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Advanced Pathophysiology 2 > GI Pathology - Exam 1 > Flashcards

GI Pathology - Exam 1 Flashcards

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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
PUD-duodenal ulcers -sites/patho
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
26
PUD-duodenal ulcers -s/s
chronic intermittent pain in epigastric region -pain 30min-2hr AFTER eating when stomach is empty -PAIN RELIEF WITH FOOD
27
Duodenal ulcer risk can be reduced with diet high in vitamin _ and _
vit A fiber
28
Inflammatory bowel diseases have unknown origin, are immune related with _ cell responses and include _ _ and _'s disease
TCell ulcerative colitis crohn's disease
29
Ulcerative colitis is an inflammatory disease that causes ulcers of the _ mucosa
colonic -sigmoid and rectum usually
30
IBD - UC -causes -patho
causes: infectious, immunologic, dietary, or genetic patho: continuous lesions, limited to mucosa and are not transmural (NOT SKIPPED)
31
IBD-UC -s/s
-diarrhea (10-20 BM/day), bloody stool, cramp -remission and exacerbations -PAIN
32
IBD-UC -tx
-FIRST LINE = 5-aminosalicylic acid (Mesalazine) -steroids and salicylate -immunosuppressive drugs -broad spect abx -colostomy or resection (increased risk colon cancer)
33
Diaphragmatic hernia -patho -s/s -tx
patho: weakness in the diaphragm, congenital ~8wks s/s: L sd most common; DIB, tachycardia, tachypnea, dim BS tx: surg
34
Hiatal hernia -patho
protrusion of upper part of stomach thru diaphragm into thorax -BRINGS ON GERD, lowers LES resting pressure
35
Hiatal hernia -s/s -tx
s/s:L sd most common; DIB, tachycardia, tachypnea, dim BS tx- wt loss, PPI, antacid, sug repair
36
GERD -patho
acid and pepsin reflux into esophagus causing esophagitis
37
GERD -causes
-resting LES tone is decreased either from TRANSIENT RELAXATION or WEAKNESS OF SPHINCTER
38
GERD -risk factors
vomiting lifting/bending coughing obesity
39
GERD -s/s
heartburn/ indigestion chronic cough laryngitis upper abd pain WITHIN 1hr eating
40
GERD -complications
-scar tissue and stricture of esophagus -aspiration -chronic sinus infection -dysplastic changes (Barrett's esophagus)
41
GERD -tx
-PPI <- most effective -H2 antagonists, prokinetic meds, antacids, pain meds -elevate HOB 6in -wt loss -quit smoking -surg - lap fundoplication
42
Cholelithiasis -patho
-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
Cholelithiasis -s/s
-epigastric pain, R hypochondrium pain -intolerance to fatty food -biliary colic (stones lodge in cystic or common bile duct) -jaundice -abd tenderness/fever
44
Cholelithiasis black v brown stones
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
Cholelithiasis -tx
-lap chole -preferred -transluminal endoscopy -endoscopic retrograde cholangiopancreatography or sphincterotomy -lithotripsy for large stones -drugs to dissolve small stones (CDCA and ursodeoxycholic acid)
46
Cholecystitis -patho -tx
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
Pancreatitis -patho
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
Pancreatitis - Acute -s/s
-resolves spontaneously -epigastric or midabd pain -N/V -fever, leukocytosis -elevated serum lipase - primary dx marker
49
Pancreatitis-Acute -tx
narcotics NG suctioning IV fluids
50
Pancreatitis - Chronic -patho
-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
Pancreatitis - Chronic -s/s -tx
continuous or intermittent abd pain tx: corticosteroids (for autoimmune), smoking and alcohol cessation, analgesics, endoscopy, surg drainage of cysts
52
Pyloric stenosis -patho -s/s -tx
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
Bowel obstruction -causes
-cancer -ulcer -spasm -paralytic ileus -adhesions
54
Bowel obstruction can be _ or _.
intestinal pyloric (acidic vomit)
55
Bowel obstruction at pylorus causes:
acid vomit
56
Bowel obstruction below duodenum causes:
neutral/basic vomit
57
Bowel obstruction that is in sm intestine causes:
extreme vomiting
58
Bowel obstruction that is in large intestine causes:
extreme constipation and less vomiting
59
Bowel obstruction - below duodenum -patho
from fibrous adhesions -neutral/basic vomit -minor change in whole body acid/base status
60
Bowel obstruction -Acute colonic pseudo-obstruction (Olgilvie syndrome)
massive dilation of large bowel -happens in pts who are critically ill, and older immobilized pts
61
Bowel obstruction - large int. -patho
most commonly from colorectal cancer, twisting (volvulus), or strictures from diverticulitis -severe constipation can cause vomiting if sm intestine is full
62
Hepatitis can be _ or _
autoimmune or viral
63
Hepatitis - Autoimmune -patho -s/s
patho: rare, chronic, progressive T Cell inflammation s/s: NO SYMPTOMS, or jaundice, fatigue, poor appetite, amneorrhea
64
Hepatitis- Autoimmune -tx
immunosuppressive therapy (steroids or with azathioprine) with remission within 24mo -relapses are common with tx withdrawal
65
Hepatitis- Viral types
-systemic, primarily affects liver -A(AKA infectious),B (AKA serum hepatitis),C,D,E
66
Hepatitis - Viral -complications
-**hepatic cell necrosis** -Kupffer cell (immune cell) hyperplasia -phagocyte infiltration of liver (obstructing bile flow and hepatocyte function)
67
Chronic active hepatitis occurs with Hep _ and _ with a predisposition to _ and hepatocellular _
B and C cirrhosis carcinoma
68
Fulminant hepatitis causes widespread hepatic necrosis and is often fatal, occurs with Hep _ (with or without Hep D infection) and Hep _
B and C
69
Hepatitis - Viral -phases
incubation prodromal (preicteric) Icteric Recovery
70
Hepatitis - Viral -Incubation phase
varies depending on virus
71
Hepatitis - Viral -Prodromal (Preicteric) phase
**starts ~ 2wks after exposure, ends when jaundice appears ** -fever, malaise, anorexia, liver enlargement/tender -HIGHLY TRANSMISSABLE
72
Hepatitis- Viral -Icteric Phase
actual phase of illness -jaundice and hyperbilirubinemia -fatigue -abd pain
73
Hepatitis - Viral -Recovery phase
-**begins with resolution of jaundice** -symptoms resolve after a few wks -chronic or chronic active hepatitis can occur
74
Hepatitis - Viral -tx
-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
Hep A -source
feces, bile serum of infected pts -risks: crowded areas, unsanitary, food/water contamination
76
Hep A -transmission
fecal-oral
77
Hep A -prevention/tx
handwashing -immunoglobulin admin before exposure or early in incubation phase -vaccines!!
78
Hep B -source
blood, saliva, semen, body fluids of infected pt
79
Hep B -transmission
contact with infected blood, body fluid, needles -maternal transmission to fetus if mom is infected in 3rd tri
80
Hep B -prevention/tx
Hep B vax
81
Hep C -source
-commonly the cause of post-transfusion Hep -implicated in infections from IV drug use and HIV
82
Hep C -transmission
Co infection with Hep B is common -80% with Hep C will have chronic liver disease
83
Hep C -prevention/tx
no vax available -antivirals
84
Hep D -source
requires Hep B for replication
85
Hep D -transmission
-
86
Hep D -prevention/t
Tx: **Pegylated interferon alpha**
87
Hep E -source
contaminated water, undercooked meat -common in african and asian countries and developing countries
88
Hep E -transmission
fecal-oral
89
Hep E -prevention/tx
vaccine in china only
90
Cirrhosis -types
-Alcoholic liver disease -Nonalcoholic fatty liver disease -biliary cirrhosis -primary sclerosing cholangitis
91
Cirrhosis -patho
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
Cirrhosis- Alcoholic liver disease -patho
-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
Cirrhosis- Alcoholic liver disease -s/s
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
Cirrhosis - Alcoholic liver disease -tx
-cessation of alcohol -rest/ nutrient dense diet -corticosteroids, antioxidants, drugs that slow fibrosis -manage complications (ascites, GIB, infection, encephalopathy)
95
Cirrhosis - NA fatty liver disease -patho
infiltration of hepatocytes with fat in absence of alcohol intake -assoc with obesity
96
Cirrhosis - biliary (Bile Canaliculi) -patho
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
Cirrhosis - Primary sclerosing cholangitis -patho
chronic inflammatory fibrotic disease of medium/large bile ducts OUT of liver
98
Acute Liver Failure -patho
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
Acute Liver Failure -s/s
anorexia vomiting abd pain progressive jaundice
100
Acute Liver Disease -tx
N-acetylcysteine antiviral drugs (for viral hepatitis) reduce the ammonia serum levels liver transplant
101
Porphyria -patho
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
Porphyria -triggers
hormonal changes during menstrual cycle fasting infections exposure to triggering drugs (etomidate)
103
Porphyria -s/s
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
Porphyria -tx
-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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