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From Flashcardlet > Patho Unit 3 > Flashcards

Patho Unit 3 Flashcards

1
Q

Ischemia

A

hypoxia due to lack of blood flow

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2
Q

PCTA

A

PerCutaneous Coronary Intervention

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3
Q

How much blood does the heart see every day?

A

6000L/day

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4
Q

Right ventricle thickness

A

.3-.5 cm

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5
Q

Left ventricle thickness

A

1.3-1.5 cm

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6
Q

Hypertrophy

A

inc. in SIZE of cells causing greater weight or ventricular thickness. Based on mass because the cells have increased in size.

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7
Q

Dilation

A

enlarged chamber

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8
Q

Cardiomegaly

A

increase in cardiac weight or size, or both (from hypertrophy and/or dilation)

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9
Q

What percent of the myocardial cells is made of mitochondria

A

23% as compared to 2% in the skeletal muscle cells.

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10
Q

How are the myocytes arranged

A

arranged circumferentially in spiral orientation.

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11
Q

Starlings law

A

as volume in the ventricle increases the stroke volume increases until the myofibrils reach optimum length, past that point then the SV starts to decrease again.

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12
Q

ANP

A

atrial naturetic peptide is released by the atria.

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13
Q

Why does diastole need to be longer than systole?

A

Because during diastole the ventricles relax and are able to refill, but more importantly the coronary arteries are only able to be perfused during diastole.

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14
Q

BNP

A

brain naturetic peptide is released by the ventricles when stretched. Levels increase significantly when a patient has CHF.

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15
Q

AV Valves

A

Mitral and Tricuspid valves

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16
Q

Semilunar Valves

A

Aortic and Pulmonic

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17
Q

Mitral Valve prolapse

A

Damage to the collagen weakens the leaflets. During systole the leaflets bulge back into the L. atrium. The murmur is heard best at the apex and is a systolic murmur.

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18
Q

Nodular calcification

A

more common in the semilunar valves.

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19
Q

Aortic stenosis

A

the cups of the aortic valve don’t open all the way d/t calcification. This is common in 80-90 year olds due to damage over time from the high pressure force.

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20
Q

Rheumatic heart disease

A

fibrotic thickening especially on the mitral valve causes stenosis causing poor drainage from the atrium to the ventricle

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21
Q

Congenital bicusp

A

increased risk of stenosis. If you see a patient that is young (even under 60 years) with aortic stenosis you have to suspect a congenital bicusp rather than tricusp.

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22
Q

Nitroglycerin

A

vasodilator that decreases blood pressure and heart rate. If a patient has an inferior wall MI (RCA supplies AV and SA nodes)- then giving them nitro will cause them to have a complete heart block.

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23
Q

SA Node blood supply

A

blood supply comes from the right coronary or the circumflex arteries.

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24
Q

AV Node blood supply

A

blood supply comes from the posterior interventricular artery (branches of the R. coornary artery in right dominant individuals)

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25
Q

Bundle of His blood supply

A

Right coronary artery

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26
Q

Bundle branches blood supply

A

Right and Left coronaries depending on whether it’s anterior or posterior.

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27
Q

Wolff-Parkinson White

A

supraventricular tachycardia that is caused by a bundle of kent (congenital) or acquired alternate pathway between atria and ventricles, causing ventricles to contract prematurely following ischemic changes.

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28
Q

Right Dominant

A

70% of people. The right coronary artery feeds the lower posterior wall of the left ventricle (via posterior descending artery)

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29
Q

Left Dominant

A

20% of people. The circumflex feeds the lower posterior wall of the left ventricle (posterior descending artery comes off circumflex a)

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30
Q

Co-dominant

A

10% of people. The Right Coronary and Circumflex arteries anastamose in the lower posterior wall of the left ventricle, so blood supply comes from both.

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31
Q

Epicardial Artery

A

the large artery on the surface of the myocardium

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32
Q

Intramural Artery

A

Smaller penetrating vessel that goes into the myocardium.

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33
Q

Endocardial ischemia

A

Ischemic damage to the interior surface of the myocardium that is supplied by the epicardial arteries. This is the area that is damaged first when a coronary artery is obstructed.

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34
Q

Transmural ischemia

A

When a coronary artery is occluded, the tissue beyond that point becomes ischemic and extends from the interior to exterior surface of the myocardium. It is full thickness ischemia.

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35
Q

inlet patch

A

a patch of gastric mucosa in the upper 1/3 or the esophagus. Can cause dysphagia, Berrett’s esophagus or adenocarcinoma.

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36
Q

Ectopic pancreatic tissue

A

pancreatic tissue found in the stomach or esophagus.

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37
Q

gastric heterotopia

A

small patches of ectopic gastric mucosa in the small bowel or colon. can causepeptic ulceration

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38
Q

Congenital duplication cysts

A

replication of the normal anatomy of the affected tissue.

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39
Q

Bronchogenic cyst

A

Broncogenic type, fluid-filled lung tissue ends up in other places in GI tract, lined by bronchial tissue (cyst of fluid filled lung tissue) needs to be removed.

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40
Q

atresia

A

assoc with polyhydraminos. Often occur at the tracheal bifurcation and is often associated with a fistula.

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41
Q

VATER

A

vertebral defects
anal atresia
tracheoesophageal fistula
renal dysplasia

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42
Q

polyhydraminos

A

excess fluid in the amniotic sac

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43
Q

imperforated anus

A

most common congenital intestinal atresia.

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44
Q

Schatzki’s ring

A

a narrowing of the lower esophagus that causes episodic dysphagia. Tx with dilation or excision. Type A = above the GE junction and covered by squamous mucosa and Type B = at the GE junction and covered by gastric mucosa

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45
Q

Plummer-Vinson syndrome

A

iron deficiency anemia, esophageal webs, mucosal lesions of the mouth and pharynx

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46
Q

esophageal ring

A

full circle or mucosa, submucosa and muscle.

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47
Q

esophageal web

A

shelf like structure of mucosa and submucosa

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48
Q

mucsularis propria

A

the muscle tissue in the esophagus that helps to move the bolus down the esophagus

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49
Q

diaphragmatic hernia

A

incomplete formation of the diaphragm allows abdominal viscera to herniate into the thoracic cavity. Webs and rings are common.

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50
Q

omphalocele

A

closure of the abdominal musculature is incomplete leaving the abdominal viscera in a membranous sac that is herniated outside of the body. 40% have other birth defects/congenital abnormalities.

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51
Q

gastroschisis

A

ventral wall defect involving all the layers of the abdominal wall leaving the abdominal viscera herniated outside the body and NOT in a membranous sac.

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52
Q

Meckel diverticulum

A

Blind outpouching of all three layers of the bowel wall. Most are in the lower colon but they can be anywhere.

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53
Q

Rule of 2s

A 
For Meckel Diverticulum:
2 ft. from iliocecal valve
2% of the population
approx. 2 in long
2x more common in males
symptoms by age 2
2 common types of ectopic tissue:  gastric and pancreatic
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54
Q

congenital hypertrophic pyloric stenosis

A

more common in males (4:1), manifests in the first 2-3 wks. of life and is assoc. with a nitric oxide synthetase deficiency that causes hyperplasia of the pyloris muscularis propia.

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55
Q

A 2 week old male is brought to the office because he has a new onset of projectile vomiting of milk (non-bilious) that is persistent. On physical exam you paplate a firm ovoid mass (“olive”) beneath the xyphoid process. What is the most likely diagnosis?

A

congenital hypertrophic pyloric stenosis

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56
Q

Hirschsprung disease

A

migration of the neural crest cells from the cecum to the rectum is arrested, so the distal intestinal segments lack Meissner submucosal and Auerbach myenteric plexus. This results in no peristalsis.

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57
Q

A baby is born and does not have its first bowel movement following birth. What is the likely diagnosis?

A

Hirschsprung disease.

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58
Q

What is the purpose of mastication?

A

break the cells, increases surface area and decreases particle size, mixes food with saliva to begin the digestion of starches (by alpha-amylase and lingual lipase), and lubricates food for swallowing.

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59
Q

Mastication innervation

A

by the 5th cranial nerve - trigeminal mandibular branch.

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60
Q

Trigeminal neuralgia

A

pain in the trigeminal nerve, exacerbated by chewing.

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61
Q

If a patient had a stroke that destroyed the left trigeminal root in the pons, what would their sx be?

A

Loss of pain and motor movement on the Left side, but when the motor cortex is involved then the loss would be on the right side.

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62
Q

Deglutination

A

swallowing

63
Q

Three stages of deglutination

A

Voluntary - initiation
Pharyngeal - passage of food from pharynx to esophagus.
Esophageal - passage of food from the esophagus to the stomach.

64
Q

Swallowing innervation

A

Afferent cranial nerves IX and X
Efferent cranial nerves IX and X
(Afferent = sensory, efferent = motor)

65
Q

If you patient presents with a brain injury and you want to assess cranial nerves IX and X you do a gag reflex test. If they gag, what does that tell you?

A

The afferent is intact, the medulla is intact and the efferent is intact. If there is no gag reflex then you worry about brainstem damage.

66
Q

What is inhibited by the medulla during swallowing?

A

The respiratory center to make sure that you don’t try to breathe and swallow at the same time.

67
Q

Primary peristalsis during the esophageal phase of swallowing, and can it occur following vagotomy?

A

the continuation of the pharyngeal peristalsis that is coordinated by the swallowing center in the medullary region. This CANNOT occur after vagotomy.

68
Q

Secondary peristalsis during the esophageal phase of swallowing, and can it occur following vagotomy?

A

if distension occurs, a wave of peristalsis is induced by the enteric nervous system and it is repeated until the bolus is cleared. This can occur after a vagotomy.

69
Q

What type of muscle makes up the upper 1/3 of the esophagus?

A

Striated muscle therefore it is innervated by the vagus.

70
Q

What type of muscle makes up the lower 2/3 of the esophagus?

A

Smooth muscle therefore it is innervated by the enteric system.

71
Q

when would a vagotomy be performed? What are the side effects.

A

When there are persistent muscle spasms or acid that is uncontrolled by medications. This is less common because PPIs are so effective now. SE include increased HR, & decreased baroreceptor reflex control.

72
Q

What is esophageal pressure like between swallows?

A

High at the sphincters and about the same as intrapleural pressure.

73
Q

What is the esophageal pressure like during swallowing?

A

UES has low pressure
Peristaltic wave has high pressure
LES and fundus have low pressure

74
Q

What kind of input do the vagus nerve and the neurotransmitter VIP have on swallowing?

A

They inhibit smooth muscle contraction (esp. on the LES and the fundus).

75
Q

nutcracker esophagus

A

lack of coordination between the longitudinal and circular smooth muscle contractions that can lead to esophageal obstruction.

76
Q

What type of obstruction is a diffuse esophageal spasm?

A

functional

77
Q

Zenker diverticulum (pharyngoesophageal diverticulum)

A

diverticulum that is located above the UES

78
Q

Traction diverticulum

A

diverticulum that is located at the midpoint of the esophagus

79
Q

Epiphrenic diverticulum

A

diverticulum that is immediately above the LES

80
Q

Achalasia (cardiospasm)

A

increased tone in the LES causes food to be retained in the esophagus so that it hypertrophies and dilates. Primary is the failure of the distal inhibitory neurons to work.

81
Q

What is the triad of achalasia?

A

Incomplete LES relaxation
Increased LES tone
Aperistalsis of the esophagus

82
Q

How can Chagas disease cause dysphasia?

A

Trypanosoma cruzi infection destroys the myenteric plexus resulting in poor peristalsis and achalasia.

83
Q

2 types of hiatal hernias

A

Sliding - the cardia is herniating above the diaphragm

Paraesophageal - a small pouch of the stomach is herniating through the diaphragm.

84
Q

Mallory-Weiss syndrome

A

longitudinal tears at the GE junction d/t severe retching or vomiting. May be deeply penetrating.

85
Q

Boerhaave syndrome

A

distal esophageal rupture that is rare but catastrophic.

86
Q

What are the causes of esophagitis?

A

GERD, candidia, herpes, CMF, pills, ulcer, alkali or acid ingestion, radiation and GVH. Many inflammatory cells (eosinophils, neutrophils or lymphocytes) within the epithelium and lamina propria.

87
Q

What is GERD?

A

increased gastric acid and/or bile in the lower esophagus because of decreased LES sphincter tone or increased abdominal pressure (obesity, pregnancy, smoking, EtOH consumption) that causes an inflammatory response, basal zone hyperplasia, elongation of the lamina propria papillae and squamous cell metaplasia.

88
Q

What is eosinophilic esophagitis?

A

increased intraepithelial eosinophils in the esophagus that causes longstanding dysphagia with solid foods, food impaction and GERD sx without improvement on therapy. Responds well to steroids and anti-interlukin drugs.

89
Q

Barrett’s esophagus and its complications

A

Long standing injury to the esophageal mucosa from gastric contents causes metaplasia to intestinal-type mucosa with goblet cells. This is the most important risk factor in the development of esophageal adenocarcinoma.

90
Q

Management of Barrett’s esophagus

A

BE w/o dysplasia: EGD every 1-3 years
BE w/low grade dysplasia: EGD every year until negative for dysplasia.
BE w/high grade dysplasia: EGD every 3 mo., resection (esophagectomy), or ablation/endomucosal resection.
BE w/intramucosal adenocarcinoma: aggressive treatment with esophagectomy or ablation/endomucosal resection depending on tumor thickness.

91
Q

Esophageal varices

A

engorged and tortuous vessels due to portal hypertension and the shunting of blood from portal to systemic venous system. Dilated vessels in the esophagus have a risk of ulceration and bleeding that can lead to death.

92
Q

You have a patient that you suspect of having varices, and you do not have the surgical support available if they start to bleed during NG tube placement, do you place the tube?

A

NO

93
Q

Assuming that you have the surgical support you need in case of severe bleeding, what type of NG tube do you use for a patient that you suspect has esophageal varices?

A

Blakemore tube - triple lumen that inflates to compress/collapse the veins to reduce bleeding risk.

94
Q

Types of esophageal Neoplasms

A

From squamous epithelium -> squamous cell carcinoma
from glandular epithelium -> adenocarcinoma
from the muscular wall -> leiomyoma

95
Q

Leiomyoma

A

the most common benign tumor that arises from smooth muscle wall that appears as a submucosal bulge on endoscopy.

96
Q

Squamous papilloma

A

hyperplastic papilliform squamous mucosa overlying a fibrovascular core that is associated with HPV.

97
Q

Squamous cell carcinoma of the esophagus

A

more common in males than females, peaks in the 5th and 6th decade, common mutations in the p53 gene, and most are in the mid esophagus (50%). Associated with EtOH, tobacco, HPV, food high in nitrates, chemical injury, polycyclic hydrocarbons (charred food) and fungus.

98
Q

Adenocarcinoma of the esophagus

A

associated with Barrett’s esophagus. Mutations in the p53 gene occurs early in the progression and this is found mostly in the distal esophagus.

99
Q

What does vagal innervation of the stomach increase?

A

secretion of mucus, HCl and pepsinogen

100
Q

What is the vascular supply to the stomach?

A

Arterial supply is segmented from the Right and Left gastric, Right and Left gastro-epiploic, short gastric and all branches of the celiac. The venous return is via the portal system.

101
Q

Gastric pits

A

shallow pits can rapidly reproduce for replacement. The gastric glands lie in these pits and produce HCl, intrinsic factor, pepsinogen I, gastrin and others.

102
Q

What do parietal cells (oxyntic) produce?

A

HCl and intrinsic factor

103
Q

What do chief cells (Zymogen) produce?

A

Pepsinogen I that is converted to pepsin in the presence of HCl.

104
Q

How do HCl and Pepsin work together?

A

HCl denatures the proteins (stretches them out) and pepsin cleaves the protein once it’s stretched.

105
Q

What do enteroendocrine cells (G Cells) produce?

A

gastrin and other endocrine products that are released into the bloodstream (NOT into the stomach!)

106
Q

What do mucous glands produce?

A

mucus and pepsinogen II

107
Q

What types of cells are prominent in the body?

A

Chief and parietal cells (acid producing cells).

108
Q

What types of cells are prominent in the fundus?

A

Mucous cells

109
Q

As you approach the pyloric sphincter, what changes in the histology occur?

A

Very few submucosal glands are seen before the sphincter and there is an increased thickness of the muscle layer.

110
Q

What things directly impact the parietal cell to produce more HCl?

A

The Vagus nerve releasing ACh, G-Cells releasing gastrin into the blood, and histamine.

111
Q

What things indirectly impact the parietal cell to produce more HCl?

A

G-Cells releasing gastrin that goes through the blood to the enteroendocrine cell, stimulating it to release histamine which then acts on the parietal cell.

112
Q

Zollinger’s syndrome

A

increased gastrin release from the pancreas (not supposed to be released from here) that causes an excess of parietal cell stimulation.

113
Q

What things inhibit parietal cells from producing HCl?

A

Somatostatin and prostaglandins inhibit the G protein system which then inhibits cAMP which in turn decreases HCl production.

114
Q

What percentage of patients don’t respond to PPIs?

A

40%

115
Q

If your patient is taking a drug that inhibits ACh and their acid is still not controlled, what other types of drugs can you try that work on another pathway?

A

H2 receptor blocker to block activation of the G-protein system, or increase somatostatin or prostaglandin in the body to inhibit the G protein system.

116
Q

Ischemic heart disease

A

imbalance between oxygen supply and oxygen demand.

117
Q

Angina pectoris

A

chest pain that is transient and reproducible, but the improvement is also predictable.

118
Q

What things increase oxygen demand?

A

Elevated systolic BP, increased ventricular volume, myocardial hypertrophy, increased HR and increased contractility.

119
Q

What things decrease oxygen supply?

A

Hypotension, decreased blood volume, vessel narrowing, and O2 delivery problem.

120
Q

What produces the symptom of pallor?

A

vasoconstriction due to the decreased cardiac output and SNS activation.

121
Q

What produces the symptom of Diaphoresis?

A

SNS activation

122
Q

What produces the symptom of dyspnea in angina pectoris?

A

decreased stroke volume causing back up into the pulmonary veins so there is transient edema and decreased O2 movement into the blood stream.

123
Q

Prinzmetal angina

A

spasm of the epicardial artery that results in no/decreased blood supply

124
Q

what is the function of beta blockers and calicum channel blockers?

A

Decrease the rate and therefore decrease the work of the heart

125
Q

What is the function of nitrates?

A

To decrease preload and afterlaod by increasing vessle diameter in the periphery therefore decreasing the work of the heart.

126
Q

MONA

A

Morphine to decrease SNS activity and therefore decrease the HR and SV, also vasodilates the periphery to decrease the afterload.
Oxygen supplement
Nitrates
Aspirin

127
Q

What is arthrectomy?

A

A small razor shaves the plaque down while suction takes up what is removed. This opens up the vessel to increase the diameter of the lumen.

128
Q

What is angioplasty?

A

ballooning of the artery to increase the diameter of the lumen.

129
Q

MI

A

persistent occlusion resulting in death of the heart muscle.

130
Q

stunned myocardium

A

the area in the periphery of the infarcted area that is edematous and dysfunctional following an MI. It is not dead and may be recovered if revascularization occurs.

131
Q

reperfusion injury

A

lactic acid, cytokines and K+ are picked up by bloodflow that returns to the infarcted tissue allowing it to be distributed throughout the body and damage other areas.

132
Q

ECG Changes with ischemia/infarction

A

Ischemia - T wave inversion or ST depression
Injury - ST elevation
Fibrosis - Q wave is pronounced downward (>1/3 the height of the R wave)

133
Q

Troponin I

A

Released from actin filaments as the myocardial tissue dies. It begins to rise 2-4 hours following myocardial injury and peaks at 48 hours.

134
Q

Complications of an MI

A

dysrhythmia, CHF, acute organic brain syndrome and ventricular wall rupture within 4-7 days post MI.

135
Q

Intra aortic balloon pump

A

can be used with cardiogenic shock to increase perfusion of the heart and brain resulting in a decreased mortality.

136
Q

Sudden cardiac death (SCD)

A

unexpected death from cardiac causes in individuals without symptomatic heart disease. Usually d/t a lethal arrhythmia.

137
Q

channelopathies

A

long QT syndromes due to problems with repolarization because of the Na/K channel.

138
Q

CHF

A

the inability to pump blood at a rate sufficient to meet the metabolic demands of the tissues or can do so only at an elevated filling pressure.

139
Q

Systolic HF

A

failure to pump blood out of the heart (low EF)

140
Q

Diastolic HF

A

failure to fill the ventricle (normal EF but low SV)

141
Q

Arginine Vasopressin (ADH)

A

causes peripheral vasoconstriction and renal fluid retention that exacerbate hyponatremia and edema.

142
Q

Natriuetic peptides (ANP and BNP)

A

protective because they decrease the preload.

143
Q

Endothelial hormones

A

endothelian vasoconstricts and is a potent growth factor for myocytes to remodel, therefore it is bad for patients with CHF.

144
Q

Endotoxin

A

from lipopolysaccharides - linked to myocyte apoptosis and release of TNF and interlukins.

145
Q

TNF alpha

A

elevated in CHF and contributes to remodeling. Also downregulates NO so it causes vasoconstriction and induces myocyte apoptosis.

146
Q

What is concentric increases in the wall thickness and what is it caused by?

A

new sarcomeres are predominantly arranged in parallel to the long axes of cells and is caused by pressure overload hypertrophy

147
Q

What is eccentric hypertrophy and what is it caused by?

A

New sarcomeres are positioned in series with the existing sarcomeres that is assocatied with volume overload hypertrophy but it increases heart weight rather than wall thickness.

148
Q

Predisposing factors to L. sided heart failure

A

ischemic heart disease, hypertension, aortic stenosis, mitral valve prolapse/regurg and myocardial disease.

149
Q

Effects of L. sided heart failure

A

Lungs: pulmonary congestion.
L Atria: chronic dilation and a. fib
Valves: S3 gallop (mitral regurg)
Brain: hypoxic encephalopathy
Kidneys: decreased urine output and pre-renal azotemia.
Systemic: fatigue, cyanosis, hypotension.

150
Q

What happens during exertion with L sided heart failure?

A

flash pulmonary edema

151
Q

Predisposing factors to R. sided heart failure

A

L sided failure, cor pulmonale

152
Q

Effects of R. sided heart failure

A

venous back up, hepato and splenomegaly, congested kidneys, subcutaneous tissue and peripheral edema, pleural and pericardial effusions in the right thoracic cavity and pericardium. Hypoxia in the brain and hypoperfusion for the kidneys.

153
Q

Diagnostic tests for HF

A

Echocardiogram and x-ray to reveal cardiothroacic ratio >0.5

From Flashcardlet (30 decks)

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