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BOARDS! > Pathoma + Secrets > Flashcards

Pathoma + Secrets Flashcards

1
Q

what are the (THREE) types of antigen associated with HBV

A
  1. ***HBsAg–surface antigen
  2. HBcAg–core antigen
  3. HBeAg–an antigen that circulates in the blood dring viral replication
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2
Q

HBsAg

A
  • most important of the three antigens
  • FIRST antigen to appear
    • core is also positive, but we dont see it
  • LAST antigen to disappear
  • if you have it YOU ARE INFECTED with Hep B!!
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3
Q

HBeAg

A
  • infectivity marker
  • indicated a HIGH INFETIVITY RATE
  • especially important in pregnant women
    • 90% of neonates will get Hep B f/m mom if she is HBeAg-POSITIVE
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4
Q

Youve just been acutely infected with HBV whats in your serum?

A
  1. serum HBsAg will become positive
  2. HBeAg will be positive soon thereafter
  3. anti-HBcAg is produced
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5
Q

!!! anti-HBcAg–why is this Ab so important

A
  1. chronicity marker (C for chronicity)
    1. IgM anti-HBcAg=acute/recent infection {Me first}
    2. IgG anti-HBcAg=chronic (>6mo of infection OR has recovered from dz)
      1. most ppl w/ HBV dont get chronic hepatitis (immune system will fix the problem)
  2. D/r window pd!!
    1. the ONLY marker that is positive: anti-HBcAg
    2. can be used to test for infxn d/r this pd
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6
Q

Window period (steps)

A
  • immune system starts to make antibodies to HBsAg and HBeAg–precipitate out effect
    • Ab isotype (G vs. M) isnt important
  • pt enters WINDOW PD
    • concentration X of HBsAg in serum
    • as body produces Ab to this Ag, Ag precipitates out of serum through immune complex formation
    • when concentration of Ab=concentration X of HBsAg–>all the HBsAg precipitates OUT and becomes UNDETECTABLE
    • (same shit happens to HBeAg and its Ab)
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7
Q

Window period (summary)

A

when the pt produces surface (“s”) and “e” Ab in equal concentrations to their antigens such that neither antibody NOR antigen is detectable in serum

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8
Q

I have been vaccinated against HBV, what AB do I have?

A

POSITIVe for: anti-HBsAg (NOT anti-HBcAg)

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9
Q

What happens after the window period?

A
  • levels of anti-HBsAg and anti-HBeAg rise over the levels of antigen
    • antibodies become detectable in the serum
  • How do you know if a pt is cured??
    • detectable levels of anti-HBsAg!!!
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10
Q

How do you differentiate between a cured pt vs. an immunized ot?

A

look for anti-HBcAg (IgG)

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11
Q

Carriers

A
  • positive for HBsAg but DO NOT HAVE Ab (even though they are otherwise asymptomatic)
  • can pass the dz to others but will not be symptomatic
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12
Q

oral herpes

A
  • usually d/t HSV-1
  • primary infection occurs in CHILDHOOD
    • lesions heal, virus remains dormant in GANGLIA of TRIGEMINAL nerve
  • reactivation d/t: stress and sunlight
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13
Q

mumps

A
  • infection with mumps virus resulting in inflamed parotid glands
  • also:
    • orchitis
    • pancreatitis
    • aseptic meningitis
  • serum amylase is INC d/t salivary gland or pancreatic involvement
  • r/o sterility (espec teens)
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14
Q

Layers of esophagus (in–>out)

[M.sM.Mp3]

A
  • mucosa
  • SUB-mucosa (under)
  • muscularis propria
    • inner circular
    • Auerbach (myenteric)
    • outer longitudinal
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15
Q

Tracheoesophageal fistula (TEF)

A
  • congenital defect
  • abnml connection b/w ESOPHAGUS and TRACHEA
  • mc: proximal E atresia with distal E arishing from trachea
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16
Q

define fistula

A

abnml connection between two (tubes)

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17
Q

TEF CP

A
  • vomiting
  • POLY-hydramnios (xs amniotic fluid)
  • abdominal distension
  • aspiration
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18
Q

Esophageal Web (+ PVS)

A
  • thin protrusion of esophageal mucosa
  • most often in UPPER E
  • cp:
    • dysphagia for poorly chewed food (gets trapped)
  • INC r/o esophageal squamous cell carcinoma
  • PVS (Plummer-Vinson syndrome):
    • SEVERE iron deficiency anemia
    • esophageal web*
    • beefy-red tongue (d/t atrophic glossitis [atrophy of mucosa])
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19
Q

Zenker Diverticulum

A
  • outpouching of pharyngeal mucosa through an ACQUIRED defect in the muscular wall (false diverticulum)
  • where? jxn of E and pharynx (pharoah)
    • above the upper esophageal sphincter
  • CP:
    • dysphagia
    • obstruction
    • halitosis (bad breath-food gets trapped and rots)
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20
Q

Mallory-Weiss Syndrome

A
  • longitudinal lacertations of mucosa (innermost layer) at the GEJ
  • cause: severe vomiting (alcoholic, bulimia)
  • CP: PAINFUL hematemesis (blood in vomit)
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21
Q

Boerhaave syndrome

A
  • complication of Mallory-Weiss syndrome
  • rupture of E leading to air in the mediastinum and subQ emphysema [air bubbles beneath skin]
  • SURGICAL EMERGENCY
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22
Q

Esophageal varices

A
  • dilated SUB-mucosal veins in the lower E
  • PP: secondary to portal HTN
    • nml: distal E vein–>L. gastric v–>portal v)
    • in portal HTN, L. gastric backs up into E vein=DILATION (VARICES)
  • asymptomatic (**r/o rupture)
  • CP: PAINLESS hematemesis (unlike PAINFUL MWS)
  • mc c/o death in CIRRHOSIS
  • [pts will also have coagulopathies-liver not functioning/not making clotting factors]
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23
Q

Achalasia Clinical Features

A
  • dysphagia for solids AND liquids
  • putrid breath
  • high LES pressure on esophageal manometry
  • BIRD-BEAK sign on barium swallow study
    • (dilated esophagus wall)
  • INC r/o esophageal squamous cell carcinoma
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24
Q

Achalasia (general)-TLES

A
  • disordered esophageal motility with inability to relax lower LES (TIGHT LES; loss of motility)
  • PP: damaged ganglion cells in myenteric (Auerbach) plexus (needed for motility and LES relaxation)
    • damage:
      • idiopathic
      • secondary to known insult: Trypanosoma cruzi infection in Chagas dz
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25
Q

GERD-rLES <gastro.esophageal.reflux.dz></gastro.esophageal.reflux.dz>

A
  • 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)
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26
Q

GERD-rLES <gastro.esophageal.reflux.dz>: Clinical features</gastro.esophageal.reflux.dz>

A
  • 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
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27
Q

Barrett Esophagus

A
  • 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
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28
Q

Esophageal carcinoma (general)

A
  • 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)
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29
Q

Esophageal Adenocarcinoma (1/2)

A
  • 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
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30
Q

Esophageal Squamous Cell Carcinoma (2/2)

A
  • 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)
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31
Q

Gastroschisis

A
  • congenital malformation
  • anterior abdominal wall leading to exposure of abdominal contents (hole in wall)
32
Q

omphalocele (omphalo-SEALED)

A
  • 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
33
Q

Pyloric Stenosis (General)

A
  • congenital HYPERTROPHY od pyloric smooth muscle
  • more common in males
  • stenosis=cant get food out=build up PRESSURE
34
Q

Pyloric Stenosis (Clinical presentation)

A
  • 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)
35
Q

Layers of the gut wall (In–>out) 2 vs. 4

A
  • two main divisions: mucosal and smooth muscle layer
  • –or– FOUR divisions <msms>
    </msms><ul>
    <li>1. Mucosa</li>
    <li>2. Submucosa</li>
    <li>3. Muscularis externa</li>
    <li>4. Serosa</li>
    </ul></msms>
36
Q

Layers of the gut wall (In–>out) [TWO]

A
  • two main divisions: mucosal and smooth mu layer
    1. MUCOSAL
      * Mucosa
      • epithelium
      • lamina prpria
      • muscularis mucosa
        * SUB-mucosa
        * + SUBmucosal plexus <meissner></meissner>
    1. SMOOTH MU LAYER
      * inner circular
      * +myenteric plexus of <auerbach></auerbach>
      * outer longitudinal
  • ALL covered by:
    • serosa-INTRA.peritoneal
    • —or—
    • adventitia-RETRO.peritoneal
37
Q

Zone ONE-liver (LR13)

A
  • PORTAL TRIAD (periportal) zone
  • affect FIRST by VIRAL hepatitis
  • ingested toxins (cocaine)
38
Q

Zone TWO-liver (LR13)

A
  • intermediate zone
  • ylw fever
39
Q

Zone THREE-liver (LR13)

A
  • pericentral vein/centrilobular zone
  • affected FIRST by ISCHEMIA
  • contains cytochrome P-450 system
  • most sensitive to METABOLIC toxins
  • site of ALCOHOLIC hepatitis
40
Q

portal triad of LIVER (bd,pv,ha)

A
  1. bile duct
  2. branch of portal vein
  3. branch of hepatic artery
41
Q

Bile and Blood-Liver zones

A
  • bile flows f/m Zone 3 to 1
  • blood flows from Zone 1 to 3
42
Q

Acute (ACIDIC) gastritis-RF

A
  • 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
43
Q

Acute (ACIDIC) gastritis General

A
  • 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)
44
Q

Chronic gastritis (general)

A
  • chronic inflamm of stomach mucosa
  • divided into two types based on underlying etiology:
      1. chronic AUTO-IMMUNE gastritis
      1. chronic H. PYLORI gastritis (more common)
45
Q

Chronic AUTO-IMMUNE gastritis (general)

A
  • 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)
46
Q

Chronic AUTO-IMMUNE gastritis (Clinical features)

A
  • 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)
47
Q

Chronic H. PYLORI gastritis (general)

A
  • 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
48
Q

Chronic H. PYLORI gastritis (CP+tx)

A
  • CP:
    • epigastric abdominal pain
  • INC r/o:
    • ulceration (PUD)
    • gastric adenocarcinoma (intestinal type)
    • MALT lymphoma (B cell lymphoma)
  • Tx: TRIPLE therapy:
      1. PPI
      1. Amoxicillin
      1. Clarithromycin (Macrolide)
    • resolves gastritis/ulcer and reverses intestinal metaplasia
  • NEG urea breath test and lack of stool Ag=eradication
49
Q

PUD (peptic ulcer dz)

A
  • 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
50
Q

PUD-Duodenal ulcer (yayyy, dinnah)

A
  • 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
51
Q

PUD-Gastric ulcer (gahhh, din)

A
  • 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
52
Q

differential diagnosis FOR ulcers

A
  • (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
53
Q

Gastric carcinoma (general)

A
  • 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
54
Q

Gastric carcinoma METS

A
  • Virchow node-spread to left supraclavicular node
  • <intestinal> Sister Mary Joseph nodule</intestinal>-spread to periumbilical region
  • <diffuse> Krukenberg tumor</diffuse>-spread to bilateral (mucinous) ovaries
55
Q

Intestinal (metaplasia) type (#1)-Gastric carcinoma

A
  • 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
56
Q

Diffuse type (#2)-Gastric carcinoma…D put a ring on it

A
  • 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])
57
Q

Diffuse type (#2)-Gastric carcinoma…SIGNET and DESMOPLASIA

A
  • 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
58
Q

duodenal atresia (general)

A
  • atresia=blind loop
  • congenital failure of duodenum to CANALIZE
  • assoc w/ Down syndrome
59
Q

duodenal atresia (Clinical features)

A
  • 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
60
Q

Meckel Diverticulum (TWO the VITELLINE)

A
  • 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
61
Q

Meckel Diverticulum (TWO the VITELLINE)

A

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
62
Q

Meckel Diverticulum (TWO to VITELLINE) can cause two other path

A
  • volvulus
  • intussusception
63
Q

Volvulus

A
  • 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
64
Q

Intus-SUS-ception (Intussusception)

A
  • telescoping of proximal segment of bowel FORWARD into distal segment
      1. telescoped segment pulled FWD by peristalsis
      1. 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
65
Q

Small Bowel Infarction (General)

A
  • 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)
66
Q

Small Bowel Infarction (Transmural VS. Mucosal) <1/2>

A
  • 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)
67
Q

Small Bowel Infarction (Transmural VS. Mucosal) <2/2>

A
  • MUCOSAL infarction occurs with MARKED HYPO-TN
68
Q

Lactose Intolerance

A
  • 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)
69
Q

Celiac dz path

A
  • 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
70
Q

Celiac dz CP

A
  • 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
71
Q

Celiac dz: complications and tx

A
  • late complications (refractory dz despite good dietary control):
    • small bowel carcinoma
    • T-cell lymphoma
  • tx: Dapsone and corticosteroids
72
Q

Celiac dz-Lab Findings

A
  • ***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)
73
Q

Tropical sprue (vs. Celiac)

A
  • 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)
74
Q

Whipple disease (MAC)

A
  • systemic tissue damage
  • MACROPHAGES loaded with Tropheryma whippelii organisms
    • partially destroyed organisms are present in MACROPHAGE lysosomes (PAS positive; stains for glycogen)
75
Q

Whipple disease (Location)

A
  • 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
76
Q

Abetalipoproteinemia

A
  • 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

BOARDS! (14 decks)

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