Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI block > Liver + Gallbladder robbins > Flashcards

Liver + Gallbladder robbins Flashcards

1
Q

What are the most common type of gallstones?

A

Cholesterol (80% in western world)

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

What are Pigment (black + brown) stones made up of?

A

Billirubin and Calcium salts = Radio opaque
**INcreased Unconjugated billirubin= Hemolysis
BROWN= Due to Infection in Bile tree
**COMMON in Asian countries

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

What are some risk factors for Cholesterol stones?

A 
Gallbladder Hypomotility 
Mucus hypersecretion= traps cholesterol crystals 
AGE
FEMALE (hormones)
Obesity (Insulin resistance)
Rapid Weight reduction 
Dyslipidemias 
Inborn errors of Bile metabolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What kind of Gallstones are seen in a patient with SCD or hereditary spherocytosis or mechanical heart valves?

A

Calcium Billirubinate = PIGMENT stones

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

Yellow pale radiolucent gallstone is most likely?

A

Cholesterol stone

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

Enlarged, tense gallbladder, with thickened walls, and edema caused by a gallstone?

A

Acute Cholecystitis

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

Patient with Severe RUQ pain lasting 6hrs. Pain radiates to shoulder, Fever, nausea, leukocytosis, and Hyperbillirubinemia?

A

Acute calculous Cholecystitis

**Jaundice= Blockage of CB duct

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

Recurrent attacks of steady epigastric pain, N/V, and intolerance to fatty foods?

A

Chronic cholecystitis

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

What is choledocholithiasis?

A

Gallstone in the biliary tree (NOT gallbladder)

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

What is Cholangitis and MCC?

A

Inflammation of the Bile ducts

Caused by Bacterial infection (e coli)

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

Pt with Right upper abdominal pain, fever, chills, and jaundice?

A

Bacterial cholangitis

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

What consequence of chronic obstruction of extrahepatic biliary tree is seen in the Liver?

A

Secondary Biliary Cirrhosis–>
Secondary inflammation
Initiates periportal fibrogenesis
Leads to Scarring and nodule formation

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

Infant with pale stool, malabsorption and inflammation and fibrosis of CB duct and progressive destruction of intrahepatic biliary tree. Liver biopsy shows Portal tract edema, fibrosis, and parenchymal cholestasis. Eventually Cirrhosis and liver failure?

A

Biliary atresia

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

What are the serum tests for Hepatocyte integrity?

A

AST
ALT
LDH

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

What are the serum tests for biliary excretion function?

A

bilirubin (serum + urine)
bile acids
ALK
GGT

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

What are the serum tests for hepatocyte function?

A 
Albumin
PT (INR)
Ammonia 
Aminopyrine breath test (hepatic demethylation)
Galactose elimination (IV)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Pt with hepatic insufficiency that progresses to Hepatic encephalopathy in 2-3 wks. What are the MCCs?

A

Acute liver failure–> massive hepatic necrosis

**MCC–> Drugs or Viral hepatitis

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

What are the signs and symptoms of Hepatic failure?

A 
Jaundice (Bilirubin >2.0)
Hypoalbuminemia--> peripheral edema
Palmar erythema 
Spider angiomas 
Hypogonadism or Gynecomastia- Increased Estrogen 
Coagulopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is defined as the systemic retention of Billirubin, bile salts, and cholesterol?

A

Cholestasis

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

What is the pathogenesis for physiological jaundice of the newborn?

A

Hepatic conjugation machinery is not fully developed–> Mild Unconjugated Hyperbilirubinemia

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

Pt develops icterus during long periods of fasting or stress caused by a decreased level of Glucoronosyltransferase (GST)?

A

Gilbert syndrome

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

What is Dubin Johnson syndrome?

A

AR defect in Transport protein responsible for Hepatocellular excretion of bilirubin glucuronides into Caniculi.

  • *Conjugated hyperbilirubinemia
  • **BLACK LIVER
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Patient with black liver has what genetic deficiency?

A

Conjugated bilirubin transport protein

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

What are the causes of Jaundice due to excess production of UNconjugated bilirubin?

A

Hemolytic anemia
Pernicious anemia
Thalassemia

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

What are the causes of jaundice due to reduced hepatic uptake of Unconjugated bilirubin?

A

Drugs

Diffuse Hepatocellular disease (Viral or drug induce hepatitis, Cirrhosis)

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

What is the cause of jaundice due to impaired bilirubin conjugation?

A

Physio of Newborn

Gilbert syndrome

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

What are the causes of jaundice caused by Conjugated bilirubinemia due to decreased Hepatocellular excretion?

A

Def in canalicular membrane transporter (Dubin johnson syndrome)
Drugs (OCT , cyclosporines)
Hepatocellular damage (viral or drug hepatitis)
Gallstone
Carcinoma in head of pancreas

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

What are some of the signs and symptoms of Cholestasis?

A 
Jaundice 
Pruritus
Skin Xanthomas (increased Cholesterol)
Elevated ALK 
Malabsorption of vitamins ADEK
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

MCCs of jaundice due to excess conjugated bilirubin?

A

Hepatitis

Intra-extra hepatic obstruction of Bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

MCC of jaundice due to excess unconjugated bilirubin?

A

Hemolytic anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are some distinctions between Acute and chronic hepatitis?

A

Acute= Less inflammation but More hepatocyte death than Chronic
**Both induce T-cell response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Which Hepatitis virus is transferred by Fecal-Oral route and does NOT have a chronic or Carrier state?

A

HAV + HEV

**Hepatitis A + E only cause AcutE infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Hepatitis virus that is ssRNA and related to Picornaviruses. What is the laboratory diagnostic test?

A

Serum Anti-HAV IgM antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are the most likely outcomes of a HBV infection?

A

60-65%–> Subclinical= 100% recovery
20-25%–> Acute= 99% recover (1% fulminant)
5-10% –> Carriers
4%–> Chronic= Hepatocellular carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is genome and route of infection for the Hepadnavirus?

A

HBV–> dsDNA
ROI= Parenteral, Sexual, perinatal
**NOT FECAL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Which viral hepatitis is associated with Daycare centers and Jails?

A

HAV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Which viral hepatitis is associated with Dialysis, Needle-sticks, and IVDA?

A

HBV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Which part of the HBV is important for establishing Persistent infection? Immunogenic? Developing hepatocellular carcinoma?

A

HBeAg-> secreted to establish persistant infection
HBsAg–> secreted and is immunogenic
HBV X protein–> HC carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Describe the clinical course of HBsAg in a HBV infection?

A

HBsAg appears before onset of Symptoms (1st)
Peaks during Overt disease
Disappears 3-6 post infection
**Anti-HBsAg does NOT rise until Acute infection is over and wks after HBsAg disappears= GAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What Antibody conferes immunity to HBV infection and is basis for current vaccines?

A

Anti-HBsAg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the significance of HBeAg, HBV-DNA, and persistent HBeAg?

A

Both signify ACTIVE viral replication
Persistent HBeAg–> progression to Chronic
**Identify INFECTIVE STATE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Ground Glass cells in liver signify?

A

HBV infection–> Hepatocytes with ER stuffed with HBsAg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the potential outcomes of Acute HCV infection?

A

15%–> Resolve

85%–> Chronic (80%stable) (20%>cirrhosis>HC carcinoma> death)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Why is it hard to develop HCV vaccines?

A

Highly variable due to infidelity of RNA replication

**Quasispecies–> infected person can carry many HCV species at once

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Which Hepatitis virus is associated with Fatty change, PROMINENT Lymphoid infiltrates, and Bile duct injury?

A

HCV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

This hepatitis virus ONLY causes infection when it is encapsulated by HBsAg?

A

HDV–> NEEDS co-infection with HBV

**D for defective= Needs another virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is the best indication of co-infection by HDV and HBV?

A

IgM against both HDV Ag a& HBcAg

**IgM= denotes current infection which is required for HDV replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Which Hepatitis virus has a HIGH mortality rate in Pregnant women (20%)?

A

HEV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Which type of Viral hepatitis is most frequently causes acute hepatitis?

A

HBV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Which type of virus almost Never cause Fulminant hepatitis?

A

HCV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What type of Hep Virus is notorious for causing a Chronic hepatitis evolving into Cirrhosis?

A

HCV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Which type of viral hepatitis is associated with Cryoglobulinemia?

A

HCV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Carrier states are prevalent in what type of viral hepatitis?

A

HBV–> infections acquired in Childhood (95%)

**Those acquired in adulthood only 10% become carriers due to Increased Maturity of Cellular immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Councilman bodies are seen in what liver infection?

A

Yellow Fever

**Councilman bodies are Eosinophilic apoptotic Hepatocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Which hepatitis virus is transferred by Blood, Birthing, and Bonking?

A

HBV

56
Q

A chronic liver disease patient presents with rigidity, seizures, confusion and Asterixis?

A

Hepatic encephalopathy

57
Q

What can cause Asterixis?

A

Severe loss of Hepatocellular function

Shunting of blood around chronic liver

58
Q

What is the pg of hepatic encephalopathy?

A

Elevated ammonia= impairs neuronal function and promotes generalized brain EDEMA

59
Q

Diffuse fibrosis and conversion of normal liver architecture into structurally abnormal nodules?

A

Cirrhosis

60
Q

What are the manifestation of ETOH on the liver?

A

Steatosis
Steatohepatitis
Cirrhosis

61
Q

What is nonalcoholic fatty liver disease associated with?

A 
METABOLIC SYNDROME 
Diabetes
Obesity 
Hypertension 
dyslipidemia
62
Q

What is the earliest change in Alcoholic liver disease?

A

Fatty liver–> accumulation begins around centrilobular hepatocytes and extends to central vein

**Soft yellow greasy liver

63
Q

What are some features of steatohepatitis?

A

hepatocyte ballooning-> swelling and necrosis
Mallory Denk Bodies-> Tangled intermediate filaments as cytoplasmic inclusions
PMN infiltration

64
Q

What characteristic feature is seen in Alcoholic HEPATITIS?

A

Mallory Denk bodies

65
Q

What is the histological appearance of Fatty liver disease?

A

Fatty hepatocytes making a “CHICKEN WIRE FENCE” appearance

66
Q

What is the “burned-out” stage of alcoholic cirrhosis?

A

Replacement of Fat with Fibrosis= Small nodules

67
Q

Causes liver cell necrosis, inflammation, fatty change. and Mallory Bodies?

A

Alcoholic hepatitis

68
Q

What is the pathogenesis of alcoholic Fatty liver?

A
  1. Excess reduced NAD from ethanol metabolism= increases Lipid synthesis
  2. Impaired assembly and secretion of lipoproteins
  3. Increased peripheral catabolism of fat
69
Q

What substance directly affects cytoskeleton organization and mitochondrial functions of hepatocytes?

A

Alcohol

70
Q

What are the causes of alcoholic hepatitis?

A

ETOH= Mito and cytoskeleton poison
Acetaldehyde= induces peroxidation disrupting cytoskeleton and membranes
ROS from oxidation of ethanol
Cytokines (TNF)

71
Q

What is the treatment for an alcoholic with hepatomegaly, mildly elevated bilirubin and ALK?

A

Fatty change== STOP ETOH reverses

72
Q

Patient with malaise, anorexia, wght loss, RUQ pain, hepatomegaly, and fever. High bilirubin, ALK, Neutrophilic leukocytosis, and elevated AST>ALT?

A

Alcoholic cirrhosis

73
Q

Chronic alcohol use is associated with what vitamin deficiencies?

A

Thiamine (B1)
B12
Folate

74
Q

What is considered the alcohol consumption threshold for developing alcoholic liver disease?

A

50-60 g/day

75
Q

What is the mechanism of NAFLD in patients with insulin resistance and obesity?

A

impaired oxidation of FA
Increased synthesis and uptake of FA
decreased hepatic secretion of VLDL cholesterol

76
Q

What is the genetic cause of disorder characterized by accumulation of body iron depositing in organs (Liver, heart, pancreas)?

A

Hemochromatosis–> HFE gene mutation

77
Q

What are the MCC of secondary hemochromatosis?

A

Acquired= Transfusions + beta Thalassemia + myelodysplastic syndromes

78
Q

Hereditary disorder causing cirrhosis, Diabetes, and skin pigmentation?

A

Hemochromatosis

79
Q

What is the function of hepcidin?

A

Down regulates the efflux of iron from intestines and macrophages into plasma and inhibit iron absorption

80
Q

What is the mechanism of damage in hemochromatosis once iron is above 20g?

A

Lipid peroxidation by iron catalyzed free radicals
Simulation of collagen formation
Direct interaction btwn iron and DNA

81
Q

AR disorder marked by accumulation of Toxic levels of Copper in Liver, brain, and eyes?

A

Wilsons disease

82
Q

What is the genetic abnormality in wilsons disease?

A

mutated ATP7B gene == encoding ATPase metal ion transporter

83
Q

What is the plasma transporter of Copper>

A

Albumin

84
Q

What accounts for 90% of the copper in the Blood?

A

Copper- alpha2 globulin complex= Ceruloplasmin

85
Q

What is the primary elimination route of Copper?

A

Bile

86
Q

What is a Kayser-Fleischer ring?

A

Eye lesion caused by Excess Copper in WILSON disease

87
Q

5 yo with ascites, jaundice, psychosis, and a dark green rings encirculing the iris?

A

Wilson disease–> Elevated copper (Ceruloplasm)

88
Q

What is the function of Alpha 1 anti-trypsin?

A

inhibition og proteases (PMN elastases during inflammation)

89
Q

What is the Pathogenesis of A1 antitrypsin deficiency mediated damage in the Liver?

A

Mutant A1AT cannot be secreted by hepatocytes= accumulation in ER and triggers Unfolded protein response causing APOPTOSIS

90
Q

What does AAT mutation ZZ cause?

A

Pulmonary emphysema and Liver injury

91
Q

Liver biopsy shows severe hepatocyte necrosis, marked inflammation with monos and Plasma cells, and burned-out cirrhosis?

A

AI Hepatitis

92
Q

What types of Abs are seen in AI hepatitis?

A

ANA
Anti smooth muscle
anti microsomal

93
Q

Most common cause of Acute liver failure necessitating transplantation In US caused by toxic metabolite produced by CYPs in acinus of zone 3 hepatocytes?

A

Acetaminophen

94
Q

What substances are known to cause hepatocellular necrosis of Zone 3 cells?

A 
Methyldopa
Phenytoin
Acetaminophen 
Halothane
Isoniazid
95
Q

What substances are known to cause Macrovesicular Steatosis?

A

Ethanol
methotrexate
Corticosteroids

96
Q

What substances are associated with causing Microvesicular steatohepatitis and Mallory Bodies?

A

Amiodarone

Ethanol

97
Q

3 yo child with permicious vomiting, and lethargy, and hepatomegaly following viral infection?

A

Reye syndrome–> microvesicular steatosis

98
Q

What are the two predisposing factors to Reye syndrome?

A

Aspirin

Viral infection

99
Q

What are the key morphological features of Reyes syndrome?

A

Hepatocellular microvesicular steatosis
Pleomorphic enlargement of matrices + loss of dense bodies.
**CEREBRAL EDEMA= swollen astrocytes
*Skeletal muscle + kidneys+ heart also show microvesicular fatty change

100
Q

What is the most common hepatic neoplasms?

A

Metastasis from:
Colon
Lung
breast

101
Q

What is a childhood hepatocellular tumor?

A

Hepatoblastoma

102
Q

What liver tumor is associated with exposure to Vinyl chlorides + Arsenic?

A

Angiosarcoma

103
Q

Well circumscribed endothelial cell lined vascular channels and intervening stroma lesions?

A

cavernous hemangiomas= benign

104
Q

Bile duct strictures separated by bland, densely collagenized stroma. No malignant potential but chains are associated with PCKD?

A

Von Meyenburg complexes

105
Q

WEll demarcated but poorly encapsulated lesions of hyperplastic hepatocytes with central stellate fibrosis in otherwise normal liver?

A

Focal Nodular Hyperplasia

  • *response to abnormal vascular flow or vascular anomaly
  • *MC in females bc grow with Estrogen or OCT
106
Q

What liver lesions is MC in women of child bearing age that grows in response to OCP and regresses with discontinuation?

A

Hepatic adenoma

107
Q

What risks are associated with Hepatic adenomas?

A
  1. Rupture causing hemorrhage esp in Pregnant females due to HIGH Estrogen
  2. Malignant transformation in those harboring Beta Catenin mutations
108
Q

What are the genetics associated with Hepatic adenomas?

A

90% somatic mutation of HNF1A or CYP1B1

10% Beta catenin= Malignant potential

109
Q

What is the precursor lesion to HCC?

A

MC-> Chronic liver failure / cirrhosis == Dysplasia over time

110
Q

What are the 2 forms of Hepatocellular dysplasia?

A

Large cell change= large, pleomorph, Large nuclei

Small cell= small, hyperchromatic, angulated nuclei

111
Q

What two things are associated with HIGH risks of HCC?

A 
HBV (East) HCV (West) 
Aflatoxin 
Alcoholic liver 
NAFLD
AAT def
Hemachromatosis
hereditary tyrosinemia
112
Q

What disorder is Most likely to give rise to HCC?

A

hereditary tyrosinemia

113
Q

What toxin is found in “moldy” grains and peanuts and can covalently bind cellular DNA causing TP53 mutations and subsequent HCC?

A

Aflatoxin–> Aspergillus

114
Q

Where do most HCC arise from?

A

Large or small dysplastic lesions in Cirrhotic livers

115
Q

What are some factors involved in the pathogenesis of HCC?

A

Inflammation and regeneration= mutations
Beta catenin or TP53 muations
HBV X antigen
Defects in DNA repair

116
Q

What is the most common path of metastasis for HCC?

A

Hematogenous–> invades Hepatic vein

117
Q

PT with rapid increase in liver size, worsened ascites, appearance of bloody ascites, fever and pain?

A

HCC

118
Q

What is the MC serological marker for HCC?

A

Alpha feto-protein

**also used in YOLK SAC tumors

119
Q

Neonate with jaundice prior to 2wk is most likely?

A

Physiological Jaundice of newborn

120
Q

Neonate with jaundice post 2wks is most likely?

A

Biliary atresia

121
Q

Newborn presents with jaundice, dark urine, acholic stools, and hepatomegaly?

A

Neonatal cholestasis

**physiological + Atresia

122
Q

Caused by nonsuppurative destruction of small and medium sized intrahepatic bile ducts leading to inflammation, fibrosis, cirrhosis, and liver failure?

A

Primary biliary cirrhosis

123
Q

What serological marker is seen in 45yo female with elevated ALK, pruritis, and history of Sjogren?

A

PBC–> Anti-mitochondrial antibodies

124
Q

What is the “Florid duct lesion?”

A

PBC lesion–> in portal tract
lymphocyte infiltrate
plasma cells
Granuloma

125
Q

35 yo male with bloody hx of bloody diarrhea, has “patchy” inflammatory/fibrotic destruction of bile duct system?

A

Primary Sclerosing Cholangitis

126
Q

Bile Duct beading (strictures and dilations) are seen in association with what GI disease?

A

Primary Sclerosing cholangitis–> IBD (UC)

127
Q

What is seen under microscopy of primary sclerosing cholangitis?

A

ONION skinning fibrosis of bile ducts

128
Q

What drugs are associated with cholestasis

(Bland) ?

A

Anabolic steroids
Contraceptive steroids
Antibiotics

129
Q

What is the most common cause of cholangitis>

A

Ascending infection caused by E coli, Klebsiella, Entercocci, Clostridium due to Obstruction

130
Q

What are some common causes of parasitic cholangitis?

A

Fasciola hepatica
schistosomiasis
cryptosporidiosis (HIV)

131
Q

What is the MCC of neonatal death caused by liver failure?

A

Biliary atresia

132
Q

Platypnea (easier to breath laying down) & Orthodeoxia (decrease in BP with upright posture) are Pathognominic for what?

A

Hepatopulmonary syndrome

133
Q

Impaired blood flow at what level of the liver will produce Eso varices, splenomegaly, and intestinal congestion only?

A

Inflow impairment

**Portal vein obstruction

134
Q

Genetic disease resulting in accumulation of glucocerbrosides within phagocytes leading to distended cytoplasms and cytoplasm looking like “wrinkled tissue paper?”

A

Gaucher Disease Type 1

**Glucocerebrosidase def

135
Q

Child splenomegaly and Lytic bone lesions, osteonecrosis, and absence of CNS deficiency has what lysosomal genetic disease?

A

Gaucher disease

  • *Ashkenazi Jews
  • *Types 2+3 CNS involvement
136
Q

What is the deficiency in Von Gierke Disease?

A

glucose-6-phosphatase def

GI block (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions