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year 2 > Path Exam 3- Liver and nutrition > Flashcards

Path Exam 3- Liver and nutrition Flashcards

1
Q

Non-alcoholic hepatitis/necrosis LFT

A

ALT & AST

  • both ~10x UL
  • greater than alkaline phosphatase
  • DIRECT bilirubin ↑ → indirect ↑ (jaundice)
  • -urine urobilinogen ↑

Alk phos & GGT- relatively normal

Chronic hepatitis:
-Prolonged PT/PTT (no improvement w/ vit K)

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2
Q

Alcoholic hepatitis/necrosis LFT

A

ALT & AST

  • AST 2x greater than ALT (↑ AST in rhabdomyalysis)
  • both ~10x UL
  • larger than alkaline phosphatase
  • DIRECT bilirubin ↑ → indirect ↑ (jaundice)
  • -urine urobilinogen ↑
  • *GGT ↑↑ due to microsomal induction
  • **neutrophilic leukocytosis
  • Mallory bodies: intracytoplasmic eosinophilic bodies
  • -irregular size & shape
  • -from cytokeratin damage
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3
Q

Cirrhosis/ chronic liver failure LFT

A
  • ALT & AST ↑
  • alk phos ↑
  • Hypoalbuminemia**
  • ↑ PT/PTT (no improvement w/ vit K)
  • Ammonia ↑↑ (Tx: lactulose- traps ammonia)
  • INDIRECT hyperbilirubinemia (variable)
  • anemic
  • Cholic acid ↓ (reduced ratio of 1ry : 2ry)
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4
Q

Cholestatic LFT

A
  • Alk Phos & GGT ↑↑
  • direct bilirubin ↑ → cholestatic jaundice
  • serum cholesterol ↑ → xanthomas
  • retained bile salts → pruritis
  • *-malabsorption; vit déficiences A, D, K
  • -if K deficient → prolonged PT/PTT that reverses w/ K
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5
Q

Fulminant failure LFT

A
  • AST & ALT ↑↑↑
  • Ammonia ↑↑ (Tx: lactulose- traps ammonia)
  • **Ferritin ↑↑↑
  • hypoalbuminemia
  • PT/PTT prolonged (no improvement w/ vit K)
  • DIRECT hyperbilirubinemia (variable)
  • -urobilinogen ↑ in urine

onset of symptoms → hepatic encephalopathy w/in 2-3 weeks

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6
Q

Space occupying lesion LFT

A

↑ T. Bili & Direct Bili

-no other significant changes

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7
Q

Acute Liver Failure causes

A

A: acetaminophen, HAV, autoimmune
B: Budd-Chiari, HBV
C: copper (Wilson’s), HCV
D: drugs/toxin, HDV
E: HEV in pregnancy
F: fatty- microvesicular type (no hepatic necrosis)
–tetracycline, valproate, pregnancy, Reye syndrome

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8
Q

Acute HBV serology

A

1) HBsAg rises (falls in acute) → Anti-HBs rises (immunity)
2) anti-HBc IgM → anti-HBc total (does not confer immunity)
3) HBeAg rises (falls before sAg)→ Anti HBe

HBeAg: infectivity; active viral replication
-persistence = progression, ↑ risk HCC
HBe-Ab → cessation of proliferation, good sign
Hbs-Ab → immunity

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9
Q

Chronic HBV serology

A
  • 1) HBsAg rises and remains elevated (NO Anti HBs)
    2) anti-HBc IgM → anti-HBc total (does not confer immunity)
  • 3) HBeAg rises (falls LATER)→ Anti HBe appear later

HBeAg: infectivity; active viral replication
-persistence = progression, ↑ risk HCC
HBe-Ab → cessation of proliferation, good sign
Hbs-Ab → immunity (doesn’t appear in chronic)

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10
Q

Three characteristics & top 3 causes of Cirrhosis

A

1) Bridging fibrous septa
2) Parenchymal nodules (micro & macro)
3) Disruption of architecture of entire liver

top 3 causes:
-Alcoholic liver disease
-Viral hepatitis
-Non-alcoholic steatohepatitis
(+ HCC = 4 primary liver insults)
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11
Q

HBV extrahepatic manifestations

A
  • membranous GN
  • most common assoc. w/ polyarteritis nodosa
  • -vasculitis → ischemia → nerves, GI, kidney
  • –aneurysms
  • serum sickness syndromes
  • -arthralgias, proteinuria, cutaneous eruptions, GI disease
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12
Q

HCV extrahepatic manifestations

A
  • Cryoglobulinemia
  • -raynauds, arthralgias, purpura
  • Membranoproliferative GN
  • Sporadic porphyria cutanea tarda (sensitive to sun)
  • ↑ type II DM
  • cutaneous vasculitis, leukocytoclastic
  • serum sickness syndromes
  • -arthralgias, proteinuria, cutaneous eruptions, GI disease
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13
Q

Clinical features of liver abscess

A
  • Fever
  • RUQ pain & tender hepatomegaly
  • Alk phos ↑
  • AST/ALT ↑ mild to moderate
  • jaundice if biliary system obstructed
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14
Q

AI hepatitis

A

Labs:

  • ANA, SMA,
  • children- LKM1

Morphology:

  • plasma cells
  • 78% female
  • interface hepatitis (piecemeal necrosis)
  • -necrosis b/w periportal parenchyma & portal tracts
  • bridging/necrosis fibrosis- b/w portal tracts
  • lymphoid infiltrates of portal tracts (dense mononuclear)
  • reactive bile duct changes
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15
Q

alpha-1 anti-trypsin deficiency

A

Labs:

  • PiZZ
  • -accumulation of misfiled Pi protein in cyto. of hepatocytes

Morphology:

  • *-PAS+
  • globular round eosinophilic inclusions
  • mallory bodies
  • *-Neonatal hepatitis** w/ cholestatic jaundice
  • clinically silent until cirrhosis in late life
  • ↑ risk HCC w/ or w/o cirrhosis
  • Associated w/ emphysema
  • prolonged conjugated bilirubinemia (dark urine, light stool)
  • most infants recover
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16
Q

NASH

A

NAFLD → NASH → NASH cirrhosis
↓ ↓ ↓
isolated HCC HCC or Decomp

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17
Q

Wilson’s disease

A

Labs:

  • Ceruloplasmin ↓
  • urine Cu ↑
  • ATP7 mutation

Morphology:

  • Cu accumulation
  • **Macronodular cirrhosis
  • Kayser-Fleishcer rings (limbus)
  • symptoms won’t appear until at least ~10yrs
  • Degeneration of lenticular nu. (putamen)
  • choreoathetoid movements
  • vacuous smile
  • drooling
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18
Q

Hemochromatosis

A

Labs:

  • HFE mutated→ hepcidin dysreg.→ excess absorption
  • % saturation ↑↑ (ferritin ↑↑)

Morphology:

  • micronodular cirrhosis
  • stain w/ prussian blue
Symptoms usually appear around 40 yrs
Classic Triad:
1) Pigment cirrhosis of liver
--HCC → free radicals (200x risk)
2) Skin pigmentation
3) DM → loss of islet cells
  • Hypogonadism (pit-hypothalm axis disruption)
  • -amenorrhea
  • -loss of libido / impotence
  • Cardiomyopathy → arryhthmias
  • arthritis / pseudogout
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19
Q

HBV morphology (acute & chronic)

A

ACUTE HEPATITIS (mimicked by drugs & AI hep)

  • T-cell infiltrates in lobules
  • ballooing degeneration → cholestasis
  • apoptosis: acidophil (councilman) bodies
  • lobular disarray
  • cholestasis

CHRONIC HEPATITIS

  • **Ground glass
  • interface hepatitis (piecemeal necrosis)
  • -necrosis b/w periportal parenchyma & portal tracts
  • bridging/necrosis fibrosis- b/w portal tracts
  • lymphoid infiltrates of portal tracts (dense mononuclear)
  • reactive bile duct changes
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20
Q

HCV morphology (acute & chronic)

A

ACUTE (mimicked by drugs & AI hep)

  • T-cell infiltrates in lobules
  • ballooing degeneration → cholestasis
  • apoptosis: acidophil (councilman) bodies
  • lobular disarray
  • cholestasis

CHRONIC HEPATITIS

  • **Steatosis
  • interface hepatitis (piecemeal necrosis)
  • -necrosis b/w periportal parenchyma & portal tracts
  • bridging/necrosis fibrosis- b/w portal tracts
  • lymphoid infiltrates of portal tracts (dense mononuclear)
  • reactive bile duct changes
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21
Q

Blood alcohol levels

A

80 mg/dl (0.08) → DUI

200 mg/dl (0.2) → inebriate occasional drinker

300-400 mg/dl → coma & respiratory arrest in unhabituated drinker

700 mg/dl → tolderated in habitual drinkers

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22
Q

Thiamine (B1) deficiency

A
  • Wernicke-Korsakoff syndrome
  • Dilated cardiomyopathy, high output failure (wet beriberi)
  • polyneuropathy (dry beriberi)
  • -toedrop, footdrop
  • weight loss
  • muscle wasting
  • edema
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23
Q

Riboflavin (B2) deficiency

A
  • Interstitial keratitis: vascularization of cornea
  • Greasy, scaling dermatitis
  • Erythroid hypoplasia
  • Glossitis
  • Cheilitis / Cheilosis
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24
Q

Niacin (B3) deficiency– Pellegra

A

3 D’s

  • dermatitis- SUN EXPOSED; scaling, desquamation, fissures
  • diarrhea- intestinal mucosal atrophy
  • dementia (neuronal loss)
  • -degeneration of posterior & lateral columns
  • death
  • glossitis

-carcinoid syndrome (uses up Tryptophan for serotonin)

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25
Q

Pyridoxine deficiency

A
  • peripheral neuropathy
  • convulsions: can only be stopped by pyridoxine
  • cheilosis
  • glossitis
  • ↑ plasma homocysteine

-long term use of isoniazid or estrogen

26
Q

Vit. C deficiency

A
  • perifollicular rash
  • bleeding gums
  • joint pain
  • subperiosteal bleed
  • impaired wound healing
  • anemia

-scorbutic rickets in children

27
Q

Folate (B9) deficiency

A

Due to:

  • ↑ use: pregnancy
  • Interference w/ absorption/metabolism
  • -ALCOHOL
  • -smoking
  • -oral contraceptive
  • -anticonvulsants
  • -chronic disease
  • Spina bifida / neural tube defects in fetus
  • megaloblastic anemia
  • Hyperhomocysteinemia: ↑ risk coronary thrombosis & stroke
28
Q

B12 deficiency

A

Due to:

  • loss of intrinsic factor
  • -AI gastritis
  • -gastric bypass/resection
  • malabsorption disease; crohn’s
  • parasite
  • Degeneration of spinal cord myelin
  • -sensory-motor defects (vibratory first lost)
  • Hyperhomocysteinemia: ↑ risk coronary thrombosis/stroke
  • glossitis
  • megaloblastic anemia (low platelets & PMN)
29
Q

Copper deficiency

A

Due to:

  • gastric surgery
  • intestinal malabsorption**
  • excess zinc
  • Myeloneuropathy
  • -muscle weakness & neurologic defects
  • abnormal collagen cross-linking

(malabsorption + neuropathy → Copper)

30
Q

Zinc deficiency

A

Acrodermatitis enteropathica

  • dermatitis around ORIFICES (eyes, nose, mouth
  • dermatitis of distal extremities
  • hypogonadism
  • impaired night vision
  • impaired immunity & healing
31
Q

Selenium deficiency

A

Protects against oxidative injury of lipids w/ vit E
-component of GSH-peroxidase

  • myopathy
  • cardiomyopathy in women & children (Keshan disease)
  • Narrow therapeutic window: significant toxicity
  • -↑ risk of prostate cancer in men
32
Q

Vit. A deficiency

A

Vit. A maintains specialized epithelium

  • Night blindness (earliest sign): ↓ rhodopsin regen.
  • Bitot spots: build up of keratin

Squamous Metaplasia

  • -conjuctiva → xeropthalmia
  • -cornea → keratomalacia → scarring→ blind
  • -bronchus → bronchopneumonia
  • -urinary tract → kidney stones
  • -pancreatic ducts

-Measles & respiratory infections is more severe w/ deficiency

33
Q

Vit. D deficiency

A

Due to:

  • limited exposure to sunlight
  • impaired fat absorption
  • deranged metabolism (liver or kidney disease)
  • ↑ fracture risk
  • Rickets in children: bowed legs, bossed head, rachitic rosary
  • Osteomalacia in adults (↓ mineralization)
  • hypocalcemic tetany
  • -convulsions
  • -Trousseau sign→ spasm w/ BP cuff
  • -Chvostok’s sign → mouth, eye muscle contract from tap
34
Q

Vit E deficiency

A

Due to:

  • fat malabsorption
  • abetalipoproteinemia
  • ***Low birth weight: immature gut

Neurologic disease

  • Spinocerebellar degeneration** (infant)**
  • -↓ or absent DTR
  • -abnormal eye movements
  • -ataxia
  • -loss position, vibratory sense, pain sense
35
Q

Causes for chronic elevations of transaminases

A 
A: α-1 Anti trypsin deficient, AI hepatitis
B: HBV
C: HCV, Copper (Wilson's disease)
D: drugs/herbals
E: ethanol
F: fat (NASH)
H: heart failure
I: iron accumulation (hemochromatosis)
36
Q

Cholestasis, cause & morphology

A
  • Extrahepatic bile duct obstruction
  • Intrahepatic bile duct obstruction
  • defects in hepatic excretion
  • Enlarged hepatocytes w/ bile droplets
  • → feathery degeneration
  • dilated bile ducts → canaliculi rupture
  • Kupffer cells phagocytose bile

At portal tracts:

  • ductular proliferation
  • edema, bile pigment retention
  • surrounding hepatocytes are swollen & degenerating
  • leads to ascending cholangitis or biliary cirrhosis
  • eventually *PMN inflammation (ascending cholangitis)
  • -bile duct epi & lumen
37
Q

Biliary cirrhosis morphology

A

Primary– small intrahepatic ducts (predicate inflammation)
Secondary– entire biliary tract

  • Intense yellow-green pigmentation
  • hard, cirrhotic- finely granular
  • dilated bile ducts
  • ↑ bile ducts
  • feathery degeneration
  • periportal mallory-denk bodies
  • -periportal fibrosis → jigsaw cirrhotic nodules
38
Q

Neonatal cholestasis causes

A
  • Idiopathic (50%)
  • Biliary atresia (33%)
  • Neonatal hepatitis:
  • -**α1-AT deficiency
  • -Alagille syndrome (paucity of bile ducts)
  • -cystic fibrosis
  • -infection (syphilis, CMV, sepsis)
  • -toxic
39
Q

vonMeyenburg Complex

A

Anomaly of the biliary tree

  • common
  • sporadic inheritance
  • bile duct hamartoma
  • -prolif. of small ducts adjacent to portal tract
  • may be under Glisson’s capsule
40
Q

Polycystic liver disease

A

Anomaly of the biliary tree

  • fairly common
  • auto. dominant
  • assoc w. polycystic kidney disease
  • multiple cysts in various organs
  • -*lined by cuboidal cells
  • -straw color fluid
  • die of renal failure
41
Q

Congenital Hepatic fibrosis

A

Anomaly of the biliary tree

  • uncommon
  • auto recessive
  • assoc. polycystic kidney disease
  • *-risk of cholangiocarcinoma
  • portal HTN w/o cirrhosis
  • curved ducts in fibrous proliferations along septal margins
42
Q

Caroli disease

A

Anomaly of the biliary tree

  • very uncommon
  • auto recessive
  • *-risk for cholangiocarcinoma
  • segmental dilations of large bile ducts
  • -may be assoc. choledocal cysts
  • portal HTN
  • intrahepatic cholistasis, cholelithiasis
  • cholangitis & hepatic abscess
43
Q

Alagille syndrome

A

Anomaly of the biliary tree

  • uncommon
  • auto dominant
  • risk of liver failure & HCC
  • portal tract bile ducts absent
  • → neonatal hepatitis
44
Q

Budd-Chiari syndrome

A
  • Hepatic vein thrombosis (outflow obstruction)
  • -obstruction of 2+ major hepatic veins
  • hepatomegaly
  • weight gain & ascites
  • aminotransferases ↑↑↑ (multi-thousands
  • Jaundice
45
Q

Peliosis hepatitis

A

impairs blood flow through the liver
-primary dilation of sinusoids

Associated w/:

  • anabolic steroids
  • rare-oral contraceptives
  • usually clinically silent
  • -fatal intra-abdominal hemorrhage may occur
46
Q

Causes of impaired intrahepatic blood flow

A
  • cirrhosis
  • sickle cell
  • DIC
  • -HELLP/eclampsia- fibrin clots in sinusoids
  • diffuse intrasinusoidal metastatic carcinoma
  • passive congestions due to heart failure
  • -centralobular hemorrhagic necrosis
  • peliosis hepatitis
47
Q

Hepatic vein & caval thrombosis

A
  • polycythemia vera
  • Inherited thrombophilias
  • -pregnancy / postpartum
  • -oral contraceptives
  • antiphospholipid syndrome
  • intra-abdominal cancer (HCC)

Hypercoagulability & sluggish flow

48
Q

Veno-occlusive disease

Sinusoidal obstruction syndrome

A
  • 1st week after BM transplant (25%)
  • hyperbilirubinemia & cholestasis

like budd-chiari but not as severe

  • tender hepatomegaly
  • ascites
  • weight gain
  • jaundice
49
Q

Causes of acute pancreatitis

A

Metabolic:

  • *alcoholism
  • hyerlipoproteinemia / hypertriglyceridemia
  • **hypercalcemia
  • drugs: furosemide
  • trypsin mutation (PRSS)
  • inhibitors of trypsin (SPINK 1)
  • CFTR

Mechanical

  • trauma, surgery, ERCP (endscopic)
  • obstructed duct
  • perforated peptic ulcer
  • ischemia
  • mumps
50
Q

Causes of chronic pancreatitis

A
  • Alcohol is most common
  • persistent obstruction
  • Hereditary
  • -PRSS → trypsin mutation
  • -SPINK → inhibitor of trypsin
  • -CFTR
  • Autoimmune → IgG4 plasma cells

Morph:

  • fibrosis
  • loss of acini
  • calcification w/in ducts
  • islets spared until late
  • hypoalbuminemia
51
Q

complications of acute pancreatitis

A
  • hypocalcemia
  • -shock
  • -ARDS
  • -acute renal failure
  • DIC
  • pancreatic abscess
  • pancreatic pseudocyst
  • duodenal obstruction (ileus ?)
52
Q

complications of chronic pancreatitis

A
  • pseudocyst
  • duct obstruction (calcification)
  • malabsorption, steatorrhea
  • secondary DM
  • pancreatic carcinoma
53
Q

pancreatic pseudocyst

A
  • develop from necrosis/hemmorhage
  • no epithelial lining
  • lined by fibrous tissue & granulation tissue
  • unilocular
  • elevated amylase
  • abdominal pain
  • mass in region of pancreas
  • may hemorrhage, infect, cause peritonitis
54
Q

Ghrelin

A
  • appetite stimulater
  • from arcuate nu. & empty stomach
  • stimulates NPY/AgRP neurons (anabolic
  • -NPY → NPYR → MCH & orexins
  • ↑ food intake
55
Q

Peptide YY

A
  • satiety signal
  • from endocrine cells of ileum; colon
  • inhibits NPY/AgRP neurons
  • -NPY → NPYR → MCH & orexins
  • decreased in Prader Willi
  • ↓ food intake
56
Q

Amylin

A
  • reduces food intake

- from β cells

57
Q

Leptin

A
  • stimulate POMC/CART (energy use)
  • -αMSH → MC4R → TRH & CRH
  • inhibits NPY/AgRP (food intake)
  • -NPY → NPYR → MCH & orexins
  • ↓ food intake
  • ↑ energy expenditure
58
Q

Adiponectin

A
  • ↑ FA oxidation → ↓ fat mass
  • insulin sensitizing
  • produced by adipocytes
  • more in lean individuals than obese

Liver:

  • ↓ FA influx
  • ↓ TG content
  • ↓ glucose production

Muscle:
-directs FA to muscle for oxidation

59
Q

Complications of obestiy

A
  • Cerebral atherosclerosis
  • stroke
  • hypoventilation
  • pickwickian syndrome (sleep apnea)
  • HTN
  • LVH
  • CHF
  • coronary atherosclerosis
  • MI
  • Non-alcoholic steatosis
  • Gallstones
  • diabetes mellitus
  • renal failure (independent or 2º to diabetes/ HTN)
  • dyslipidproteinemia (↑ chol, TG, LDL, ↓ HDL)
  • osteoarthritis / gouty arthritis
  • reproductive dysfunction
  • coagulopathy (DVT & PE)
60
Q

Osteopathic structural changes of obesity

A
  • Flattened thoracic curve: T3-T5
  • ↓ lumbosacral curve
  • L5 ant. S1
  • sacral extension
  • -B/L intermittent lumbar radiculopathy
  • -lumbosacral instability
  • -constant low back pain

year 2 (15 decks)

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