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Pathophysiology 2200 > mod 7 > Flashcards

mod 7 Flashcards

1
Q

What does GERD stand for? Development and most frequent clinical manifestation.

A

gastroesophageal reflux disease.

development: stomach returns its contents to the esophagus - due to relaction of the lower esophageal sphincter.
- can be spontaneous, neutralized cleared in minis - esophagitis can occur.

longterm: fibrosis and pancreatic lesions
manifestations- increase gastric volume and pressure

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2
Q

Dyspepsia

A

upset stomach

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3
Q

Gastroparesis

A

slowing of food movement in the stomach “paresis” = slowing.

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4
Q

What increases the likely-hood of GERD?

A

infancy - positional + reduced sphincter (colic)
^ intra-abdominal pressure (obesity + prego)
smoking
foods that relaxes LES (eg. after dinner, coffee, alcohol and fats)
people with lupus have more issues

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5
Q

what is a peptic ulcer?

A

A break in the protective mucosal lining of the lower esophagus, stomach or duodenum.
could be multi, acute, chronic, superficial or deep.

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6
Q

Describe melena

A

black foul smelling stool from digestion - has blood.

“coffee grounds” lower gi

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7
Q

describe hematemesis + complications

A

vomiting of blood - lower gi tract

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8
Q

what are the 3 other complications of peptic ulcers

A

hemorrhage: causes hematemesis or melena
perforation: ulcer erodes thru call to the peritoneum.
penetration: same, not erosion into another organ (eg. liver)

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9
Q

Identify and describe the pathophysiology of peptic behind the effects of the two risk factors that develop peptic uclers

A

Helicobacter Pylori - passes through the mucosal lining of the stomach.
- neutralizes the gastric juices in the stomach, causes the thick mucosal lining
to “liquify” and then it is able to penetrate through.

NSAIDS - interfere with prostaglandin synthesis
- prostaglandins inhibit acid secretion + stimulate mucus + bicarbonate secretions. The NSAIDS can decrease the prostaglandins synthesis and decrease these effects which can lead to the acid touching the layer, causing ulceration.

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10
Q

Two similarities between duodenal ulcers and gastric ulcers?

A

Gastric: occurs in the stomach common in older folks (55-65) 1/4

  • h.pylori and NSAIDS (chronic)
  • more chronic than duodenal ulcers and duration.
  • pain immediate after eating

Duodenal: duodenum

  • greater frequency w/ other types (young folks, most common in male)
  • mainly h.pylori and NSAIDS
  • pain 2-3 hours after eating
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11
Q

What are the main treatments for peptic ulcers?

A

antibiotics
reduce acidity
- antacids
- proton pump inhibitor (interferes with H_ secretion from the parietal cells)
- h2 receptor antagonists (block action of histamine which HCL secretes)
minimally invasive surgical resection of uclers.

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12
Q

Two diseases that make up inflammatory bowel disease

A

Ulcer Colitis

Chron’s disease

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13
Q

Typical ages of ulcer colitis vs crohn’s

A
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14
Q

Regions of the bowel affected by ulcer colitis vs crohn’s

A

ulcer: large intestine

crohn’s: anywhere in the gi tract (mouth to anus)

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15
Q

The appearance of inflammed tissues: crohn’s vs ulcer colitis

A

ulcer: inner most layer

crohn’s: any part

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16
Q

risk factors of crohn’s

A 
NSAIDS
obesity
smoking
age
ethnicity
genetics
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17
Q

risk factors of ulcer colitis

A

smoking
contraceptive
being white

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18
Q

clinical manifestations of crohn’s

A
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19
Q

clinical manifestations of ulcer colitis

A
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20
Q

define tenesmus

A

feeling of passing stool even though it is empty

21
Q

toxic megacolon

A

defines seriousness of a condition

22
Q

common cause of croup?

A

laryngealtrachbronchitis ltb

23
Q

What is retraction

A

Funky looking dents from ab cavity mf

24
Q

What is celiac disease?

A

A malabsorbptive disease where the mucosa fails to absorb digestive nutrients
- sprue or gluten-sensitive enteropathy

25
Q

What is the development of celiac disease

A

T cell mediated immune disorder

  • person with it can show an intense immune reaction to gluten protein of cereal grains.
  • The inflammation brought on by immune reaction damages small intestinal villous epithelium, interfering with the absorption of macro and mico-nutrients.

Appears early on during infantry, can develop in older adults.

26
Q

clinical manifestations of celiac disease

A 
failure to thrive
ab pain
diarrhea w/fatty acids
malabsorption of nutrients leading to
  - ostoporosis, seizures, anemia, short statue, pregnancy

primary: remove gluten from diet

27
Q

Liver disorders - define portal hypertension and its causes

A

abnormally high bp in the portal venous system
- caused by disorders that obstruct blood flow, thru portal or vena cava and thrombosis of hepative beings, severe r sided heart failure, alcoholic cirrhosis etc.

It can result in complications such as ascites, splenomegaly _ portosystemic shunts w/ accompany esophageal varices

28
Q

What is ascites and two causes

A

It is accumulation of fluid in the perineal cavity
caused by portal hypertension and release serum protein production by the liver, decrease osmotic pressure of capillaries, more retention of fluid in tissues that seeps into the peritoneal cavity fluid in abdominal cavity pushes on the diaphragm - causes breathing issues.

29
Q

how can ascites be treated and what could happen if moved too quickly

A

by paracentesis (drainage of the abdominal cavity using a needle)
it relieves breathing
- collapse lungs

30
Q

Development of carices associated with the portal system and most common clniical manifestation

A

veins drain directaly back to the v.c and hepatic protal vein
if pressure becomes greater, there is a increase resistance for the blood to flow from esophagus into the portal syste,
collateral veins will develop between

31
Q

Where are two other places where collateral shunts can occur due to portal hypertension? Name the varices that result

A 
Between veins on abdominal wall
caput medusae (varices) and/or hemorrhoids (rectum)
32
Q

Hepatic encephaolopahty development and clinical manifestations

A

Liver dysfunctions + collateral vessels that shunt blood past the liver to allow toxins to remain in the blood stream and reach the brain
ammonia - urea most hazardous and the neurotransmission is affected
may display personality changes, memory loss, confusion, coma and asterixis

33
Q

Define asterixis

A

Flapping of hands

34
Q

Define icterus and describe its two causes that are related to GI organs

A

It is jaundice
RBC are broken down in the spleen and liver - breakdown bilirubin, liver can excrete into bile.
- Excess bilirubin
Green/yellow tinge on skin caused by hyperbilirubinemia

3 causes
- too many rbc being broken down, obstruction (common_ and prcoess disruption

35
Q

Why are feces clay colored and urine dark with jaundice

A

The bilirubin is excreted into feces and passes through, it goes everywhere.

36
Q

Where does jaundice often occur first

A

The sclera of the eye then skin

37
Q

Why does splenomegaly occur with liver disorders and how blood cell numbers can be affected

A

spleen enlargement due to portal hyper tension (shunting to splenic vein)
formed elements take longer to filter thru enlargement of spleen, leads to increase the rate of removal (increase time to remove)
result = anemia, thrombocytopenia, leukopenia

38
Q

Define aute hepatitis and outline its common causes and diagnostic features

A 
Hep A(infectious), B(serum), C, D, E - all can cause
HBV AND HCV can cause chronic liver diseases and liver cancer
- causes destruction of hepatocytes, scarring + hyperplasia of hepative macrophages 
0if intra-hepatic ducts are damaged, obstruction and jaundice can occur (most damage with hcv and hbv)
39
Q

Damage done by acute hepatitis to the liver

A

done by contamination + body fluids

- more rapid progression with hbv, hcb, hdv and hiv

40
Q

The stages of typical acute viral hepatitis infection

A

Prodromal stage - viral inflammatory effect

  • 2 weeks after exposure, ends with jaundice (urine and feces changes)
  • marked by fatigue, vomiting, headache, cough, low grade fever. Disease = very infectious during this stage.

Icteric Stage - Live effects

  • 2-6 weeks
  • jaundice, dark urine, clay coloured stool, liver is enlarged + tender - palpation causes pain

Convalescent Stage - healing and repair

  • begins with resolution - 6-8 weeks after exposure
  • liver remains large and tender. Live returns to normal function.
  • 2-12 weeks after onset of jaundice
41
Q

Define and describe chronic hepatitis, causitive organism and possible result

A

persistent of clinical manifestations

  • remain abnormal for longer than 6 months (HBV/HCV surface antigen persists.
  • virus persists in hepatocytes providing a prolonged immune response, extending liver damage.
42
Q

Define cirrhosis + cause and 3 disorders that can lead to it

A

It is irreverisble infallmatory, fibrotic liver disease
0caused b direct damage and inflammation
from man disorders (HBV, HCV, excessive alcohol consumption, prolonged exposure to drugs + toxins, hepatoxin.

It can lead to hepatomegagly, splenomegagly, ascites, portal hypertension, hepatic encephaolpathy and esophageal varices.

43
Q

Define hepatotocin

A

Toxins that can affect the liver

44
Q

Disorders that result from cirrhosis

A

Fibrosis - release of inflammatory mediators by leukocytes + activation of fibroblasts

45
Q

Describe two types of alterations that occur in the liver during the development of cirrhosis

A

liver metabolism and structur

46
Q

What is the “treatment” for cirrhosis

A

No treatment

  • rest,
  • vitamin
  • good nutrition
47
Q

Define liver failure

A

inability to perform normal function of the liver

- may need a liver transplant

48
Q

Name and describe the clinical manifestations of liver failure

A
  • Fetor hepaticus - chronic musty odor of breath
    anemia, thrombocytopenia, leukopenia (clotting factor loss that leads to purpural, petechiae, spider angioma, and epistaxis
  • hemolysis - changes in rbc lipid membrane
  • hepatorenal syndome (kidney failure, oliguria decrease bv thru bleeding)
  • hepative encephaolopathy

Pathophysiology 2200 (7 decks)

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