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git patho v bare bones Flashcards

1
Q

most common benign neoplasm of oropharynx

A

squamous cell papilloma

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2
Q

most common malignant neoplasm of oropharynx

A

SCC: squamous cell carcinoma

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3
Q

what is sialolithiasis?

A

calculi causing ductal obstruction (mostly in submandibular glands)

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4
Q

what are the causes of sialadenitis? (viral, bacterial, autoimmune)

A

viral: mumps (bilateral inflammed parotid glands)
bacterial: staph aureus, strep viridans
autoimmune: sjogren syndrome

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5
Q

most common benign neoplasms of salivary glands (2)

A

pleomorphic adenoma> warthin tumour

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6
Q

what is atresia?

A

a condition in which an orifice or passage in the body is (usually abnormally) closed or absent

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7
Q

what is achalasia?

A

swallowing disorder that affects the esophagus (esophagus muscles do not contract properly and do not help propel food down toward the stomach)

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8
Q

what is diaphragmatic hernia?

A

incomplete formation of diaphragm→ abdominal viscera herniates into thoracic cavity

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9
Q

what are varices?

A

an abnormally dilated vessel with a tortuous course

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10
Q

how are oesophageal varices formed?

A

liver cirrhosis→ portal HT→ formation of collateral channels to divert flow fr portal vein→ collateral veins get congested & dilated (varices)→ variceal rupture→ hematemesis, melena

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11
Q

what are mallory-weiss tears?

A
  • longitudinal superficial mucosal tears near the GEJ (junction between distal esophagus and the proximal stomach (cardia))
  • associated with severe retching/vomiting due to acute alcohol intoxication
  • clinical: hematemesis
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12
Q

what is gerd?

A

reflux of gastric contents into lower esophagus, due to transient lower esophageal sphincter relaxation triggered by gastric distenstion

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13
Q

what is barrett esophagus?

A
  • complication of chronic gerd
  • intestinal metaplasia within esophageal squamous mucosa
  • associated with increased risk of adenocarcinoma
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14
Q

common malignant neoplasms of oesophagus (2) + location

A
  1. SCC (upper 2/3 of oesophagus)
  2. adenocarcinoma (lower 1/3)
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15
Q

what are the causes of pyloric stenosis? (4)

A
  1. congenital: hyperplasia of pyloric muscularis propria→ obstruct gastric outflow
  2. benign, acquired: antral gastritis
  3. benign, acquired: peptic ulcers close to pylorus
  4. malignant, acquired: carcinomas of distal stomach/pancreas→ fibrose→ narrow pyloric channel
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16
Q

what is acute gastritis?

A

sudden onset of stomach mucosal injury/inflammation with NEUTROPHILS present
(damaging forces»protective mech)

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17
Q

gastritis vs gastropathy

A

gastritis: mucosal injury with NEUTROPHILS
gastropathy: mucosal injury with rare/absent inflamm cells

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18
Q

what is zollinger-ellison syndrome

A
  • neuroendocrine tumours (GASTRINOMA) in small intestine or pancreas
  • trophic effects on gastrin→ hypersecretes gastric acid
  • present w duodenal ulcers or chronic diarrhoea
  • treatment: PPIs
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19
Q

what is peptic ulcer disease?

A
  • chronic mucosal ulceration in duodenum/stomach
  • penetrates muscularis mucosa/deeper
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20
Q

what are the risk factors of peptic ulcer disease? (4)

A
  1. H. pylori infection
  2. NSAIDs
  3. cigarette use
  4. CVS disease
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21
Q

clinical presentations of peptic ulcer disease (4)

A
  • epigastric burning/aching
  • pain occurs 1-3hrs after food, worse at night, relieved by alkali/food
  • penetrating ulcers can refer pain to back, left upper quadrant, chest
  • n+v, bloating, belching, weight loss
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22
Q

what is the pathophysiology behind h.pylori gastritis?

A
  • in almost all pts w duodenal ulcers, and most pts w gastric ulcers/chronic gastritis
  • antral inflammation→ increased gastrin production→ increase HCl production→ gastric/duodenal peptic ulcer
  • long standing infection→ involves body & fundus→ atrophic gastritis w reduced parietal cell mass & intestinal metaplasia→ decreased ulcers but increased risk of adenocarcinoma
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23
Q

what is the pathophysiology of autoimmune atrophic gastritis?

A
  • chronic gastritis
  • CD4+ T cells direct against parietal cell components→ loss of parietal cells→ defective acid & IF production
  • defective HCl prod→ achlorhydria/hypochlorhydria→ stimulates gastrin release→ hypergastrinemia & G-cell hyperplasia→ neuroendocrine cell hyperplasia
  • defective IF production→ defective ileal vit B12 absorption→ B12 deficiency & pernicious anemia
  • atrophy & intestinal metaplasia→ increased adenocarcinoma risk
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24
Q

malignant neoplasm of stomach

A

adenocarcinoma

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25
Q

metastasis of gastric carcinoma/adenocarcinoma

A
  • lymph node: invovles virchow node (left supraclavicular node0
  • distant metastasis: liver, periumbilical region (sister mary joseph nodule), bilateral ovaries (krukenberg tumour)
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26
Q

what is duodenal atresia?

A

congenital failure of duodenum to canalise

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27
Q

what is the most common congenital GIT anomaly?

A

meckel diverticulum

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28
Q

what is meckel diverticulum?

A

congenital outpouching of all 3 layers of bowel wall (true diverticulum)

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29
Q

what is volvulus?

A

twisting of bowel along mesentery→ obstruction & disruption of blood supply→ infarction

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30
Q

what is the most common cause of intestinal obstruction in children?

A

intussusception

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31
Q

what is intussusception?

A

segment of bowel sliding forward into distal segment→ obstruction

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32
Q

pathophysiology of lactose intolerance

A

lactase deficiency→ lactose accumulates in intestine lumen→ osmotic diarrhoea

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33
Q

what is celiac disease?

A

congenital damage of small bowel villi due to gluten exposure (immune mediated)

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34
Q

what are the causes of acute appendicitis?

A

adults: luminal obstruction eg faecolith (stone made of feces in intestine)
children: lymphoid hyperplasia

increase intraluminal pressure→ compromise venous outflow→ bacterial proliferation→ acute inflammation

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35
Q

what are the clinical presentations of acute appendicitis?

A

early: periumbilical pain, fever, n/v
late: pain localises to RIF (right iliac fossa)/mcburney’s point

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36
Q

what is inflammatory bowel disease?

A
  • autoimmune, chronic relapsing bowel inflammation (bloody diarrhoea, abdominal pain)
  • associated w colonic adenocarcinoma
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37
Q

types of IBD (2)

A
  1. crohn’s disease
  2. ulcerative colitis
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38
Q

site of crohn disease vs UC

A

crohn disease: any GIT area
UC: only rectum (always) and colon

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39
Q

what is anorectal atresia?

A

congenital anorectal malformation→ absent anal opening at birth (failure of cloacal diaphragm to involute)

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40
Q

what is hirschsprung disease?

A

congenital failure of ganglion cells to descend into myenteric & submucosal plexus→ aganglionic segment cant relax→ no coordinated peristalsis→ functional obstruction!!→ massive dilatation of bowel proximal to obstruction (risk of rupture)

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41
Q

what is colonic diverticula?

A

wall stress e.g. vasa recta traverse muscularis propria→ outpouching of mucosa & submucosa

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42
Q

how does colonic diverticula lead to diverticulitis?

A

faecolith gets trapped in diverticula pouch→ infection→ diverticulitis

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43
Q

what are the causes of ischemic bowel disease?

A
  • atherosclerosis of SMA
  • arterial thromboembolism
  • venous thrombosis
    etc
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44
Q

what is pseudomembranous colitis?

A

antibiotic use→ disrupt normal colonic microbiome→ C. difficile overgrowth!!!→ severe inflammation of inner lining of colon

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45
Q

what are the causes of intestinal tuberculosis? (3)

A
  1. consumption of milk products containing mycobacterium bovis
  2. consumptiom of sputum fr person with active mycobacterium tuberculosis
  3. spread from distant TB sites
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46
Q

microscopic signs of intestinal tuberculosis (2)

A
  1. caseating granulomas (epithelioid histiocytes, langhan giant cells, central caseating necrosis)
  2. ziehl-neelson stain for acid-fast bacilli
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47
Q

what is amoebiasis?

A

colonic disease caused by entamoeba histolytica (protozoa)→ flask-shaped ulcers

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48
Q

what is familial adenomatous polyposis?

A
  • autosomal dominant disorder w numerous adenomatous colonic polyps
  • due to inherited APC mutation
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49
Q

what is cholestasis?

A

any condition that causes retention of bile: impaired bile formation or obstruction of bile flow

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50
Q

clinical presentations of cholestasis

A

tissue deposition of bilirubin (bile pigments)→ jaundice, icterus

others: pruritus, skin xanthomas (fat buildup under skin surface), intestinal malabsorption/vit ADEK deficiencies

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51
Q

what is extrahepatic biliary atresia?

A
  • complete/partial obstruction of extrahepatic biliary tree lumen
  • within first 3 months of life
  • jaundice, pale stools, tea coloured urine (obstructive jaundice)
  • 1/3 of neonatal cholestasis cases
52
Q

what is cholangitis?

A

inflammation of the bile duct system

53
Q

what is primary biliary cholangitis (PBC)?

A

chronic, progressive condition that causes inflammation→ destruction of bile ducts

54
Q

what is primary sclerosing cholangitis (PSC)?

A

chronic liver disease→ bile ducts inside & outside liver become inflammed & scarred→ become narrowed/blocked

55
Q

what is choledochal cyst?

A

congenital anomaly of biliary tree (usually common bile duct)→ abnormal dilatation→ obstructs bile flow

56
Q

where does gallbladder carcinoma spread to? (direct and metastasis)

A

usually adenocarcinoma

direct invasion: liver, stomach, duodenum
metastasis: liver, regional lymph nodes, lungs

57
Q

what is cholelithiasis?

A

gallstones

58
Q

what are the symptoms of cholelithiasis?

A
  1. RUQ/epigastric pain
  2. biliary colic (usually after fatty meal)
59
Q

what is cholecystitis?

A

gallbladder inflammation

60
Q

what is calculous acute cholecystitis?

A

obstruction of neck/cystic duct by a stone causing chemical irritation & inflammation

61
Q

what is acalculous acute cholecystitis?

A
  • cystic duct obstruction & cholecystitis in the absence of stones
  • e.g. lack of gallbladder stimulation→ gallbladder stasis→ concentration of bile salts→ bile sludge→ build up of pressure→ ischemia
62
Q

what is chronic cholecystitis?

A
  • repeated acute cholecystitis, or without previous attacks
  • commonly associated w cholelithiasis!!
63
Q

why are most liver diseases chronic by the time of clinical presentation?

A
  • liver has enormous functional reserve→ mild liver damage may not be clinically detected
  • liver disease is usually an insidious process
64
Q

what is the progression of acute hepatitis/mild liver injury?

A

acute hepatitis→ liver regeneration & repair

65
Q

what is the progression of massive liver injury?

A

massive liver injury→ acute liver failure

66
Q

what is the progression of chronic hepatitis/persistent liver injury?

A

chronic hepatitis→ fibrosis/cirrhosis→ chronic liver failure or acute-on-chronic liver failure

67
Q

what is acute liver failure?

A
  • occurs within 26 weeks of initial liver injury (no pre-existing liver disease)
  • diffuse injury without obvious cell death
68
Q

what are the causes of acute liver failure? (3)

A
  1. drugs/toxins
  2. acute hepatitis A/B/E
  3. autoimmune hepatitis
69
Q

what is chronic liver failure?

A

progressive deterioration of liver functions for more than six months e.g. chronic hepatitis

70
Q

what are the causes of chronic liver failure? (3)

A
  1. chronic hep B/C
  2. NAFLD
  3. ALD
71
Q

what is cirrhosis?

A

scarred & permanently damaged liver (dense fibrous tissue formation)→ shrunken, firm, nodular liver

72
Q

what is acute-on-chronic liver failure?

A
  • unrelated ACUTE injury supervenes on CHRONIC disease
    OR
  • CHRONIC disease itself has a flare of/ACUTE activity that directly leads to liver failure
73
Q

what are the consequences of liver failure? (5)

A
  1. coagulopathy (impaired hepatic synthesis of coagulation factors)
  2. hepatic encephalopathy (liver dysfunction→ brain dysfunction)
  3. cholestasis (obstruction to bile flow)
  4. portal HT
  5. hyperestrogenemia (palmar erythema, spider angioma, hypogonadism, gynecomastia)
74
Q

what is the causes of portal HT?

A

prehepatic:
- increased resistance: thrombosis/narrowing of portal vein
- increased flow: splenomegaly/arterial vasodilation→ increased splenic blood flow

intrahepatic: cirrhosis/non-cirrhotic

posthepatic:
- hepatic vein outflow obstruction
- heart problems eg RH failure

75
Q

effects of portal HT (4)

A
  1. increased pressure in peritoneal capillaries→ ASCITES
  2. portosystemic shunting of blood→ devt collateral channels→ ANORECTAL & ESOPHAGEAL VARICES
  3. shunting of NH3 fr GIT into general circulation→ HEPATIC ENCEPHALOPATHY
  4. splenomegaly→ anemia, leukopenia, thrombocytopenia
76
Q

which hepatitis viruses are transmitted fecal-orally?

A
  1. Hep A (SHELLFISH!)
  2. Hep E (water borne too)
77
Q

which hepatitis viruses are transmitted parenterally?

A
  1. Hep B
  2. Hep C (mainly blood, sexual & vertical are rare due to low circulating viral levels)
  3. Hep D
78
Q

which hep virus’s genomes are RNA?

A

Hep A, C, D, E

79
Q

which hep virus’s genomes are DNA?

A

hep B

80
Q

which hep viruses have available vaccines?

A

hep A, B, D (HDV is protected by HBV vax)

81
Q

which hep viruses DONT have available vaccines?

A

hep C, E

82
Q

explain how there may be hep A epidemic in singapore?

A

low exposure to HepA→ youths have no antibodies→ are susceptible

introduction of infected material eg raw SHELLFISH→ epidemic

83
Q

what is the pathophysiology of hep B virus?

A

enters blood→ infects hepatocytes→ viral DNA polymerase synthesizes missing DNA portions→ host RNA polymerase synthesizes mRNA→ produce more viral DNA→ progeny HBV releases by budding

some viral DNA may integrate into host cell genome→ carrier

84
Q

what is the progression of disease of HBV carriers?

A

5-15% of infected become carriers (HBsAg detected in blood > 6mths)→ 10-30% develop chronic helpatitis→ cirrhosis→ liver cancer

1% carriers/year develop anti-HB (immune)→ recover :)

85
Q

what is the epidemiology of HCV?

A
  • hosts: infected humans & chimps
  • 60-80% of infected become carriers→ chronic hepatitis
86
Q

what is the epidemiology of HDV?

A
  • mostly associated w IVDA
  • infects HBV carriers (uses HBV coat to infect cells, aka HBV is a helper virus)
87
Q

which virus has special effect on pregnancy?

A

Hep E!!
high mortality rate of 25% in pregnant women & fetus

88
Q

rank the severity of symptoms of the different hepatitis viruses

A

HAV/HCV &laquo_space;HBV «HDV
HEV is self limiting w no sequelae

89
Q

what are the viruses that can cause hepatitis? (5)

A
  1. yellow fever virus
  2. EBV
  3. CMV
  4. rubella
  5. hantaviruses
90
Q

what are the most common hepatitis virus causes of acute hepatitis?

A
  1. HBV (50%)
  2. HAV (20-30%)
  3. HCV (5%)
  4. HEV (<5%)
91
Q

what are the most common hepatitis virus causes of chronic hepatitis?

A
  1. HBV (70%)
  2. HCV (20%)
92
Q

which hepatitis viruses does NOT cause carriage and chronic hepatitis?

A
  1. Hep A
  2. Hep E
93
Q

what are the most common hepatitis virus causes of liver cancer?

A
  1. HBV (70%)
  2. HCV (20%)
94
Q

what are the mechanisms of drug & toxin induced liver injury?

A
  1. direct toxicity
  2. through hepatic conversion of xenobiotic→ active toxin
  3. through immune mediated mechanisms
95
Q

what are the most common hepatotoxins causing liver failure? (acute + chronic)

A

acute: acetaminophen
chronic: alcohol…

96
Q

what are the risk factors of alcoholic liver disease (ALD)? (4)

A
  1. severity depends on dose & duration
  2. gender: females
  3. ethnic & genetic differences e.g. in detoxifying enzymes
  4. comorbid conditions eg concomitant liver pathologies like viral hepatitis
97
Q

what is the progression of ALD?

A

normal liver→ steatosis (fatty liver)→ steatohepatitis (hepatocellular inflammation and damage in response to the accumulated fat)→ cirrhosis→ hepatocellular carcinoma

steatosis & steatohepatitis can resolve/reverse w abstinence

98
Q

what are non-alcoholic fatty liver diseases (NAFLD)

A

spectrum of disorders that present with hepatic steatosis/fatty liver in absence of/low alcohol consumption

99
Q

what are the causes of NAFLD? (2)

A

associated w metabolic syndrome! buildup of fat in liver
1. insulin resistance→ dysfunctional lipid metabolism, increased production of inflamm cytokines
2. oxidative injury→ liver cell necrosis (fat laden cells are highly sensitive to lipid peroxidation pdts)

100
Q

what is the progression of NAFLD?

A

NAFLD→ isolated fatty liver (>80%) :))
NAFLD→ non-alcoholic steatohepatitis (NASH) :(→ NASH cirrhosis (11% over 15 yrs)→decompensation or HCC

101
Q

what is metabolic associated fatty liver disease (MAFLD)?

A

basically same as NAFLD lol,,, just better criteria model

102
Q

what are the diagnostic criterias of MAFLD?

A

detection of liver steatosis + at least one of:
- overweight/obesity
- T2DM
- clinical evidence of metabolic dysfunction

103
Q

what are the manifestations of impaired blood inflow to the liver? (3)

A

e.g. portal vein obstruction, intra/extrahepatic thrombosis

  • esophageal varices
  • splenomegaly
  • intestinal congestion
104
Q

what are the manifestations of impaired INTRAHEPATIC blood flow? (4)

A
  • ascites
  • esophageal varices
  • hepatomegaly
  • elevated ALT/AST
105
Q

what are the manifestations of impaired hepatic vein OUTFLOW? (5)

A
  • ascites
  • hepatomegaly
  • elevated ALT/AST
  • abdominal pain
  • jaundice
106
Q

what is a common non-neoplastic cause of liver mass?

A

focal nodular hyperplasia (FNH)

107
Q

what is FNH?

A

non neoplastic!!
-due to focal alterations in hepatic blood supply
- well-demarcated but poorly encapsulated pale nodule typically with central fibrous scar
- background non-cirrhotic liver

108
Q

what are 3 benign neoplastic cause of liver mass?

A
  1. hepatocellular adenoma (HCA)
  2. bile duct adenoma
  3. haemangioma
109
Q

what are haemangiomas?

A

benign neoplasm of connective tissue
- hypervascular, venous malformations forming noncancerous mass (angioma)
- most common benign liver tumour
complication: rupture→ intraperitoneal leeding, thrombosis

110
Q

what are hepatocellular adenomas?

A

benign neoplasm of hepatocytes
- pale, soft +/- hemorage in a non-cirrhotic background

111
Q

what are the malignant neoplastic causes of liver mass? (3)

A
  1. hepatocellular carcinomas (HCC)(90%)
  2. cholangiocarcinoma (CC)(10%)
  3. hepatoblastoma
112
Q

what is HCC?

A

malignant neoplasm of hepatocyte
- associated w HBV infections, younger pts in absence of cirrhosis

113
Q

what is CC?

A

malignant neoplasm of bile duct (both within & outside liver)
- 2nd most common primary malignant tumour of liver)
- risk factors (eg HBV, HCV, PSC)→ chronic inflammation & cholestasis→ promotes somatic mutations or epigenetic alterations

114
Q

what is hepatoblastoma?

A

malignant neoplasm
- rare but most common liver tumour of early childhood (<3yo)
- associated w FAP, Beckwith Wiedemann syndrome

115
Q

what are the common primary sites of malignant neoplasms that metastasize to the liver? (4)

A

colon, breast, lung, pancreas

116
Q

what is zollinger-ellison syndrome?

A

gastrin-secreting tumor of the pancreas→ stimulates H+ secretion by parietal cells (no negative feedback)

117
Q

what is pancreas divisum?

A

congenital: foetal CBD and pancreatic duct fail to fuse→ enter duodenum separately

118
Q

what is annular pancreas?

A

congenital: pancreas wraps around duodenum like a ring→ stenosis/obstruction

119
Q

what is ectopic pancreas?

A

congenital: pancreatic tissue in non-pancreatic sites eg stomach, intestines

120
Q

what is pancreatic agenesis?

A

congenital: missing parts of the pancreas

121
Q

what is acute pancreatitis?

A
  • reversible parenchymal injury
  • inappropriate release & activation of pancreatic enzymes→ destroy pancreatic tissue→ breakdown of pancreatic protective mech→ autodigestion of pancreas→ acute inflammatory reaction
122
Q

what is the pathogenesis of acute pancreatitis?

A
  1. duct obstruction → accumulation of enzyme rich fluid in pancreatic interstitium (raised intrapancreatic ductal pressure)→ edema→ impaired blood flow & → acinar cell injury (ischaemia)
  2. oxidative stress (eg alcohol) → release and activation of intracellular proenzymes → acinar cell injury
  3. defective intracellular transport (e.g. alcohol) → deliver proenzyme to lysosomal compartment→ intracellular activation → acinar cell injury

acinar cell injury→ activated enzymes→ acute pancreatitis

123
Q

what is chronic pancreatitis?

A
  • repeat episodes of acute pancreatitis, cause fibrosis (absent in acute)
  • prolonged inflammation of pancrease
  • irreversible destruction of EXOCRINE parenchyma, late stage destruction of ENDOCRINE parenchyma
124
Q

what is the etiology of chronic pancreatitis?

A
  • usually middle aged males
  • most common cause is long term alcohol abuse
125
Q

what are pancreatic pseudocysts?

A

non-neoplastic cysts presenting after acute pancreatitis or traumatic injury

126
Q

what are the common solid pancreatic neoplasms?

A
  • ductal adenocarcioma
  • acinar cell carcinoma

Gastro (20 decks)

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