Module 3 Flashcards

Respiratory and GI (117 cards)

1
Q

Define anaphylactoid reactions

A

An allergic reaction that is not mediated by an antigen-antibody reaction.

It is present like anaphylaxis but does not require a previous exposure to occur. For example, an anaphylactoid reaction to IV medication produces an excessive release of histamine in some patients; N-acetylcysteine (NAC), vanco, opioids, NSAID’s.

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2
Q

IgE stands for what?

A

Immunoglobulin E

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3
Q

GERD stands for what?

A

gastro-esophageal reflux disease

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4
Q

Classically, a weak BLANK has been the mechanism held responsible for GERD

A

lower esophageal sphincter

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5
Q

PEEP stands for what?

A

positive end-expiratory pressure

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6
Q

Oxygen dissociation curve

What causes a left shift?

A

decrease temperature

decreased pCO2

decreased 2,3-BPG

Decrease hydrogen ions (increased pH)

“with left shift, the tissue is left behind”

higher affinity for O2

alkalotic

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7
Q

Oxygen dissociation curve

What causes a right shift?

A

increase temperature

increased pCO2

increased 2,3-BPG

increased hydrogen ions (decreased pH)

“give oxygen to the tissue” / Bohr effect

lesser affinity for O2

acidosis

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8
Q

oxygen dissociation curve

what is the Hb saturation (%) when the partial pressure of oxygen is 60 mmHg?

A

90%

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9
Q

oxygen dissociation curve

what is the Hb saturation (%) when the partial pressure of oxygen is 45 mmHg?

A

75%

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10
Q

Esophagus is how long?

A

25-30 cm

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11
Q

What are the two main bands of the Esophagus?

A

upper 1/3rd is skeletal

distal 2/3rd’s is smooth

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12
Q

These are my symptoms; what am I?

retrosternal burning pain may radiate to the neck or jaw

regurgitation, dysphagia, water-brash (hypersalivation)

worse with bending over, lying, or large meals

relieved with liquids, antacids, standing or sitting

A

GERD

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13
Q

What are some risk factors for GERD?

A

weak/relaxed LES

pregnancy, obesity

Drugs - calcium channel blockers and beta blockers (class 4 and 2)

hiatus hernia

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14
Q

What are some risk factors for esophagitis?

A

GERD

corrosive/irritants - draino, pine sole

infectious - HIV, AIDS, DM, chemo
- Candida (yeast infection), HSV (herpes)

Radiation/chemotherapy- to nearby structures

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15
Q

These are my symptoms; what am I?

odynophagia

retrosternal aching burning stabbing CP

thrush

oral lesions - herpes

GERD

A

esophagitis

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16
Q

esophageal obstruction

BLANK is the most common cause of food impaction.

A

meat

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17
Q

these are my symptoms; what am I?

painless, massive hematemesis, melena

hemodynamic instability

stigmata of chronic liver disease

A

esophageal varices

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18
Q

these are my symptoms; what am I?

hematemesis, melena

Hx vomiting/retching; often ETOH

CP/epigastric pain

A

Mallory Weiss tear

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19
Q

explain pathophysiology of me

mucosal tears at the gastric esophageal junction

wrenching / vomiting with non-relaxed LES

A

Mallory Weiss tear

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20
Q

explain pathophysiology of me

portal hypertension (cirrhosis)

dilated tortuous veins in the submucosa

hemorrhoids or varicose veins

A

esophageal varices

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21
Q

Somatic pain?

Visceral pain?

Referred pain?

A

Somatic = specific

visceral = diffuse

referred = felt elsewhere

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22
Q

pathophysiology of me?

(1) Helicobacter pylori

(2) nonsteroidal anti-inflammatory drug use such as aspirin

(3) hypersecretion of HCl, as occurs in Zollinger–Ellison syndrome, a gastrin-producing tumour, usually of the pancreas.

A

peptic ulcer

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23
Q

most common cause of lower gi bleeding?

A

upper gi bleeding

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24
Q

layers of the stomach from the innermost to outermost?

A

mucosa

submucosa

muscularis

serosa

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25
4 parts of the stomach?
cardia - attaches to the esophagus - cardiac sphincter is the other side of LES fundus body - the largest portion of the stomach antrum - attaches to small bowel
26
definition inflammation of the gastric mucosa?
gastritis
27
definition a breach in the mucosa which extends through the muscularis mucosa into the submucosa or deeper?
ulcer
28
usual pain characteristics page 1098 Sander's initially periumbilical or epigastric; colicky; later becomes localized to RLQ.
appendicitis
29
usual pain characteristics page 1098 Sander's sudden or gradual onset; generalized of localized, dull or severe and unrelenting; guarding; pain on deep inspiration
peritonitis
30
usual pain characteristics page 1098 Sander's severe, unrelenting RUQ or epigastric pain; may be referred to the right subscapular area
cholecystitis
31
usual pain characteristics page 1098 Sander's dramatic, sudden, excruciating LUQ, epigastric, or umbilical pain; may be present in one or both flanks; may be referred to the left shoulder
pancreatitis
32
usual pain characteristics page 1098 Sander's lower quadrant; increases with activity
pelvic inflammatory disease
33
usual pain characteristics page 1098 Sander's epigastric, radiating down the left side of the abdomen, especially after eating; may be referred to their back
diverticulitis The left side because it most commonly affects the sigmoid colon (LLQ). Asian decent is most common on RLQ. Cramping may cause referred pain to patients lower back.
34
usual pain characteristics page 1098 Sander's abrupt onset in RUQ; may be referred to the shoulders
perforated gastric or duodenal ulcer
35
usual pain characteristics page 1098 Sander's abrupt, severe, spasmodic; referred to epigastrium, umbilicus
intestinal obstruction
36
usual pain characteristics page 1098 Sander's referred to hypogastrium and umbilicus
volvulus
37
usual pain characteristics page 1098 Sander's steady throbbing midline over aneurysm; may radiate to back, flank
leaking abdominal aneurysm
38
usual pain characteristics page 1098 Sander's episodic, severe, RUQ, or epigastrium lasting 15 minutes to several hours; may be referred to subscapular area, especially right
biliary colic
39
usual pain characteristics page 1098 Sander's intense; flank, extending to groin and genitals; may be episodic
renal calculi
40
usual pain characteristics page 1098 Sander's lower quadrant; referred to shoulder; agonizing with rupture
ectopic pregnancy
41
usual pain characteristics page 1098 Sander's lower quadrant, steady, increases with cough or motion
ruptured ovarian cyst
42
usual pain characteristics page 1098 Sander's intense; LUQ, radiating to left shoulder; may worsen with elevation of foot of the bed
splenic rupture
43
physical signs in patients with acute abdominal pain - page 1099 Sander's pain in the chest or epigastrium when the McBurney point is palpated, a possible sign of appendicitis
Aaron sign
44
physical signs in patients with acute abdominal pain - page 1099 Sander's periumbilical blue discoloration; may indicate retroperitoneal hemorrhage, pancreatic hemorrhage, or rupture of an AAA
Cullen sign
45
physical signs in patients with acute abdominal pain - page 1099 Sander's blue discoloration of the flanks; may indicate retroperitoneal hemorrhage, pancreatic hemorrhage, or AAA rupture
grey turner sign
46
physical signs in patients with acute abdominal pain - page 1099 Sander's severe left shoulder pain; may indicate splenic rupture or rupture of an ectopic pregnancy
kehr sign
47
physical signs in patients with acute abdominal pain - page 1099 Sander's pain when dropping from standing on the toes to the heels with a jarring landing; may indicate localized peritonitis due to acute appendicitis
Markle sign
48
physical signs in patients with acute abdominal pain - page 1099 Sander's tenderness midway between the anterior-superior iliac spine and the umbilicus; may indicate acute appendicitis
McBurney sign
49
physical signs in patients with acute abdominal pain - page 1099 Sander's cessation of inspiration during examination of the RUQ; may indicate acute cholecystitis
Murphy sign
50
physical signs in patients with acute abdominal pain - page 1099 Sander's pain with flexed right hip rotation; may indicate appendicitis
obturator sign
51
physical signs in patients with acute abdominal pain - page 1099 Sander's pain when raising a straight leg against resistance; may indicate appendicitis, right-side AAA
Psoas (iliopsoas) sign
52
physical signs in patients with acute abdominal pain - page 1099 Sander's pain in RLQ of the abdomen when the LLQ is palpated; possible sign of appendicitis
Rovsing sign
53
BLANK is a commonly encountered, self-limited, infection-producing inflammatory change within the larger airways. It is often caused by one of the following: influenza syncytial virus, or coronavirus. The predominant cough may be productive and can last up to three weeks. Sputum purulence usually indicates sloughed inflammatory airway cells and, taken alone, does not indicate a bacterial etiology.
Bronchitis
54
BLANK is the active inhalation of any non-gaseous foreign substances into the lung. It often occurs when fluids such as vomitus, saliva, blood, or neutral liquids, enter the airway.
aspiration
55
BLANK is manufactured by special cells in the gastric mucosa.
Hydrochloric acid
56
BLANK is classified as acute or chronic, inflammation of the gastric mucosa and has various etiologies.
Gastritis
57
What are some causes of acute gastritis?
Helicobacter pylori * NSAIDS/ASA * Alcohol * severe stress shock/hypotension caustic and toxic ingestions chron's idiopathic
58
Gastritis why is chronic NSAID use bad for this disease?
Nonsteroidal anti-inflammatory drugs inhibit prostaglandin synthesis, thereby decreasing mucus and bicarbonate production and mucosal blood flow, allowing ulcer formation. HCO3 and mucus protect the stomach
59
Gastritis why is H. pylori bad for this disease?
production of cytotoxic chemicals, breakdown of protective mucus, and inflammatory immune response.
60
Gastritis why is ETOH bad for this disease?
the direct toxic effect on the epithelium
61
These are my S/Sx, what am I? Burning epigastric pain The pain also may be described as sharp, dull, an ache, or an “empty” or “hungry” feeling. Pain may be relieved by milk, food, or antacids, presumably due to buffering and/or dilution of acid, or vomiting. Pain recurs as the gastric contents empty, and the recurrent pain may classically awaken the patient at night or early morning.
peptic ulcer disease
62
The acronym CPAP stands for?
Continuous positive airway pressure
63
The acronym BIPAP stands for?
Bi-level positive airway pressure
64
Contraindications for CPAP are what?
‐ Respiratory/cardiac arrest ‐ Agonal respirations ‐ Facial trauma or burn ‐ Unresponsive to speech ‐ Inability to maintain a patent airway ‐ Vomiting ‐ Active upper GI bleed ‐ Suspected Pneumothorax ‐ Systolic BP less than 90 ‐ Unable to sit up
65
Intrinsic PEEP (auto-PEEP) is usually about BLACK cm of water.
5
66
when people are pursed lip breathing, what is happening to the lungs?
keeps the alveoli open
67
Dimenhydrinate what class of drug is it?
Antiemetic
68
Dimenhydrinate what are the indications?
Indications  Symptomatic relief of nausea and drug-induced nausea and vomiting  To potentiate the effects of analgesics  Motion sickness
69
Dimenhydrinate what are the contraindications?
Contraindications  Glaucoma  Chronic lung disease  Difficulty in urination secondary to prostatic hypertrophy  Comatose states  Patients who have received a large amount of depressants including alcohol.
70
Dimenhydrinate what are the adverse reactions?
Adverse Reactions  Drowsiness - CNS depressant effects may be potentiated when used in conjunction with alcohol  Dizziness  Dry mouth, excitement and nausea have been reported
71
Diphenhydramine what class of drug is it?
Class Antihistamine + Anticholinergic
72
Diphenhydramine what are the indications?
Indications  Symptomatic relief of allergies, allergic re-mechanism of Actions, anaphylaxis, acute dystonic re-mechanism of Actions due to phenothiazines, motion sickness
73
Diphenhydramine what are the contraindications?
Contraindications  Asthma, glaucoma, pregnancy, hypertension, narrow-angle glaucoma, infants  Patients taking monoamine oxidase inhibitors  Children with chronic lung disease
74
Diphenhydramine what are the adverse reactions?
Adverse Reactions  Sedation, hypotension, seizures, visual disturbances, vomiting, urinary retention, palpitations, dysrhythmias, dry mouth and throat  Paradoxical CNS excitation in children
75
Diphenhydramine, what is the dose we can give to a patient on a call?
25 mg administered over two minutes after dilution with 10 ml of normal saline via IV repeat once if needed in 15 minutes
76
Diphenhydrate, what is the dose we can give to a patient on a call?
Administer DIMENHYDRINATE 25 mg IV over two minutes after dilution with 10 ml of normal saline. If the patient develops nausea and/or vomiting, this may be repeated in 15-30 minutes if required. An additional dose of 25-50 mg IV may be repeated every 6 hours as needed.
77
what is gastroenteritis?
inflammation of the stomach and intestines
78
BLANK #1 (deflated, air-filled spaces within the lung parenchyma) often develop in patients with emphysema from the destruction of alveolar walls. BLANK #2 (air-containing spaces between the lung and visceral pleura) also may develop. When BLANK #1 collapse or BLANK #2 rupture, they increase the diffusion defect seen in these patients and also can lead to pneumothorax.
#1 = bullae #2 = blebs
79
__|-----\___ The graphic representation of ETCO2 is displayed as a waveform (measured in mmHg) on a capnograph throughout the respiratory cycle. Each waveform on the capnograph consists of four phases. Phase 1 (A-B) Phase 2 (B-C) Phase 3 (C-D) Phase 4 (D-E)
Phase 1 (A-B) Respiratory baseline - represents air that is exhaled from the conducting airways with little to no detectable carbon dioxide, because this air did not participate in gas exchange. Phase 2 (B-C) expiratory upstroke - represents the mixture of air from the anatomic dead space and alveolar gas. It is here that carbon dioxide concentration begins to rise. Phase 3 (C-D) expiratory alveolar plateau - represents a plateau as alveolar gas is exhaled (alveolar plateau). Phase 4 (D-E) inspiration down stroke - represents inspiration (inspiration washout), where the end-tidal volume (the peak concentration) and then there is a sharp decline in carbon dioxide concentration.
80
anatomy structures of the small intestine?
duodenum - 25-30 cm jejunum - 2.5m ileum - 3m
81
anatomy of the large intestines?
cecum ascending colon transverse colon descending colon sigmoid colon anal canal
82
definition BLANK is defined as that originating proximal to the ligament of Treitz, whereas lower GI bleeding originates more distally.
Upper GI bleeding
83
pathophysiology of gastroenteritis
damage to mucosal gi surfaces inflammation hemorrhage and erosion of the mucosa and submucosa
84
These are my S/Sx, what am I? diarrhea vomiting diffuse abdominal pain anorexia fluid loss/dehydration fever
gastroenteritis
85
what am I? inflammation of the large bowel/rectum S/Sx bloody mucoid diarrhea, cramps, colicky pain replacing and remitting fever and weight loss
ulcerative colitis
86
what am I? inflammation anywhere in the GI tract? patchy but most common in small and large bowel S/Sx diarrhea, cramping abdominal pain, fever, weight loss 50% have Melena relapsing and remitting course
crohn's disease
87
what am I? anywhere skip lesions - patchy large intestine thick wall malabsorption due to anorexia liner ulcers fistulae poor response to surgery
crohn's disease
88
what am I? colon and rectum diffuse involvement - continuous large intestine thin wall no malabsorption superficial ulcers no fistulae good response to surgery
ulcerative colitis
89
what am I? usually in the sigmoid colon, although all can be involved. defects in the wall where blood vessels penetrate are weak spots
diverticulosis
90
what has to happen for diverticulosis to turn into diverticularitis?
BRBPR is usually painless but can be massive LLQ pain, fever, diarrhea perforation, diffuse, peritonitis, sepsis, shock, even death
91
what am I? pathophysiology obstruction of lumen increased intraluminal pressure, distention, and decreased blood flow ischemia, bacterial infection, eventual perforation and abscess
appendicitis
92
The most common cause of Small bowel obstruction is?
adhesions following abdominal surgery.
93
what am I? obstipation N/V, anorexia cramping abdominal/epigastric pain, waxes and wanes distention high-pitched "tinkling" bowel sounds diffuse tender abdomen +/- peritoneal signs if perforation/ischemia
bowel obstruction
94
what am I? skin - jaundice, spiders angiomas, palmar erythema, bruising breathe - fetor hepaticus trunk - ascites, gynecomastia, testicular atrophy extremities - edema, muscle atrophy, asterixis, palmar erythema
cirrhosis
95
What am I? Cholelithiasis and alcohol abuse are the most common causes, but there are many potential etiologies.
pancreatisis
96
Pathophysiology autoantibodies against beta cells complete lack of insulin abrupt onset, young, not obese, ketosis;DKA insulin-dependent what am I?
Diabetes Mellitus 1
97
resistance of tissue and organs to insulin what am I?
Diabetes Mellitus 2
98
pathophysiology of hypoglycemia? why is the pt act altered?
lack of glucose in brain
99
describe what happens in DKA
The shift from carbohydrate metabolism to fat metabolism results in the formation of ketone bodies (ketoacids). Ketone bodies are acids, so their continuous production leads to metabolic acidosis. Often the respiratory system at least partially compensates for the acidosis; this is Kussmaul respirations. The kidney's ability to clear the acid is overwhelmed by the continuous production of ketone bodies, such that profound acidosis eventually occurs. This acidosis, along with the usually severe dehydration (diuresis) can lead to death. Hyperkalemia, secondary to acidosis, also leads to cardiac dysrhythmias, some of which may be lethal.
100
These are my S/Sx, what am I? polydipsia, polyuria, polyphagia visual blurring, weakness N/V, abdominal pain tachycardia, Kussmaul's respirations, dry skin and mucus membranes hypotension decreased LOC
DKA
101
pathophysiology, what am I? mostly elderly pts gradual onset Insufficient insulin to prevent hyperglycemia enough insulin to prevent ketosis triggering stress (infection, MI) profound dehydration from prolonged glycosuria/volume loss
Hyperosmolar hyperglycemic state
102
Which has a higher ABG glucose level? DKA or HHS?
HHS
103
What is histamine?
Histamine is a protein released by mast cells and basophils. It promotes vascular permeability and causes dilation of capillaries and venules and contraction of smooth muscle in the GI tract and bronchial tree. An associated increase in gastric, nasal, and lacrimal secretions also occurs, resulting in tearing and rhinorrhea. The increased capillary permeability allows plasma to leak into the interstitial space, thereby reducing the amount of intravascular volume available for the heart to pump. The profound body-wide vasodilation further reduces cardiac preload, which in turn decreases stroke volume and cardiac output. Collectively, these responses lead to flushing, urticaria, angioedema, and hypotension. Although the onset of action for histamine is rapid, its effects are short-lived, because they are quickly broken down by plasma enzymes.
104
What is the dose of epi in the anaphylaxis protocol for A and adolescents?
Adult = 1:1000 IM 0.3 mg q 10 minutes if: 1) Symptoms or signs of upper airway obstruction not improved 2) Signs of shock not improved 3) Severe bronchospasm still present ACP If the patient’s condition deteriorates despite two doses of IM EPINEPHRINE ¤ Administer EPINEPHRINE, (1:10,000) 0.1 mg IV slowly over 5 minutes Adolescents = 1:1000 IM 0.3 mg q 10 minutes if: 1) Respiratory compromise 2) Reduced BP or signs of end-organ dysfunction 3) Gastrointestinal symptoms ACP If the patient’s condition deteriorates despite two doses of IM EPINEPHRINE ¤ Administer EPINEPHRINE, (1:10,000) 0.1 mg IV slowly over 5 minutes
105
What is Virchow Triad?
factors contribute to clot formation; hypercoagulability, stasis, and vessel injury. Status - Extended travel, Prolonged bed rest, Obesity, Advance age, Varicose veins Venous injury/trauma - Surgery of the thorax, abdomen, pelvis, or legs, Burns, Long bone fractures, Fractures of the pelvis or legs Hypercoagulability - Malignancy (especially with metastasis), Use of oral contraceptives, Pregnancy, Autoimmune disorders, Congenital or acquired coagulation disorders
106
How does a pulmonary embolism happen?
It most often is caused by migration of a thrombus from the large veins of the lower extremities, but it also can occur as a result of fat, air, sheared Venous catheters, amniotic fluid, or tumor tissue. The clot or ambulous dislodges and travels through the venous system to the right side of the heart. From there, it travels to the pulmonary arteries, extracting the blood supply to a section of the lung.
107
What is capnography?
the measurement of exhaled carbon dioxide
108
Presentation of pulmonary embolism?
classic triad - dyspnea - hemoptysis - pleuritic CP other symptoms - cough - fever/rigors - syncope -palpitations/anxiety
109
ECG Findings for pulmonary embolism?
sinus tach new RBBB S1Q3T3 right axis deviation atrial fibrillation
110
Preload defintion?
ventricular wall tension at the end of diastole - not blood returning to the heart stretch on the ventricular fibres just before contraction
111
afterload definition?
ventricular wall tension during contraction resistance that must be overcome for forward flow
112
what is cardiac output?
the volume of blood ejected per minute HR x stroke volume
113
what is ejection fraction?
the percentage of blood ejected from the left ventricle normal is 55-75% the heart is never empty. 30% is severe heart failure
114
what is ventricular hypertrophy?
LV muscle is thickened inwardly
115
these are my S/Sx, what am I? dependent edema RUQ Pain JVD peripheral edema hepatomegaly
right-sided heart failure
116
what are the causes of right-sided heart failure?
cardiac causes - left-sided heart failure - pulmonary stenosis - RV infarction pulmonary disease - COPD, ARDS, infections, sarcoid pulmonary vascular disease - PE, pulmonary hypertension
117