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ACP Year 1 > Module 3 > Flashcards

Module 3 Flashcards

Respiratory and GI

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
Q

4 parts of the stomach?

A

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

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26
Q

definition

inflammation of the gastric mucosa?

A

gastritis

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27
Q

definition

a breach in the mucosa which extends through the muscularis mucosa into the submucosa or deeper?

A

ulcer

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28
Q

usual pain characteristics page 1098 Sander’s

initially periumbilical or epigastric; colicky; later becomes localized to RLQ.

A

appendicitis

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29
Q

usual pain characteristics page 1098 Sander’s

sudden or gradual onset; generalized of localized, dull or severe and unrelenting; guarding; pain on deep inspiration

A

peritonitis

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30
Q

usual pain characteristics page 1098 Sander’s

severe, unrelenting RUQ or epigastric pain; may be referred to the right subscapular area

A

cholecystitis

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31
Q

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

A

pancreatitis

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32
Q

usual pain characteristics page 1098 Sander’s

lower quadrant; increases with activity

A

pelvic inflammatory disease

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33
Q

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

A

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.

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34
Q

usual pain characteristics page 1098 Sander’s

abrupt onset in RUQ; may be referred to the shoulders

A

perforated gastric or duodenal ulcer

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35
Q

usual pain characteristics page 1098 Sander’s

abrupt, severe, spasmodic; referred to epigastrium, umbilicus

A

intestinal obstruction

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36
Q

usual pain characteristics page 1098 Sander’s

referred to hypogastrium and umbilicus

A

volvulus

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37
Q

usual pain characteristics page 1098 Sander’s

steady throbbing midline over aneurysm; may radiate to back, flank

A

leaking abdominal aneurysm

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38
Q

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

A

biliary colic

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39
Q

usual pain characteristics page 1098 Sander’s

intense; flank, extending to groin and genitals; may be episodic

A

renal calculi

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40
Q

usual pain characteristics page 1098 Sander’s

lower quadrant; referred to shoulder; agonizing with rupture

A

ectopic pregnancy

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41
Q

usual pain characteristics page 1098 Sander’s

lower quadrant, steady, increases with cough or motion

A

ruptured ovarian cyst

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42
Q

usual pain characteristics page 1098 Sander’s

intense; LUQ, radiating to left shoulder; may worsen with elevation of foot of the bed

A

splenic rupture

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43
Q

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

A

Aaron sign

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44
Q

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

A

Cullen sign

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45
Q

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

A

grey turner sign

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46
Q

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

A

kehr sign

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47
Q

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

A

Markle sign

48
Q

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

A

McBurney sign

49
Q

physical signs in patients with acute abdominal pain - page 1099 Sander’s

cessation of inspiration during examination of the RUQ; may indicate acute cholecystitis

A

Murphy sign

50
Q

physical signs in patients with acute abdominal pain - page 1099 Sander’s

pain with flexed right hip rotation; may indicate appendicitis

A

obturator sign

51
Q

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

A

Psoas (iliopsoas) sign

52
Q

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

A

Rovsing sign

53
Q

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.

A

Bronchitis

54
Q

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.

A

aspiration

55
Q

BLANK is manufactured by special cells in the gastric mucosa.

A

Hydrochloric acid

56
Q

BLANK is classified as acute or chronic, inflammation of the gastric mucosa and has various etiologies.

A

Gastritis

57
Q

What are some causes of acute gastritis?

A

Helicobacter pylori *

NSAIDS/ASA *

Alcohol *

severe stress

shock/hypotension

caustic and toxic ingestions

chron’s

idiopathic

58
Q

Gastritis

why is chronic NSAID use bad for this disease?

A

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
Q

Gastritis

why is H. pylori bad for this disease?

A

production of cytotoxic chemicals, breakdown of protective mucus, and inflammatory immune response.

60
Q

Gastritis

why is ETOH bad for this disease?

A

the direct toxic effect on the epithelium

61
Q

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.

A

peptic ulcer disease

62
Q

The acronym CPAP stands for?

A

Continuous positive airway pressure

63
Q

The acronym BIPAP stands for?

A

Bi-level positive airway pressure

64
Q

Contraindications for CPAP are what?

A

‐ 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
Q

Intrinsic PEEP (auto-PEEP) is usually about BLACK cm of water.

A

5

66
Q

when people are pursed lip breathing, what is happening to the lungs?

A

keeps the alveoli open

67
Q

Dimenhydrinate what class of drug is it?

A

Antiemetic

68
Q

Dimenhydrinate what are the indications?

A

Indications
 Symptomatic relief of nausea and drug-induced nausea and vomiting
 To potentiate the effects of analgesics
 Motion sickness

69
Q

Dimenhydrinate what are the contraindications?

A

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
Q

Dimenhydrinate what are the adverse reactions?

A

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
Q

Diphenhydramine what class of drug is it?

A

Class
Antihistamine
+
Anticholinergic

72
Q

Diphenhydramine what are the indications?

A

Indications
 Symptomatic relief of allergies, allergic re-mechanism of Actions, anaphylaxis,
acute dystonic re-mechanism of Actions due to phenothiazines, motion sickness

73
Q

Diphenhydramine what are the contraindications?

A

Contraindications
 Asthma, glaucoma, pregnancy, hypertension, narrow-angle glaucoma, infants
 Patients taking monoamine oxidase inhibitors
 Children with chronic lung disease

74
Q

Diphenhydramine what are the adverse reactions?

A

Adverse Reactions
 Sedation, hypotension, seizures, visual disturbances, vomiting, urinary retention,
palpitations, dysrhythmias, dry mouth and throat
 Paradoxical CNS excitation in children

75
Q

Diphenhydramine, what is the dose we can give to a patient on a call?

A

25 mg administered over two minutes after dilution with 10 ml of normal saline via IV repeat once if needed in 15 minutes

76
Q

Diphenhydrate, what is the dose we can give to a patient on a call?

A

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
Q

what is gastroenteritis?

A

inflammation of the stomach and intestines

78
Q

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.

A

1 = bullae

#2 = blebs

79
Q

__|—–\___

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)

A

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
Q

anatomy structures of the small intestine?

A

duodenum - 25-30 cm

jejunum - 2.5m

ileum - 3m

81
Q

anatomy of the large intestines?

A

cecum

ascending colon

transverse colon

descending colon

sigmoid colon

anal canal

82
Q

definition

BLANK is defined as that originating proximal to the ligament of Treitz, whereas lower GI bleeding originates more distally.

A

Upper GI bleeding

83
Q

pathophysiology of gastroenteritis

A

damage to mucosal gi surfaces

inflammation

hemorrhage and erosion of the mucosa and submucosa

84
Q

These are my S/Sx, what am I?

diarrhea
vomiting
diffuse abdominal pain
anorexia
fluid loss/dehydration
fever

A

gastroenteritis

85
Q

what am I?

inflammation of the large bowel/rectum

S/Sx
bloody mucoid diarrhea, cramps, colicky pain
replacing and remitting
fever and weight loss

A

ulcerative colitis

86
Q

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

A

crohn’s disease

87
Q

what am I?

anywhere
skip lesions - patchy
large intestine thick wall
malabsorption due to anorexia
liner ulcers
fistulae
poor response to surgery

A

crohn’s disease

88
Q

what am I?

colon and rectum
diffuse involvement - continuous
large intestine thin wall
no malabsorption
superficial ulcers
no fistulae
good response to surgery

A

ulcerative colitis

89
Q

what am I?

usually in the sigmoid colon, although all can be involved.

defects in the wall where blood vessels penetrate are weak spots

A

diverticulosis

90
Q

what has to happen for diverticulosis to turn into diverticularitis?

A

BRBPR is usually painless but can be massive

LLQ pain, fever, diarrhea

perforation, diffuse, peritonitis, sepsis, shock, even death

91
Q

what am I?

pathophysiology

obstruction of lumen
increased intraluminal pressure, distention, and decreased blood flow
ischemia, bacterial infection, eventual perforation and abscess

A

appendicitis

92
Q

The most common cause of Small bowel obstruction is?

A

adhesions following abdominal surgery.

93
Q

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

A

bowel obstruction

94
Q

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

A

cirrhosis

95
Q

What am I?

Cholelithiasis and alcohol abuse are the most common causes, but there are many potential etiologies.

A

pancreatisis

96
Q

Pathophysiology

autoantibodies against beta cells

complete lack of insulin

abrupt onset, young, not obese, ketosis;DKA

insulin-dependent

what am I?

A

Diabetes Mellitus 1

97
Q

resistance of tissue and organs to insulin

what am I?

A

Diabetes Mellitus 2

98
Q

pathophysiology of hypoglycemia?

why is the pt act altered?

A

lack of glucose in brain

99
Q

describe what happens in DKA

A

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
Q

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

A

DKA

101
Q

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

A

Hyperosmolar hyperglycemic state

102
Q

Which has a higher ABG glucose level?

DKA or HHS?

A

HHS

103
Q

What is histamine?

A

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
Q

What is the dose of epi in the anaphylaxis protocol for A and adolescents?

A

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
Q

What is Virchow Triad?

A

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
Q

How does a pulmonary embolism happen?

A

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
Q

What is capnography?

A

the measurement of exhaled carbon dioxide

108
Q

Presentation of pulmonary embolism?

A

classic triad
- dyspnea
- hemoptysis
- pleuritic CP

other symptoms
- cough
- fever/rigors
- syncope
-palpitations/anxiety

109
Q

ECG Findings for pulmonary embolism?

A

sinus tach
new RBBB
S1Q3T3
right axis deviation
atrial fibrillation

110
Q

Preload defintion?

A

ventricular wall tension at the end of diastole
- not blood returning to the heart

stretch on the ventricular fibres just before contraction

111
Q

afterload definition?

A

ventricular wall tension during contraction

resistance that must be overcome for forward flow

112
Q

what is cardiac output?

A

the volume of blood ejected per minute

HR x stroke volume

113
Q

what is ejection fraction?

A

the percentage of blood ejected from the left ventricle

normal is 55-75%

the heart is never empty.

30% is severe heart failure

114
Q

what is ventricular hypertrophy?

A

LV muscle is thickened inwardly

115
Q

these are my S/Sx, what am I?

dependent edema
RUQ Pain

JVD
peripheral edema
hepatomegaly

A

right-sided heart failure

116
Q

what are the causes of right-sided heart failure?

A

cardiac causes
- left-sided heart failure
- pulmonary stenosis
- RV infarction

pulmonary disease
- COPD, ARDS, infections, sarcoid

pulmonary vascular disease
- PE, pulmonary hypertension

117
Q
A

ACP Year 1 (1 decks)

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