Pathoma + Secrets Flashcards

Question

GERD-rLES

Answer 1

* reflux of acid from the stomach d/t REDUCED LES tone (diaphragm usually helps with this) * RF (6): * alcohol * tobacco * obesity * fat-rich diet * caffeine * sliding hiatal hernia (cardia is in esophagus hourglass)

Answer 2

* heartburn (mimics cardiac chest pain) * asthma (adult-onset) * cough-can irritate airway as acid shoots up * damage to enamel of teeth * Late complications: * ulceration with stricture (narrow lumen) * Barrett esophagus * fibrosis b/c stem cells are destroyed

Answer 3

* metaplasia of lower esophageal mucosa (innermost layer) * f/m: stratified. squamous. epithelium * to: NON-ciliated. columnar. epithelium (with goblet cells) * in 10% of GERD pts * PP: response of lower esophageal stem cells to scidic stress * may progress to dysplasia and adenocarcinoma

Answer 4

* two main types: adenocarcinoma or squamous cell carcinoma * presents late poor prognosis) * s.s: * progressive dysphagia (solids to liquids) * weight loss * pain * HEMATEMESIS * \*\*Squamous (extra): * hoarse voice (recurrent laryngeal nerve involvement) * cough (tracheal involvement)

Answer 5

* malig proliferation of **GLANDS** * mc type of esophageal ca in the WEST (**AdenoAmerica**) * arises from pre-exisiting **Barrett esophagus** * usually involves LOWER 1/3 of the E * RF: * fat (obesity) * GERD * smoking

Answer 6

* malig of squamous cells * m/c E ca WORLDWIDE * usually arises UPPER 2/3 * RF (irritation): * **alchohol and tobacco** (mc causes) * very hot tea * **achalasia** * esophageal web (**PVS**) * esophageal injury (lye ingestion)

Answer 7

* congenital malformation * anterior abdominal wall leading to exposure of abdominal contents (hole in wall)

Answer 8

* PERSISTENT herniation of bowel into umbilical cord * PP: failure of hearniated intestines to *return to body* cavity during development * contents are **COVERED** by peritoneum and amnion of the umbilical cord

Answer 9

* congenital HYPERTROPHY od pyloric smooth muscle * more common in males * stenosis=cant get food out=build up PRESSURE

Answer 10

* born NML * presents two weeks after birth as: * projectile NON-bilious vomiting * d/t build-up in pRESURE * NON-bilious b/c bile is in duodenum hasnt reached there yet * VISIBLE peristalsis * olive-like mass in the abdomen * tx: myotomy (cut away the muscle)

Answer 11

* two main divisions: mucosal and smooth muscle layer * --or-- FOUR divisions

1. Mucosa
2. Submucosa
3. Muscularis externa
4. Serosa

Answer 12

* two main divisions: mucosal and smooth mu layer * 1. MUCOSAL * Mucosa * epithelium * lamina prpria * muscularis mucosa * SUB-mucosa * + SUBmucosal plexus * 2. SMOOTH MU LAYER * inner circular * +myenteric plexus of * outer longitudinal * ALL covered by: * serosa-INTRA.peritoneal * ---or--- * adventitia-RETRO.peritoneal

Answer 13

* PORTAL TRIAD (periportal) zone * affect FIRST by VIRAL hepatitis * ingested toxins (cocaine)

Answer 14

* intermediate zone * ylw fever

Answer 15

* pericentral vein/centrilobular zone * affected FIRST by ISCHEMIA * contains cytochrome P-450 system * most sensitive to METABOLIC toxins * site of ALCOHOLIC hepatitis

Answer 16

1. bile duct 2. branch of portal vein 3. branch of hepatic artery

Answer 17

* bile flows f/m Zone 3 to 1 * blood flows from Zone 1 to 3

Answer 18

* **CURLING** ulcer (severe burn) * extends through mucosal INTO SUB.mucosal * hypo-volemia leads to DEC blood supply * **CUSHING** ulcer (INC ICP) * INC stim of vagus nerve=INC acid production (via INC ACh) * **NSAIDS** * DEC PGE2 * PG usually: DEC acid, INC blood flow, stim mucosa * Heavy **ALCOHOL** consumption=DIRECT toxin * **CHEMO-**therapy-knockout cells thatre turning over * **SHOCK** * DEC blood flow * multiple (stress) ulcers may b seen in ICU pts

Answer 19

* acidic damage to the stomach mucosa * d/t **IMBALANCE** between mucosal defenses and acidic environment * *Defenses*: * **mucin** layer (produced by foveolar cells) * **bicarb** secretion by surface epithelium * normal **bloody supply** * provides nutrients and picks up leaked acid * *acid damage* results in: * superficial inflamm * erosion (loss of superficial epithelium) * ulcer (loss of mucosal layer)

Answer 20

* chronic inflamm of stomach mucosa * divided into two types based on underlying etiology: * 1. chronic AUTO-IMMUNE gastritis * 2. chronic H. PYLORI gastritis (more common)

Answer 21

* a.i. destruction of gastric PARIETAL ces (located in stomach body and fundus) * assoc w/ Ab vs. parietal cells and/or IF * path mediated by T-cells (type 4 HS)

Answer 22

* atrophy of mucosa with intestinal metaplasia * achlorhydria with: * INC gastrin leveles * b/c of lost neg feedback * antral G-cell hyperplasia * megaloblastic (pernicious) anemia d/t lack of IF (no Vit B12) * INC r/o gastric adenocarcinoma (intestinal type)

Answer 23

* d/t H. pylori-induced acute and chronic **INFLAMM** * **mc form of gastritis** (90%) * H. pyori UREASES and PROTEASES along with inflamm weaken mucosal defenses * **ANTRUM**=mc site

Answer 24

* CP: * epigastric abdominal pain * INC r/o: * ulceration (PUD) * gastric adenocarcinoma (intestinal type) * MALT lymphoma (B cell lymphoma) * Tx: **TRIPLE therapy**: * 1. PPI * 2. Amoxicillin * 3. Clarithromycin (Macrolide) * resolves gastritis/ulcer and reverses intestinal metaplasia * NEG urea breath test and lack of stool Ag=eradication

Answer 25

* SOLITARY mucosal ulcer involving proximal DUODENUM (90%)...or distal stomach/GASTRIC (10%) * **DUODENAL ulcer (90%)** is almost always d/t H. pylori...rarely d/t ZE syndrome * ZE: tumor that produces excess gastrin * parietal cells make lots of acid * cause PUD * H. pylori: in **PRE-PYLORIC** area of gastric ***ANTRUM*** * **GASTRIC ulcer** (10%): * 75% H. pylori * other: NSAIDS, bile reflux

Answer 26

* CP: epigastric pain that IMPROVES WITH MEALS (b/c of protective mechs) * diagnostic endoscopic bx: ulcer with HYPER.trophy of Brunner glands * usually arises in ANTERIOR duodenum * ...when in POSTERIOR duodenum: BAD NEWS BEARS * rupture may lead to: * bleeding from the GDA (gastroduodenal artery) * --or-- * acute pancreatitis

Answer 27

* aka distal stomach (only 10% of the ulcer locations-proximal duodenum is the other 90!) * causes: * 75%: H. pylori * other: NSAIDS, bile reflux * CP: * epigastric pain that WORSENS with meals * ulcer usually on LESSER CURVATURE of the (pyloric) antrum * rupture carries risk of bleeding from LEFT GASTRIC ARTERY

Answer 28

* (proximal) duodenal ulcers (90% of PUD ulcer locations) are almost never malig * duodenal carcinoma is EXTREMELY rare * (distal stomach) **gastric ulcers** (10% of PUD ulcer locations) can be caused by **gastric carcinoma** (INTESTINAL subtype) * benign peptic ulcers: * small (\<3cm) * sharply demarcated ("punched out") * surrounded by radiating folds of mucosa * MALIG peptic ulcers: * large * irregular * HEAPED UP margins * bx required for definitive diagnosis

Answer 29

* malig proliferation of surface pitherlial cells (adenocarcinoma) * subclasified into: intestinal type (more common) and diffuse type * CP: * presents late with weight loss * abdominal pain * anemia * early satiety (DIFFUSE type) * rarely: acanthosis nigricans -or- Leser-Trelat sign * AN: thickening and darkening of skin in axillary regions * LT sign: dozens of severe keratoses all over the skin

Answer 30

* **Virchow node**-spread to *left _supraclavicular_* node * ** Sister Mary Joseph nodule**-spread to *_periumbilical_* region * ** Krukenberg tumor**-spread to bilateral (mucinous) *_ovaries_*

Answer 31

* presents as: * large irregular ulcer * HEAPED up margins * most commonly involves: LESSER CURVATURE of the antrum (similar to gastric ulcer (10% of PUD) * RF: * intestinal metaplasia * d/t: H. pylori * d/t: a.i. gastritis * nitrosamines in smoked food (Japan) * bloodtype A

Answer 32

* characterized by: SIGNET RING cells that diffusely infiltrate the gastric wall * DESMOPLASIA results in thickening of stomach wall (LINITIS PLASTICA) * NOT assoc w/ H. pylori, intestinal metaplasia, or nitroasmines (unike intestinal type [#1])

Answer 33

* signet ring cell: * nucleus pushed off to the edge by productionof mucin by tumor cells * desmoplasia: * reactive response of the stroma * **fibrous** formation=LINITIS PLASTICA

Answer 34

* atresia=blind loop * congenital failure of duodenum to CANALIZE * assoc w/ Down syndrome

Answer 35

* atresia=blind loop * CF: * **polyhydramnios**=TOO MUCH amniotic fluid-can swallow and digest it * **distention** of stomach and blind loop of duodenum * pyloric sphincter stays tight between them * DOUBLE BUBBLE sign * **bilious vomiting**-buildup of food, bile there too, will get regurged

Answer 36

* outpouching of all THREE layers of the bowel wall * stool gets stuck there in umbilical area-can FEEL it (ew) * arises due to failure of VITELLINE DUCT to involute * VITELLINE DUCT-vital for receiving nutrients during early development

Answer 37

RULE of TWOs * see in TWO% of pop-mc congenital anomaly of the GI tract * TWO inches long (lol) * located in the small bowel within TWO feet of the ileocecal valve * can present d/r the first TWO years of life w/: * BLEEDING (due to heterotopic gastric mucosa) * twisting volvulus * telescoping intussusception * obstruction (mimics appendicitis) * \*\*most cases asymptomatic * \*\*PLUS: ECTOPIC pancreatic -or- gastric tissue

Answer 38

* volvulus * intussusception

Answer 39

* twisting of bowel along its mesentery * results in obstruction and disruption of blood supply with infarction * most common locations: * **sigmoid** colon (elderly)-LLQ * **cecum** (young adults)-RLQ * Meckel assoc

Answer 40

* telescoping of *proximal* segment of bowel **FORWARD** into *distal* segment * 1. telescoped segment pulled FWD by **peristalsis** * 2. obstruction and disruption of blood supply with **infarction** (blood is being pulled fwd as well!) * infarction: currant jelly stools!! * assoc w/ a **leading edge** (focus of traction) * *kids* mc cause: **lymphoid hyperplasia** * i.e. due to ***rotavirus*** * terminal ileum * lots of *Peyers patches*, has thick wall * intussusception into the cecum * adults mc cause: tumor

Answer 41

* small bowel is highly susceptible to ischemic injury * needs A LOT of **ATP** b/c its doing a lot of digestion and absorption * Clinical features: * abdominal pain * bloody diarrhea * DEC bowel sounds (its less active)

Answer 42

* **TRANSMURAL** infarction occurs with: * *thrombosis* of the **mesenteric vein** * **polycythemia vera**-RBCs too many=THICK blood and INC r/o thrombosis * **LUPUS** anti-coagulant * -or- *thrombosis/embolism* of the **SMA** (superior mesenteric artery) * embolism can be caused by: * **a-fib**...leads to thrombus: lack of motility of ATRIUM, it can break off, embolize, and lodge itself in the SMA * **vasculitis**-Ex: PAN-polyarthritis nodosum (if with abdo complaints)

Answer 43

* MUCOSAL infarction occurs with MARKED HYPO-TN

Answer 44

* DEC fxn of the lactase enzyme in the **BRUSH BORDER of ENTEROCYTES** * lactase nml fxn: lactose--\> glucose + galatose * CP: abdominal distension and diarrhea (upon consumption of milk products) * undigested lactose is ***OSMOTICALLY* ACTIVE** (will draw water with it) * deficiency may be **congenital** (rare AR d/o) -or- **acquired** (often develops in *late* CHILDHOOD) * temporary deficiency seen after **small bowel infection** (lactase is highly susceptible to injury)

Answer 45

* immune-mediated damage of small bowel villi d/t gluten exposure * assoc w/ HLA-DQ2 and DQ8 (=hypersensitivity) * gluten's most pathogenic component: GLIADIN * deamidated GLIADIN is presented by APC via MHC.c2 to helper T-cells * helper T-cells mediate tissue damage

Answer 46

* *Children*: * abdominal distension * diarrhea * FTT * *Adults*: * chronic diarrhea * bloating * small herpes-like vesicle may arise on skin:**dermatitis HERPE-tiformis** * d/t IgA deposition at the *tips of dermal papillae* * resolves with GF diet

Answer 47

* late complications (refractory dz despite good dietary control): * small bowel carcinoma * T-cell lymphoma * tx: Dapsone and corticosteroids

Answer 48

* \*\*\*IgA Ab against: * endomysium-connective tissue that ensheaths each muscle fiber * tTG * --or-- GLIADIN * IgG Ab are also present-useful for diagnosis in indivs with IgA deficiency * duodenal bx: * **flattening** of *villi* * **HYPER-plasia** of *crypts* * INC intraepithelial **lymphocytes** * damage is most prominent in the duodenum (Jejunum and ileum are less involved)

Answer 49

* tropical regions * after infectious diarrhea * responds to AB * \*\*damage most prominent in **jejunum and ileum** (*secondary vit B12 or folate deficiency* may ensue--duodenum less commonly involved)

Answer 50

* systemic tissue damage * MACROPHAGES loaded with *Tropheryma whippelii* organisms * partially destroyed organisms are present in MACROPHAGE lysosomes (**PAS positive;** stains for glycogen)

Answer 51

* classic site of involvement: **SMALL BOWEL LAMINA PROPRIA** (layer of mucosa)\*\* * macrophages compress lacteals * chylomicrons (repackaged FA) canNOT be transferred from enterocytes to lymphatics (--\>thoracic duct--\>blood) * results in **FAT malabsorption and steatorrhea** * other common sites on involvement: * synovium of jts (arthritis) * cardiac valves (endocarditis) * lymph nodes * CNS

Answer 52

* AR deficiency of apolipoprotein B-48 (chylomicron) --and-- B-100 (VLDL + LDL) * d/t L-o-F: MTP gene * Clinical features: * malabsorption-due to defective chylomicron formation * absent plasma VLDL and LDL * deficient ADEK

Pathoma + Secrets Flashcards

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