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Advanced Pathophysiology 2 > GI Pathology - Exam 1 > Flashcards

GI Pathology - Exam 1 Flashcards

1
Q

Carcinoid syndrome
-patho
-causes

A

causes: endogenous secretion of serotonin and kallikrein

patho-paraneoplastic syndrome from tumors

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2
Q

Carcinoid Syndrome
-s/s

A

flushing
N/V
diarrhea
-less often: HF, emesis, bronchoconstriction, hepatomegaly, endocardial fibrosis, retroperitoneal and pelvis fibrosis

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3
Q

Carcinoid Syndrome
-treatment

A

octreotide (somatostatin analogue)
-decreases serotonin release from tumor

-avoid beta blockers, will increase serotonin release from tumor (phenylephrine ok)

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4
Q

Hirshsprung’s Disease
-patho
-causes

A

patho: poor regulation of activity of colon, swollen colon, shrunken rectum; causes obstructions

causes: lack of ganglionic cells in myenteric (auerbach) plexus and submucosal (meissner) plexus

-more common in males, siblings of pts with this disease, and pts with Down Syndrome

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5
Q

Hirschsprung’s
-s/s
-tx

A

S/s: newborn fails to have BM in 48hr, swollen abdomen, green/brown vomit, constipation/diarrhea, failure to gain weight

Tx- high fiber, fluids, stool softeners, isotonic enemas, surgery

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6
Q

Mendelson’s Syndrome
-patho
-tx

A

patho: hypoxia, pulm edema, infiltrates following aspiration

Tx- vent support, bronchodilators prn, abx if culture is +

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7
Q

Mallory-Weiss Tear
-patho/causes
-tx

A

patho: laceration at junction of esophagus and stomach from mallory-weiss syndrome/ tearing from extreme vomiting

s/s-hemataemesis

tx- heals on its own, cautery/clip possibly, medications to decrease acid

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8
Q

Gastrinoma/ Zollinger-Ellison Syndrome
-patho
-s/s

A

patho: non-beta cell tumor of pancreas or G cell tumor; increased parietal cell mass constantly stimulates; low pH inactivates pancreatic lipase causing bile salts to increase

s/s: steatorrhea and hypokalemia; duodenal ulcers, diarrhea

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9
Q

Ketoacidosis
-causes

A

Lack of insulin
-body can’t use available glucose
-ketosis occurs, breaking down fat for fuel

Insulin deficiency
-excess of glucagon
-promotes breakdown of stored fats, producing ketones
-body thinks it needs more glucose so it breaks down other sources

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10
Q

Ketoacidosis
-effects

A

-excess glucose acts as osmotic diuretic
-polyuria
-polydipsia
-polyphagia
-possible weight loss
-Kussmaul breathing (acetone breath)
-high BG, ketonuria
-N/V abd pain
-confusion
-weakness/fatigue
-acidosis from anaerobic break down/ketones

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11
Q

Acute liver failure
-patho

A

patho: severe impairment/necrosis of liver cells WITHOUT preexisiting liver disease or cirrhosis

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12
Q

Leading cause of acute liver failure is _ _.

A

Acetaminophen overdose
-give N-acetylcysteine

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13
Q

Acute liver disease
-s/s

A

anorexia
vomiting
abd pain
progressing jaundice
ascites
GIB
coag issues
encephalopathy(ammonia accumulation-late)
portal HTN, elevated bilirubin

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14
Q

Acute liver failure
-tx

A

-antiviral therapy (improves cases of viral hepatitis)
-lower the serum ammonia level
-liver transplant

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15
Q

Portal HTN
-patho

A

HTN in portal vein (normal = 5-10mmHg, HTN is >10mmHg)
-increased resistance to portal flow from either obstruction in liver or reduction of flow in biliary channels

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16
Q

Portal HTN
-tx

A

beta blockers- prevent variceal bleeding
no definitive tx, liver transplant is best option

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17
Q

There is normally a _ - _ mmHg difference between CVP and portal venous system pressure, _ difference = bleeding/varices

A

0-5mmHg difference
increased

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18
Q

About _% of CO flows thru liver.

A

30%
-if obstruction occurs, can drop CO or cause systemic HoTN from poor venous return

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19
Q

PUD is ulceration in the _ _ of the lower esophagus, stomach, or duodenum

A

mucosal lining
-when acid and pepsin overcome ability of mucosa to defend itself

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20
Q

PUD
-causes

A

Causes of:
high acid/peptic content
irritation
poor blood supply
poor secretion of mucus
infection (H. Pylori)

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21
Q

PUD
-risk factors

A

-genes
-H.Pyloir infection
-habitual use of NSAIDs
-excessive drinking, smoking
-acute pancreatitis
-COPD
-obesity
-cirrhosis
-age >65y

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22
Q

PUD-Gastric ulcers
-sites/patho

A

common site: antral region adjacent to acid-secreting mucosa

Patho:
-common cause=H.Pylori;
-primary defect is increased permeability to H+ ions
-pepsinogen converted to pepsin too early
-histamine release increases HCl
-gastric secretion is normal or less than normal

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23
Q

PUD-gastric ulcer
-s/s

A

pain IMMEDIATELY after eating
-chronic
-anorexia, vomiting, wt loss

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24
Q

PUD-BOTH GASTRIC AND DUODENAL ULCER
-tx

A

Antacids-neutralize gastric contents, pH, inactivate pepsin, relieve pain

PPI +anticholinergics- suppress acid secretion

Bismuth + combo abx + vit C- kill H.Pylori

Sucralfate and colloidal bismuth- coat ulcer

Surg resection

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25
Q

PUD-duodenal ulcers
-sites/patho

A

mosre common than gastric ulcers bc less protection than stomach

patho:
-higher # of parietal cells in duodenum secreting acid
-high gastrin level
-rapid gastric emptying (chyme is acidic_
-cigarette smoking increasing acid

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26
Q

PUD-duodenal ulcers
-s/s

A

chronic intermittent pain in epigastric region
-pain 30min-2hr AFTER eating when stomach is empty
-PAIN RELIEF WITH FOOD

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27
Q

Duodenal ulcer risk can be reduced with diet high in vitamin _ and _

A

vit A
fiber

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28
Q

Inflammatory bowel diseases have unknown origin, are immune related with _ cell responses and include _ _ and _’s disease

A

TCell
ulcerative colitis
crohn’s disease

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29
Q

Ulcerative colitis is an inflammatory disease that causes ulcers of the _ mucosa

A

colonic
-sigmoid and rectum usually

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30
Q

IBD - UC
-causes
-patho

A

causes: infectious, immunologic, dietary, or genetic

patho: continuous lesions, limited to mucosa and are not transmural (NOT SKIPPED)

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31
Q

IBD-UC
-s/s

A

-diarrhea (10-20 BM/day), bloody stool, cramp
-remission and exacerbations
-PAIN

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32
Q

IBD-UC
-tx

A

-FIRST LINE = 5-aminosalicylic acid (Mesalazine)
-steroids and salicylate
-immunosuppressive drugs
-broad spect abx
-colostomy or resection (increased risk colon cancer)

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33
Q

Diaphragmatic hernia
-patho
-s/s
-tx

A

patho: weakness in the diaphragm, congenital ~8wks

s/s: L sd most common; DIB, tachycardia, tachypnea, dim BS

tx: surg

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34
Q

Hiatal hernia
-patho

A

protrusion of upper part of stomach thru diaphragm into thorax
-BRINGS ON GERD, lowers LES resting pressure

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35
Q

Hiatal hernia
-s/s
-tx

A

s/s:L sd most common; DIB, tachycardia, tachypnea, dim BS

tx- wt loss, PPI, antacid, sug repair

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36
Q

GERD
-patho

A

acid and pepsin reflux into esophagus causing esophagitis

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37
Q

GERD
-causes

A

-resting LES tone is decreased either from TRANSIENT RELAXATION or WEAKNESS OF SPHINCTER

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38
Q

GERD
-risk factors

A

vomiting
lifting/bending
coughing
obesity

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39
Q

GERD
-s/s

A

heartburn/ indigestion
chronic cough
laryngitis
upper abd pain WITHIN 1hr eating

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40
Q

GERD
-complications

A

-scar tissue and stricture of esophagus
-aspiration
-chronic sinus infection
-dysplastic changes (Barrett’s esophagus)

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41
Q

GERD
-tx

A

-PPI <- most effective
-H2 antagonists, prokinetic meds, antacids, pain meds
-elevate HOB 6in
-wt loss
-quit smoking
-surg - lap fundoplication

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42
Q

Cholelithiasis
-patho

A

-too much water, cholesterol in bile
-decreased secretion of bile acids(reduced CCK)
-decreased resorption of bile salts from ileum (reduced CCK)
-gallbladder smooth musc stasis
-genes
-inflamed epithelium

43
Q

Cholelithiasis
-s/s

A

-epigastric pain, R hypochondrium pain
-intolerance to fatty food
-biliary colic (stones lodge in cystic or common bile duct)
-jaundice
-abd tenderness/fever

44
Q

Cholelithiasis
black v brown stones

A

black:
-formed in sterile environment
-made of calcium bilirubinate polymer from hyperbilirubinbilia

brown:
-bacterial infection of bile ducts
-made of calcium soaps, unconjugated bilirubin, cholesterol, FA, and mucin

45
Q

Cholelithiasis
-tx

A

-lap chole -preferred
-transluminal endoscopy
-endoscopic retrograde cholangiopancreatography or sphincterotomy
-lithotripsy for large stones
-drugs to dissolve small stones (CDCA and ursodeoxycholic acid)

46
Q

Cholecystitis
-patho
-tx

A

inflammation of gallbladder (acute or chronic)

s/s- fever, leukocytosis, rebound tenderness, abd muscle guarding

tx- pain mgmt, fluids and lytes, fasting, abx, if GB is perffed, immediate chole

47
Q

Pancreatitis
-patho

A

injury or damage to panc cells and ducts cause leakage of panc enzymes(trypsin, lipase, and chymotrypsin) into its tissue, inflaming and eating itself

-can leak into the bloodstream and injure vessels and other organs

48
Q

Pancreatitis - Acute
-s/s

A

-resolves spontaneously
-epigastric or midabd pain
-N/V
-fever, leukocytosis
-elevated serum lipase - primary dx marker

49
Q

Pancreatitis-Acute
-tx

A

narcotics
NG suctioning
IV fluids

50
Q

Pancreatitis - Chronic
-patho

A

-most common cause = alcohol abuse
-repeated exacerbations ->chronic changes
-destroys ACINAR cells and ISLETS OF LANGERHANS
-parenchyma is destroyed and replaced with fibrous tissue, calcifications, obstructions, and cysts

51
Q

Pancreatitis - Chronic
-s/s
-tx

A

continuous or intermittent abd pain

tx: corticosteroids (for autoimmune), smoking and alcohol cessation, analgesics, endoscopy, surg drainage of cysts

52
Q

Pyloric stenosis
-patho
-s/s
-tx

A

patho: blocking/narrowing of pylorus, messes up gastric emptying

s/s: acidic projectile vomiting IMMEDIATELY AFTER eating, wt loss, persistent hunger

tx- surg - pyloromyotomy

53
Q

Bowel obstruction
-causes

A

-cancer
-ulcer
-spasm
-paralytic ileus
-adhesions

54
Q

Bowel obstruction can be _ or _.

A

intestinal
pyloric (acidic vomit)

55
Q

Bowel obstruction at pylorus causes:

A

acid vomit

56
Q

Bowel obstruction below duodenum causes:

A

neutral/basic vomit

57
Q

Bowel obstruction that is in sm intestine causes:

A

extreme vomiting

58
Q

Bowel obstruction that is in large intestine causes:

A

extreme constipation and less vomiting

59
Q

Bowel obstruction - below duodenum
-patho

A

from fibrous adhesions
-neutral/basic vomit
-minor change in whole body acid/base status

60
Q

Bowel obstruction
-Acute colonic pseudo-obstruction (Olgilvie syndrome)

A

massive dilation of large bowel
-happens in pts who are critically ill, and older immobilized pts

61
Q

Bowel obstruction - large int.
-patho

A

most commonly from colorectal cancer, twisting (volvulus), or strictures from diverticulitis
-severe constipation can cause vomiting if sm intestine is full

62
Q

Hepatitis can be _ or _

A

autoimmune or viral

63
Q

Hepatitis - Autoimmune
-patho
-s/s

A

patho: rare, chronic, progressive T Cell inflammation

s/s: NO SYMPTOMS, or jaundice, fatigue, poor appetite, amneorrhea

64
Q

Hepatitis- Autoimmune
-tx

A

immunosuppressive therapy (steroids or with azathioprine) with remission within 24mo
-relapses are common with tx withdrawal

65
Q

Hepatitis- Viral
types

A

-systemic, primarily affects liver
-A(AKA infectious),B (AKA serum hepatitis),C,D,E

66
Q

Hepatitis - Viral
-complications

A

-hepatic cell necrosis
-Kupffer cell (immune cell) hyperplasia
-phagocyte infiltration of liver (obstructing bile flow and hepatocyte function)

67
Q

Chronic active hepatitis occurs with Hep _ and _ with a predisposition to _ and hepatocellular _

A

B and C
cirrhosis
carcinoma

68
Q

Fulminant hepatitis causes widespread hepatic necrosis and is often fatal, occurs with Hep _ (with or without Hep D infection) and Hep _

A

B and C

69
Q

Hepatitis - Viral
-phases

A

incubation
prodromal (preicteric)
Icteric
Recovery

70
Q

Hepatitis - Viral
-Incubation phase

A

varies depending on virus

71
Q

Hepatitis - Viral
-Prodromal (Preicteric) phase

A

**starts ~ 2wks after exposure, ends when jaundice appears **
-fever, malaise, anorexia, liver enlargement/tender
-HIGHLY TRANSMISSABLE

72
Q

Hepatitis- Viral
-Icteric Phase

A

actual phase of illness
-jaundice and hyperbilirubinemia
-fatigue
-abd pain

73
Q

Hepatitis - Viral
-Recovery phase

A

-begins with resolution of jaundice
-symptoms resolve after a few wks
-chronic or chronic active hepatitis can occur

74
Q

Hepatitis - Viral
-tx

A

-restrict physical activity PRN
-low-fat, high carb diet if bile flow is obstructed
-avoid contact with blood/body fluids with pts with Hep B or C

75
Q

Hep A
-source

A

feces, bile serum of infected pts
-risks: crowded areas, unsanitary, food/water contamination

76
Q

Hep A
-transmission

A

fecal-oral

77
Q

Hep A
-prevention/tx

A

handwashing
-immunoglobulin admin before exposure or early in incubation phase
-vaccines!!

78
Q

Hep B
-source

A

blood, saliva, semen, body fluids of infected pt

79
Q

Hep B
-transmission

A

contact with infected blood, body fluid, needles
-maternal transmission to fetus if mom is infected in 3rd tri

80
Q

Hep B
-prevention/tx

A

Hep B vax

81
Q

Hep C
-source

A

-commonly the cause of post-transfusion Hep
-implicated in infections from IV drug use and HIV

82
Q

Hep C
-transmission

A

Co infection with Hep B is common
-80% with Hep C will have chronic liver disease

83
Q

Hep C
-prevention/tx

A

no vax available
-antivirals

84
Q

Hep D
-source

A

requires Hep B for replication

85
Q

Hep D
-transmission

A

-

86
Q

Hep D
-prevention/t

A

Tx: Pegylated interferon alpha

87
Q

Hep E
-source

A

contaminated water, undercooked meat
-common in african and asian countries and developing countries

88
Q

Hep E
-transmission

A

fecal-oral

89
Q

Hep E
-prevention/tx

A

vaccine in china only

90
Q

Cirrhosis
-types

A

-Alcoholic liver disease
-Nonalcoholic fatty liver disease
-biliary cirrhosis
-primary sclerosing cholangitis

91
Q

Cirrhosis
-patho

A

irreversible inflammatory, fibrotic disease disrupting liver function/structure
-nodular and fibrotic tissue decreases hepatic function
-biliary channels become obstructed and cause portal HTN
-portal HTN shunts blood away and causes necrosis from ischemia
-most common causes: alcohol abuse and viral hepatitis

92
Q

Cirrhosis- Alcoholic liver disease
-patho

A

-alcohol oxidizes and damages hepatocytes

-mild form: fatty liver (steatosis) - reversible if drinking stops here

-moderate: steatohepatitis - inflammation and necrosis is happening

-severe: alcoholic cirrhosis (fibrosis)- toxic effects from alcohol affect immune function, oxidative stress from lipid peroxidation, malnutrition; hormone degradation doesn’t occur properly, ammonia builds up, FA and enzyme/protein synth is decresed

93
Q

Cirrhosis- Alcoholic liver disease
-s/s

A

Nausea
anorexia
fever
abd pain
jaundice
spider angiomas
amenorrhea
loss of body hair
gynecomastia
edema
varices
coag issues
anemia/ splenomegaly
hepatopulmonary syndrome
elevated AST, ALT, ALP bilirubin, PTT, LOW albumin

94
Q

Cirrhosis - Alcoholic liver disease
-tx

A

-cessation of alcohol
-rest/ nutrient dense diet
-corticosteroids, antioxidants, drugs that slow fibrosis
-manage complications (ascites, GIB, infection, encephalopathy)

95
Q

Cirrhosis - NA fatty liver disease
-patho

A

infiltration of hepatocytes with fat in absence of alcohol intake
-assoc with obesity

96
Q

Cirrhosis - biliary (Bile Canaliculi)
-patho

A

cirrhosis begins in bile canaliculi and ducts
-autoimmune (primary biliary cirrhosis): T Cell and antibody mediated destruction of INTRAhepatic bile ducts
-obstructive (secondary biliary cirrhosis): obstruction of bile ducts

97
Q

Cirrhosis - Primary sclerosing cholangitis
-patho

A

chronic inflammatory fibrotic disease of medium/large bile ducts OUT of liver

98
Q

Acute Liver Failure
-patho

A

severe impairment or necrosis of liver without preexisting disease or cirrhosis
-main cause: acetaminophen OD
-hepatocytes become edematous, patchy areas of necrosis and inflammatory cell infiltrates disrupt parenchyma
-irreversible

99
Q

Acute Liver Failure
-s/s

A

anorexia
vomiting
abd pain
progressive jaundice

100
Q

Acute Liver Disease
-tx

A

N-acetylcysteine
antiviral drugs (for viral hepatitis)
reduce the ammonia serum levels
liver transplant

101
Q

Porphyria
-patho

A

enzyme defect causing altered heme synth and overproduction/ accumulation of precursors in liver
-**Delta-aminolevulinic acid (ALA) and porphobilogen (PBG) **
-prophyrins or pophyrin precursors accumulate and type of porphyria depends on which accumulates

102
Q

Porphyria
-triggers

A

hormonal changes during menstrual cycle
fasting
infections
exposure to triggering drugs (etomidate)

103
Q

Porphyria
-s/s

A

vary widely between 9 different forms, non-specific
Most common presentation:
-acute abd pain
-seizures
-confusion
-hallucinations
-progressive motor neuropathy causing paralysis or resp failure
-tachycardia/HTN
-skin lesions/blisters/rash
-frailty
-red urine

104
Q

Porphyria
-tx

A

-Hemin 3-4mg/kg Iv Q day for 4 days - fixes deficiency of regulatory heme and down regulates ALAS
-IV glucose for mild attacks (same effect)
-avoid triggering drugs (reglan, barbs, sulfa drugs, rifampin)
-treat other symptoms

Advanced Pathophysiology 2 (4 decks)

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