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D&T 4: Exam 3 > Path > Flashcards

Flashcards in Path Deck (99)
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1
Q

Arsenic Poisoning

A

Found in soil and well water; some herbicides

Acute: Decreased mitochondrial oxidation causing some CNS and cardiovascular abnormalities

2-8 weeks: Peripheral neuropathy, tinnitus

Chronic: Lung and skin cancer, anemia, hyperpigmentation of the soles of the feet

2
Q

Cadmium poisoning

A

Exposure thru food, mining, electroplating, nickel batteries

Causes COPD, Cancer, Renal tubular damage, Osteoporosis

3
Q

Organochlorides

A

Halogenated compounds that resist deactivation such as DDT, dioxins, PCBs

Anti-androgenic; Dioxin will also cause incurable acne, hyperkeratosis (picture of Ukranian dude)

4
Q

Smoking effects on pregnancy

A

Pre-term delivery

Intrauterine growth retardation

Spontaneous abortion

Sudden Infant Death Syndrome

5
Q

Effects of estrogen hormone replacement therapy

A

Reduces osteoporotic fractures BUT

Increased risk of: hepatic adenoma, thromboembolism, and breast cancer

-Could help prevent CVD if started before 60

6
Q

Acetaminophen OD

A

Overwhelmed glutathione reductase system =» hepatic centrilobular necrosis w/ fulminant liver failure

Tx: N-acetylcysteine (restores glutathione)

7
Q

Methamphetamines

A

Increases release of dopamine

Signs: Euphoria, mydriasis, hyperpyrexia, increased BP and HR

Chronic: Psychosis, paranoia, violence

8
Q

MDMA

A

Increases serotonin release; causes a euphoria, hallucinations, mydriasis, and hyperpyrexia

9
Q

Prognostic factors for a burn

A
  1. Surface area
  2. Depth of burn
  3. Other internal injuries
  4. Prompt rehydration and antibiotic admin.
10
Q

Consequences of severe burns

A

Hypovolemia (most pressing)

Hypermetabolic state

Infection

Injury to airway (will show oral or bronchial charring)

11
Q

Heat stroke findings

A

Core temp >40 degrees

Vasodilation

Tachycardia, arrhythmias

Hyperkalemia

12
Q

Plumbism

A

Pb2+ exposure occurs w/ old homes, mining, car batteries, some kids toys and it will compete w/ Ca2+ for binding shit

-Most Pb2+ is absorbed into the bones and teeth making “Lead Lines” at metaphyseal plates (actually consist of Ca2+)
=»Decreased fracture healing and bone growth

*Has a half-life of 20 yrs

-Also causes a hypochromic, microcytic anemia due to interference w/ Hb synthesis
=»Increased free protoporphyrin, basophilic stipling, and ringed sideroblasts in the bone marrow

Clinical: Child- decreased mental function, behavior issues, hearing loss
Adult- headache, memory loss, wrist and foot drop

13
Q

Hepatic Encephalopathy

A

Hyperammonemia

=»Behavior abnormalities, hypotonia, EEG changes

14
Q

Hepatic microvesicular steatosis

A

Can be seen w/ fatty liver of pregnancy or tetracycline toxicity

Multiple small fat globules can be seen in hepatocytes

15
Q

Regenerative liver nodules

A

Regeneration of liver cells in the canal of Hering; originate from progenitors of parenchymal and bile duct cells?

16
Q

Feathery degeneration of hepatocytes

A

Indicative of cholestasis within the canaliculi or hepatocytes

17
Q

Tx of cholestasis

A

Intrahepatic =» Liver transplant

Extrahepatic =» Surgery to remove obstruction

18
Q

Detecting IgG HAV viral levels

A

Total HAV Ig - IgM HAV= IgG HAV

19
Q

Why is the host response inadequate to HBV?

A

The virus inserts itself into the host DNA

Therefore, tx is targeted at preventing cirrhosis and HCC

20
Q

Most variable region of HCV genome

A

E2 envelope protein; target of anti-HCV antibodies

Polymerase lacks proofreading =» constant mutations

21
Q

HCV treatment

A

Pegylated IFN-a, ribavirin

Response depends on HCV genotype
***Best outcome if HCV type 2 or 3

22
Q

Appearance of HBV infected hepatocytes

A

Cytoplasm has “ground-glass” appearance (filled w/ HBV particles) w/ a granular periphery

23
Q

HCV histology

A

Has an “interface” appearance; lymphoid follicles are found beyond the portal tracts

24
Q

Type I AI Hepatitis

A

ANA, ASMA (+)

Middle-aged adults and older people usually

Possible assoc. W/ HLA-DR3 or DR4

25
Q

Type II AI Hepatitis

A

Anti-LKM-1 antibodies that attack CYP2D6

Classically in young, european adults

26
Q

OCPs damage to liver

A

Can cause: Hepatocellular cholestasis

               Hepatic adenomas (risk of rupturing)    

               Vascular thromboses (Budd-chiari syndrome)
27
Q

Ethanol effects on the liver

A

Fatty liver disease (fat droplets, ballooning necrosis, steatohepatitis w/ mallory-denk bodies)

Heptocellular carcinoma

28
Q

Acetaminophen effects on the liver

A

Massive, acute hepatocellullar necrosis

29
Q

Methotrexate effects on the liver

A

Fatty liver disease

Fibrosis and sclerosis

30
Q

Histology of alcoholic liver disease

A

Mallory-denk bodies (cytoplasmic, eosinophilic inclusions made of ubiquinated intermediate filaments)

Neutrophil sattelitosis (produce free radicals in damaged area)

31
Q

Effects of alcohol on the liver

A

Hypoxia

Oxidative stress

Steatosis

Mitochondrial membrane dysfnxn

32
Q

Hepatocellular steatosis

A
  1. Increased NADH shunts more substrates towards lipid synthesis
  2. Impaired assembly and secretion of lipoproteins
  3. Increased peripheral catabolism of fat =» increased FAs in the blood
33
Q

Gold standard for biopsy of NAFLD

A

Liver biopsy

Also used for grading (notes degree of inflammation, necrosis, and steatosis) and staging (notes fibrosis)

34
Q

Non-alcoholic steatohepatitis

A

More progressive form of NAFLD; MCC of elevated liver enzymes

Tx: Treat the IR to prevent steatosis and hepatocellular carcinoma

35
Q

NAFLD “Hit” theory

A

First hit: Insulin resistance causing increased glucose levels

Second hit: Acute steatosis leads NAFLD; denoted by hepatocellular oxidative injury causing necrosis and inflammation

36
Q

Pediatric NAFLD

A

Will see more diffuse steatosis and portal fibrosis as well as a mononuclear cell infiltrate

37
Q

HAV structure

A

naked,ssRNA (+) member of the picornaviradae family

Capsid consists of VP1, 2, and 3; 1 and 3 are antigenic ***

*Contains a single ORF (open reading frame) that produces a long, single polypeptide whose proteolysed products produce the viral structural and regulatory proteins

38
Q

HAV Hepatocyte cellular receptor

A

Infects hepatocytes via HAVcr1/TIM1 (class I integral protein)

TIM1= T-cell immunoglobulin mucin family I

Tropism is determined by the asialoglycoprotein receptor, determines the uptake of the virus

39
Q

HAV Auxiliary factor

A

IgA1y =» special ligand on HAVcr1/TM1 that forms IgA-HAV complex enhancing interaction w/ the hepatocyte receptor

**KNOW THIS

40
Q

Depression in elderly

A

Can be mistaken for dementia

41
Q

Drugs w/ a black box warning in elderly

A

Dopamine antagonists

42
Q

Breastmilk jaundice

A

Breast milk contains B-glucuronidase which converts conj. back to unconj. bilirubin

Tx: Stop breastfeeding ya dingus

43
Q

UGT1A1 gene

A

Gene that encodes for bilirubin-UDP-glucuronosyl transferase; is deficient in Type I Crigler-Najjar (produces severe kernicterus) and has decreased fnxn in the milder Type II Crigler-Najjar (mild jaundice treated w/ lifelong phototherapy)

44
Q

MRP2 gene

A

Encodes for transporter protein for conj. bilirubin into the bile canaliculi; is mutated in Dubin-Johnson syndrome (causes relapsing non-pruritic jaundice and increased conj. bilirubin)

45
Q

Hepatic giant cell transformation

A

Unique response of young liver to injury; will see multinucleated, giant hepatic cells alongside apoptotic, eosinophilic bodies

-Can also see some extramedullary hematopoiesis occurring

***Seen during neonatal cholestasis

46
Q

Kasai procedure

A

SI is attached to the liver in order to bypass the atretic biliary duct and resume normal bile flow; can be done if liver transplant is not possible

47
Q

C282Y mutation

A

Cysteine =» Tyrosine substitution at amino acid 282 in the HFE gene; causes primary hereditary hemochromatosis

-Defective hepcidin gene leads to uncontrolled absorption of iron and deposition in parenchyma when storage iron levels get too high

Clinical: Classic triad= hepatomegaly, hyperpigmentation, DM (Yellow Diabetes); can also see arrhythmias

Tx: Therapeutic phlebotomy

48
Q

ATP7B gene

A

Encodes for a copper-transporting ATPase in the trans-Golgi network in the canaliculi

defective protein causes Wilson’s disease (also called hepatolenticular degeneration) leading to:

  1. decreased copper excretion into the bile
    • is usually performed by ATP7B promoting copper storage into lysosomes which interact w p62/dynactin and are then exocytosed into the bile
  2. decreased incorporation into ceruloplasmin
    * >4mg in liver biopsy indicates disease, even if sx arent present yet
49
Q

Rhodanine stain

A

Indicates copper levels inside of hepatocytes; important because increased glycogen on histo can resemble viral hepatitis histo

50
Q

SERPINA1 gene

A

Located on Cr. 14 and encodes for AAT; PiZZ is the homozygous (ZZ) mutated form causing the most severe disease

-Overall, the disease is due to a defect in the migration of Pi from the ER to the Golgi apparatus; will accumulate in the ER and cause autophagocytosis and hepatocyte destruction

Tx: Liver transplant

51
Q

Stages of Primary Biliary Cirrhosis

A

Portal: Portal inflammation, bile duct damage w/ “florid duct lesion” **** KNOW

Peripheral: Ductal proliferation, periportal inflammatin/fibrosis

Septal: Bridging fibrosis, ductopenia

Cirrhosis (last stage)

-Pts. have increased ALP, GGT, and anti-mitochondrial abs*

Tx: Ursodiol (a natural bile acid); possible transplant

52
Q

Potential sequelae of Primary Sclerosing Cholangiitis

A

Hepatocellular carcinoma

Cholangiocarcinoma

Autoimmune Hepatitis

Chronic pancreatitis

53
Q

Rokitansky-Aschoff sinuses

A

Deep crypts or sinuses formed during chronic cholecystitis; can also see lymphoid follicle formation beneath it

Will also see subserosal fibrosis with a gray-white wall

54
Q

Caroli’s Disease

A

Congenital, nonobstructive, segmental multifocal dilatation of the intrahepatic bile ducts

  • When isolated= disease
  • When present w/ fibrosis “syndrome”

Clinical: Presents in early childhood w/ jaundice, fever, pain, Cholangitis, increased ESR, increase ALP and GGT

-Increased risk of cholangiocarcinoma

55
Q

Alagille Syndrome

A

AD disorder characterized by paucity of the hepatic bile ducts; caused by mutations in JAG1/NOTCH2***

-Biopsy shows cholestasis and decreased number of bile ducts

Clinical: Presents in infant, cholestasis, xanthomas, pruritis

Labs: Conjugated hyperbilirubinemia, Increased ALP and GGT, hyperlipidemia

Clinical: Malabsorption, cholestasis, hypoplastic pulmonary tree, vertebral arch defects, hyperplastic facies

Tx: Liver transplant

56
Q

Hepatic infarct of Zahn

A

Atrophy and hemostasis of the liver but NO gross necrosis

-due to acute thromboses in the small intrahepatic portal vein radicles `

57
Q

Peliosis hepatitis

A

Blood-filled cysts in the liver w/ an incomplete endothelial lining; generally asymptomatic but can rupture and cause severe bleed

Causes: Steroids, OCPs, toxins, tamoxifen, MTX, AIDS, hairy cell leukemia

58
Q

Sinusoidal obstructive Syndrome

A

Obstruction of the hepatic sinusoids causing endothelial sloughing and perivascular fibrosis and ECM deposition

Causes: Chemotherapeutics, Pt containing drugs, herbal teas, BM transplant

Tx: Anticoagulation; defibrotide

59
Q

Focal nodular hyperplasia

A

Vascular malformation of AV anastamoses w/ localized overgrowth of liver cell components; assoc. w/ OCP use in 20-40 yr. old women; has no malignant potential

Histo: Solid mass w/ dystrophic artery formation and possible inflammatory infiltrate

60
Q

MCC of benign hepatic tumor

A

Cavernous hemangioma; vascular lesion of dilated, communicating vessel channels

  • Consists of discrete, subcapsular red-blue nodules that are lined by a single layer of endothelial cells
  • Typically incidentally found in females, do have potential to rupture tho
61
Q

Kasabach-Meritt syndrome

A

Microangiopathic anemia w/ consumption coagulopathy

Erythrocytosis

Bleeding

-Presence of hepatic cavernous hemangiomas

62
Q

MCC of primary hepatic malignant tumor

A

HCC; mostly arise from chronic cirrhosis (takes 10 yrs) but can arise from aflatoxin exposure, Hemochromatosis, primary biliary cirrhosis, autoimmune hepatitis

  • Increasingly due to NAFSH
  • AFP=serum marker, however, this is also increased in cirrhosis, pregnancy, and chronic HCV (so it’s nonspecific)
63
Q

Fibrolamellar variant of HCC

A

Arises in younger pts. that have no underlying liver disease; has the same clinical manifestations (fever, RUQ pain, fatigue, sweating)

-Better prognosis than normal HCC tho

Presents as a firm, unencapsulated mass that on histo appears w/ large, eosinophilic cells w/ abundant fibrolamellar (thick fibrosing) stroma

64
Q

CA 19-9

A

Indicates cholangiocarcinoma for this test; can be due to primary sclerosing cholangitis, clonorchis sinensis infxn, chemicals, chronic cholecystitis

-Whipple procedure used to tx

65
Q

Metastatic tumors to the liver

A

Adults: Colon, breast, lung, pancreas

Kids: Neuroblastoma, Wilm’s tumor, rhabdomyosarcoma

66
Q

Intrahepatic cholestasis of pregnancy

A

May be due to mutations in phospholipid translocator, ATP cassette transporter B4; may cause cholestasis

-Typically benign but not always

Clinical: Sx. appear in third trimester typically in multiparous women; have history of cholestasis w/ OCP use

-**Pruritis, dark urine, pale stool, conjugated hyperbilirubinemia, increased ALP and GGT, ***Increased bile salts

67
Q

Most common cause of liver transplant in children

A

Biliary atresia; could also do a Kasai procedure

68
Q

Most common route to acute hepatic failure

A

Chronic liver disease

69
Q

Hepatorenal syndrome

A

Hepatic failure causing venous congestion causes the renal artery to constrict which leads to a transient loss of renal fnxn

-Resolves once liver fnxn returns

70
Q

Perisinusoidal stellate cell

A

Stimulated by inflammatory cytokines released by damaged hepatocytes to produce more collagen in the space of Disse

➡️fibrosis

71
Q

RBC zinc-bound protoporphyrin

A

Increased with Plumbism

72
Q

Main toxicity areas of cadmium

A

Bone, kidney, lung

-Toxic to the tubules in the kidney and the alveolar macros in the lung

73
Q

Cancers assoc. With polycyclic hydrocarbons

A

Lung and bladder

74
Q

Polymorphism

A

Variant allele present in at least one percent of the population

75
Q

Most infectious phase of viral hepatitis

A

The end of the prodromal period

76
Q

In what pts. Can HDV infxns be serious

A

IV drug abusers

77
Q

Assertive mating

A

Choice of mating based on Phenotype

78
Q

Which type of hepatitis may not respond to immunosuppression?

A

Type II

79
Q

Dane particle

A

A complete infectious particle of HBV, has an envelope with all three infectious antigens

80
Q

pgRNA

A

Pregenomic RNA: is a few nucleotides shorter than precore RNA and lacks the start codon for HBeAg

⭐️ encodes viral polymerase and HBcAg

⭐️serves as a template for genome synthesis

81
Q

‘5 epsilon structure of HBV

A

Portion of pgRNA that associates with HBcAg and binds to HBV polymerase (Pol)

⭐️terminal protein domain serves as protein primer for Reverse Transcriptase leading to the formation of new DNA

82
Q

Pol-DNA oligo complex

A

Consists of the newly synthesized HBV DNA associating with the 5 epsilon structure on pgRNA

⭐️pairs with the ‘3 end of pgRNA to prime reverse transcription to synthesize the negative strand of the virus

This will serve as the template for incomplete synthesis of the positive strand

83
Q

Where does the HBV envelope come from

A

ER membrane

84
Q

What part of the brain is CO specifically toxic to?

A

The globus Pallidus

85
Q

Increased urinary corproporphyrin I to corproporphyrin III ratio

A

Gilbert syndrome

86
Q

NonPruritic jaundice

A

Probs Dubin-Johnson syndrome

87
Q

Canalicular cholestasis

A

Will see mild portal inflammation due to bile plugs activating Kupfer cells

-Assoc. With sepsis

88
Q

Ductal cholestasis

A

Dilated canals of Hering, bile plugs

Progresses to sepsis ➡️ worse prognosis

89
Q

Most common form of biliary atresia

A

Perinatal form: Biliary tree is normally developed at birth and then destroyed, usually by viruses like CMV, ROTAVIRUS, REOVIRUS

90
Q

What condition can ulcerative colitis exist with

A

Primary Sclerosing Cholangitis

91
Q

Conditions contributing to cholesterol stone formation

A

Cholesterol supersaturation

Hypo motility of gall bladder

Increased mucous secretion

accelerated nucleation of cholesterol

92
Q

Conditions contributing to pigmented gallstone formation

A

Chronic hemolysis

Ileal dysfnxn

Bacterial infection of the biliary tree
-or ascaris or clonorchis

93
Q

Chronic cholecystitis may grow what organism

A

E. Coli

94
Q

Von-Meyenburg complexes

A

Hamartomas of ductal structures found within hyalinized stroma

-Assoc. W/ ADPKD OR PCLD

95
Q

Congenital Hepatic ️Fibrosis

A

Fibrotic liver possibly with fibrovascular projections into ducts

-Can be assoc. With ARPKD, Caroli’s disease

96
Q

Tx of Sinusoidal obstructive disease

A

Anticoagulation

Defibrotide

97
Q

Klatskin tumor

A

A Cholangiocarcinoma that has a Hilar location; causes symptoms of biliary obstruction

98
Q

Tumor assoc. With FAP or Beckwith-Wiedemann syndrome

A

Hepatoblastoma

99
Q

Severe complication of eclampsia

A

Hematoma scan dissect under Glissons capsule and rupture producing COAGULATIVE necrosis

-prior to this, you can also see general lab signs of hepatic dysfnxn