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Applied Patho > Exam 2 > Flashcards

Exam 2 Flashcards

wks 3-5

1
Q

Azotemia

A

increased BUN w/in the bloodstream

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2
Q

Creatinine

A

muscle tissue breakdown

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3
Q

BUN

A

waste product of protein

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4
Q

Thrombocytopenia

A

bruising easily; bleeding under skin

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5
Q

A healthy urinary tract is sterile T or F

A

true; normal flora are confined to the urethra opening

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6
Q

UTI big 3 clinical manifestations

A
  • burning
  • urgency
  • frequency
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7
Q

what is the cause of nephrolithiasis

A

cause is unknown; dependent on what stones are composed off

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8
Q

What is the priority of treating kidney stones(nephrolithias)

A

reducing pain/ pain management

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9
Q

parietal cells secrete

A

hydrochloric acid and intrinsic factors

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10
Q

goblet cells secrete what

A

mucous; protective layer

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11
Q

What are G cells and what do they secrete

A

gastric cells; gastrin

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12
Q

H. pylori secretes what

A

urease

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13
Q

NSAIDs pathophysiologic mechanism

A

inhibits or blocks prostaglandin E leading to decreased mucosa

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14
Q

A physical and anatomical change to the colon

A

Cathartic colon

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15
Q

obstipation

A

sensation to defecate with no stool or gas

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16
Q

Where are a large number of goblet cells located

A

LARGE intestine

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17
Q

big concern with UC Attack

A

fluid and electrolyte loss

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18
Q

What is bleeding that originates distal to the ileocecal valve called

A

Lower GI Bleed

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19
Q

inflammatory erosion in the stomach or duodenal lining

A

peptic ulcer disease

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20
Q

Small intestine absorbs what

A

vit B12 and other vitamins

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21
Q

Large intestine absorbs what

A

water and electrolytes

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22
Q

Celiac disease is autoimmune & genetic T or F

A

TRUE

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23
Q

endoscopy

A

scope through the mouth through the esophagus and into small intestine

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24
Q

H2 antagonist do what

A

inhibits histamines in stomach which increases mucous

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25
Q

Malabsorption affects what

A
  • muscle mass
  • rep function
  • immune function
  • vitamin deficiencies
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26
Q

Ulcerative colitis patho

A
  • cytotoxic t cells increase number of B and plasma cells
  • increase IgG & IgE
  • leading to inflammation and atrophy
  • leads to formation of pseudopolyps
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27
Q

Crohns in characterized by

A

cobblestone appearance and skip lesions

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28
Q

Only diagnosis/ test to decipher between UC and Crohns

A

Colonoscopy

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29
Q

Upper GI bleed is where

A

esophagus, stomach, and duodenum

30
Q

UGIB Patho

A

rupture, tear, or perforation

31
Q

What labs to check with GI bleeds

A
  • CBC; check clotting
  • BUN; has blood been digested
  • Hgb/Hct; how fast does blood clot
32
Q

As we get older what happens to GI motility

A

GI motility and secretions decrease leading to slowing digestion and emptying and thus deceased absorption

33
Q

How is H. pylori transmitted

A

person to person
- bacteria can be spread by fecal contamination of food or water
- most prevalent in developing countries

34
Q

Does Ulcerative Colitis have a cure?

A

YES; Crohns does NOT

35
Q

What medication is given during an acute phase of IBD

A
  • corticosteroids
  • antidiarrheals
  • fluids/ electrolytes
  • NPO diet
36
Q

EXCRETES metabolic waste

A

KIDNEY

37
Q

Secretes lipase, amylase, trypsin, and chymotrypsin
- start to autodigest w/ a blockage

A

PANCREAS

38
Q

Where is bile stored

A

The gallbladder

39
Q

What is the difference between conjugated and non-conjugated bilirubin

A
  • Conjugated is water soluble and non is NOT water soluble
40
Q

converts amino acids and glycerol into glucose when the body’s store of glucose is inadequate

A

LIVER

41
Q

Abnormal fluid buildup in the third spacing

A

Ascites

42
Q

Where does conjugation of bilirubin occur

A

LIVER

43
Q

What organ stores glucose and glycogen

A

LIVER

44
Q

What is bilirubin

A

breakdown of aged RBCs

45
Q

glycogenesis

A

liver stores glucose and glycogen

46
Q

glycogenolysis

A

breakdown of glycogen

47
Q

gluconeogenesis

A

convert amino acids and glycerol into glucose
- MAKE NEW

48
Q

Pre hepatic liver dysfunction

A
  • Excessive RBC hemolysis
  • before it gets to the liver
49
Q

Intrahepatic dysfunction

A
  • hepatocellular injury
  • liver CANNOT conjugate bilirubin
  • unconjugated bilirubin accumulates and causes jaundice
50
Q

Post hepatic dysfunction

A
  • bile duct obstruction
  • increased levels of conjugated bilirubin circulating causes pot hepatic jaundice
51
Q

Portal hypertension

A

increased resistance with in the portal vein
- portal vein becomes narrow with lots of pressure
- caput medusa

52
Q

What does the liver synthesize/ make

A

Albumin

53
Q

Gallbladder spasmodic pain is known as

A

Biliary colic

54
Q

During a gallbladder attack you should avoid food and be NPO T or F

A

True; ng tube placement to relieve n/v

55
Q

Calculus cholecystitis

A

An obstruction of the gallbladder
- gallstones
- 90% of cases

56
Q

Acalculous cholecystitis

A

No obstruction present
- 10% of cases

57
Q

Murphys sign is to test for what organ

A

GALLBLADDER

58
Q

Pancreas role; ENDOCRINE

A
  • releases into the blood
  • pancreas produces insulin, glucagon, ect
59
Q

Pancreas role; EXOCRINE

A
  • secretes digestive enzymes into the ducts
  • amylase, tripsin, lipase, bicarb
60
Q

Pancreatitis is

A

autodigestion of the pancreas by its own enzymes

61
Q

Cullen sign is

A
  • pancreatitis
  • discoloration around umbilicus
  • brighter in color; pinks and reds
62
Q

Grey turner sign is

A
  • pancreatitis
  • discoloration at the flanks/ backside
63
Q

Amylase breaks down

A

carbs into glucose

64
Q

Lipase breaks down

A

fats

65
Q

protease breaks down

A

proteins

66
Q

Acute pancreatitis is reversible; chronic is not T or F

A

TRUE

67
Q

What medications should you avoid with cirrhosis

A

NARCOTICS

68
Q

Cirrhosis patho

A

liver cells are DESTROYED and replaced with fibrotic tissue
- loss of normal function
- caused from ETOH or nonalcoholic fatty liver disease

69
Q

Can gallstones lead to pancreatitis

A

yes; result from untreated gallstones

70
Q

Accessory organs

A

liver, pancreas, gallbladder

71
Q
A

Applied Patho (11 decks)

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