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GI/Endo/Repro > Assessment 3 > Flashcards

Assessment 3 Flashcards

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1
Q

Cystinuria

A

Defect in transport of cystine, lysine, arginine, ornithine

Poor absorption in kidneys/intstines

Cystine accumulates in urine (least soluble)

Treat w/ lots of water

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2
Q

Hartnup disease

A

Defect in transport of neutral AA (Ile, Leu, phe, Thr, Trp, Val)

Intestine and kidneys

D173N mutation

Lack of tryptophan, treat with try and niacin supplements

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3
Q

Cystinosis

A

Cannot transport cystine out of lysosome

Autosomal recessive, ESRD by 7-10yrs

Treat with cysteamine - reacts with cystine and end products leave lysosome

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4
Q

Pyruvate TA

A

Pyruvate –> Alanine

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5
Q

OAA TA

A

OAA –> Asp

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6
Q

a-KG TA

A

a-KG –> Glutamate

Alanine to Pyruvate

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7
Q

Transaminations all require…

A

Vitamin B6

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8
Q

Biosynthesis of Serine

A

3PG –> Phosphopyruvate –> phosphoserine –> Serine

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9
Q

Glycine synthesis

A

Serine –> Glycine

Serine hydroxymethyl transferase, creates N5/N10 methylene THF

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10
Q

Most stable THF?

A

N5 Methyl THF

All THF forms go towards that

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11
Q

Degradative reactions involving THF: Serine

A

Serine comes from 3PG which comes from Glucose

Glucose carbons —–> end up in THF compound

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12
Q

Degradative reactions involving THF: Formate

A

Make N10 formyl THF

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13
Q

Degradative reactions involving THF: Histidine degradation

A

Make N5-formimino THF

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14
Q

Biosynthetic reactions with THF

A

dUMP to TMP (N5/N10 methylene THF)

Glycine to Serine

Homocysteine –> methionine (N5 Methyl THF)

Purine biosynthesis (N10 formyl THF)

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15
Q

S Adenosylmethionine

A

Used in all methyl transferase reactions except homocysteine –> methionine

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16
Q

Phe –> Tyr

A

Enzyme: Phenylalanine hydroxylase

Cofactor: Tetrahydrobiopterin

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17
Q

AA degraded into which 7 families

A 
Acetoacetyl-CoA
Acetyl CoA
Pyruvate
a-KG
Succinyl CoA
Fumarate
Oxaloacetate
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18
Q

Leucine degraded into…

A

Acetyl CoA

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19
Q

Leucine/Lysine degraded into…

A

Acetoacetyl-CoA –> Acetyle CoA

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20
Q

AA degradation cycle

A

Pyruvate –> Acetyl CoA + OAA –> Citrate –> aKG –> Succinyl CoA –> Fumarate –> Oxaloacetate

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21
Q

Ketogenic AA

A

Leucine

Lysine

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22
Q

Phenylalanine degradation

A

Phe –> Tyr –> x –> Homogentisic acid –> Fumorylacetoacetate –> Fumarate + Acetoacetate

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23
Q

Alcaptonuria

A

Buildup of homogentisic acid in urine

Black urine

Arthritis

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24
Q

Phenylketonuria

A

Cannot breakdown Phe:

Classical - no enzyme
Other - lack of THB

Buildup of TA product phenylpyruvate, phe, phenyllactate

Restrict Phe diet

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25
Tyrosinemia Type I and II
Type I: Lack of fumarylacetoacetate hydrolase Early death Type II: Defect in tyrosineaminotransferase, buildup of Tyr Treat both with low Phe and Tyr diet
26
Nitisinone
Treatment for Type 1 tyrosinemia Blocks homogentisic acid production
27
Bilirubin production
Heme degraded --> biliverdin --> bilirubin --> Attached to albumin --> Carried in blood to liver
28
Bilirubin in hepatocytes
Albumin released, bilirubin enters hepatocytes --> Conjugated with glucoronic acid, water soluble --> excreted to bile and deconjugated by bacteria in intestines --> most leaves in feces
29
Hemochromatosis
Defect in HFE gene - excessive iron absorption Excessive iron accumulation, especially in liver Autosomal recessive Hemosiderin (iron storage) deposition = damage to liver, pancreas, heart Micronodular cirrhosis, diabetes, brown skin Phlebotomy can be useful treatment
30
Wilson Disease
Copper accumulation - liver, brain, eye ATP7B gene mutation (copper transporting ATPase) - Failure to incorporate copper into ceruloplasmin which takes copper to bile Rare disease Kayser Fleischer rings (copper in cornea)
31
Alpha-1 antitrypsin deficiency
Inhibitor of proteases, when not there --> tissue damage Increase risk for hepatocellular carcinoma Cirrhosis
32
Acute fatty liver of pregnancy
Very rare Microvesicular steatosis Fetus causes inherited metabolic disorder in mother
33
Adult Polycystic kidney disease
Mutation in gene encodinc polycystin-1 (transmembrane glycoprotein) Loss of function of stress response on ciliary membranes = abnormal fluid filled cysts
34
Familial hypercholesterolemia
Mutation in gene encoding LDL receptor on hepatocytes Increased blood cholesterol Heterozygotes have 1/2 LDL receptors, homozygotes have none
35
Gilbert syndrome
Fluctuating hyperbilirubinemia in response to stress, fasting, exercise UGT1A1 mutation
36
Bilirubin conjugator
UGT1A1
37
Bilirubin transport proteins
Albumin/bilirubin transporter: OATP2 Conjugated bilirubin tranporter: MRP2
38
Control points for bilirubin clearance
1. Uptake 2. Conjugation 3. Secretion
39
CAR agonist
Increases bilirubin metabolism and clearance
40
Unconjugated hyperbilirubinemia
Increased production - hemolysis Decreased uptake - OATP2 Impaired conjugation
41
Crigler-Najjar type I vs type II
Type 1: No UGT1A1 activity, high levels of bilirubinemia Kernicterus Type II: Reduced UGT1A1 activity, usually benign
42
Indinavir and UGT1A1
Huge increase in bilirubinemia with Gilbert syndrome Inhibits UGT1A1
43
Kernicterus treatment
Expose to light, photoisomerization of Bilirubin
44
Dubin Johnson Syndrome
MRP2 mutation Cannot excrete conjugated bilirubin Black livers - lipofuscin melanin complex
45
Rotor syndrome
Conjugated bilirubin secreted back into blood (MRP3) cannot be taken back into hepatocyte OARP1B1/3 defect
46
Bilirubin and inflammation
Heme oxygenase suppresses inflammation Activated leukocytes upregulate HO = increased bilirubin = slow inflammation
47
Neurotransmitters developed from tyrosine
Dopamine Norepinephrine Epinephrine Need B6 and THB
48
Serotonin
Derived from tryptophan B6 and THB
49
GABA
Derived from glutamate
50
Histamine
Derived from histidine B6
51
Homocystinemia/uria
Buildup of homocysteine Optic lens issues, osteoporosis, mental retardation B6 can lower levels in 50% of cases (lower affinity of B6 by enzyme)
52
Defective enzymes that can lead to homocystinemia
1. Cystathionine beta synthase (Homocysteine --> Cystathionine) 2. N5/N10 methylene THF reductase (N5/N10 methylene THF --> N5 methyl THF) 3. Methionine synthase (N5 methyl THF --> THF and Homocysteine --> Methionine)
53
Elevated homocysteine effects
Decrease endothelial growth Increase smooth muscle cell proliferation - can exacerbate atherosclerosis Block coagulation cascade --> clots/thrombosis
54
Homocysteinemia treatment
Vit supplements: B6, folic acid, B12
55
Neural tube defects and homocysteine
Does not have direct effect But can monitor levels of functional folate by checking homocysteine levels Increased homocysteine = decreased functional folate
56
Vit B12
Obtain from milk/meat, absorbed via intrinsic factor Methyl cobalamin: Used Methionine synthase reaction Adenosyl cobalamin: Methly malonyl coa --> succinyl coa
57
B12 deficiency - neurological problems
Lack of B12 = lack of methionine = lack of SAM SAM needed for DNA methylation
58
Betaine pathway
Choline --> Betaine --> Dimethylglycine Homocystein --> methionine in final step
59
Branched chain amino acid metabolism, step 1 and 2
1. Transamination, B6 required | 2. Branched chain alpha keto acid DH
60
Isoleucine metabolism final product
Succinyl CoA + Acetyl CoA Ketogenic and Glucogenic
61
Leucine metabolism final products
Acetyl CoA Ketogenic only
62
Valine metabolism final products
Succinyl CoA Glucogenic
63
Maple syrup urine disease
Defect in branched chain alpha keto acid DH Buildup of branched chain amino acids
64
Glycine metabolism pathways
1. Glycine Serine 2. Glycine cleavage enzyme = CO2, N5/N10, NH4 3. Oxidase to Glyoxylate, transaminate back to Glycine
65
Primary Oxaluria type 1
Lack of glycine transaminase Buildup of Glyoxylate and subsequently oxalate kidney stones
66
Non ketotic hyperglycinemia
Glycine cleavage enzyme defect Elevated glycine in CSF and plasma --> Neurological defects because glycine is inhibitory neurotransmitter
67
Heme synthesis
Succinyl CoA + Glycine --> delta aminolivulenic acid --> x2 --> Porphobiliniogen --> Heme
68
Lead poisoning
Inhibits heme synthesis Affects Aminolevulinic acid Dehydratase
69
Porphyria
Class of defects in heme biosynthesis Photophobia, eat rare meats
70
AST/ALT ratio in NAFLD
AST/ALT less than 1
71
AST/ALT ratio in alcoholic liver disease
AST/ALT >1
72
NASH vs hepatic steatosis
NASH has fibrosis, not to extent of cirrhosis Hepatic steatosis has fatty droplets only
73
Ballooning degeneration
NASH Cells swell and fill with fluid, nuclei in center
74
Cirrhosis
Extensive fibrosis around regenerating nodules Large web of fibrosis and noticeable cell damage Collagen deposition in Space of Disse = blockage of hepatocytes to blood
75
Mechanisms of death in cirrhosis
Liver failure Portal hypertension Hepatocellular carcinoma
76
Alcoholic liver disease
Cirrhosis preceded by hepatic steatosis and alcoholic hepatitis Mallory bodies surrounding hepatocytes Alcohol metabolizing enzymes create more NADH and H = more lipid synthesis = fatty droplets
77
Hyperdynamic circulation
Portal hypertension = body response to dilate arteries = BP Drop = more salt/water retained = even more edema
78
Ascites
Fluid in peritoneal cavity Hypoalbuminemia, hyperdynamic circulation
79
NAFLD
Due to hyperlipidemia, obesity etc Steatosis more common than NASH
80
NAFLD lab findings
AST/ALT
81
NAFLD guidelines
Weight loss reduced hepatic steatosis Loss of body weight helps steatosis but need more for necroinflammation improvement Exercise may help
82
NASH treatment?
Vitamin E
83
Intrahepatic cholestasis vs extrahepatic
Intrahepatic: Defective bile secretion or intrahepatic bile duct disease Extrahepatic: Mechanical obstruction or injury of large bile ducts outside of liver
84
Cholestasis clinical features
Jaundice Pruritis Malabsorption
85
Cholestasis lab findings
Elevated ALP, GGT, 5NT Elevated conjugated bilirubin
86
Secondary biliary cirrhosis
Prolonged obstruction of extrahepatic biliary tree Fibrosis of liver --> cirrhosis
87
Intrahepatic cholestasis histology
Centrilolobular Intracellular and canalicular Hepatocyte necrosis
88
Extrahepatic cholestasis histology
Bile duct/bile plugs Edema and acute inflammation of portal tracts
89
Cholelithiasis
Gall stones Can be asymptomatic Cholesterol (80%) and pigment stones
90
4 F's of gall stones
Female Forties Fat Fertile
91
Biliary colic
Severe RUQ pain post prandial Fatty food intolerance
92
Acute cholesytitis
Murphys sign Palpable gall bladder Elevated ALP and leukocytosis
93
Acute cholecystitis complications
Gangrenous cholecystitis Emphysematous Stone in bile duct Gall bladder hydrops
94
Acute cholecystitis treatment
Early cholestectomy Intraoperative cholangiogram to rule out common bile duct stones Electrolytes/fluid
95
Choledocolithiasis
Stones in biliary tree Obstruction can lead to ascending cholangitis - bacterial infection of bile ducts
96
Acute Cholangitis
Bacterial infection of biliary tree Inflammation aggravated E. coli, Clostriidium, Enterobacter
97
Charcot triad
Abdominal pain, fever, jaundice
98
Reynolds Pentad
Charcot triad + hypotension, altered menta status
99
Clinical features of acute cholangitis
Charcot triad Reynolds Pentad Elevated WBC
100
Acute pancreatitis
Can be caused by stone in Ampulla of Vater, occlusion of pancreatic duct
101
Acute pancreatitis clinical
Elevated amylase/lipase Hypocalcemia Leukocytosis
102
Biliary atresia
Luminal obstruction of biliary tree Congenital
103
Biliary atresia treatment
Kasai portoenterostomy Liver transplant
104
Primary sclerosing cholangitis
Cholestatic liver with fibrosis and inflammation Narrowing/obstruction of larger bile ducts --> cirrhosis Males>females 70-75% coexisting IBD
105
PSC ERCP
segmental constrictions String of beads
106
PSC clinical/lab features
Fatigue, pruritis, jaundice Antinuclear antiboy Anti smooth muscle anti body p-ANCA
107
PSC cirrhotic stage
Biliary cirrhosis 3-6 years after presentation
108
Cholangiocarcinoma
Rare PSC is risk factor Poor prognosis Painless jaundice, clay stool, cola urine Obstructive jaundice labs (GGT, ALP, Bilirubin increase)
109
Courvoisier Sign
Jaundice + Palpable gall bladder Painless jaundice
110
Primary biliary cirrhosis
Granulomatous destruction of intrahepatic bile ducts Female>Male Hepatocellular carcinoma risk Pruritis, fatigue, jaundice (late) Can be asymptomatic
111
PBC treatment
Ursodeoxycholic acid Cholestyramine - bind bile salts in intestines to enhance excretion Immunosuppressants liver transplant
112
Autoimmune hepatitis
Female predominance Immune system attacks hepatocytes High IgG and gama globulin Liver biopsy Prednisone, azathioprine
113
Autoimmune hepatitis Type 1
More common, all ages Antinuclear antibody Anti smooth muscle antibody Anti actin antibody
114
Autoimmune hepatitis type 2
Girls and women, children 2-14 Anti livery kidney microssome Anti liver cytosol-1
115
Most common HIV transmission
Male to male sexual contact
116
5 body fluids that transmit HIV
``` Blood Semen/pre semen Rectal secretions Vaginal secretions Breast milk ```
117
HIV Transmission types (3)
Sexual (horizontal transmission) Blood exposure: Needles, IV drug use, transfusions Vertical transmission: Fetus in birth canal or in utero, breast milk
118
Postive male/Negative female prevention
Donor insemination Sperm washing IVF w/intracytoplasmic sperm injection
119
Positive female/Negative male prevention
Intra-uterine insemination | IVF
120
HIV risk by type of exposure: Sexual
``` Least risk Insertive vaginal Receptive vaginal Insertive anal Receptive anal Highest risk ```
121
HIV risk by type of exposure: Blood exposure
``` Least risk Needle share Needle stick Mucous membrane exposure Transfusion Most risk ```
122
Best HIV diagnosis
HIV Ag/Ab test + Ab differentiation test Earlier diagnosis
123
Newborn HIV test
Newborns carry maternal Ab HIV RNA quantitation at different time frames AZT for 6weeks
124
Acute HIV infection
2-6 weeks after exposure 1. Mono like illness, adenopathy and pharyngitis 2. Rash on trunk 3. Neurological symptoms
125
HIV infection: first 3 months
Huge rise in viral count, decline in CD4 count HIV immune response occurs and viral load decreased to steady state level
126
HIV monitoring
Viral load CD4 cell count
127
Steps of HIV progression
1. Binding/Fusion 2. Uncoating 3. Reverse transcription 4. Integration 5. Proviral transcription 6. Translation 7. Cleavage 8. Assembly, maturation, release
128
Binding and Fusion drugs
CCR5 antagonist Fusion inhibitor: Enfuviritide - side effect, injected, no bueno
129
Uncoating
Virus fused with CD4 membrane, viral RNA released into cytoplasm
130
Reverse Transcription
Viral RNA transcribed into DNA
131
Reverse transcription drug classes
NNRTI: Prevents binding of RT to HIV RNA NRTI: Allows RT and HIV RNA binding, chain terminator, eventually DNA degrades
132
NNRTI drugs
Efavirenz - dreams Rilpivirine - Need food Entravirine: CYP450
133
NRTI drugs
Zidovudine - AZT, children born to HIV+ mothers Lamivudine (3TC) - Hep B Emtricitabine (FTC) - Hep B Abacavir - Hypersensitivity, HLAB5701 Tenofovir (TDF/TAF) - decreased bone density, renal toxicity
134
Integration drugs
-tegravir Raltegravir - Rash, myopathy Elvitegravir Dolutegravir - hypersensitivity
135
Proviral transcription
Viral DNA reprograms CD4 machinery to produce Viral RNA and viral mRNA
136
Translation
Ribosomes use viral mRNA to create proteins/enzymes in polyprotein
137
Cleavage
Proteases cut polyprotein and release enzymes/proteins needed for creation of new HIV virus
138
Protease inhibitors
Ritonavir (RTV): First PI, used as booster Lopinavir (LPV): Increase cholesterol/TG Darunavir (DRV): Hypersensitivity Atazanavir (ATV): Kidney stones, UGT1A1 inhibitor
139
HIV clearance evasion
Rapid replication Mutagenesis Latency Down regulation of MHC on infected cells Structure Infection of sanctuary sites
140
Chronic HIV infection
Latency phase, generally asymptomatic Immune system able to limit replication, virus lays dormant Avg 8-10 years
141
Immune defects in HIV+
Low CD4 Dysregulation: altered cytokines, impaired response to antigens, hypergammaglobulinemia
142
When to start ART
All HIV patients, differs based on baseline CD4 levels
143
Absolute indications for ART
``` Hep B/C HIV associated neuropathy HIV associated neurocognitive disorders Pregnancy Malignancy AIDS defining disease ```
144
ART start: 3 medications
2 NRTI + integrase inhibitor OR protease inhibitor
145
Morphological changes with ART
Lipodystrophy Lipohypertrophy Lipoatrophy
146
HIV mutagenesis
Mutation rate of 1/10,000 Mutation occurs during Reverse Transcription
147
CD4 response after ART
``` Increased numbers Response to non HIV antigens Decreased inflammatory cytokines No response to HIV antigens Response to new antigens ```
148
AIDS definition
CD4
149
Candidiasis
Oral thrush CD4
150
PCP/PJP
Pneumocystits iroveci (carinii) Pneumonia CD4
151
Cryptococcal Meningitis
CD4100 for 3mo, undetectable, start ART
152
Toxoplasmosis
CD4
153
Mycobacterium Avium
CD4
154
AIDS defining cancers
Kaposi Sarcoma Non hodgkins lymphoma: EBV Cancer of cervix/anus/rectum: HPV
155
Biochemical nutritional evaluation
Albumin Transferrin Prealbumin Retinol binding protein
156
Pregnancy nutrition
Energy: +340 2nd tri, +450 3rd tri Protein +25 Carbs Iron +50% Folate +50%, B12
157
Food to avoid during pregnancy
Vit/mineral mega doses Fish w/mercury Soft cheeses/food poisoning risks
158
Lactation nutrient needs
+500 kcal energy All more than during pregnancy, nutrient dense foods Inadequate diet = reduced milk quantity and deprives mother of nutrient stores
159
Infancy nutrients
Energy and protein highest/kg in infancy 30g fat Vit/minerals highest than during adulthood
160
Infancy food guidelines
Solid foods @4-6 months Introduce foods singly at intervals, 3-5 days Iron rich/vit C
161
Childhood nutrients
Energy need increases, but per kg decreases Carb: Fiber = age +5 High quality protein Fat: 30-40% 1-3yrs 25-35% 4-18
162
Nutrient concerns in childhood
Iron Vit D: Fortified milk/cereal Fluoride: Water
163
Adolescence
Puberty/growth spurt Tanner staging Energy, protein, vit/mineral increase
164
Acute Liver Failure Definition
Coagulation abnormality, mental alteration No preexisting cirrhosis Illness less than 26 weeks
165
Acute liver failure stats
2000 cases anually 33% mortality, 40% survival without transplant >65% survival with transplant
166
ALF etiology
Mainly drugs, esp acetaminophen Hep A/B Unknown
167
ALF classification
Hyperacute: 7d Acute: 8-28d Subacute: 29-60d
168
ALF type and cause
Subacute: Drug Acute: Acetaminophen, Hep A Acute: Hep B
169
Acetaminophen toxicity
Enhanced P450 --> NAPQI toxicity Doses >15g Hepatic dysfunction at day 3
170
Acetaminophen overdose treatment
Glutathione precursors
171
Hep B ALF
1% pt with Hep B, 8% ALF is HBV .4% mortality
172
Hep A ALF
Less than 1% Hep A pts Elevated creatinine
173
ALF complications
``` Jaundice Infection Hepatic encephalopathy Coagulopathy Metabolism issue Renal failure ```
174
Hepatic encephalopathy treatment
Airway protection Lactulose - meh Sedation
175
Coagulopathy
Decreased synthesis of clotting factors Decreased platelets
176
Infection and ALF
80-90% Sepsis is leading cause of death G+
177
Phase I enzymes
Minor structural changes, oxidation CYP
178
Phase II enzymes
Large molecular additions Transferases: UGT
179
CYP3A4
Most common CYP used by many drugs
180
CYP2D6
Neurological drugs | Genetic polymorphism
181
Rifampicin
Most important CYP3A4 inducer Results in other drug concentration reduction
182
Most powerful CYP competitive inhibitor
Ketoconazole Huge increase for other drug
183
Hepatitis A Virus
Single serotype Acute disease, no chronic infection Usually asymptomatic Lifelong immunity after immune response
184
Hep A transmission
Fecal oral Personal contact Blood exposure (RARE)
185
Hep A pathogenesis
Survives in stomach and enters blood --> liver Replicates in hepatocytes, not cytotoxic Excreted in stool before jaundice Immune mediated damage to liver
186
Hep A clinical features: Incubation, symptoms
Avg incubation: 28-30 days Cholestasis, dark urine, clay stool, jaundice Jaundice more likely as age increases
187
Hep A antibody history
IgM detectable 5-10 days before symptoms IgG 4 weeks post infection then mass rise
188
Hep A diagnosis
Serum HAV IgM antibody
189
Hep A prevention
Hygiene Sanitation Vaccination: Recombinant (pre), Immune globulin (post)
190
Hep E
Acute asymptomatic in developing countries Enteric zoonotic transmission Very rare in developed countries
191
HEV pathogenesis
15-60 day incubation Replication in hepatocytes, feces excretion Ab pain, anorexia, fever, hepatomegaly, jaundice
192
HEV natural history (Ig and enzymes)
Large ALT rise at around 6 weeks post infection IgM rise faster than IgG
193
HEV mortality
Relatively low but 20% in pregnant women
194
HEV diagnosis/prevention
Antibody assays available but inconsistent anti HEV IgG/IgM HEV RNA detection No antivirals
195
HEP B
DNA virus with RNA intermediate 350mil infected Multiple genotypes with differing progression/response rates
196
HBV transmission
Blood, semen, vaginal
197
HBV pathogenesis
Multiple viral proteins: Surface, core, E, Polymerase, X Detectable protein is HBsAG (surface) Not cytotoxic, immune mediated damage
198
HBV pathogenesis
2-3 month incubation Jaundice Low acute case mortality 15-25% chronic case fatality
199
HBV diagnosis
Choestasis AST/ALT elevation IgM anti HBsAg = acute infection HBsAg+ = infectious HBeAg correlates with infectiousness
200
Acute HBV natural history: Virus, enzymes, Ag, Ig
Large rise of virus within weeks = large rise in antigen, decline at 3mo IgM anti HBc at clinical onset then declines @6months Anti HBsAg = resolution of disease, viral load/Ag undetectable
201
Chronic HBV natural history
Large rise in DNA/HBsAg Antigen persists = chronic IgG HBc rises and persists IgM anti HBc decrease = chronic
202
Immunity with HBV vaccination serology
``` HBsAg = negative anti-HBc = negative anti-HBs = positive ```
203
Immunity with HBV infection serology
HBsAg = negative anti HBc = positive anti HBs = positive
204
Chronic HBV infection serology
HBsAg = positive Anti HBc = positive Anti HBs = negative IgM anti HBc = negative
205
Acute HBV infection serology
HBsAg = positive Anti HBc = positive anti HBs = positive IgM anti HBs = negative, rises after resolution of disease
206
HBV prevention/treatment
Vaccine: HepB IG, Recombinant Treatment: IFN Polymerase inhibitors - Lamivudine, Tenofivir, Emtricitabine
207
Hep C
Leading cause of liver transplant RNA virus
208
Hep C transmission
IV drugs Transfusion/transplantation Sexual and perinatal but much lower than HBV
209
HCV natural history
Exposure (20% resolved) Chronic (Some stable/variable progression) Cirrhosis (Some slowly progressive) HCC/Transplant/Death - 25yrs
210
HCV diagnosis
HCV antibody - Not good early/acute HCV RNA - Better Abnormal liver enzymes
211
Acute HCV natural history
Large ALT rise with HCV RNA detection Huge anti HCV after a few months
212
Chronic HCV progression
HCV RNA detection Large initial ALT rise, then decline, then variable spikes Anti HCV increase like in acute
213
HCV vaccine
NONE
214
Sofosbuvir
2014: NS5B polymerase inhibitor
215
Boceprevir/Telaprevir
NS3/4A protease inhibitors
216
Hep D
HBV coinfection Derived from HBV Cytotoxic effect on hepatocytes No bueno
217
Hep D detection
Anti HD Ab detected via ELISA HBV vaccination protects from HDV HBV antivirals DO NOT reduce HDV
218
ALF and urea
Liver can't create urea so ammonia leaves and goes to brain Ammonia becomes glutamate, osmotic pressure increase --> increase intra cranial pressure
219
NAS scoring system categories
Steatosis Lobular inflammation Ballooning degeneration Fibrosis
220
ALF liver transplant contraindications
Uncontrolled intracranial hypertension Prolonged systemic hypotension Sepsis/ARDS
221
Lab parameters for liver transplant
Creatinine INR Total Bilirubin
222
Achilles heel of liver transplantation
Biliary complication Bile leaks/obstruction/strictures
223
Porcelain gall bladder
Wall thickening and calcium deposition Increased risk of gall bladder carcinoma
224
PSC treatment
Endoscopic balloon dilation Endoscopic stent Liver transplant
225
PSC histology (Stain and presentation)
Trichrome stain Onion skin fibrosis
226
Klatskin Tumor
Cholangiocarcinoma arising at hepatic hilum No gall bladder distention
227
PBC Lab findings
Antimitochondrial antibodies Increased IgM Elevated ALP but NORMAL total bilirubin
228
Cirrhosis - 3 morphological characteristics
1. Bridging fibrous septa 2. Regenerative parenchymal nodules 3. Architectural disruption throughout entire liver
229
Hepatic stellate cells
When activated, deposit collagen into Space of Disse
230
Intra/pre/post hepatic portal hypertension
Intra: Cirrhosis Pre: Portal vein thrombosis Post: Hepatic vein thrombosis
231
Clinical consequences of Portal Hypertension
Congestive Splenomegaly Hepatic Encephalopathy Portosystemic venous shunts with risk of bleeds Ascites
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Chronic liver disease signs
Caput medusae (PH) Jaundice/Scleral icterus (Hyperbilirubinemia) Asterixis (flapping tremor) Encephalopathy (Ammonia) Gynecomastia/spider angiomas (Androgen/estrogen metabolic dysfunction) Palmar erythema (Red palms)
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Ultrasound benefits
Bile duct dilation Gall bladder Hepatic vasculature Obese patients ruin everything
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CT benefits
Optimal with contrast Visualize ductal dilation Better assessment of pancreas and level of obstruction Gall stones can't be seen though
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MRI benefits and contraindications
Evaluate hepatic parenchyma Level and etiology of obstruction Biliary and pancreatic ducts via MRCP Contraindications: Pacemakers, obesity
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Nuclear Medicine
Functional assessment of biliary system Sensitive to diagnosis of acute cholecystitis
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Iminodiactetic acid analogues
Nuclear medicine technique Uptake by hepatocyte, transport into bile canaliculi, excreted into biliary system Flows into gall bladder
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Endoscopy
ERCP: Direct access to papillae, can extract stones or place stents
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PTC
Percutaneous Transhepatic Cholangiography Access biliary system through skin/liver Dilate/stent strictures
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Neonatal jaundice TORCH
Etiologies ``` Toxoplasmosis Other Rubella CMV Herpes ```
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Ascending Cholangitis bacteria
E Coli Enterococcus faecalis Klebsiella Pneumoniae Ascending because bacteria starts in intestines then moves up bile duct to liver
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Entamoeba Histolytica
Ingest cysts, trophozoites burrow into intestines, can get into liver Anchovy paste nastiness Liver abscesses Treat with Metronidazole
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Physiological jaundice of newborn
Takes time for baby to start conjugating bilirubin High levels dangerous, goes to brain = kernicterus
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Simple cyst
Thought to be congenital Common - 5%
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Liver abscess - pyogenic
Induce pus formation E. Coli Klebisella pneumoniae Strep Bacteroides Drain Metronidazole, clindamycin 3rd gen cephalosporin
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Hydatid Cyst
Echinococcus granulosis - tapeworm (cestode) Live in intestinal lumen (definitive host), Tissue cysts (intermediate hosts) Humans are accidental hosts Liver and lungs Surgery, albendazole (blok glu uptake)
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Ascariasis
Nematode - roundworm Common infestation Travel up lungs and into GI tract and grows --> to liver causing abscesses Mebendazole
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Fasciolasis
Liver flukes - flatworms Watercress salad
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Schistosoma
Swimmers itch Katayama fever Eggs in liver = granulomatous reaction, fibrosis, portal hypertension Eosinophilia Risk of hepatocellular carcinoma

GI/Endo/Repro (8 decks)

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