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term 4 > ders path > Flashcards

ders path Flashcards

1
Q

guaiac test

A

tests for occult blood in stool(turns blue)

-ulcerative colitits, chrons, colorectal cancer

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1
Q

how to get leukoplakia

A

HPV, friction(ill fitting dentures), pipe smoking tobacco
-same risk factors for oral SCC, and erythroplakia

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2
Q

Red velvety eroded area
* Poorly circumscribed
* Typically marked dysplasia,
and intense inflammation
with vascular dilation

A

Erythroplakia

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3
Q

hairy oral leukoplakia microscopic features

A

Hyperkeratosis and acanthosis seen microscopically

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4
Q

plummer vinson syndrom sx

A

iron def anemia, esophageal webs, glossitits

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5
Q

plumber vinson syndrom ->

A

SCC
-partial obstruction causes progressive dysphagia

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6
Q

pseudoalchesia

A

secondary:
Chagas disease (Trypanosoma cruzi)
* Diabetic autonomic neuropathy
* Infiltrative disorders: malignancy, amyloidosis, sarcoidosis

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7
Q

what conditions are associated with esophageal varicies

A

decompensated cirrhosis and hepatocellular carcinoma (HCC)
-significant cuase of death in cirrhosis
via vericeal hemmorage

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8
Q

what changes morphologically under go with GERD

A

Hyperemia(so much blood flow), basal zone hyperplasia, and elongation of lamina propria all happen reactively
-will also see eosinophils NOT neutrophils

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9
Q

risk factors that cause scc of esophagus

A

achlasia, hot beverages/spicy foods, HPV, diet deficient in fruit and veggies, alochol and tobacco, plumber vinson

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10
Q

esophageal SCC metastisis

A

direct stread to mediastinal trachea and heart

lymphatic spread to Cervical, Mediastinal Paratracheal; Tracheobronchial; Gastric and celiac nodes

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11
Q

how to get congenital vs aquires pyloric stenosis

A

congential: trisomy 18, turner syndroms, esophageal atresia

aquired: peptic ulcer, chronic antral gastritis, malignency (inflammatoion and fibrosis cuases closing of opening)

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12
Q

acute erosive gastritis vs chronic non erosive gastritis

A

both non neoplastic, irritation to stomach from not enough protection to too much irritant
acute: NSAIDS, alcohol, iron, ulcers, AI
chronic: H pyloir, AI/pernicious anemia, systemic diseases

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13
Q

H Pylori associations

A

Diffuse antral gastritis(+- increase acid productin) and
Multifocal atrophic gastritis, both chronic gastritis(not neccesarily pernicious anemia).

Also Peptic Ulcers, Gastric carcinomas, and a MALToma/gastric lymphoma
-if inflammation is limited to antrium there will be inc gastrin. inc in parietal cells and inc acid
-if inflammation spreads to body, fundus will more likely be gastric carcinoma because will be gastric atrophy, dec parietal cells, dec acid

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14
Q

test to diagnose H Pylori

A

non invasive: urea breath, saliva or fecal PCR
invase: rapid urease test

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15
Q

AI gastritis complications

A

gastric carcinoma(gland destruction and atrophy, dec acid, dec intrinstic factor)
carcinoid tumor (causes endocrine hyperplasia)

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16
Q

what are risk factors that cause peptic ulcers

A
  • Helicobacter pylori infection
  • NSAIDs (potentiated by corticosteroids and inhibition of prostaglandins, besides that it is also a direct irritant!)
  • Zollinger-Ellison syndrome (PUD of stomach, duodenum, and jejunum bc of pancreatic tumor and too much gastric acid)
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17
Q

what are the differences between two types of gastric adenocarcinoma

A

intestinal: from chronic gastritis and intestinal metaplasia, H pylori, atrophy

diffuse:E-cadherin (CDH1) germline mutation. Signet ring cells, no gland formation, hard and plasticy = Linitis plastica

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18
Q

Krukenberg tumor

A

bilateral ovarian
spread of adenocarcinoma of stomach

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19
Q

Virchow node

A

active in adenocarcinoma of stomach

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20
Q

Blumer shelf

A

palpable mass on digital rectal exam suggesting stomach adenocardinoma metastasis to rectouterine pouch (pouch of Douglas)

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21
Q

Sister Mary Joseph nodule

A

subcutaneous periumbilical metastasis of stomach adenocarcinoma

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22
Q

Most common mesenchymal tumor of the abdomen

origin?
morphology?
mutation?

A

Gastrointestinal Stromal Tumor (GIST), most commonly in the stomach
-arise from the interstitial cells of Cajal, or pacemaker cells, of the
gastrointestinal muscularis propria
-solitary, well-circumscribed, fleshy, submucosal mass composed of thin, elongated spindle cells or plumper epithelioid cells
-Ckit (tyrosine kinase) gain of function mutations

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23
Q

Congenital anomaly due to incomplete involution of vitelline duct

other features:

A

meckles diverticulum

-in the right lower quadrent
-rule of 2s
-true diverticulum

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24
Q

meckles diverticulum complications

A

hemmorage and peptic ulcer
intersusseption and internal blockage
diverticulitis and fistule

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25
Q

HLA DQ2 (majority) and HLA DQ8

also…

A

celiac
also Anti gliadin antibodies
2. Antiendomysial antibodies(antibodies actually target tTG-2 enzyme
within endomysium).
3. Anti-tissue transglutaminase2 (tTG2)antibodies

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26
Q

Reduced villous : crypt ratio
* Villous blunting and crypt
hyperplasia
* Crypt elongation
* Lymphoplasmacytic infiltrate in
lamina propria
* Increased intraepithelial
lymphocytes (CD8+)

A

celiac

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27
Q

celiac disease complications

A

t cell lymphoma, iga nephropathy, dermititis herpetiformis

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28
Q

Whipple Disease

A

Multi-visceral chronic disease involving the small intestine, joints, heart and CNS
> malabsorptive diarrhea due to impaired villous absorption and lymphatic drainage.

triad: diahreah, weight loss, and arthritis. extra intestinal sx continue years after malasbortive, also cardiac neurologic, adn pulmonary problmes

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29
Q

mucosa laden with distended macrophages in lamina propria- contain PAS positive granules; Partially digested bacilli. This infects the intestines absorptive ability

A

whipple

-mycobacterium can also present like this(both PAS posi) so use zeil nelson to differntiate

PAS positive a1AT def

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30
Q

what can cause intestinal obstructions

A
  • Hernias
  • Intestinal adhesions
  • Intussusception(most common in young children- if they get rota there is a hypertrophy of peyer patches and then there is drag )
  • Volvulus

or paryltyic mucosa like hirchspurg

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31
Q

acute appendicitis etiology

A

Stasis of luminal contents by a fecalith/fecal block→increase in intraluminal pressure→
impaired venous outflow plus bacterial proliferation → ischemia and inflammation.

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32
Q

Neutrophilic infiltration of the muscularis propria

A

acute appendicitos

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33
Q

complication include peritonitis, pyelephlebitis(infalmmed thrombosis of the portal vein), portal venous thrombosis, liver abscess, and bacteremia

A

acute appendicitis

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34
Q

tumors of the appendix

A

-carcinoid is most common and is begign
-begnin mucinous cystadenomas
-malignent mucin producing cystadenocarcinoma
both Characterized by mucinous epithelial proliferation, extracellular mucin (mucin can dissect through and cause rupture–> PSEUDOMYXOMA PERITONEI

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35
Q

PSEUDOMYXOMA PERITONEI

A

from a ruptured appendix mucin neoplasm
-Tenacious, semisolid mucin fills the abdomen

  • spreads to: Adenocarcinoma of ovary, colon, pancreas
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36
Q

Associated with RET mutation in most inherited cases

A

Hirschsprung

-causes failure of neuroblasts from the neural crest to migrate to the end of gastrointestinal tract causing a loss of smooth muscle relaxation(via NO) in the rectum and causes obstruction

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37
Q

aganglionosis

A

Distal intestinal segment lacks both the Meissner submucosal plexus and the Auerbach myenteric plexus)Enteric Nervous System absent (no meissner or myenteric plexus of nerves)

seen in hirschpurng

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38
Q

complication of hirschpung dx

A

perforation and peritonitits

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39
Q

Acquired pseudo-diverticular (all layers not involved) flask-like outpouchings of the colonic mucosa and submucosa through the colonic wall

A

diverticular disease

-at the sight of the signoid colon
-form contispation

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40
Q

extraintestinal sx of IBD

A

more prevelant in UC
-migratory polyarthritis, alkylating spondylosis, erythma nodulosum, PSC, clubbing

intraintestinal = malabsorption more related to chrons

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41
Q

string sign

A

chrons strictures

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42
Q

backwash ileitis

A

aka toxic mega colon from ulcerative colitis

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43
Q

inflammatory infiltrates, crypt abscesses, crypt distortion, PSC

A

associatiations of both UC and Chrons

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44
Q

pseudopolyps

A

UC

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45
Q

infective agents of infective enterocolytis

A

bacteria: *salmonella, *mycobacterium, shigella, ecoli, yersinia, campylobacter
viral: CMV
parasite: Entamoeba histolytica

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46
Q

infective form and tansmission of amebic colitis

A

cystic form
feacal oral transmission

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47
Q

mimics pancreatitis

A

Entamoeba histolytica, amebic colitis

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48
Q

moa of Entamoeba histolytica

A
  1. Attatch to colonic epithelium via adhesin
    2 .Epithelial breakdown via protease***
  2. invade lamina propria into submucosa
  3. recuit neutrophils**
  4. lateral submucosal breakdown
  5. flash shaped ulcer
  6. bloody diahrea*
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49
Q

complication of Entamoeba histolytica

A

amebic liver abcess

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50
Q

erythrophagocytosis diagnostic for what

A

dignostic for active amebic enterocolitis
-Stool analysis shows presence of ingested red blood cells within
trophozoites which is pathognomonic
-Stool analysis can also show cysts with multiple nuclei, if seen alone it is
not specific for active disease (can be seen in carrier state)

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51
Q

what cuases typhoid fever
-transmission?

A

Salmonella enterica, and its two subtypes, typhi and paratyphi
-fecal oral, food, water

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52
Q

MOA of S. typhi

A
  1. Bacteria endocytized (brough in) by the endothelila cells and the Microfold M cells via T3SS to go into submucosa
  2. evade immune system via Capsular Vi antigen which inhibits phagocytosis and inflammation
  3. Engulfed in the submucosa by macrophages. can survive in macrophage and not phagocytize by T3SS.
  4. Macrophages take to other lymphoid tissue and causes enlargement of primary and secondary lymphnode tissues…Peyer patches enlarge into sharply delineated, longitudinal plateau-like elevations (may be longitdinal formation of ulcerations from inflammation above the peyer patch)

salmonella

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53
Q

typhoid nodules (aggregates of macrophages) in liver and spleen (hepatosplenomegaly) as well as other tissue such as peyer patches and mesenteric lymph nodes

A

progression of typ[hoid fever> step ladder fever

-ulcer above the submucosa of peyer patch is oval shape in longitudinal orientation

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54
Q

typhoid fever diagnosis

A

culture from bone marrow!

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55
Q

PSEUDOMEMBRANOUS COLITIS aka

A

Antibiotic-associated colitis/ diahreah

-predominently from clostridium diff
-also associated with PPI and immuno comprimose

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56
Q

Superficially damaged crypts distended by mucopurulent exudate which erupt in pseudomembranous colitis

A

mushroom cloud

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57
Q

sx for acute ischemic colitis vs chronic ischemic colitis

A

maybe from a thrombo embolysm
sudden onset pain, bloody diahreah, desire to deficate, coagulative necrosis of the musclar propia, exudate and fibrosis on serosa

-chronic from atherosclerosis or hypoperfusion(splenic flexture) cuases intestinal angina, strictures and can mimic inflammatory bowel disease

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58
Q

Mucosal epithelial hyperplasia projecting as a mass in the lumen in the left colon

A

Hyperplastic Polyps
-piling up of epithelium

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59
Q

non malignent polyps

A

hyperplastic

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60
Q

Nodular protrusions of the mucosa with a serrated surface

A

Hyperplastic Polyps

-right side colon cancer (MSI,HPNCC, nonconventional)

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61
Q

Typically pedunculated, smooth-surfaced, reddish lesions
* Focal disorganization of the epithelium and lamina propria with cystically dilated
glands/ tubules filled with mucin and inflammatory infultrate in the lamina propria

A

juvinile polyp

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62
Q

-Large and pedunculated with a lobulated contour
-Arborizing (branch-like) network of smooth muscle in lamina propria.

A

PEUTZ JEGHER SYNDROME

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63
Q

mucocutaneous
hyperpigmentation

A

PEUTZ JEGHER SYNDROME
-dark blue to brown macules on the lips, nostrils, buccal mucosa, palmar surfaces of the hands, genitalia, and perianal region

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64
Q

complications of peutz jegher

A

intussuspetion,
inc risk of malignencies(colonies, pancreatic, breast

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65
Q

convential vs non convential adenomas

A
  • Conventional adenomas - tubular, villous, tubulovillous (
  • Non-conventional - Sessile serrated adenomas. (right)
    -Presence of epithelial dysplasia (risk of malignancy) with no invasion-tall, hyperchromatic crowded nuclei
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66
Q

clinical features of adenomas

A

asymtomatic, anemia from occult blood loss, intercusseption
villous adenoma can cause hypokalemia

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67
Q

APC tumor suppressor gene on chr. 5q

A

Familial Adenomatous Polyposis
-needs two hits
-causes 1000+ polyps

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68
Q

Gardner Syndrome

A

FAP + osteomas of the mandible, skull, and long bones + epidermal cysts + desmoid and thyroid tumors + dental abnormalities

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69
Q

Turcot Syndrome

A

FAP + CNS tumors

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70
Q

MSH2, MLH1

A

mismatch repair mutation causes HNPCC

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71
Q

Mucinous and signet ring cell

A

Hereditary Non-Polyposis Colon Cancer

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72
Q

neoplasm that Usually arise at sites of chronic inflammation

A

MALT (b cell ) lymphoma
ex. peyers patch
from H pylori chronic gastritis

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73
Q

acute liver failure association

A

encephalopathy
acetometaphen damage
heptitis virus infectin
autoimmune hepitits

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74
Q

Liver is small and shrunken due to loss of parenchyma → can lead to decline in
serum transaminases

A

acute liver failure

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75
Q

large zones of hepatocyte loss with areas flooded with RBCs
interspersed by occasional islands of surviving/ regenerating hepatocytes

A

acute liver failure

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76
Q

what causes cronic liver failure

A

hep b/c, NAFLD, AFLD, AI hepatitis

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77
Q

Condition marked by the diffuse transformation of the entire liver into regenerative
parenchymal nodules surrounded by fibrous bands with variable degrees of vascular shunting

A

cirrhosis

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78
Q

cirrosis pathogenesis, what cells

A

Activation of Hepatic stellate cells (Ito) responsible for hepatic fibrosis

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79
Q

Pruritis due to persistent cholestasis
* Hyperestrogenemia due to impaired metabolism
➢ Palmar erythema, Spider Angioma
➢ Hypogonadism and Gynecomastia in males
* Hypogonadism in women can occur due to disruption of hypothalamic
pituitary axis function

A

cirrhosis

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80
Q

cirrhosis complications

A

Hepatic encephalopathy
* Bleeding from esophageal varices
* Bacterial infections (resulting from damage to gut mucosal barrier and
Kupffer cell dysfunction)
* Development of hepatocellular carcinoma

81
Q

Chronic, progressive hepatitis, presence of autoantibodies, and therapeutic response to immunosuppression

A

AI hepetitis

82
Q

Interface hepatitis, lymphoplasmacytic activity in portal tract and lobule, Regenerating hepatic rosettes

A

AI hepetitis

83
Q

Steatosis
* Steatohepatitis (NASH): ballooning, Mallory hyaline (Mallory-Denk bodies)
* Fibrosis around central vein

A

ALD, NAFLD, Wilsons disease(with central fat necrosis)

84
Q

Autoimmune disease characterized by progressive nonsuppurative, inflammatory destruction of small and medium sized intrahepatic bile duct

A

PBC
-resulting from T lymphocyte–mediated destruction

85
Q

PBC diagnosis

A

Antimitochondrial antibodies. Elevated serum alkaline phosphatase and γ-glutamyl transferase→both are markers of cholestasis(flow bile blockage from liver to duodenum)

86
Q

PBC features morphological and clinical

A

*Lymphocytic and/or granulomatous bile duct destruction (florid duct lesion)
* Profound cholestasis→feathery degeneration; Mallory Denk bodies(also seen in Wilson disease)
* May progress to cirrhosis

Clinical features: Fatigue, pruritus and jaundice.

87
Q

Chronic cholestatic liver disease with segmental inflammation and obliterative fibrosis of intrahepatic and extrahepatic bile ducts with dilation of preserved segment

A

PSC

88
Q

Excess iron deposited in parenchymal organs such as the liver and pancreas → followed by

A

heart, joints, and endocrine organs

hemochromatosis

89
Q

Hemochromatosis mutation,or can be caused by?

A

autosomal recessive mutations in HFE gene most commonly (excessive iron absorption)

can also be causes by transfusions, alcohol, HEPETITIS C

90
Q

hemosiderosis

A

Excess iron in cells (no symptoms)

91
Q

Autosomal recessive disorder that affects copper metabolism in body.

A

wilson dz

92
Q

wilson dz mutation

A

mutations in the ATP7B gene on chromosome 13, which is responsible for encoding a protein that helps transport copper out of the liver.

93
Q

wilson dz morphology

A

Liver: non-specific changes including
* Fatty change with focal hepatocyte necrosis
and Mallory Denk bodies
* Acute fulminant hepatitis, chronic hepatitis, cirrhosis
-deposition in the neuronal gangia causes CNS sx
-deposition in eye causes sunflower cataracs

94
Q

Periodic acid–Schiff (PAS) stain of the liver, highlights the characteristic magenta cytoplasmic granules→round-to-oval cytoplasmic globular inclusions of misfolded protein

A

alpha 1 AT

95
Q

Long term use of oral contraceptives and anabolic steroids are associated with the development in some patients

A

hepatic adenoma

96
Q

hepatoblastoma spreads to

A

Spreads to lungs, lymph nodes and peritoneum

97
Q

types of hepatoblastoms

A
  • Epithelial type: composed of small polygonal fetal cells or embryonal cells forming
    acini, tubules, or papillary structures vaguely recapitulating liver development
  • Mixed epithelial and mesenchymal type: contains foci of mesenchymal
    differentiation that may consist of primitive mesenchyme, osteoid, cartilage, or striated muscle
98
Q

Strong propensity for invading vascular channels (portal vein, Inferior Vena Cava)

A

hepatocellular carcinoma

99
Q

Variant of hepatocellular carcinoma
* Younger age
* No association with HBV or cirrhosis
* AFP normal
* Outcome similar to HCC in non-cirrhotic live

A

Fibrolamellar Carcinoma

-AFP also normal in cholangiocarcinoma

100
Q
  • Usually, single hard tumor with fibrous bands traversing through it (scirrhous)
  • Well differentiated polygonal cells in cords or nests, separated by fibrous septa
A

Fibrolamellar Carcinoma

101
Q

Malignancy of the biliary tree, arise from intra and extra hepatic bile ducts
how does it present?

A

Cholangiocarcinoma
-presents as multifocial liver lesions)

102
Q

risk factors for cholangiocarcinoma

A

PSC, gallstones, benzidine, nitrosamines
parasitic infections: Clonorchis sinensis and Opisthorchis viverini

103
Q

what neoplasms metastitize to the liver

A

-adenocarcinomas of the colon, stomach, pancreas
-breast
-lung
-neuroendocrine tumors
-melanoma
-neuroblastoma
-Wilms tumor
-leukemia

104
Q

Risk factors: advancing age, female gender, oral contraceptives, obesity, rapid weight reduction

A

Cholelithiasis (cholesterol stones)

105
Q

Primarily in the setting of bacterial infections of the biliary tree and parasitic
infestations
* Risk factors: chronic hemolysis, biliary infection

A

pigmented biliary stones- cholelithiasis

106
Q

Primary complication of gallstones

A

Acute calculous cholecystitis(inflammation of the gallbladder)
-from flow obstruction

107
Q

Results from gall bladder stasis and ischemia→cystic artery is an end artery with no collateral circulation

A

Acute acalculous cholecystitis
-bc of hypotension sepsis, immunosupression, infection

108
Q

Mucosal phospholipase converts lecithin to lysolecithin
→Damage to glycoprotein layer of mucosa →Further release of prostaglandins from mucosa
→ Cumulatively leads to mucosal & mural inflammation
→Increased intraluminal pressure will can cause ischemia
→Superimposed bacterial contamination

A

pathogenesis of cholecystisis due to obstruction of flow

109
Q

PORCELAIN GALL BLADDER

A

extensive dystrophic calcification from multiple acute cholecytisis attacks causes chronic cholecystitis

-Bluish discoloration and brittle consistency of gallbladder(inc risk of cancer)

110
Q

Mirizzi syndrome

A

gallstone impacted in the cystic duct causing compression of
common hepatic duct and obstructive jaundice
type of Choledocholithiasis (bile duct stone)

111
Q

agents that cause CHOLANGITIS (bile duct inflammation)

A

E.coli, S.faecalis,
Enterobacter

112
Q

sx for cholangitis

A

charcots triad (fever, right upper quadrant pain and jaundice)

113
Q

An autosomal recessive systemic disorder of exocrine glands characterized by:
* Chronic pulmonary disease
* Deficient exocrine pancreatic function
* Other complications of inspissated mucus in a number of organs, including the small intestine, liver and the reproductive tract

A

cystic fibrosis

114
Q

cystic fibrosis mutation

A

Gene on chromosome 7 (7q31.2) encodes for a protein called the CF transmembrane conductance regulator (= CFTR)
* Major function of the CFTR protein in the sweat gland ducts → reabsorb luminal chloride ions and augment sodium reabsorption through the epithelial sodium channel (ENaC)

with defective Cl transport: high sweat salt concentration, thick luminal secretions

115
Q

Bronchiectasis
* Pancreatitis
* Diabetes
* Neonatal intestinal obstruction * Azoospermia, infertility

A

cystic fibrosis

116
Q

acute pancreatitis laboratory findings

A
  • Raised amylase levels in first 24 hours
  • Followed by lipase within 72-96 hours
  • Hypocalcemia (calcium used in fat necrosis)
117
Q

acute pancreatitis complications

A
  • Acute Respiratory Distress Syndrome (ARDS)
  • Acute Tubular Necrosis (ATN)
  • Pancreatic abscess – later in the course of the disease
  • Pseudocysts
118
Q

pancreatic adenocarcinoma accosiation

A

smoking
KRAS mutation

-usually in the head, then body, then tail

119
Q

Features of obstructive jaundice – tumor in the head of pancreas
* Trousseau’s syndrome (migratory thrombophlebitis) may be present.
* Release of platelet activating factors and procoagulants from tumor
* No single specific marker but sometimes raised CA 19-9

A

pancreatic adenocarcinoma

120
Q

what vaccines are available for food borne pathogens

type?

A
  1. rotavirus given at 2 months(2 live attenuated oral- common AE is intussusseption)
  2. cholera (attenuated with ctxA delected). give to travelers or for outbreaks
  3. typhoid (2- Vi capsular polysachoride, and Ty21a live attenuated oral
  4. Hepetitis A
121
Q

common food poisoning organisms

A

bacteria: staph aureus, Clostridium botulism

marine/algae: Ciguatera, Scombroid, Shellfish, Pufferfish

122
Q

Associated foods: sliced meat, ham, poultry, *puddings, *potato or egg salad, *mayonnaise, *cream pastries

A

staph aureus

123
Q

what makes you stick with staph aureus food poisoning

A

enterotoxin ST:heat stable and activate guanylate cyclast
-also used in B.cereus

124
Q

Large, G +ve, motile, rods, anaerobic, spores forming,
neurotoxin

A

clostridium botulism

-spores germinate when at low O2 concentrations and they are heat resistant but the toxin is heat liable

125
Q

-Disease often starts with nausea,vomiting,abdominal pain,diarrhea,and dry mouth with sore throat.
– Eventually CNS symptoms develop:
* Cranial nerve palsies-doubl evision,blurred vision,drooping eyelids, slurred speech, difficulty swallowing, dry mouth and muscle weakness ***Symmetric descending flaccid paralysis, respiratory failure, death

A

clostridium botulism

126
Q

moa of botulism toxin

A

Binding presynaptically to high-affinity recognition sites on the *cholinergic nerve terminals and decreasing the release of acetylcholine, causing a neuromuscular blocking effect.

127
Q

toxin activates voltage dependent sodium channels

where to be found

A

Ciguatoxin
found in barracuda, black grouper & amberjacks

128
Q

Ciguatera Fish Poisoning presentation

A

GI (3-6 hrs post ingestion) - diarrhea, nausea, vomiting, abdominal pain/cramps

– CNS (3-72 hrs post ingestion) - peri-oral paresthesias, pruritus without urticaria, a metallic taste in the mouth, painful dentition, painful urination, blurred vision, and temperature- related dysesthesias

– CVS (within hours) - bradycardia, heart block, hypotension

129
Q

Scombroid poisoning
-how does it happen and from where

A

from tuna, mackerel, mahi mahi, swiss cheese
pimproper storage allows bacterial overgrowth causing build up of histidine > histamine

130
Q

major agents causing esophagitis

A
  1. candida spp, 2. HSV, 3. CMV,

also can be caused from immunosupresion (cancer, transplant, HIV, diabetes)

131
Q

Multinucleated giant cells with ground-glass nuclei and eosinophilic inclusions

A

HSV

132
Q

intranuclear or intracytoplasmic inclusion bodies (Owl’s eye inclusions)

A

CMV

133
Q
  • Gram negative
  • Curved to spiral (1-3 turns)
  • Motile: 5-6 polar flagella
  • Microaerophilic: 2-5% O2, 5-10% CO2
  • Oxidase positive
  • Urease positive
A

H Pylori

134
Q

Helicobacter pylori: Virulence Factors
-colonization
-immune escape
-disease induction

A

Colonization:
* Adhesins: BabA and SabA
* Outer membrane proteins
* Flagella: Bacterial movement to epithelial surface
* Urease: Neutralize gastric acid

Immune escape:
* Lipopolysaccharides
* Exotoxins: Suppress phagocytosis, Block effector T cell response

Disease induction:
* Type IV secretion system :Injection of effectors
* Secretory enzymes
* Exotoxins-Caga+, Vaca
* Effectors

135
Q

Cytotoxin associated gene A+(CagA+) strains have inc risk of:

A

from H pylori
inc risk of peptic ulcers and oncogenesis (facilitates malignent transformation of gastric epithelial cells)

136
Q

Forms anion-selective channels in vacuole membranes➔swelling * Inserts in mitochondrial membranes➔mitochondrial death➔
induction of apoptosis

A

VacA toxin from H pylori

137
Q

Production of ammonia increases pH

A

principle of urease invasive test for H pylori (urease produces ammonia)

138
Q

agents of appendicitis and pseudoappendicits

A

E coli, B. fragilis, Peptostreptococci, Pseudomonas

Pseudoappendicitis by Yersinia
enterocolitica

139
Q

Grey Turner sign
Cullen sign

A

pancreatitis
GT sign is flank ecchymosis
Cullen is perumbilical ecchymosis

140
Q

what mirobe causes intrabdonimal access

A

Bacteroides fragilis- GNAR
-cna really cause abcess anywhere

can also include resident GI microbes(E coli, klebsiella)

141
Q

bacteriodes fragilis virulence factors

A

-adhesive surface pilli
-antiphagocytic capsule
-penicillin resistant bc beta lactamase production
LPS endotoxin is less toxic than other gram -

142
Q

major nosocomial pathogen

A

Clostridium difficle

-primary cause of anti biotic associated diahreah in the hospital

143
Q

G+ bacillus
anaerobe
endospore formation
motile
oppertunistic
toxin produces

risk factors?

A

clostridium difficile
-only the toxin forming stains thrive with antibiotic otherwise there are non toxic versions in the normal GI. A and B toxin.
- risks to C diff is antibiotic use, hospitalization, PPI, older, exposure to health care worker(may cause initial endospore formation, then add antibiotic and get full sx)

144
Q

toxic mega colon

A

complication of:
ulcerative colitis
C difficile

145
Q

C diff toxin and virulence factor

A

A and B toxin. TcdA-enterotoxin binds to brush border. TcdB-cytotoxin(depolymerized actin and disrupts cytoskeleton)

flagella and adhesin

146
Q

toxin leads to an inflammatory cascade

A

C difficile

147
Q

pseudomembranes

A

adherent white yellow plaques

somewhere inbetween mild diahrea sx and severe toxic megacolon sx.

148
Q

diagnosis for C diff

A

(GDH)EIA for Glutamate Dehydragenase
EIA for toxin A or B

-no culture

149
Q

tests for diagnosing inflammatory diahrea

A

only preformed in certain situations:
-stool lactoferrin tests for WBC(inflammatory diahrea)
-stool RBC
-ova and parasite stool test(done under special circumstance)

150
Q

in US stool culture will be for

A

camylobacter(with CAMPY micro-aerobic conditions), shigella, and salmonella

e coli needs special request

macconkey will have ecoli fermenting lactose and shigella and salmonella not fermenting(clear)

shigella -salmonella agar has salmonella black H2S produced. and shigella green/cleart H2S not produced

151
Q

Enterobacteriaceae members

similarities

A

Escherichia** Shigella** Salmonella** Yersinia**
Klebsiella* Proteus*

all facultative anaerobes
Gram -ve, non-spore forming, rod shaped bacteria. all motile except shigella and klebsiella

152
Q

Gram -ve bacilli (Rods)
Facultative anaerobes
Motile
* Rapid Fermenter of Lactose
* Catalase Positive
* Oxidase Negative

A

e coli

grow pink on mc conkey agar

153
Q

ETEC virulence factor

A

Mucosal adherence with pili/fimbrae(CFA- colonization factor antigens).

Exotoxin/enterotoxin production: Heat-labile and stable toxin ( LT and ST). Both 1A 5B(acitve and binding)
LT-similar to cholera and inc Camp
ST- inc guanilate cyclase(in staph aureus poisoning)

both of these virulence factors are plasma encoded

154
Q

1o cause of “Traveller’s Diarrhoea”
pathogenesis?

A

ETEC
-injest contaminasted foos, strong attatchment to SI and release of LT and ST to cause electrolyte disturbance, no invasion

155
Q

infintile diahrea
pathogenesis?

A

EPEC
-no LT, ST, CFA like seen in ETEC
-plasmid encodes for adherence factor Bundle Forming Pilli(BFP)
-also does not invade like ETEC but will cause attatchment-effacement lesion and will cover the whole top surface area to a dec in absorption leading to diahrea (food borne illness)

156
Q

Single curved Gram-ve rods, 2 - 4μm long
– (May be linked end to end) forming “S” shapes – Motile (single polar flagellum)
– Non-spore forming
– Facultative anaerobes
– Oxidase +ve

A

vibrio cholera

oxidase is key test done for diagnosis

157
Q

ferments sucrose and mannose
acid sensitive
halo tolerant

A

vibrio cholera

158
Q

Bacteriophage encoded AB toxin

A

cholera toxin CtxA
-very similar effect to LT toxin of ETEC and will cause electrolyte imbalance via inc in camp

causes rice water stool
-food borne illness

159
Q

Thiosulphate-citrate-bile salts-sucrose (TCBS) agar

A

sucrose acts as a differentiating agent for Vibrio CHOLERA(not another type of vibrio)
sucrose+ yellow dots

160
Q

Gram-positive
* Large anaerobes
* Non-motile rods
* Spore-forming
*Members of the intestinal microflora of humans and most other animals

A

clostridium perforingens

type A causes the food borne infection

161
Q

clostridium perforingens pathogenesis

A

injestion from food source, sporulation in SI(conditions are perfect) and will release CPE (an LT type toxin which causes *cytotoxic acitivty and *alters membrane permeability, causing electrolyte imbalance and diahrea

can see enterotoxin in feces

162
Q

Gram +ve rods
Arranged in chains
Aerobic
Spore former
Emetic toxin & Enterotoxin

A

bacillus cereus

emetic is if injesting preformed toxin(resemble Staph aureus and injest ST NEUROtoxin found in rice/grains)
entereotoxin if ingesting pathogen-acts identically to C-perforingens with LT toxin inc camp

163
Q

Non-enveloped
Icosahedral nucleocapsid
ss +ve sense RN

A

norovirus -

164
Q

winter vomitting disease
pathogenesis

A

norovirus
-transmitted fecal oral, food, water
SI is perfect conditions for multiplication, transient lesions produced- microvilli shortened and intrercellular spaces wider, no damage to large intestine and no fecal leukocytes, shed in feces

165
Q

Wheel-shape,
Non-enveloped
double-capsid structure (3 layers counting core)
ds RNA

whats in core and whats on capsid

A

rotavirus

core has rna dep rna polymerase
capsid has VP4- P antigen for Protease sensitive ATTATCHMENT and VP7-G antigen for Glycoprotein

166
Q

rota virus pathogenesis

A

kinda similar to noro
- ingest fecal oral or water and multiply in the SI. Causes SI microvilli dmaage and atrophy(decreasing surface area of SI and dec production of disaccharides). Normal columnar epithelium at the villus tips is replaced by irregular cuboidal, cryptlike cells, leading to multiple defects in fluid and electrolyte regulation in the affected intestinal mucosa. NSP4 protein acts like a toxin and inc net fluid excretion, shed in the faeces

167
Q

Non-enveloped,
icosahedral symmetry
* Smooth or slightly indented outer shell
* ss +ve sense RNA

A

Astroviruses

like noro also peaks in winter
like rota virus pathogenesis with infection there is villi shortening and decreased intestinal enzyme activity(sx are milder here than rota)

168
Q

Icosahedral protein shell capsomeres
ds DNA
Pentons

A

adenovirus

main taget is the respiratory system, but can also infect small intestine

169
Q

Coccidian Protozoan that causes chronic diahrea

A

Cryptosporidium
-especially in AIDS pts
called persistent diahrea in children of endemic countried
-can cause some mild villopus blunting

170
Q

which oocytes resist disinfectant including chlorination

A

cryptosporidium
acid fast thick walled oocyte is shed in feaces (diagnostic and infective stage)

171
Q

Gram-positive, facultatively intracellular,
Non-spore forming, halophilic, beta-hemolytic (beta hemolysin), coccobacilli (short rods).tumbling motibily

A

Listeria
-tumbling motility
-readily multiplies in the fridge(putting unpasturized milk and raw cheeses(soft)/meat in the fridge aint gunna cut its)
-Only Gram-positive organism that has an endotoxin

motile at 30°C and below

172
Q

Transplacental vertical transmission

Vaginal transmission- during birth of neonate

A

listeria

effects pregnant women and neonates

173
Q

listeria pathogenesis

A

-Invades epithelium via InlA and InlB
-will go in a vacuole
-vacuole rupture via pore forming toxin LLO +PlcA and PlcB
-now an replicate freely in the cytoplasm
-when it is time to spread to the next cell. ActA expression forces host to polymerize actin. rocket propell
-into the next with a double vacuole which will just get taken care of by LLO…

174
Q

listeria diagnosis

A

with blood culture!

175
Q

No known animal reservoir
* Non-motile
* Non-encapsulated
* Gram –ve rods
Acid stable
***Intracellular
(does not ferment lactose
H2S negative)

A

shigella
-similar to EIEC with toxin and has a low infectious dose
-H2S negative, does not ferment lactose

Food, Flies, Feaces, Fingers…not animal
-exposure risk at day care! day care exposure also to yersinia

176
Q

shigella virulence factors and pathogenesis

A

Endocytosis the M cell: attatch and T3SS
Phagosome lysis, and macropahge apoptosis, IL 1 release : T3SS
Endotoxin: O
Exotoxin: shigella toxin only in shigella D
-Stays intracellular to avoid humoral immunity
-actin rockets

NAD glycohydrolase: destroys NAD causing cell death

does not invade into the blood stream

177
Q

Bacillary dysentery
causes inhibition of?

A

from the shigella toxin(only in shigella dysteneria)

-enterotoxic(adheres to SI and blocks absorption), neurotoxic(abdonimal cramping), cytotoxic(1A 5 B structure…B bing to glycolipid, A active causes irreversible inhibition of 60 S ribsomoal subunit

178
Q

reactive arthritis

A

conjuctivitis, urethritis, arthritis

cant see, cant pee, cant climb a tree

Shigella, Salmonella, Yersinia, (1% c. jejuni)

179
Q

Gram-negative, rod-shaped
* Motile
* Facultative anaerobic
* Non spore-forming
Lactose fermenter
major surface antigens?

A

E coli

major surface antigens: K=capsule, H=flaHgella, O: LipOPS

180
Q

EIEC pathogenesis
no virulence factors given

A

similar to Shigella
-Endocytosis into M cell. Invades the LI where macrophage will eat it.
-Lysis of phagolysosome
-replicates in cytoplasm
-actin rocket
destroys colonic cells , does not invade the system.

181
Q

Characterized by the presence of aggregative adherence fimbriae (AAF

A

EAEC

-helps with attatchment to intestinal mucosa and triggests host immune responce with enhanced mucus biofilm production**
-there is no intracellular jouney like EPEC and ETEC

AAF binds to MUC1

182
Q

O157:H7

resoviour?

A

SLT- shigela like toxin of EHEC, STEC, VTEC

-resovior in cattle and sheep

183
Q

STEC presentation

A
  1. Hemoragic colitis( 3 days after injestion) = bloody diahrea,,,started as watery
  2. About one week after the diahrea there is HUS(microangio anemia with shistocytes, thrombocytopenia, and acute renal failure)
  3. if elder can develpoe TTP which is HUS with mental presentation
184
Q

STEC pathogenesis

A

-injestion (cattle and sheep resoviour)
-attatchment similar to EPEC(Bundle Forming Pilli(BFP))
-phage encoded toxin-cytotoxin/verotoxin(Stx-1 is similar to shigella, also Stx-2…both are AB toxins and blocks rRNA)
-this causes the hemoragic colitis
-toxin enters the blood! and binds to glomerular epithelium cuasing the HUS

185
Q

Gram negative rods
* Do not ferment lactose
* Motile
acid labile
H2S positive

major surface antigens?

A

Salmonella

surface manigens: O-LPS cell wall
H= flaHgella
Capsular Vi

colorless on mac conkey agar(doesn ferment lactose)

186
Q

pathogenesis of salmonella

A
  1. Attatchment and invasion of eplithelial via SPI-1and T3SS
  2. Invade M cells/macrophage of Peyer patch
  3. Intracellular survival via SPI-2 and T3SS
  4. replicate INSIDE vacule
  5. macropahge disseminatesto different organs…this is when it becomes typhoid fever
    transport to liver, spleen, bone marrow in macrophage, colonization in gallbladder, bacteremia and replication in bile. bile renters intestines
187
Q

macular rash on trunk

A

salmonella typhi

-other dx for salmonella is blood(amenia, leukopenia, NO eosinophils)

188
Q

curved-spiral rods
* Gram -ve
* Motile (single polar flagellum)
* Microaerophilic
* Oxidase +ve

resovior?
toxin?

A

campylobacter jejunilarge animal

-resovior: esp kittens and puppies, also commercial poltery, cows, sheep

-toxin: endotoxin, enterotoxin(watery diahrea),cytotoxin(bloody diarrhea)

oxidase catalase test is the definitive diagnosis

189
Q

Symptoms appear 3-5 days after ingestion
* Vomiting – slight
* Diarrhea - often profuse
* Abdominal pain - often severe
* Prostration – often severe
* Pyrexia – often present
* Other symptoms – blood-stained feces

A

campylobacter jejuni

similar clinical presentation for salmonella and shigella

190
Q

Guillain-Barré syndrome

A

paralysis starting form the feet
c. jejuni
-antibodies against c. jejuni cross react with GM1 ganglioside in the myelin sheaths bc they look similar and leads to their destruction

191
Q

pseudoappendicitis

toxin and effect?

A

yersinia

ST enterotoxin(inc cGMP)

191
Q

Psychrotroph

resovior?

A

Yersinia

resovior: pigs*, any farm animalor rodent. fish and shellfish. risk with unpasturized milk, cheese
-ink risk if you have iron overload!

192
Q

Gram -ve,
Glucose +ve
Sucrose +ve
Catalase +ve
Oxidase -ve

A

Yersinia

193
Q

bipolar-staining,
coccobacilli

A

Yersinia

194
Q

Not agglutinated by anti O1 sera

A

non cholera vibrio
and halophilic(likes salt, vibrio cholera is halo tolerant)

195
Q

enterotoxin & haemolysin

A

Vibrio parahaemolyticus

196
Q

Vibrio vulnificus is concern for

sx?

A

Patient with underlying liver conditions

-acute gastroenteritis, necrostizing skin, invasive sepsis

197
Q

Capsule
* Heme receptors, siderophores (iron acquisition)
* Fibronectin binding protein, pili (adherence)
* Metalloprotease, hemolysin, cytolysin, phospholipase (extracellular products)
* Endotoxin
* Flagellum

A

Vibrio vulnificus virulence

198
Q

Vibrio vulnificus diagnosis

A

Screening of stool samples
oxidase activity

TCBS) agar - for both vuln and parahaemocyticus

sucrose test - for both vuln and parahaemocyticus

term 4 (13 decks)

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