctioning

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103
Q

The majority of hyperthyroidism pathologies are attributed to what 3 disease processes?

A

Graves disease
toxic multinodular goiter
toxic adenoma

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104
Q

What population is graves more common in?

A

Females aged 20-40, more common to female to men in a 7:1 ratio

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105
Q

First line treatment for Graves?

A

antithyroid drug, either methimazole or propylthiouracil (PTU)

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106
Q

In an emergent case, what drugs would you give to a Graves patient?

A

IV BBs, glucocorticoids, and PTU usually necessary (BBs don’t affect the abnormality but may relieve symptoms by impairing the conversion of T4 to T3)

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107
Q

What is the other name of severe hypothyroidism?

A

Myxedema

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108
Q

What are the 2 most common causes of hypothyroidism?

A

Ablation of the gland by radioactive iodine or surgery and idiopathic though likely autoimmune in nature with antibodies blocking TSH receptors

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109
Q

What autoimmune disorder creates a goiter and hypothyroidism in middle-aged women?

A

Hashimoto thyroiditis

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110
Q

What type of hypothyroidism responds to TRH with an elevation in TSH?

A

Primary hypothyroidism

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111
Q

If TRH does not cause an increase in TSH, what gland is not working?

A

Pituitary gland

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112
Q

Drug of choice to treat hypothyroid?

A

L-thyroxine (synthroid)

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113
Q

What can trigger a myxedema coma?

A

Most common in elderly women (who have had hypothyroidism for awhile) triggered by infection, trauma, cold and CNS depressants

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114
Q

What is the primary treatment of myxedema coma?

A

L-thyroxine (synthroid) or L-triiodothyronine

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115
Q

In most cases, a goiter is associated with what kind of thyroid dysfunction? Treatment?

A

A compensated euthyroid state. TX = synthroid

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116
Q

With goiters/thyroid tumors, what could indicate an increased risk of airway obstruction?

A

Preop hx of dyspnea in upright or supine position is predictive of possible AW obstruction during GA

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117
Q

What are the most serious complications from thyroid surgery?

A

Laryngeal nerve injury (bilateral injury may warrant a trach), hypoparathyroidism from inadvertent damage (look for hypocalcemia in the first 48 hours post op) and hematoma compressing the trachea (again, emergency trach)

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118
Q

What hormone stimulates the adrenal cortex to produce cortisol, which facilitates the conversion of NE to EPI in the adrenal medulla?

A

ACTH (adrenocorticotropic hormone)

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119
Q

Describe the process of the cortex to convert NE into epi

A

Hypothalamus releases CRH -> Anterior pituitary releases ACTH -> adrenal cortex converts NE into epi

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120
Q

What 2 adrenal hormones cause sodium retention and K excretion?

A

Aldosterone and cortisol

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121
Q

What is the ratio of pheochromocytoma Ne/Epi ratio?

A

85:15 NE:EPI which is inverse of normal for the body, 15:85 NE:EPI

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122
Q

DOC for pheochromocytoma?

A

Phenoxybenzamine

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123
Q

What are the 2 forms of Cushing syndrome (hypercortisolism)?

A

ACTH-dependent: high plasma ACTH stimulates the adrenal cortex to produce excessive cortisol

ACTH-independent: excessive cortisol production by abnormal adrenocortical tissue that is not regulated by CRH and ACTH

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124
Q

What is a common cause of ACTH-dependent and independent Cushing’s (hypercortisolism)?

A

Independent = small cell lung carcinoma
Dependent = benign or malignant adrenocortical tumors

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125
Q

S/sx of Hypercortisolism (Cushings)?

A

Sudden weight gain, usually central w/↑facial fat(moon face), ecchymoses, HTN, glucose intolerance,muscle wasting, depression, insomnia

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126
Q

What test can differentiate hypercortisolism (Cushing) from ectopic ACTH syndrome?

A

High-dose dexamethasone suppression test

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127
Q

What is the treatment of choice in hypercortisolism (Cushing)?

A

transsphenoidal microadenomectomy if microadenoma is resectable (if not, 85-90% resection of the anterior pituitary)

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128
Q

What is Hyperaldosteronism (Conn Syndrome)?

A

Excess secretion of aldosterone from a functional tumor (aldosteronoma) that acts independently of a physiologic stimulus

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129
Q

What nonspecific s/sx may indicate Hyperaldosteronism (Conns)?

A

HTN, hypokalemia, hypokalemic metabolic acidosis

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130
Q

What diagnostic criteria is highly suggestive of hyperaldosteronism (Conns)?

A

Spontaneous hypokalemia in presence of systemic HTN

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131
Q

Treatment of Hyperaldosteronism (Conns)?

A

Competitive aldosterone antagonist (Spironolactone), K+ replacement, antihypertensives, diuretics, tumor removal, possible adrenalectomy

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132
Q

What lab value is suggestive of hypoaldosteronism?

A

Hyperkalemia in the absence of renal insufficiency

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133
Q

Treatment of hypoaldosteronism?

A

liberal sodium intake and daily administration of fludrocortisone

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134
Q

What are the 2 types of adrenal insufficiency?

A

Primary: Adrenal glands unable to produce enough glucocorticoid, mineralocorticoid, and androgen hormones (usually d/t autoimmune adrenal destruction)

Secondary: hypothalamic-pituitary disease or suppression leading to failure in the production of CRH or ACTH

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135
Q

What test indicates adrenal insufficiency?

A

Cortisol stress test: baseline cortisol is less than 20 ug/dL and remains less than 20 after ACTH stimulation

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136
Q

Treatment of adrenal insufficiency?

A

Steroids

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137
Q

What are the 3 most common causes of primary hyperparathyroidism?

A

benign parathyroid adenoma (90%)
carcinoma (<5%)
parathyroid hyperplasia

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138
Q

Treatment of hyperparathyroidism?

A

Surgical removal of abnormal portions of gland

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139
Q

What is secondary hyperparathyroidism?

A

compensatory response of the parathyroid glands to counteract a separate disease process producing hypocalcemia.

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140
Q

What is unique about secondary hyperparathyroidism in regards to calcium levels?

A

Because secondary hyperparathyroidism is adaptive, it rarely produces hypercalcemia

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141
Q

Secondary hyperparathyroidism treatment?

A

controlling the underlying disease, normalizing phosphate levels in pts with renal disease by administering a phosphate binder

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142
Q

What is the most common cause of low or absent PTH?

A

inadvertent removal of parathyroid glands, as may occur during thyroidectomy

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143
Q

Most dangerous complication of parathyroid damage/removal?

A

Low calcium related laryngospasm

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144
Q

What is the most common cause of chronic hypocalcemia?

A

Chronic renal failure

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145
Q

Hypoparathyroidism Tx?

A

Calcium replacement, vitamin D

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146
Q

What are the 6 hormones the anterior pituitary secretes? What 2 are stored but not made by it?

A

GH, ACTH, TSH, FSH, LH, and prolactin. Vasopressin and oxytocin are stored in the AP (made by the hypothalamus)

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147
Q

What lab value indicates acromegaly? Treatment?

A

Elevated IGF-1 (insulin like growth factor). Tx = surgical excision of the adenoma, if surgery is not feasible, use a somatostatin analogue

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148
Q

Airway concerns with acromegaly?

A

Distorted facial anatomy can interfere with ventilation, large tongue/epiglottis = higher chance of airway obstruction, glottic opening may be narrowed, use of a smaller ET tube and fiber optic intubation is common

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149
Q

What is diabetes insipidus?

A

the absence of vasopressin (ADH) c/b destruction of posterior pituitary (neurogenic DI) or failure of renal tubules to respond to ADH (nephrogenic DI)

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150
Q

How do you differentiate nephrogenic vs neurogenic DI?

A

Desmopressin
In neurogenic it causes urine-concentration, but has no effect in nephrogenic

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151
Q

Neurogenic vs nephrogenic DI treatment?

A

Neuro = DDAVP
Nephro = low salt/protein diet, diuretics and NSAIDs

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152
Q

What is SIADH?

A

Some stimulus is making the body secrete more ADH (many potential causes). This causes urine to become very concentrated

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153
Q

SIADH treatment?

A

fluid restriction, salt tablets, loop diuretics & ADHantagonists-Demeclocycline

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154
Q

What is the defined value for HTN?

A

BP of 130/80 or greater of either SBP or DBP

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155
Q

What is isolated systolic, isolated diastolic and combined BP values?

A

IS = SBP greater than 130, DBP less than 80
ID = SBP less than 130, DBP greater than 80
Combined = 130/80 or greater in both

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156
Q

What is the widened pulse pressure in HTN a risk factor for?

A

CV morbidity as it correlates with vascular remodeling and stiffness

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157
Q

What are some common causes of secondary HTN in middle aged adults?

A

hyperaldosteronism, thyroid dysfunction, OSA, Cushings, and pheochromocytoma

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158
Q

What are the common causes of secondary HTN in children?

A

renal parenchymal disease or coarctation of the aorta

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159
Q

What is the common cause of secondary HTN in adolescents?

A

Coarctation of the aorta

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160
Q

Common causes of secondary HTN in young adults?

A

Thyroid dysfunction, fibromuscular dysplasia and renal parenchymal disease

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161
Q

Common causes of secondary HTN in the elderly?

A

Atherosclerotic renal artery stenosis, renal failure, hypothyroidism

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162
Q

Define resistant, controlled resistant and refractory HTN

A

Resistant = on 3+ antihypertensives at max dose
Controlled resistant = 4+ antihypertensives
Refractory = uncontrolled on 5+ BP drugs

163
Q

What e-lytes are inversely related to HTN and CVA?

A

Dietary K and Ca intake

164
Q

How much does BP drop with weight loss?

A

1 mmHg per Kg of weight lost

165
Q

How does initial HTN therapy change in black adult patients?

A

Start with a CCB or thiazide (in the other populations, ARBs/ACE are effective)

166
Q

Renal artery stenosis is a common cause of secondary HTN, how do you treat it?

A

Renal artery repair; if not feasible, start ACE/ARBs with/without diuretics (use ONLY if the stenosis is in one kidney, if both kidney vessels are stenotic you can accelerate renal failure)

167
Q

At what BP would you start considering to cancel a non-emergent surgery?

A

BP of 180/110 or greater (in general, elevated BP is not a direct reason to delay surgery without other risk factors)

168
Q

What external s/sx are associated with: a Pheo? Renal artery stenosis?

A

Pheo = flushing, sweating & palpitations
RAS = renal bruit

169
Q

Stoppage of what BP med is associated with rebound effects? Increase CV events?

A

Rebound effect = BB
Increase in CV events = CCB

170
Q

Poorly controlled HTN is frequently accompanied with_____that generally makes surgery more complicated?

A

Dehydration, especially if on a diuretic

171
Q

At what pressure is PIH (pregnancy induced HTN) showing evidence of encephalopathy and end-organ dysfunction? At what pressure is intervention needed?

A

DBP greater than 100 and immediate intervention for a BP greater than 160/110

172
Q

DOC of peripartum HTN?

A

Labetalol

173
Q

What drug is the DOC for rapid arterial dilation?

A

sodium nitroprusside

174
Q

What CCB has a very short DOC with selective arteriolar vasodilating properites?

A

Clevidipine

175
Q

What is the value that supports a diagnosis of pulmonary HTN?

A

mean pulmonary artery pressure (mPAP) greater than 20

176
Q

What is precapillary PH? Isolated Postcapillary? Combined?

A

Pre = PVR greater than 3, PAWP less than 15 or normal
Post = normal PVR, PAWP greater than 15
Combined = PVR greater than 3, PAWP greater than 15

177
Q

What is the common cause of isolated postcapillary PH?

A

increased pulmonary venous pressure, usually d/t elevated LAP c/b valve disease or LV dysfunction

178
Q

What type of PH causes a systemic to pulmonary shunt?

A

High flow PH

179
Q

What value is elevated in all 3 types of PH?

A

mPAP

180
Q

What is the math formula to calculate PVR?

A

PVR = mPAP - PAWP / CO

181
Q

What echo findings support a diagnosis of PH?

A

RA and RV enlargement with elevated peak tricuspid regurgitation velocity

182
Q

What mPAP values are indicative of mild, moderate and severe PH?

A

mild = 20 - 30 mmHg
Mod = 31 - 40 mmHg
Severe = greater than 40 mmHg

183
Q

What rare inherited mutation can cause PH?

A

A mutation in bone morphogenetic protein receptor type 2 (BMPR2)

184
Q

What makes PH hard to diagnose?

A

S/sx are vague and can only be clinically confirmed with a right heart cath. Furthermore, many cases are idiopathic without a known cause or identifiable risk factor

185
Q

What are the 3 main classes of vasodilator drugs used to treat PH?

A

Prostanoids, endothelin receptor antagonists and nitric oxide/guanylyl cyclase pathway drugs

186
Q

Of the prostanoid drugs, what is the only one shown to reduce mortality?

A

Epoprostenol

187
Q

How do prostanoids work?

A

Mimic the effect of prostacyclin to produce vasodilation while inhibiting platelet aggregation. They also have anti-inflammatory effects and may reduce proliferation of vascular smooth muscle cells

188
Q

How do Endothilin Receptor antagonists (ERAs) work?

A

The vascular endothelial dysfunction associated with PAH involves an imbalance btw vasodilating (nitric oxide) and vasoconstricting (endothelin) substances. ERAs have been shown to improve hemodynamics and exercise capacity

189
Q

How do Nitric oxide/guanylate cyclase drugs work?

A

nitric oxide produces pulmonary vasodilation by stimulating guanylate cyclase and cGMP formation in smooth muscle cells. This effect is transient because nitric oxide is quickly bound by hgb and degraded by phosphodiesterase type 5

190
Q

What drug can help nitric oxide exert its effect longer?

A

PD-5 drugs

191
Q

Chronic PH therapy is generally directed towards what drug class?

A

PD-5 inhibitors

192
Q

With suspected moderate/severe PH, what is indicated prior to surgery?

A

A right heart cath

193
Q

85-90% of PH patients are responsive to what drug intervention?

A

Inhaled nitric oxide, though other targeted therapy such as CCBs may still be beneficial

194
Q

What is the primary intraoperative goal in managing PH?

A

Primary intraoperative goal is maintaining optimal “mechanical coupling” btw the right ventricle and pulmonary circulation to promote adequate left-sided filling and systemic perfusion

195
Q

Why must interventions involving changing the hearts mechanics (inotropy, preload) with PH must be done with extreme caution?

A

Any change to myocardial oxygen supply/demand can be catastrophic in PH

196
Q

What is the hallmark of PH in terms of cardiovascular pathophysiology?

A

Increased RV afterload, leading to RV dilation, increased wall stress, and RV hypertrophy

197
Q

Why is elevated RV pressure problematic for coronary flow?

A

the elevated RV pressure leads to increased coronary flow during diastole,making the RV more vulnerable to systemichypotension, worsening the 02 supply/demandmismatch and potentially causing myocardial ischemia

198
Q

Why is thoracic surgery problematic for patients with PH?

A

It is common to collapse a lung during thoracic surgery, this can have atelectasis problems, systemic hypoxia problems, and the HPV response can further increase RV afterload

199
Q

What is the difference between pre-heart failure and heart failure classification?

A

Pre = structural changes but no s/sx
Failure = s/sx now present, like SOB and fatigue

200
Q

What are the other names of HFrEF and HFpEF?

A

HFrEF (SF) = systolic HF
HRpEF (DF) = diastolic HF

201
Q

What type of dysfunction is present in both types of HF?

A

Diastolic dysfunction

202
Q

What type of HF is more likely to have modifiable risk factors?

A

HFrEF or systolic HF

203
Q

List the incidence rates of HFpEF, HFrEF and borderline HFpEF

A

HFpEF = 52%
HFrEF = 33%
HFpEP (borderline EF, 40-49%) = 16%

204
Q

What is the primary determinant of HFpEF? HFrEF?

A

HFpEF (DF) = LV diastolic dysfunction (LVDD)
HFrEF (SF) = contractile dysfunction

205
Q

What 3 factors determine LVDD?

A

HR, loading conditions and myocardial contractility

206
Q

What type of HF is this?

A

HFrEF (note that SV is decreased, which means that EF is also decreased, the contractility slope is decreased and compliance is unchanged)

207
Q

What type of HF is this?

A

HFpEF (DF) (SV is unchanged, slope of contractility is unchanged, but the compliance of the LV is decreased)

208
Q

What must be avoided in LVDD?

A

Tachycardia - it greatly exacerbates the condition as the LV is already stiff

209
Q

What s/sx are more common to HFpEF? HFrEF?

A

pEF = paroxysmal nocturnal dyspnea, pulmonary edema, dependent edema
rEF = S3 gallop

210
Q

What type of HF is harder to diagnose?

A

HFpEF (DF) - there may be little to no s/sx at rest. Can be diagnosed via a cath

211
Q

What pressure measurements are indicative of HFpEF and a strong predictor of mortality?

A

mPCWP (wedge pressure) of greater than 15 at rest, or 25 during exercise

212
Q

What is an early radiographic sign of LV failure & pulmonary venous HTN?

A

distention of the pulmonary veins in the upper lobes of the lungs

213
Q

What are Kerley lines?

A

A honeycomb pattern reflecting interlobular edema & may be present in HF

214
Q

What are the 3 diagnostic criteria of the ACC/AHA for HFpEF?

A

HF s/sx, EF greater than 50% and evidence of LVDD

215
Q

What HF measurement criteria includes several echo related measurements alongside HF s/sx?

A

The ESC criteria

216
Q

Is an EKG sensitive to HF?

A

No because the rhythm changes are generally related to an underlying pathology to the HF (LVH, MI, conduction abnormalities)

217
Q

What are 2 important biomarkers that can help diagnose HF?

A

BNP and N-terminal pro-BNP

218
Q

Is BNP higher or lower in HFrEF or HFpEF?

A

Higher in HFrEF (SF) (d/t dilation & eccentric remodeling as BNP is related to LV end-diastolic wall stress)

HFpEF (DF) is more concentric hypertrophy with a normal-ish LV chamber size and lower LV end-diastolic wall stress

219
Q

What lab values measure the inflammatory component of CHF?

A

CRP (C-reactive protein) and GDF15 (growth differentiation factor-15)

220
Q

What does the NYHA classification focus on? ACC/AHA?

A

NYHA = degree of physical limitation
ACC/AHA = presence and severity of HF

221
Q

What are the basic treatments for HFpEF (DF) and HFrEF (SF)?

A

DF = mitigate s/sx, treat related conditions, exercise and weight loss
SF = BBs and ACE

222
Q

When are thiazide diuretics indicated in HF?

A

If the patient has poorly controlled HTN, may prevent the onset of HFpEF

223
Q

What type of HF do ACE/ARBs have the most benefit?

A

HFrEF (SF)

224
Q

what is CRT?

A

Cardiac resynchronization therapy, or biventricular pacing, this more synchronous beating may improve CO and is recommended for NYHA class III or IV, or with EF less than 5% (are you even conscious at this point???) or QRS of 120 - 150

225
Q

Why are ICDs valuable in HF patients?

A

̴~50% HF deaths are d/t sudden cardiac dysrhythmias

226
Q

Describe the basic function of an LVAD

A

A mechanical pump(s) can take over partial or total function of the damaged ventricle and facilitate restoration of normal hemodynamics and perfusion

227
Q

What is de novo HF?

A

HF presentation in a patient for the first time

228
Q

What is the leading cause of de novo HF?

A

Cardiac ischemia from coronary occlusion

229
Q

First line treatment for acute HF?

A

Diuretics (assuming hemodynamic stability), if not stable, hemodynamic support may be needed to get the patient stable first

230
Q

Are vasodilators able to improve outcomes in HF?

A

No, they do not improve outcomes

231
Q

How do vasopressin receptor antagonists (Tolvaptan) work?

A

They reduce the arterial constriction, hyponatremia, and the volume overload associated with AHF

232
Q

What are the 2 basic classes of + inotropes used in HF?

A

Catecholamines (epinephrine, norepinephrine, dopamine, dobutamine) stimulate β-receptors on the myocardium to activate adenylyl cyclase to increase cAMP

PDE-inhibitors (milrinone) indirectly increase cAMP by inhibiting its degradation

233
Q

How does IABP help modulate HF?

A

improves LV coronary perfusion by reducing LVEDP

234
Q

What ratio in an IABP is ideal for tachycardia?

A

1:2

235
Q

How much does IABP improve CO?

A

by 0.5-1 L/min

236
Q

Is a peripheral or central VAD able to provide complete ventricular decompression?

A

Central

237
Q

What type of VAD requires a sternotomy or thoracotomy for placement?

A

Central VAD

238
Q

What is the downside of a peripheral VAD?

A

Consists of a small pump & controller, which is helpful for transport, but generates heat, causing more hemolysis and lower flows

239
Q

What is the relationship of lung perfusion and ECMO? Ideal anesthetic plan?

A

ECMO reduces lung perfusion, meaning inhaled anesthesia won’t work as well, and TIVA becomes the primary choice

240
Q

With HF, what is a hard stop to doing surgery?

A

Acute decompensation, recent change in clinical status, or in de novo acute heart failure

241
Q

What are the 2 categories of cardiomyopathy?

A

Primary (confined to heart muscle)
Secondary (pathophysiologic cardiac involvement in the context of a multiorgan disorder)

242
Q

What is cardiomyopathy?

A

a group of myocardial diseasesassociated with mechanical and/or electrical dysfunction that usually exhibit ventricular hypertrophy or dilation

243
Q

What is the most common genetic CV disease?

A

Hypertrophic cardiomyopathy

244
Q

How does HCM (hypertrophic cardiomyopathy) usually present in terms of anatomical changes?

A

hypertrophy of the interventricular septum and the anterolateral free wall

245
Q

Most common cause of death in HCM?

A

Dysrhythmias

246
Q

What is unique about myocardial ischemia in HCM?

A

It is present whether or not you have CAD

247
Q

What EKG abnormalities are generally present in HCM?

A

high QRS voltage, ST-segment and T-wave alterations, abnormal Q waves, and left atrial enlargement

248
Q

What is the EF in HCM?

A

Generally greater than 80% unless in terminal/end stage

249
Q

What is the anti-arrhythmic of choice in HCM?

A

Amiodarone

250
Q

How does disopyramide help in HCM?

A

Disopyramide has a negative inotropic effect, improving LVOT obstruction and heart failure symptoms

251
Q

What are some surgical strategies in HCM?

A

Septal myomectomy
Cardiac cath w/injection to induce ischemia of the septal perforator arteries
Echocardiogram-guided percutaneous septalablation

252
Q

What is DCM (dilated cardiomyopathy)?

A

a primary myocardial disease characterized by LV or biventricular dilatation, biatrial dilation, decreased ventricular wall thickness, and systolic dysfunction w/o abnormal loading conditions or CAD

253
Q

What echo findings are consistent with DCM?

A

4 chamber dilation

254
Q

What is the primary condition leading to cardiac transplantation?

A

DCM

255
Q

What is stress cardiomyopathy?

A

“Apical ballooning syndrome”is a temporary primary cardiomyopathycharacterized by LV apical hypokinesis w/ischemic EKG changes, however the coronary arteries remain patent

256
Q

What is peripartum cardiomyopathy?

A

Rare primary cardiomyopathy, form of dilated cardiomyopathy of unknown cause that arises during the peripartum period (3rd trimester-5 months postpartum)

257
Q

Diagnostic criteria for peripartum cardiomyopathy?

A

development of HF in the period surrounding delivery
absence of another explainable cause
LV systolic dysfunction with a LVEF <45%

258
Q

What is secondary cardiomyopathy?

A

Secondary cardiomyopathies are d/t systemic diseases that produce myocardial infiltration and severe diastolic dysfunction

259
Q

Most common cause of secondary cardiomyopathy? Less common causes?

A

Common = amyloidosis
Less common = hemochromatosis, sarcoidosis, and carcinoid tumors

260
Q

What would make you suspect secondary cardiomyopathy?

A

S/sx of HF but no evidence of cardiomegaly or systolic dysfunction

261
Q

What is cor pulmonale?

A

RV enlargement (hypertrophy and/or dilatation) that may progress to right-sided heart failure

262
Q

Common causes of cor pulmonale?

A

pulmonary hypertension,myocardial disease, congenital heart disease, or any significant respiratory, connective tissue, or chronic thromboembolic disease

263
Q

What is the most common cause of cor pulmonale?

A

COPD

264
Q

What EKG changes are suggestive of cor pulmonale?

A

RA/RV hypertrophy, R. Axis deviation and rBBB

265
Q

If a PH patient has a + response to vasodilators during a heart cath with sustained response, what drug class would you start them on?

A

A CCB

266
Q

What are the 4 groups of obstructive respiratory diseases that influence anesthetic management?

A

Acute upper respiratory tract infection (URI)
Asthma
Chronic obstructive pulmonary disease (COPD)
Miscellaneous respiratory disorders

267
Q

What accounts for 95% of URI cases?

A

Infectious nasopharyngitis

268
Q

What scoring system is used to determine the risk of proceeding with surgery in URI patients?

A

COLDS

269
Q

What are some anesthetic management strategies in an URI patient?

A

Hydration, reduce secretions, limit airway manipulation, anesthetize airway, LMA > ET, intubate like you would an asthmatic patient

270
Q

What infiltrates the airway mucosa causing inflammation?

A

eosinophils, neutrophils, mast cells, T cells, B cells, and leukotrienes

271
Q

Main inflammatory mediators of asthma?

A

histamine, prostaglandin D2, and leukotrienes

272
Q

At what FEV1 value are asthma patients typically symptomatic?

A

less than 35%

273
Q

What ABG values would you expect to find in symptomatic asthma?

A

Hypocarbia and respiratory alkalosis

274
Q

During an asthma attack, at what FEV1 value is PaCO2 likely to increase?

A

Less than 25%

275
Q

What CXR findings may be present with severe asthma?

A

hyperinflation and hilar vascular congestion due to mucous plugging and pulmonary HTN

276
Q

1st line treatment in asthma? Secondary options?

A

1st line = short acting B2 agonists
Secondary: inhaled corticosteroids, daily inhaled B2 agonists, inhaled muscarinic antagonists, leukotriene modifiers, and mast cell stabilizers

277
Q

What treatment is reserved for severe asthma?

A

Systemic corticosteroids

278
Q

What is the only non-pharmacologic treat for refractory asthma?

A

Bronchial thermoplasty

279
Q

What are the 2 most common corticosteroids used to treat acute severe asthma?

A

Hydrocortisone and methylprednisone

280
Q

What FEV1, FVC and FEV1/FVC ratios indicate a risk of periop respiratory complications?

A

FEV1 or FVC less than 70% predicted or ratio of less than 65%

281
Q

When do you give stress-dose steroids in an asthma patient?

A

If they have been on systemic corticosteroids within the past 6 months

282
Q

What is the basic progression of COPD?

A

1) pathologic deterioration in elasticity or recoil within the lung parenchyma, which normally keeps the airwaysopen
2) pathologic changes that decrease bronchiolar wall structure, allowingthem to collapse during exhalation
3) increased velocity through the narrowed bronchioles, which lowers intrabronchial pressure andfavors airway collapse
4) active bronchospasm and obstruction resulting from increased pulmonary secretions
5) destruction of lung parenchyma, enlarged air sacs, and development of emphysema

283
Q

What are some common PFT findings in COPD?

A

FEV1:FVC <70%, an increased FRC & TLC, and reduced diffusing lung capacity for carbon monoxide (DLCO)

284
Q

What CXR findings suggest emphysema?

A

Hyperlucency and Bullae

285
Q

What are the 2 phenotypes of COPD?

A

Multiorgan loss of tissue (MOLT) phenotype of COPD, is associated with airspace enlargement, alveolar destruction,loss of bone, muscle, and fat tissues, and carries higher rates of lung cancer

Bronchiticphenotype is associated w/ bronchiolar narrowing and wall thickening and is usually accompanied by metabolic syndrome and cardiac disease

286
Q

What changes to A1-antitrypsin occur in COPD?

A

A1 = low, which allows trypsin to start breaking down lung tissue

287
Q

In COPD, what is the treatment of high eosinophils? What does low levels indicate?

A

High = indicate inhaled glucocorticoids
Low = increased risk of PNA

288
Q

Describe the treatment progression of COPD

A
  1. Stop smoking. 2. long-acting inhaled muscarininc-antagonists/long-acting B2 agonists, 3. inhaled glucocorticoids
289
Q

What is the minimum PaO2 goal in COPD?

A

60 mmHg or greater

290
Q

What surgical treatment may be indicated in severe refractory COPD?

A

Lung volume reduction surgery (either VATS or median sternotomy)

291
Q

What therapies can reduce postop pulmonary complications with COPD?

A

Preoperative chest physiotherapy such as deep breathing, coughing, incentive spirometry, and pulmonary physical therapy can reduce postop pulmonary complications

292
Q

What is most predictive of pulmonary complications in COPD?

A

Clinical findings such as smoking, wheezing, and productive cough are more predictive of pulmonary complications than spirometric tests

293
Q

How long should patients cease smoking to optimize surgical outcomes?

A

At least 6 weeks prior to surgery, though 8 weeks has the maximum benefits

294
Q

How long do the sympathomimetic effects of nicotine last?

A

20-30 minutes

295
Q

E1/2 time of CO?

A

4-6 hours

296
Q

When does normal immune function of the lungs recover after smoking cessation?

A

6 weeks

297
Q

What is bronchiectasis?

A

Irreversible airway dilation, inflammation and chronic bacterial infection

298
Q

Why is a bacterial superinfection so devastating in bronchiectasis?

A

Once a bacterial superinfection is established, it is nearly impossible to eradicate, and daily expectoration of sputum persists

299
Q

What is the gold standard to diagnose lung pathologies like COPD and Bronchiectasis?

A

CT

300
Q

What are the key treatments of bronchiectasis?

A

abx and chest physiotherapy to improve expectoration

301
Q

What is the basic pathophysiology of cystic fibrosis?

A

autosomal recessive disorder of the chloride channels leading to abnormal production and clearance of secretions. This decreases chloride transport, which decreases Na transport and water, which causes dehydrated viscous secretions, luminal obstructions and destruction/scarring of glands/tissues

302
Q

What can diagnose cystic fibrosis?

A

Diagnostic criteria: a sweat chloride concentration >60 mEq/L along with clinical sx (cough, purulent sputum, exertional dyspnea) or family history of the disease

303
Q

What condition is almost universal in cystic fibrosis?

A

Chronic pansinusitis and COPD is also extremely prevalent

304
Q

Basic treatments for cystic fibrosis?

A

Sx control, pancreatic enzyme replacement, 02 therapy, nutrition, prevention of intestinal obstruction

305
Q

What is the main non-pharmacologic treatment of cystic fibrosis?

A

Enhance the clearance of secretions (chest physiotherapy, High-frequency chest compression with an inflatable vest and airway oscillation devicesare alternative methods of physiotherapy). Bronchodilators may help if the patient is known to have a beneficial response to it

306
Q

What creates the thick viscosity of mucus in cystic fibrosis?

A

Neutrophils and degradation products

307
Q

What can you give to a CF patient if hepatic function is poor or exocrine pancreatic function is impaired?

A

Vitamin K

308
Q

What are some goals to optimize a CF patient for surgery?

A

Optimize PFTs, control infection, and facilitate removal of airway secretions

309
Q

What is primary ciliary dyskinesia?

A

Congenital impairment of ciliary activity in respiratory tract,epithelial cells and sperm tails and ciliated ovary ducts

310
Q

What happens in primary ciliary dyskinesia as a result of impaired ciliary activity?

A

chronic sinusitis, recurrent respiratory infections, bronchiectasis and infertility

311
Q

What is the triad of Kartagener syndrome?

A

Chronic sinusitis, bronchiectasis, and situs inversus (chest organ position is inversed)

312
Q

What is isolated dextrocardia?

A

The heart is on the other side of the body

313
Q

What type of anesthesia is preferred for primary ciliary dyskinesia?

A

RA > GA

314
Q

What are some basic interventions in dextrocardia/sinus inversus?

A

Reverse EKG positions, LIJ preference for central lines, uterine displacement should be to the right, if using a double lumen ET is needed you may need a R DLT placement

315
Q

What is bronchiolitis obliterans?

A

epithelial and subepithelial inflammation leading to bronchiolar destruction and narrowing

316
Q

What findings on CT indicate severe Bronchiolitis obliterans?

A

Air trapping and bronchiectasis

317
Q

What are some common causes of central airway obstruction?

A

Tumors, granulation from chronic infection and airway thinning from cartilage destruction

318
Q

What can cause tracheal stenosis?

A

Prolonged intubation or a tracheostomy tube

319
Q

When does tracheal stenosis become symptomatic?

A

When the lumen is less than 5 mm

320
Q

What is the most successful treatment of tracheal stenosis?

A

surgical resection & reconstruction with primary re-anastomosis

321
Q

Describe the lab values associated with euthryoid sick syndrome. Common cause?

A

Low T3/4 and normal TSH. Likely a stress response in critically ill patients, may also be surgery related

322
Q

What type of BB must be avoided in treatment of a pheochromocytoma?

A

First line treatment is alpha blockade, so you must avoid non-selective BBs. If you give a non-selective BB before an alpha blocker, the blocked vasodilatory B2 receptors results in unopposed alpha agonism leading to vasoconstriction and hypertensive crisis.

323
Q

In hyperaldosteronism (Conn syndrome), describe plasma renin activity in primary vs secondary hyperaldosteronism

A

Primary = renin activity is suppressed
Secondary = renin activity is high

324
Q

What is the difference between Addison’s disease and adrenal insufficiency?

A

In AI, there is only a glucocorticoid deficiency unlike Addison’s

325
Q

What is the basic difference between primary vs secondary adrenal insufficiency?

A

Primary = Adrenal glands unable to produce enough glucocorticoid, mineralocorticoid, and androgen hormones

Secondary = hypothalamic-pituitary dz or suppression leading to failure in the production of CRH or ACTH

326
Q

1/3 of Crohn’s disease patients have what additional s/sx?

A

Inflammatory issues; arthritis, dermatitis, kidney stones

327
Q

What common heart/BP medication is NOT a first line therapy for treatment of HTN?

A

BBs

328
Q

What changes to FEV1, FVC and FEV1/FEV ratio would you expect with RLD?

A

FEV1 and FVC are decreased, the FEV1/FEV ratio is either normal or increased

329
Q

What changes to TLC in RLD would you expect in mild, moderate and severe disease?

A

Mild = 65-80% predicted value
Moderate = 50 - 65% predicted value
Severe = < 50% predicted value

330
Q

What kind of lung issue is pulmonary edema (RLD vs obstructive)? What does it appear like on CXR?

A

RLD, and bilateral, symmetric perihilar opacities on CXR

331
Q

When does diffuse alveolar damage related to increased permeability of the capillaries occur in pulmonary edema?

A

Generally with ARDS

332
Q

What are the s/x related to cardiogenic pulmonary edema?

A

marked dyspnea, tachypnea, elevated cardiac pressures, and SNS activation that is more pronounced than that seen in pts with increased-permeability pulmonary edema

333
Q

What is the physiology of negative pressure pulmonary edema?

A

Attempted negative pressure ventilation against a closed airway (numerous causes, tumor, laryngospasm, epiglottis, OSA) that draws fluid in from the alveolar capillaries.

334
Q

Treatment of negative pressure pulmonary edema?

A

Usually self limiting, supplemental O2, if mechanical ventilation needed it is usually brief, s/sx usually clear in 12-24 hours

335
Q

What is the physiology of neurogenic pulmonary edema?

A

D/t CNS injury, a massive outpouring of SNS impulses from the injured CNS causesgeneralized vasoconstriction and blood volume shifting into the pulmonary circulation -> the now pulmonary HTN/hypervolemia can injure blood vessels in the lungs

336
Q

What is re-expansion pulmonary edema?

A

Occurs during rapid expansion of the lung (such as relief of pneumothorax) . It is related to 3 factors: the amount of air/liquid that was in the pleural space (1L or more increases the risk), duration of collapse (greater than 24 hours increases risk) and speed of re-expansion

337
Q

In drug-induced pulmonary edema, your patient has a history of cocaine use. They have pulmonary edema that has not responded to several doses of diuretics, what do you suspect has occured?

A

The drug induced pulmonary edema has progressed to diffuse alveolar hemorrhage

338
Q

Most other pulmonary edema’s involve protein concentration changes or SNS/drug induced vasoconstriction. What makes high altitude pulmonary edema unique from the other pulmonary edema’s?

A

It has vasoconstriction due to the HPV reflex, not SNS outflow

339
Q

In severe pulmonary edema, what are your Vt, RR and PEEP goals?

A

Vt = lower than normal Vt
RR = 14 - 18
PEEP = less than 30 cmH2O

340
Q

What is a common cause of chemical pneumonitis?

A

Aspirated gastric fluid -> atelectasis and leakage of intravascular fluid into the lungs causing capillary permeable pulmonary edema

341
Q

If the pt aspirated gastric content while supine, where would you expect to find evidence of the edema on CXR?

A

superior segment of the RLL

342
Q

If chemical aspiration is suspected, what steps should you take to help treat the patient?

A

Suction the oropharynx, Trendelenburg position (doesn’t prevent reflux, but can prevent gastric contents in the oropharynx from moving into the airway), start O2 and PEEP, Do not start Abx unless pt becomes symptomatic with + cultures

343
Q

What is EVALI?

A

E-cig vaping associated lung injury

344
Q

What additives in E-cigs contribute to EVALI?

A

tetrahydrocannabinol (THC), vitamin E acetate, nicotine, cannabinoids (CBD), and other oils have been associated with EVALI

345
Q

Tx of EVALI?

A

Abx, steroids and supportive care

346
Q

What is the most commonly reported finding in Covid related RLD?

A

a drop in diffusing capacity, risk of is made worse if you need to be ventilated

347
Q

What lab value is suggestive of acute respiratory failure?

A

PaO2 less than 60 with O2 supplementation without a R to L shunt with an abrupt increase in PaCO2 and decrease in pH

348
Q

What is the lab value difference in chronic vs acute respiratory failure?

A

Chronic = normal pH with elevated PaCO2
Acute = decrease in pH and elevated PaCO2

349
Q

3 goals in acute respiratory failure treatment?

A

1) a patent airway 2) hypoxemia correction 3) removal of excess C02

350
Q

Why is CPAP preferable to NC, venture mask, NRB or T-piece in maintaining oxygenation?

A

It can provide greater than 50% O2 concentrations and improve moderate to severe VQ mismatches

351
Q

What is the difference between volume cycled ventilation vs pressure limited?

A

Volume = variable pressure per breath to reach a set Vt
Pressure = variable volume until a certain pressure is hit

352
Q

What are the primary modes of volume cycled ventilation?

A

A/C (assist control) and SIMV (synchronized intermittent mandatory ventilation)

353
Q

What is the primary disadvantage of volume cycled ventilation?

A

the inability to compensate for leaks in the delivery system

354
Q

Describe A/C ventilation

A

a set RR ensures the set number of breaths even if there is no inspiratory effort. If negative pressure is sensed, a tidal volume will be delivered

355
Q

Describe SIMV ventilation?

A

allows SV, while providing a predefined minute ventilation. The circuit provides sufficient gas flow and periodic mandatory breaths that are synchronous with the pt’s inspiratory efforts

356
Q

Advantages of SIMV over A/C?

A

continued use of respiratory muscles, lower mean airway and mean intrathoracic pressure, prevention of respiratory alkalosis, and improved pt–ventilator coordination

357
Q

1 factor that predisposes a patient to nosocomial PNA? What is the usual cause of nosocomial PNA?

A

Intubation (think VAP). Most common cause is aspiration of infected/contaminated secretions around the ETT

358
Q

Treatment of nosocomial sinusitis?

A

antibiotics, replacement of nasal tubes with oral tubes, decongestants and head elevation to facilitate sinus drainage

359
Q

Common cause of hypoxia r/t mechanical ventilation? Less common?

A

Common = Atelectasis
Less common = tension PTX and PE, which are usually accompanied by HoTN

360
Q

3 main causes of arterial hypoxemia? Which of these conditions does increased FiO2 not improve it?

A

V/Q mismatch, right-to-left pulmonary shunting, and hypoventilation
FiO2 does not improve oxygenation during R/L shunting

361
Q

What are the chronic hypoxemic responses to PaO2 less than 50?

A

Carotid body–induced increase in alveolar ventilation
Hypoxic pulmonary vasoconstriction to divert pulmonary blood flow away from hypoxic alveoli
Increased SNS activity to increase COP and enhance tissue oxygen delivery

362
Q

What does a VD:VT ratio of 0.6 indicate?

A

An increase in the ratio of dead space to alveolar space (normal is 0.3)

363
Q

What should you suspect in an increase in VD:VT ratio?

A

ARF, decrease in CO or pulmonary embolism

364
Q

2 common causes of alkalemia?

A

Mechanical hyperventilation and diuretic use

365
Q

How much CO does a shunt typically have?

A

2-5%

366
Q

Basic guidelines that can help guide if someone is ready for extubation?

A
  • Vital capacity of >15 mL/kg
  • Alveolar-arterial oxygen difference of <350 cmH2O while breathing 100% 02
  • Pa02 of >60 mm Hg with an Fi02 of <0.5
  • Negative inspiratory pressure of more than −20 cmH2O
  • Normal pHa
  • RR <20
  • VD:VT of < 0.6
367
Q

3 options to help trial a vent wean?

A

SIMV, which allows progressively fewer mandatory breaths until pt breathing on their own

Intermittent trials of total removal of mechanical support and breathing through a T-piece

Use of decreasing levels of pressure support ventilation

368
Q

What mediator is responsible for the inflammation in ARDs?

A

Proinflammatory cytokines

369
Q

Long term complications of ARDs?

A

fibrosing alveolitis with persistent arterial hypoxemia and decreased pulmonary compliance

370
Q

What does proning do in accomplish in ARDs?

A

Exploiting gravity to help recruit lung units and improve V/Q matching

371
Q

What is intrinsic restrictive lung disease’s other name?

A

ILD

372
Q

Examples of ILD related pathologies?

A

Sarcoidosis
Hypersensitivity Pneumonia
Pulmonary Langerhans Cell Histiocytosis
Pulmonary Alveolar Proteinosis
Lymphangioleiomyomatosis

373
Q

What is sarcoidosis?

A

Systemic granulomatous disorder that involves many tissues, most commonly the lungs and intrathoracic lymph nodes (can affect many organ systems)

374
Q

What test may diagnose sarcoidosis?

A

Kveim skin test

375
Q

What drug class can suppress the s/sx of sarcoidosis and treat hypercalcemia?

A

Corticosteroids

376
Q

What is hypersensitivity pneumonitis?

A

diffuse interstitial granulomatous inflammation in the lungs after inhalation of dust containing fungi, spores, or animal or plant material

377
Q

Treatment of hypersensitivity pneumonitis?

A

antigen avoidance, glucocorticoids, and lung transplant

378
Q

What is pulmonary langerhans cell histiocytosis?

A

In this disease the inflammation is usually around smaller bronchioles, causing destruction of the bronchiolar wall and surrounding parenchyma. Usually affects the upper/middle zones of the lung (strong association with smoking)

379
Q

langerhans cell histiocytosis tx?

A

smoking cessation, systemic glucocorticoids, and symptomatic support

380
Q

What is Pulmonary Alveolar Proteinosis (PAP)?

A

Disease characterized by lipid-rich proteinaceous material in the alveoli

381
Q

What can cause Pulmonary Alveolar Proteinosis (PAP)?

A

May occur independently or assoc w/ chemotherapy, AIDS, or inhaledmineral dust

382
Q

What is unique about anesthesia airway management in pulmonary alveolar proteinosis (PAP)?

A

Airway mgmt during anesthesia for lung lavage includes DLT to lavage each lung separately and optimizing oxygenation during the procedure

383
Q

Pulmonary Alveolar Proteinosis (PAP) treatment?

A

whole-lung lavage under GA to remove the alveolar material and improve macrophage function

384
Q

What is Lymphangioleiomyomatosis?

A

Rare multisystem disease causing proliferation of smooth muscle of theairways, lymphatics, and blood vessels that occurs most frequently in women of reproductive age.

385
Q

Treatment of Lymphangioleiomyomatosis?

A

Sirolimus (immunosuppressive)

386
Q

What are Chronic extrinsic restrictive lung diseases?

A

Chronic extrinsic RLD is often d/t disorders of the thoracic cage that interfere with lung expansion (such as thoracic deformities, scoliosis, kyphosis etc)

387
Q

2 types of costovertebral skeletal deformities?

A

Scoliosis and kyphosis

388
Q

What is pectus carinatum?

A

Pigeon chest - sternum projects outwards, cause is unknown, usually a cosmetic concern

389
Q

Common cause of flail chest? Treatment?

A

Cause = rib fractures, Treatment = positive pressure ventilation

390
Q

What is a tension pneumothorax?

A

Gas entering the pleural space during inspiration that can’t escape during exhalation (medical emergency)

391
Q

What direction does the trachea deviate in a pneumothorax?

A

Towards the unaffected side (away from the pneumo)

392
Q

What is the relationship of pulmonary compromise to the degree of respiratory compromise during anesthesia if the patient has a mediastinal mass?

A

They do not correlate, even asymptomatic patients can develop severe airway obstruction during anesthesia

393
Q

What are the “other” nonpulmonary causes of restrictive physiology?

A

Asphyxiating thoracic dystrophy “Jeune syndrome:” autosomal recessive disorder with skeletal dysplasia and multiorgan dysfunction

Fibrodysplasia ossificans: hereditary disorder c/b a genetic variation in bone morphogenetic protein (BMP) type 1

Poland syndrome: partial or complete absence of pectoral muscles, commonly affecting one side. Pts may also have paradoxical respiratory motion due to the absence of multiple ribs

394
Q

What is the common cause of extrathoracic RLD?

A

Neuromuscular disorders; unlike thoracic cage disorders, the cough is preserved, however ventilation may be impaired when asleep (may lead to the development cor pulmonale)

395
Q

What breathing changes occur in quadripelgia?

A

The loss of SNS tone from the spinal cord causes unopposed PNS stimulation = mild bronchial constriction (anti-cholinergic bronchodilators can reverse this)

396
Q

What physical changes may cause RLD?

A

Obesity, pregnancy

397
Q

What is the major contraindication to pleural biopsy?

A

Coagulopathy

398
Q

Pneumothorax occurrence rate during diagnostic biopsy procedures?

A

Pneumothorax occurs in 5-10% of pts after transbronchial lung biopsy and in 10-20% after percutaneous needle biopsy of peripheral lung lesions

399
Q

What is mediastinoscopy?

A

Blunt dissection of the pretracheal fascia to permit biopsy of the paratracheal lymph nodes

Risk = pneumo, mediastinal hemorrhage, air embolism, RLN injury

Pressure from the scope may exert pressure on the right innominate artery, causing loss of pulses in the right arm and compromise of right carotid artery blood flow

400
Q

What levels of ACTH and CRH would you expect to find in ACTH dependent and independent cushings?

A

Ind = high plasma ACTH
Dep = low plasma ACTH and CRH

401
Q

In general, does medical management work better in HFrEF or HFpEF? Lifestyle changes?

A

Medical management works well in HFrEF (little benefit in HFpEF). Treatment = BBs, ACE-I
Lifestyle changes works well in HFpEF

402
Q

What concentration of proteins and secretory products would you expect to find in the ISF if pulmonary edema is related to increased capillary permeability? If pulmonary edema related to increased hydrostatic pressure?

A

Increased capillary permeability = increased concentration of proteins/secretory products in the ISF

Increased hydrostatic = decreased concentration of proteins/secretory products in the ISF

403
Q

What is the classic lab value presentation of sarcoidosis?

A

Hypercalcemia. Other lab markers: serum amyloid A, adenosine deaminase, and serum soluble IL2 receptor

Semester 2 TxWes (16 decks)

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