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Pathophysiology > Cardio and GI Pathology > Flashcards

Cardio and GI Pathology Flashcards

1
Q

when do you see Kerley B-lines?

A

Left sided heart failure

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2
Q

What are heart failure cells?

A

Mac’s w/ Hemosiderin in them IN the alveoli

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3
Q

Where does Right sided heart failure usually come from, and if not that….what else would it be?

A

Usually comes from Left sided failure, but can also come from Cor-pulmonale (Pulmonary HTN)

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4
Q

What kind of heart failure shows a heavy and engorged liver?

also splenomegaly

A

right sided

because of close vessel proximity of liver to right heart

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5
Q

Tetralogy of falot and TGF are what kind of shunt?

A

Right to left shunt

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6
Q

What are the 3 left to right shunts

A

ASV, VSD, AV septal defect

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7
Q

of all the L to R ASD types shunts, the persistent oval window (90% of all ASD’s) is called…?

A

Secundum ASD

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8
Q

This L to R ASD is from a defect located near AV valves

A

Primum ASD

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9
Q

This L to R ASD is from an abnormal connection of right pulmonary veins with superior vena cava of the right atrium

A

Sinus Venosum ASD

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10
Q

What are the 4 features of the Tetralagy of Fallot

A

VSD, overriding aorta, pulmonic stenosis, right vent hypertrophy.

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11
Q

if a infant has cyanosis of the lower half of the body what type of coarctation does the patient have?

A

a coarc WITH a PDA

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12
Q

If later in life a patient notices weaker lower pulses, and upper limb HTN, what type of coarc does the patient one

A

a coarc WITHOUT a PDA

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13
Q

True or false: pulmonic stenosis/atresia commonly occurs by itself?

A

no, often associated with Right vent failure, PDA, or hypoplastic right ventricle.

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14
Q

what are roth spots?

A

white lesions surrounded by hemmorage in the retina, classic sign of pericarditis

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15
Q

what are janeway lesions?

A

red painless maculopapular lesions on hands and feet

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16
Q

what are splinter hemmorages?

A

linear lesions under the neails (microemboli)

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17
Q

what are osler nodes?

A

painful nodes in hands and feet

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18
Q

what carditis will you need to meet duke criteria of : + culture of strep and/or HACEK group, staph aerus. Positive echo with valvular vegitation, and new heart murmur?

A

Endocarditis

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19
Q

Tricuspid valve prolapse leads to what heart failure?

A

right sided heart failure

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20
Q

what cardiomyopathy often leads to sudden death?

A 
hypertrophic cardiomyopathy
(vent and septal wall thickening encroaching/dysfunctioning on valves
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21
Q

this “S” sound is common in children, and in adults may indicate decompensating heart failure.

A

s3 gallop

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22
Q

this cardiomyopathy shows fibrous changes in the myocardium that decreases the ability of the chambers to enlarge (relax), and accept sufficient volume of blood.

A

restrictive pericarditis

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23
Q

rheumatic fever can cause what 2 issues in the heart?

A

aortic stenosis and mitral valve stenosis

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24
Q

marfans causes what in the heart?

A

mitral valve prolapse (weakening chordae tendinae)

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25
Q

failure to relax

A

achalasia

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26
Q

esophagus above LES dilates, mytenteric plexus may be absent, and dysfunction of inhibitory neurons and NO and VIP transmitters

A

primary achalasia

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27
Q

when achalasia may be due to chagas, polio, diabetic autonomic neuropathy, malignancy

A

seconday achalasia

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28
Q

most common type of diverticula

A

false diverticula: only mucosa and submocosa involved

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29
Q

diverticulum immediately distal to the UES

A

Zenker (will be halitosis)

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30
Q

diverticulum at midpoint of esophagus

A

traction

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31
Q

laceration of the esophagus common in excess vomiting

A

mallory-weiss syndrome (frank blood)\

varices is darker.

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32
Q

inflammatory disease from reglux of gastric content

A

reflux esophagitis

eosiniphils show up BEFORE n’phils and lymphocytes

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33
Q

what correlates with degree of reflux damage…clinical features or the duration?

A

duration

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34
Q

what type of metaplasia in reflux esophagitis

A

basal (walls thicken)

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35
Q

what type of metaplasia in barret esophagus

A

columnar (goblet cells show up)

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36
Q

red velvety mucosal patch is what disease?

A

barret esophagitis

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37
Q

patchy or entire esophagus covered by gray-white pseudomembrane

A

candidiasis esophagitis

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38
Q

punched out ulcers

A

herpes esophagitis

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39
Q

intracytoplasmic and intranuclear inclusion in the vascular epithelium in the base of the ulcers

A

CMV esophagitis

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40
Q

what are the %’s of carcinoma of the esophagus from proximal, mid, and distal?

A

20 - 50 - 30

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41
Q

tumors of the esophagus are usually

A

malignant

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42
Q

what is the cell type of esophageal carcinoma?

A

sqamos cell

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43
Q

gray white plaque thickenings (as opposed to pseudomembrane candidiasis)

A

malignant esophogeal carcinoma

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44
Q

Barret’s esophagus usually leads to what type of malignancy

A

Adrenocarcinoma (malignant tumor WITH glandular differentiation)

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45
Q

what does Adenocarcinoma look like?

A

Flat or raised patches of intact mucosa in the distal portion, either nodular or infiltrative (more aggressive)

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46
Q

Pancreatic heterotopsias

A

pancreatic tissue in the stomach

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47
Q

diaphragmatic hernia

A

development of the stomach in the thoracic cavity

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48
Q

a patient with projectile vomiting, non-bilious regurg, and visible ovoid mass in region of pyloris has

A

pyloric stenosis

49
Q

how does stress affect GI tract?

A

sympathetic outflow increases with stress

50
Q

the presence of n’phils ABOVE the basement membrane, with possible erosion and edema signifies what pathology?

A

acute gastritis

51
Q

the most common cause of chronic gastritis is…

A

H. Pylori infection

52
Q

how does H Pylori cause ulcer formation in chronic gastritis

A

H Pylori produces an enzyme urease which urea into amines with increase stomach Ph allowing further colonization of H Pylori. It then express cytotoxins that form peptic ulcers

53
Q

in chronic gastritis, how does the body respond locally

A

Nphils fight in the grandular and surface epithelial cells, lymphoid aggregates, increased mitosis in neck region of gastric glands. columnar metaplasia (same as barrets). Atrophy, dysplasia (removal of cells faster than proliferation)

54
Q

where are peptic ulcers most likely to occur

A

first portion of the duodenum

55
Q

are peptic ulcers usually solitary/diffuse, and acute/chronic?

A

solitary, and chronic

areas exposed to gastric juices

56
Q

Are peptic ulcers sharply punched out with clean appearance or the opposite?

A

peptic ulcers are sharply demarcated, and punched out, with clean appearance

57
Q

what is the clean appearance of peptic ulcers due to?

A

pepsin removing the debris

58
Q

what are the 4 layers of a peptic ulcer?

A

thin fibroid debris
n’phils with inflammator infiltrate
granulation tissue w/ monocytes
fibrous collagenous base

59
Q

how does peptic ulcer disease usually manifest?

A

pain 1-3 hours after foot, occasional first presenting symptom might be microcytic hypochromic anemia

60
Q

what is more deadly? perforation or bleeding from peptic ulcer

A

perforation

61
Q

what is more common from peptic ulcer? bleeding or perforation

A

bleeding

62
Q

what differentiates acute gastritis ulceration from peptic ulcer disease?

A

acute gastritis ulceration is caused by a strong external source such as STRESS OR NSAIDS (could be endogenous however like stress)

63
Q

stress ulcers can take the shape of..shock, burns, TBI (ICH increase), sepsis, etc….true or false?

A

True

64
Q

What is the classic presentation of acute gastric ulceration?

A

MULTIPLE lesions, small, found anywhere with no scarring, and can heal completely.

65
Q

what are two physical types of polyps that are benign?

A

sessil (no stalk)

pedunculated (stalk)

66
Q

which other type of usually benign polyp has a higher malignant potential?

A

adenomatous polyp

67
Q

what are inflammatory polyps?

A

submucosal “abscesses” with eosinophils

68
Q

What are hamartomatous polyps?

A

a bunch of hodge-podge cells that dont belong, they are benign, and dont invade anywhere.

69
Q

what do we also call hamartomatous polyps?

A

Peutz-Jergen’s polyps

70
Q

these lesions of poorly defined borders with heaped up rings are OPPOSITE to what other pathology with clean, well demarcated lesions?

A

Peptic ulcer disease

We are talking here about gastric carcinoma

71
Q

Where do gastric carcinomas commonly occur?

A

lesser curvature

BUT ulcerative lesions on greater curvature are likely malignant if you see them

72
Q

if you detect gastric carcinoma, if the prognosis good?

A

no, it is often too late.

73
Q

besides H pylori, what are some other causes of gastric carcinoma?

A

smoking, nitrates (food preservatives), water, pickled foods, etc.

74
Q

which histological subtype of gatric carcinoma shows identifiable precursor lesions?
intestinal, or diffuse?

A

Intestinal

diffuse has no precursor lesions

75
Q

What are Signet Ring Cell?

A

“Diffuse” type gastric carcinoma cells with nucleus pushed to the side. ASSUME CANCER

76
Q

early gastric carcinoma…

advanced gastric carcinoma…..

A

…stops at submucosa (better prognosis)

…extends into the muscular wall

77
Q

what is the term for growth that protrudes up into the lumen

A

exophytic

78
Q

Gastric carcinoma, and many other cancers, often metastasize to what nodule above the clavicle?

A

Virchow (sentinel) supraclavicular nodule

79
Q

A pt. presents with weight loss, anorexia, nausea, and dysphagia, she likely has

A

gastric carcinoma

80
Q

What gastric pathology shows B-Cell MALT lymphomas, and h pylori?

A

Gastric lymphomas

treat with antibiotics, kills 50% of them

81
Q

T or F: colon contains vili?

A

false

82
Q

a string like gut lumen is called a________, and occurs most often in the___________?

A

atresia, duodenum

83
Q

what is the rule of 2’s in meckel’s diverticulum?

4 of them

A

2% of population, 2 inches long, 2 feet from colon, before age 2.

84
Q

If you dont have a meissner or auerbach plexus in the (usually sigmoid) colon present, what are you?

A

toxic megacolon / Hirschsprung’s Disease

85
Q

Viruses can often shorten vili, destroy brush borders, and more by damaging mucosal epithelium, in what pathology?

A

Diarrhea

86
Q

What do we call diarrhea from ingestion of pre-formed toxins like…staph aureus, v. cholera, c. perfringens, b. cereus?

A

Enterotoxin mediated diarrhea

self limited to 1 day

87
Q

can organisms preformed or not, become sytemic causing systemic symptoms?

A

yes

88
Q

osmolarity of stool needs to only be ______mOsm/L higher than plasma to cause osmotic diarrhea

A

50 mOsm/L

89
Q

output needs to exceed what amount to be considered diarrhea

A

500ml/day

90
Q

if you see yellow pastry like diarrhea think….

A

malabsorption

91
Q

what can increase osmotic diarrhea?

A

bile salts, magnesium salts, lactulose therapy, dissacharides

92
Q

Zollinger ellison syndrome is…

A

so much HCL produced that pancreatic enzymes will not work.

93
Q

how does celiac disease work?

A

gluten triggers inflammatory response from CD8 (cytotoxic t-cells) and its “transglutaminase” antibodies to attack body’s villi. Causes malabsorption of all nutrients. Causing osmotic diarrhea.

94
Q

Shigella, salmonella, c. jejuni, and e. histolyca all cause….?

A

dysentery, the infectious type

an exudative disease

95
Q

what causes the IBS type of dysentery?

A

Presence or absence of some kind of gut flora and mediated by CD4+ T cells

96
Q

Crohn’s is a type of dysentery causing IBS that is what type of reaction from the body?

A

Delayed type hypersensetivity reaction

it occurs anywhere between mouth to anus

97
Q

It presents many findings in the gut, but namely

skip lesions….which are what?

A

several sharply demarcated areas with intact mucosa between them.

98
Q

and string sign, which is what?

A

thick and rubbery small intestine, providing for a narrowed lumen

99
Q

what is ulcerative colitis?

A

a continuous lesion in the colon starting in the rectum and travelling proximally.

100
Q

Ulcerative colitis shows psuedopolyps, which are?

A

Islands of healthy muscosa within a large ulcerative lesions.

101
Q

Vascular infarction of the bowel is reversible, until it involves what layer?

A

the muscularis layer

grade: transmural

102
Q

which type of hemmorhoid is painful?

A

external (inferior) hemmorhoids from the pudendal nerve. (superior is splanchnic)

103
Q

which is the only type of diverticulum that can be seen in the ascending colon?

A

true diverticulum

104
Q

acquired/false diverticula are comonly found where and contain how many layers of GI?

A

descending and sigmoid, containing 2 layers.

105
Q

what is a consequence of endometriosis or crohns that can lead to adhesions

A

internal herniation

106
Q

intusucception in an adult signifies presence of a…

A

tumor

107
Q

twisting of the loops of the bowel…..

A

volvulus

108
Q

how common are small intestine tumors?

A

exceedingly rare (3-5% of all GI tumors)

109
Q

TRUE OR FALSE, crohns pt’s can increase risk of small intestine tumors?

A

true

110
Q

what is the risk for malignancy in hyperplastic (smooth, nipple like lesioned) polyps in the colon?

A

virtually none

111
Q

polyps that are 1-3cm, smooth or slighly lobulated, occuring in the context of polyposis (50-100), mean what?

A

risk of malignancy

112
Q

in what condition do 5–2500 polyps develop?

A

Familial Adenomatous Polyposis

prophylactic colonectomy recommended

113
Q

When colorectal lesions appear later in life “de-novo”, this is called?

A

lynch syndrome

hereditary non-polyposis colorectal cancer syndrome

114
Q

What age bracket [10 year group] is most likely to get colorectal carcinoma?

A

60-80

115
Q

what are the risk factors for colorectal carcinoma?

A

caloric intake, refined carbs, red meat, and decreased protective micronutrients and fiber.

116
Q

in the proximal colon of colorectal carcinoma you see pedunculated polyps…what do you see in the descending colon?

A

a “napkin ring”, annular lesions with heaped up borders and beaded boundaries, with an ulcerated center.

117
Q

with endocrine cell tumors, the appendix and rectum do not mets, but what tumors in what two areas of the lower GI do?

A

Ileum and Colon

118
Q

what may be the confirmatory diagnosis for acute appendicitis?

A

elevated white count

Pathophysiology (7 decks)

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