GI pathology Flashcards

1
Q

● Telescoping of SI into adjacent segment; obstruct + ischemia; < 2 yoa
● Sx: sudden colicky pain w/ vomiting, lethargy, “red currant jelly”
● PE: sausage shaped mass in RUQ, epigastric, or peri-umbilical region

A

Intussusception

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

● Enlarged colon but NOT due to obstruction
● RFs: medications or Hirschsprung’s disease (mesenteric plexus never develops) or UC / pseudo membrane colitis
● Sx: constipation, abdominal pain, fecaloma, fever, abdominal tympany
● Complications: Chaga’s disease, colonic rupture (EMERGENT)

A

Megacolon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

● Twisting of GIT -> obstruction,

RFs: midgut infants, colon adults

● Etiology: chronic constipation or laxative use in adults, unknown infants
● Sx: no bowel sounds, abdominal pain & distention, vomiting, ischemia

A

Volvulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

● Protrusion of abdominal contents through weakened part of wall
● Indirect (passes canal into scrotum) or direct (directly into inguinal canal), femoral (more common in females)
● RFs: males; 75% inguinal
● Sx: mass (maybe reducible), painless, heaviness
o Incarcerated: pain, enlarged, discoloured, N/V, fever, abd. distention w/ possible bowel obstruction
o Strangulated: blue/red/purple discoloration, significant abd pain, peritoneal signs  gangrene

A

Hernia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

● Loss of lower esophageal motility ->tight esophageal sphincter -> lumen enlarges as food accumulates / stasis
● RFs: surgery, severe erosive esophagitis –> damages mesenteric plexus, Chaga’s disease, amyloidosis (amyloid proteins deposit in tissues), cancer, AI
● Sx: dysphagia, regurgitation, chest pain, night cough, aspiration
● Complications: aspiration pneumonia, cancer

A

Achalasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

● Ileum obstruction from motor dysfunction –> paralysis
● Etiology: surgery, SC injury above T5, opioids, hypothyroidism (slows GIT)
● Sx: constipation, lack of bowel sounds, N/V, dyspepsia, belching (excess)

A

Adynamic Ileus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

● Part of the stomach herniates through the esophageal hiatus of the diaphragm
● Two types: (1) Sliding – when esophagogastric junction is above the diaphragm (95%), and (2) Paraesophageal – junction is below diaphragm
● Etiology: female (pregnancy), age, decreased fiber, obesity, ascites

A

hiatal hernia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

which inflammatory disease

● Infection of appendix –> inflame, pus –> necrosis, gangrene w/ ischemia
● RFs: adolescents, < 30 yoa, low fiber diet, Abx use
● Sx: Migrating, severe pain from umbilicus to RLQ
o MANTRELS Score: 7+ = likely, 5-6 = doubtful, 3-4 = negative
▪ Migratory pain (1)
▪ Anorexia (1)
▪ Nausea (1)
▪ Tenderness (1)
▪ Rebound tenderness (1)
▪ Elevated temperature (1)
▪ Leukocytosis – high WBCs (2)
▪ Shift to the left – more immature WBCs (1)
● PE: (+) peritoneal signs (rebound tenderness, guarding, rigidity)
● Dx: abdominal x-ray, CT, U/S; REFER for surgery (untreated  gangrene)

A

appendicitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

which inflammatory disease:
“-losis” = out pouch; “-itis” = out pouch + infection from bacterial release
● Results in inflame of bowel wall in sigmoid colon/rectum (75%), perforation, fistula, or abscess (25%)
● RFs: low fiber diet, obesity, sedentary lifestyle, older age
● Sx: LLQ pain, low fever, alternating constipation/diarrhea, N/V
● PE: fistulas (connection)  pneumaturia (gas in urine), feculent vaginal d/c, cutaneous or myofascial infection; abscess, perforation, peritoneal signs

A

DIVERTICULAR disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

which inflammatory disease:

inflammation of small intestine; could from ischemia (arterial/venous obstruction)
● Etiology:

  • viral, bacterial or parasitic infection (food poisoning, stomach bug or the stomach flu).
  • secretory (pathogenic), exudative, osmotic, malabsorptive, deranged motility
A

enteritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

which inflammatory disease:

Erosion of mucosa in the esophagus;

Etiology: H pylori, Zollinger-Ellison (severe hyper-chlorhydria causing recurrent ulcers)

● RFs: GERD, smoking, bulimia
● Sx: substernal burn after eating, difficulty swallowing solid foods, chronic cough & laryngitis, SOB, hoarseness

A

esophageal ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

● which inflammatory disease:

Local erosion of the stomach or SI;

RFs: H. pylori  chronic gastritis, NSAIDs, stress, Zollinger-Ellison syndrome

● RFs: smoking, chronic NSAID use, cirrhosis, aspirin, COPD, low fibre, stress, corticosteroids
● Sx: burning after meals, dyspepsia, nausea, belch, melena, guarding
o Gastric wall: pain right after meals w/ NO relief from food or antacids
o Duodenum: pain 2-3 hours after meals, better w/ food & antacids
● Dx: breath test (H. pylori), gastrin, endoscopy; Tx: PPI, Abx
● Complications: high reoccurrence rate, GI bleeding, perforation, cancer

A

peptic ulcer disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q


which imflammatory disease:

Inflame entire stomach; erosive (severe) or non-erosive (metaplastic)
● Sx: pain w/ food, dyspepsia, N/V, no appetite, melena (black stool)

A

gastritis (acute)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

inflamation of the stomach lining

Two main types: (BOTH present with chronic dyspepsia-indigestion)
● Fundal Type A (immunologic):
o MOA: parietal cells of the fundus destroyed by CD4+ T cells  lowers gastric acid secretion  malabsorption of nutrients
o Complications: anemia, autoimmune thyroiditis, celiac, ulcer
● Antral Type B (H pylori infection): PUD, lymphoma, purpura

A

gastritis - chronic!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

which inflammatory disease:
● Retrograde flow of stomach acid into esophagus, bc of failure of lower esophageal sphincter
● Sx: < after meals, chronic cough, wheeze sore throat, globus
● Dx: based on clinical sx; endoscopy, biopsy (rare); Tx: HPI or PPIs

A

GERD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

● GERD damages esophagus leads to inflammation & disrupted peristalsis
● RFs: obesity, hiatal hernia, lying down after meals, restrictive clothing around the waist, hypo- or hyper-chlorhydria
● Sx: substernal burning after meals, chest pain, cough, laryngitis
● Complications: Barrett’s esophagus

A

esophagitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

which inflammatory disease:

due to GERD

tissue that is similar to the lining of your intestine replaces the tissue lining your esophagus

● simple squamous to INTESETINAL epithelium; esophageal structures develop
● RFs: long-standing untreated GERD; Sx: chronic retrosternal/epi pain
● Dx: endoscopy, biopsy; cannot be diagnosed clinically
● Complications: esophageal cancer from dysplasia

A

Barret Esophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

which inflammatory disease

● Chronic inflammation of ONLY the descending colon & rectum; NO skip/granulomas

continuous rectal lesions

● RFs: NSAIDs or Jewish
● Sx: bloody, mucoid diarrhea, wax/wane, fever, fatigue, arthralgia
● Complications: arthritis, ankylosing spondylitis (fused spine, from HLA B27 gene), uveitis, CRC, toxic megacolon, osteoporosis

A

IBD-UC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

which inflammatory disease

● Chronic inflammation of ileum & colon w/ skip lesions & granulomas
● Can occur anywhere in GIT; inflammation present btwn wax/wane attacks
● RFs: AI, smoking, Jewish, FHx, stress, low fiber, NSAID, lack of breastfeed
● Sx: pain, diarrhea, fatigue, anal fistulae, adhesions, adhesions, strictures
● Complications: anemia (B12, folate, iron malabsorption), uveitis, arthritis, adhesions, CRC, urolithiasis

A

IBD-Crohn’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

which congenital cdx

● Esophagus doesn’t form properly -> no connection to stomach -> fistulation of trachea
● Sx: drooling, coughing, choking, regurgitation of all food, aspiration pneumonia if there’s a tracheoesophageal fistula

A

esophageal atresia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

which congenital cdx

● Membrane (thin fold of tissue) obstructs esophagus; congenital if affecting lower 2/3 & acquired if upper 1/3 (iron deficiency, bullous disease, rejected graft, celiac)

● Sx: chest pain, dysphagia

A

Esophageal Webs & Rings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

which congenital cdx

● Outpouching of all layers of the small intestine (usually the ileum) from vitelline duct not degrading after birth;

RFs: ectopic tissue interferes

● Sx: asx or painless hematochezia (blood from anus), obstruction, volvulus

A

Meckel Diverticulum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

which congenital cdx:

● Hypertrophy of pylorus causing constriction / obstruction of stomach outlet
● RFs: males, Jewish, FHx
● Sx: severe vomiting in neonates, insufficient urination, hunger, dehydration, metabolic alkalosis  electrolyte imbalances

A

pyloric stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

which abdominal cavity cdx:

● Liver cirrhosis/damage to hepatocytes -> congestion of portal venous system -> fluid buildup in peritoneal cavity

(fluid collects in spaces within your abdomen, from high pressure in certain veins of the liver (portal hypertension) and low blood levels of a protein called albumin)

● Labs: serum ascites albumin gradient (SAAG – measures albumin) is the GOLD standard indicator for ascites
o High SAAG > 1.1 = portal venous system pushing fluid out
o Low SAAG < 1.1 = inflammation or cancer

● Sx: abdominal distention, (+) fluid transmission across abdomen, shifting dullness, pressure on other abdominal organs
o High SAAG = normal glucose & low WBC (no infection/immune process)
o Low SAAG = low glucose & low pH & high WBC (bc inflame/cancer)

A

Ascites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

which abdominal cavity cdx

● Inflam. of peritoneum from visceral -> parietal as infected organ contacts wall

o Visceral pain diffuse; parietal is better innervated / localized pain
● RFs: appendicitis, PID, trauma, puncturing foreign body, bacterial, TB
● Sx: “acute abdomen sx” pain, tenderness, rebound tenderness, guarding, N/V

● Complications: intestinal paralysis from severe inflam., shock, abscess, death

A

Peritonitis / Adhesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

which vascular cdx

● Engorged veins in esophagus from chronic alcoholism or portal HTN
● RFs: alcoholism; Sx: bleeding, severe epigastric pain, liver disease
● Complications: high risk of rupture & death

A

esophageal varices

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

● Dilated veins of anal canal; RFs: low fiber diet -> constipation, pregnancy

● Sx: rectal pain, bleeding, itch, rectal prolapse -> thrombotic or inflamed

A

hemorrhoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

necrosis due to inadequate blood supply to the affected area

Two types:
● Transmural – all GI layers, causes ischemic enteritis (inflam.)
● Partial – only mucosa, incomplete occlusions of superior mesenteric artery from athero., shock, or heart failure

A

infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

● Abnormal, dilated, and fragile blood vessels in the colon
● Most common vascular issue of GIT; healthy blood cells degenerate from age
● RFs: renal failure, age, CVD; Sx: bleeding, asx unless massive hemorrhage  anemia, hematochezia (anus), hematemesis (oral)

A

Vascular Ectasis of the Colon

30
Q

which neoplasm cdx

● Squamous cell origin; RFs: Barrett’s esophagus, alcoholism, smoking, H. pylori eradication (H pylori reduces stomach acid  less reflux  less dysplasia)
● Sx: dysphagia, hoarseness from damage to recurrent laryngeal nerve, cachexia; poor prognosis

A

Esophageal Cancer

31
Q

which neoplasm cdx

Adenocarcinoma (looks like an ulcer) either diffuse or intestinal; Asia & Africa
● Etiology: diffuse (high meat/low F/V) & intestinal (high salt, gains, nitros)
● Sx: vague GI upset, fatigue, weight loss, anorexia; Dx missed unless ulcer or metastasis occurs

A

gastric cancer

32
Q

T/F intestinal neoplasms are common , secondary to celiac or IBD

A

F: they are extremely rare

33
Q

● Dx: serum alpha-fetoprotein (AFP) is common tumor marker

● RFs: chronic hepatitis B/C, alcoholism, aflatoxin (carcinogen); Asia & Africa

● Sx: asx until later stage or jaundice, easy bruising, ascites, cachexia

A

Hepatocellular Carcinoma/liver cancer

34
Q

● Squamous cell origin; RFs: chewing tobacco, smoking, alcohol, HPV

● Sx: any mouth sore that does not heal within 14 days should be considered

● Leukoplakia are white benign patches; Erythroplakia reddish, precancerous

A

oral (Leukoplakia)

35
Q

For pancreatic cancer. what type of tumor?
Starts in the _________ epithelium in the pancreatic head causing blockage of the __________________

A

Adenocarcinoma that starts in the ductal epithelium in the pancreatic head causing blockage of the common bile duct

36
Q

● Neoplastic change in pancreatic head; ductal adenocarcinoma (80%); unrelated to gallstones & GB
● RFs: smoking, African descent, diet/alcohol
● Sx: vague epigastric pain + weight loss + jaundice  ASSUME PC
● PE: Courvoisier’s sign – non-tender, palpable GB + mild jaundice
● Dx: CT, MRCP; Prognosis: poor , 5YR survival ratio

A

Pancreatic Cancer

37
Q

● 3rd most common cancer; adenocarcinomas; screening begins at 50 yoa
● RFs: chronic UC, high fat low fiber diet, polyps, strong FHx
● Sx: depending on location (polyp  bleed  detect on FOBT)
o R: systemic sx  fatigue, weight loss, iron deficiency, RLQ mass
o L: constipation, abd pain, reduced stool caliber, rectal bleeding
o Rectum (70%): obstruction, tenesmus, rectal bleed, mass on DRE
● Labs: CBC for microcytic anemia; Dx: FOBT (+), colonoscopy
● Spread will go to the liver (hepatomegaly) & lungs; 5YR survival

A

colorectal cancer

38
Q

what kind of tumor is colorectal cancer commonly?
On which side does it cause obstruction? (left or right)

A

Commonly adenocarcinoma of the rectal or colonic epithelium
Left sided tumors = obstruction
Right sided tumors = NO obstruction

39
Q

which infectious disease

● Inflam. of SI & colon; Types: Abx associated, pseudo membrane colitis, ulcerative
● Sx: diarrhea, N/V, abdominal pain, fever, chills

A

Enterocolitis

40
Q

esophagitis microbes

A

candida or HSV

41
Q

● Inflammation of the gums
o Gingivitis: -calculus causes inflammation of gingival tissues
o Periodontitis: inflammation in periodontal ligament, alveolar bone, cementum of teeth
● RFs: Poor oral hygiene, acute stress, aging, infection, mouth breathing
● Acute necrotizing ulcerative gingivitis/Vinvent’s angina/Trench mouth:
o Severe form in patients with decreased resistance to infection
o mixed infx Borrelia vincentii & Fusobacterium
o Young adults, poor hygiene, not contagious

A

Gingivitis / Periodontitis

42
Q

● Oral inflammation; Microbe: Candida albicans;

RFs: Abx, children, elderly

● Sx: local white membranous lesion

A

ORAL THRUSH

43
Q

what condition?
White patches (ESP. on tongue) that BLEED when scraped off , inflamed base, bad breath, dry mouth

A

ORAL THRUSH

44
Q

● Severe oral inflammation from HSV 1; Sx: cold sore, fever

A

Herpetic Stomatitis:

45
Q

● Also called “canker sores”; RFs: food allergies, Crohn’s, celiac, iron & B vitamin deficiencies, or idiopathic

A

Aphthous Stomatitis:

46
Q

● Diffuse hepatic inflammation cause by specific hepatotropic viruses (< 6 mo)

A

viral hepatitis

47
Q

which infectious disease has these phases

Sx: (two phases)

o Viral prodrome: anorexia, N/V, malaise, low fever, dull RUQ pain

o Icteric phase: jaundice, dark urine, acolic stool, hepatomegaly, splenomegaly, cervical lymphadenopathy (complication  fulminant hepatic failure)

Chronic: vague abdominal pain, fatigue, depression, headache, rarely jaundice

A

viral hepatitis

48
Q

● which infectious disease

Labs: CBC, liver enzymes, LFTs, viral serology
o High AST, 20x higher ALT, mildly high bilirubin + ALP
o Viral Abs: IgM anti-HAV, HBsAg (surface), IgM anti-HBs, anti-HCV

Tx: supportive UNLESS

red flags! encephalopathy (high NH4+ in brain  cognitive changes), prolonged INR (slow clotting), severe vomiting, hypoglycemia (LV can’t convert to glucose  imbalance elevates insulin)
● 5 types of viral hepatitis:
o HAV: acute, contaminated food/water, fecal/oral
o HBV: acute or chronic, seafood or contaminated food/water, fecal/oral, HBsAg in serum indicates an active infection
o HCV: acute or chronic, unprotected sex or childbirth, HCV IgG Ab
▪ More likely to lead to autoimmune conditions
o HDV: acute or chronic, infection with HBV (higher susceptibility)
o HEV: fecal/oral, more common in underdeveloped countries

A

viral hepatitis

49
Q

● Inflammation of parotid gland; usually related to mumps or S aureus
● Sx: bilateral, submaxillary / sublingual swelling, tenderness, fever (24-72 hrs

A

Parotitis

50
Q

● Sudden inflame of pancrease + hemorrhage due to auto-digestion by enzymes & hemorrhagic fat necrosis
● RFs: I GET SMASHED
o Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps/Malignancy, Autoimmune, Scorpion Sting, HyperTGs/Ca2+, ERCP, Drugs

● Sx: severe, constant epigastric pain; radiates to the back; N/V, sit up/forward, fever (toxic metabolites), abdominal distention

● PE: Cullen’s sign (umbilical ecchymosis), Grey Turner’s (flank ecchymosis), guarding & reduced bowel sounds

● Labs:** elevated serum amylase & lipase (enzyme) **– almost always !!!!!
● REFER to ICU; prognosis usually good but could develop abscess

A

Acute Pancreatitis

51
Q

● Long-standing inflammation w/ irreversible morphological changes of pancreas
● RFs: alcohol & idiopathic
● Labs: may or may not have elevated amylase and lipase

● Sx: persistent/intermittent epigastric pain; late stages -> steatorrhea (fat in stool) & diabetes mellitus d/t decreased endocrine/exocrine function/v patho

A

Chronic Pancreatitis

52
Q

what type of pancreatitis:
● Alcohol dehydrates  less fluid  enzymes can’t move  precipitate  pressure builds  blocked enzymes digest pancreas  inflame, edema, hemorrhage

A

Alcohol Induced Pancreatitis

53
Q

what type of GB cdx

● Gallstones in the GB and ducts; 80% asymptomatic
● 85% cholesterol stones, others are pigment stones (bilirubin or alcohol mix calcium) - hardened deposits of digestive fluid
● RFs: fat/fasting, fertile, forty, family history, First Nations
● Sx: Dull ache, biliary colic in RUQ, if asymptomatic, no treatment

A

Cholelithiasis

54
Q

● what type of GB cdx

Inflammation of GB from obstruction of cystic duct (immune response); reoccurrence; consider if symptoms > 12 hrs

● RFs: bacterial, exogenous estrogen exposure

● Sx: severe RUQ pain (hours, days), radiates to R shoulder, fever (low), N/V, anorexia, Charcot’s triad (fever, RUQ pain, jaundice) REFER for surgery

● PE: (+) Murphy’s Sign: sharp inhale w/ palpation of GB 🡪 Most predictive!!

● Complications: cholangitis (lethal) or cholelithiasis stones obstruct duct

A

cholecystitis

55
Q

what type of GB cdx

1 or more stones in the** common bile duct**; risk of impacting pancreas
● Bile can’t leave -> begins to compromise LV function -> jaundice fluctuates
● Sx: RUQ pain – colicky or constant, fever, N/V, loss of appetite
o Fluctuating jaundice – duct blocks and unblocks
o Acholic stool – light, no bile
● PE: (+) Murphy’s Sign

A

Choledocholithiasis

56
Q

what type of liver cdx

impairment in excretion of bile
Bile stops moving & builds up in liver -> damages hepatocytes

● Etiology: gallstones, tumors, metabolic dysregulation (no secretions), drugs, primary biliary sclerosis, primary sclerosing cholangitis (“fit liver” picture)
● RFs: mixing medications
● Sx: ITCH (pruritus), jaundice, fatigue – vagueness makes Dx difficult
● Complications: intrahepatic cholestasis of pregnancy  stillbirth, prematurity, abnormal clotting

A

Cholestasis

57
Q

● Sclerosing or fibrosis replaces hepatocytes; > 75%  liver failure
● RFs: chronic hepatitis B or C, alcohol
● Sx: fatigue, hard, shrunken liver, jaundice

A

Cirrhosis

58
Q

● Severe and rapid hepatocellular injury (< 8 wks); from viral (HBV) or drugs
● Sx: malaise, low fever, urticaria, pruritis, hepatomegaly, RUQ pain, hepatic encephalopathy (confusion, altered consciousness, coma)
● Labs: CBC, high liver enzymes, LFTs (high bilirubin, INR), LDH (lactate dehydrogenase)

A

Fulminant Hepatic Failure (ACUTE)

59
Q

**● Decompensation of liver; inability to regenerate; complete loss of function
**● Areas of decompensation:
o Encephalopathy: cognitive decline  drowsiness, tremors (Asterixis: wrist quiver), disoriented  stupor, hyperactive reflexes  coma
o Excretory dysfunction: can’t conjugate bilirubin  buildup  jaundice
o Coagulopathy: decreased clotting + easy bruising
o Hypoalbuminemia: edema + portal HTN from…
▪ Caput medusa: dilated superficial veins of abdomen (shunt)
▪ Ascites: low albumin  alters pressure to push fluid out  increases blood volume  fluid accumulates (PE: shifting dullness)
o Hormones: abnormal catabolism of hormones leaves ADH, aldosterone & estrogen to buildup in blood  gynecomastia, testicular atrophy

● Labs: high (or normal) AST + ALT, PT/INR, low albumin, LDH
o Acute failure: high LE, Chronic: mild or high, Acute/Chronic: high bilirubin

A

Hepatic Failure (CHRONIC)

60
Q

**an autosomal recessive disorder of bilirubin metabolism within the liver

ET: decreased UDP-glucuronosyltransferase activity and impaired uptake of bilirubin

**● Sx: jaundice; Labs: elevated unconjugated bilirubin

A

Gilbert Syndrome

61
Q

● Liver damage from alcohol consumption; cholestasis buildup damages hepatocytes  fibrosis around central vein  venous obstruct  cirrhosis
● Related to steatosis (fat deposits) as fatty acids are made with alcohol conversion
● Sx: fever, hypotension, jaundice, tachycardia, malnourishment
● PE: palpable, tender liver (ALWAYS tender in cirrhosis, NOT hepatomegaly), ascites
● Labs:* AST: ALT > 2:1* (ONLY time, B6 def) & elevated enzymes + LFTs
o High bilirubin & leukocytes
● Prognosis: Reversible if alcohol is avoided, but cirrhosis is not reversible

A

Alcohol-Related Liver Disease

62
Q

● Inflammation of liver from medication (acetaminophen, OCP, Abx); can’t clear metabolites  buildup & damage hepatocytes
● Excess dosing 10-15g/day or 4-6g/day in epilepsy & alcoholics
● RFs: any disease that caused liver injury
● Sx: N/V, jaundice, hepatic encephalopathy, acute renal failure, death
● Labs: CBC, liver enzymes (all high), LFTs (high bilirubin + INR)
● Dx: EMERGENT, gastric lavage/oral charcoal; prognosis based on blood [ ]

A

Drug-Induced Hepatitis

63
Q

what type of liver cdx

Inflammation + damage from **fat buildup **unrelated to alcohol; metabolic
● RFs: obesity, insulin resistance, dyslipidemia, metabolic syndrome, weight loss
● Sx: fatigue, malaise, mild RUQ pain, hepatomegaly, unexplained splenomegaly, portal HTN (could cause fluid buildup in spleen)
● Complications: cirrhosis, hepatocellular carcinoma, liver failure, encephalopathy

A

Non-Alcohol Steatohepatitis (NASH)

64
Q

liver disease when immune system is attacking the liver

Unknown cause; RFs: other AI conditions, viral infection, medications
● Sx: (similar to acute hepatitis) weight loss, fatigue, behavioural changes, epistaxis (sign of upper GI hemorrhage from poor clotting), easy bruising
● Complications: liver failure, chronic liver disease, anemia (from bleed)

A

Autoimmune Hepatitis

65
Q

what type of liver cdx

From elevated pressure in portal venous system, originating from:
o Pre-hepatic: portal vein thrombosis, congenital abnormality
o Intra-hepatic: from liver cirrhosis
o Post-hepatic: CHF, hepatic vein thrombosis, IVC pathology, constrictive pericarditis
● Sx: hepatic encephalopathy, ascites, splenomegaly, mild pancytopenia (trapped blood in the spleen), varicose veins, caput medusae, jaundice
● Complications: renal failure, variceal rupture (esophagus), bacterial peritonitis

A

portal HTN

66
Q

what type of liver cdx

Bilirubin accumulates in extrahepatic tissues -> yellow skin coloration
● Accumulation of
o Unconjugated (indirect) bilirubin from hemolytic anemia / hemorrhage
o Conjugated (direct) bilirubin from obstruction (stones), hepatitis, cirrhosis, drugs, or pregnancy

A

jaundice

67
Q

what def./reabsorption cdx:

● Low/no HCl acid in stomach; RFs: aging, drugs, pernicious (B12) anemia
● Sx: asx or dyspepsia, gastric upset
● Complications: infection (easier to colonize), nutrient malabsorption (B12), dysbiosis, gastric cancer

A

achlorhydria

68
Q

what type of def/reabsorption cdx:

Gluten (gliadin) intolerance; immune cells attach gliadin on villi of jejunum  flattens microvilli  decreased absorption  osmosis pulls fluid in
● Sx: (unmanaged) bulky, frothy, greasy, yellow, or gray stools; nutrient malabsorption  weight loss, borborygmi, flatus, muscle wasting, fatigue
● Complications: autoimmunity (IBD, thyroiditis), anemia, osteoporosis (from chronic inflammation), intestinal lymphoma, dermatitis herpetiformis (rash)
● Dx: endoscopy to observe microvilli (gold standard)

A

Celiac disease

69
Q

● Malabsorption of lactose from lactase enzyme deficiency; remains in gut
● Sx: gas, bloating, diarrhea, diffuse abdominal pain

A

Lactase Deficiency

70
Q

name the enzyme deficiencies

  1. ● Deficiency of hexosaminidase A; needed to breakdown toxins in brain/SC  buildup & degrade CNS  severe mental/motor impairment
    ● RFs: Ashkenazic Jews
  2. ● Deficiency of alpha-L iduronidase (IDUA)  accumulation of heparan sulfate & dermatan sulfate in the heart, brain, liver & other organs
    ● Sx: progressive mental deterioration, dwarfism, stubby fingers, cloudy cornea
  3. ● Deficiency of lysosomal alpha glucosidase  glycogen accumulates in the liver, heart & skeletal muscle
    ● Sx: fatal from cardiorespiratory failure
A
  1. Tay Sach’s
  2. Hurler’s disease
  3. Pompe’s disease
71
Q

● Viral infection 12hr-3days, oral-fecal route, viruses-> epithelium damage-> osmotic diarrhea, vomiting

● Microbes: Salmonella, E. coli, Campylobacter jejuni, Shigella, Yersinia enterocolitica (“Gastroenteritis is SECSY”)
o Secretory: cholera
o Bloody: enterohemorrhagic E. coli (EHEC)

A

Gastroenteritis

72
Q

● RFs: Antacid drugs or hypochloridria, immunosuppression, exposure to infected person or contaminated food, lack of breast feeding, children, elderly, immunocompromised
● Sx: Diarrhea, sometimes cramping/pain, presence of blood and/or pus, systemic symptoms (fever, arthralgias, myalgias), highly frequent or unremitting bowel movements
● Complications:
o Blood or pus, recurrent diarrhea, signs of serious electrolyte disturbances including hypotension, dizziness, sunken fontanelles, severe dehydration lack of urination or tear production and/or skin tenting.
o Dysentery can lead to sepsis and death.
o Hemolytic uremic syndrome is life-threatening complication of EHEC.
o Viral diarrhea is leading

A

Gastroenteritis