Quiz 2 Flashcards
1
Q
A disproportionate elevation in serum aminotransferases compared to alk phos. with elevation of serum bilirubin follows what pattern of liver test abnormalitites?
A
Hepatocellular pattern
2
Q
A disproportionate elevation in alk phos. compared to serum aminotransferases with possibly elevated serum bilirubin follows what pattern of liver test abnormalities?
A
Cholestatic pattern
3
Q
An AST:ALT value of over 2 is most likely to be due to what pathology?
A
Alcoholic fatty liver disease
4
Q
Is a hepatic or non-hepatic cause most likely for isolated hyperbilirubinemia?
A
Hepatic
5
Q
What are three possible causes for unconjugated hyperbilirubinemia?
A
1) Physiologic in newborns
2) Hemolysis
3) Impaired conjugation (Gilbert syndrome or Crigler-Najjar)
6
Q
What is generally indicated by conjugated hyperbilirubinemia (generally accompanied by abnormal liver enzymes)?
A
Hepatitis (aute or chronic) or biliary obstruction; but there are numerous causes
7
Q
AST and ALT elevated 50x normal may be an indiciation of what?
A
“Shock liver” as seen in septic shock, AKA ischemic hepatitis
also hepatic infarction and fulminant liver failure (as in tylenol overdose)
8
Q
What are the three components that make of total energy expenditure (TEE)?
A
TEE= BMR + Physical activity + thermic affect of food (usually ~10%)
9
Q
How is indirect calorimetry used to measure TEE in a clinical setting?
A
It involves using RQ through conversions used to estimate TEE
10
Q
What is the respiratory quotient (RQ)?
A
The ratio of CO2 released to O2 absorbed during respiration
11
Q
Why can O2 be used to estimate energy expenditure?
A
90% of O2 is used by Cytochrome C oxidase (complex IV of ETC), and thereby can be used to estimate energy expenditure
12
Q
How can protein oxidation be calculated in an inpatient setting?
A
Measuring urinary nitrogen excretion
13
Q
What effect does fever have on BMR with a 1 degree C increase in temperature?
A
10-12% increase/degree C
14
Q
What two groups of patients stand to benefit most from indirect calorimetry?
A
1) Patients with severe burns or trauma
2) Severely obese patients
15
Q
How is enteral nutrition provided?
A
Directly into the stomach/small intestine
16
Q
How is parenteral nutrition provided?
A
Into a central/peripheral vein
17
Q
In cases where the GI tract is non-functional, should parenteral or enteral nutrition begin immediately?
A
Parenteral nutrition
18
Q
At what point should a patient on parenteral nutrition also be given enteral nutrition?
A
As soon as the ability to digest/absorb resumes (even if parenteral nutrition is continued)
19
Q
What is the physician’s role in a hospital setting in nutrition support?
A
1) Determine if nutrition support is necessary
2) Determine method and route of nutrition provision
20
Q
What is the dietician’s role in a hospital setting in nutrition support?
A
1) Determines amount,type, and rate of formula
2) Determines free water flushes for enteral nutrition
21
Q
Who might work with a dietician to establish a macro and micro nutrient prescription?
A
A pharmacist
22
Q
What peptide hormone is triggered by food in the stomach and precipitates acid secretion into the stomach?
A
Gastrin
23
Q
The presence of proteins, fats, and lowered duodenal pH triggers the release of what hormone?
A
Cholecystokinin (CCK), which precipitates secretin and other intestinal hormones
24
Q
What are four complications that can occur with enteral feeding?
A
1) Aspiration pneumonia
2) Refeeding syndrome
3) Diarrhea
4) Altered glucose, lipid, acid-base balance
25
What are three complications that can occur from long-term parenteral feeding?
1) Micronutrient deficiencies
2) Liver/gallbladder disease (from overfeeding)
3) Catheter-related infection
26
What are three complications of underfeeding?
- Poor wound healing
- Weakness
- Malnutrition
27
What are three complications of overfeeding?
- Hyperglycemia
- CO2 retention
- Fatty liver
28
T/F: A child who loses 70% of their small bowel can fully recover absorption and digestion?
True
29
What is the pathophysiology of refeeding syndrome?
After a period of nutrition depravation, feeding can rapidly move glucose into cells along with phosphorous, potassium, and magnesium, causing serum levels to sharpy drop
30
What are three potential complications of refeeding syndrome?
- Cardiac arrest
- Neuromuscular complications
- Respiratory dysfunction
31
What practices can be avoided and implemented inorder to prevent refeeding syndrome (2 of each)?
Avoid
1) Avoid sudden overfeeding
2) Avoid excess glucose
Implement
1) Replace phosphorous, potassium, and magnesium
2) Provide thiamin (helps with glucose metabolism in malnourished patients
32
One of what two HLA mutations is carried by nearly all celiac patients?
HLA-DQ2
HLA-DQ8
33
What are classic symptoms of celiac disease? Are they common or uncommon?
Chronic diarrhea, weight loss, failure to thrive
Uncommon
34
What are 5 common non-classical symptoms of celiac disease?
1) Iron deficiency (also hypocalcemia)
2) Abdominal discomfort and bloating
3) Altered bowel habits mimicking IBS
4)Peripheral/central neurologic disorders
5) Osteoporosis
35
What condition can present in celiac patients due to deposition of IgA into dermal papillae following sensitization of gut mucosa by gluten? How often does it present in celiac patients?
Dermatitis herpetiformis
Around 1 in 6 patients
36
What deficiency could affect the results of an anti-TTG IgA screening test for celiac disease?
IgA deficiency
37
Following a positive anti-TTG IgA screen in adults, what are the next steps for confirming a diagnosis of celiac disease?
Endoscopy, followed by duodenal biopsy if necessary
38
Between celiac disease, gluten sensitivity, and wheat allergy; which presents with enteropathy? Which presents with detectable autoantibodies?
Celiac disease (both)
39
Between celiac disease, gluten sensitivity, and wheat allergy; which is almost completely restricted to HLA-DQ2 or HLA-DQ8 mutations? Can the other two conditions present with those mutations?
Celiac disease
Absolutely, they are common mutations in gluten sensitivity and wheat allergy
40
What are three major risks of untreated celiac disease?
1) Lymphoma (other small bowel cancers as well)
2) Osteoporosis
3) Nutritional deficiencies (most types, especially Iron)
41
What percentage of US adults have IBD (ulcerative colitis or Crohn's disease)?
1.3%
42
What is the peak age of onset for IBD?
15-25 years old
43
What are 5 risk factors for IBD?
1) Infections
2) Antibiotics
3) Low fiber, high refined-sugar diet
4) NSAID use
5) Stress
44
When is celiac disease likely to present?
In childhood or adulthood
45
Should a patient refrain from ingesting gluten before serologic testing for anti-IgA TTG?
No, the exact opposite
46
Is smoking a risk factor for UC or CD?
it is a risk for CD, somewhat protective against UC
47
Where can Crohn's disease affect the GI tract?
48
Where can Ulcerative colitis affect the GI tract?
49
Between Ulcerative colitis and Crohn's disease, which is more likely to present with abdominal pain, and abdominal mass, and intestinal obstruction?
Crohn's disease
50
Between Ulcerative colitis and Crohn's disease, which is more likely to present with bloody diarrhea?
Ulcerative colitis
51
Between Ulcerative colitis and Crohn's disease, which is more likely to present with perianal disease and/or fistulae?
Crohn's disease
52
Between Ulcerative colitis and Crohn's disease, which is more likely to present with systemic symptoms?
Crohn's disease
53
In the diagnosis of IBD, what is another likely cause of similar symptoms to rule out?
Infection
54
What are the three pillars of diagnosis for IBD?
1) Endoscopy
2) Histology (biopsy)
3) Radiological criteria
55
What blood work and serologic markers can be used to diagnose IBD?
CBC, ESR, CRP
ASCA
anti-OmpC
anti-CBir1
pANCA
56
What is the signifiance of testing for calprotectin and lactoferrin in the diagnosis of IBD?
They will be elevated in inflammation (such as IBD) but NOT in IBS
57
What are 3 kinds of quick onset medications for treating IBD?
1) Corticosteroids
2) Anti-TNF agnets
3) JAK inhibitors
58
What are 2 kinds of longer onset medications for treating IBD?
1) Azathioprine/6MP
2) Methotrexate
59
Is IBD curable? Why is there an emphasis on balance in treatment?
It is not; treatment is managed based on symptoms
It is important to assess the risks of treatment (cancer, infection, other side effects) against the symptoms the patient is experiencing
60
Which lab values are positioned in which spot on these templates?
61
What two situations can create a false positive result on a urea breath test?
1) PPI use
2) GI bleed
62
Is AST or ALT more specific for hepatic injury?
ALT (AST is found also in heart, brain, kidney, and skeletal muscle)
63
Alkaline phosphatase (Alk phos/ALP) is derived mostly from what two organs/structures?
Liver and bones
64
What other lab value can be used in tandem with ALP in order to determine hepatic or extrahepatic injury?
GGT
65
T/F: Albumin levels will be normal in in acute liver injury and high in advanced liver disease?
False; albumin will be normal in acute liver injury, but will be LOW in advanced liver disease
66
Where are nearly all coagulation factors produced?
the liver
67
While platelets are not precise to liver function, they can help gauge what?
Severity of liver disease
68
How is absolute risk reduction (aRR) calculated?
aRR = CER - EER
CER- control event rate
EER- experimental event rate
69
What is selection bias?
A distortion in the integrity of the data due to a sample selection that does not accurately reflect the target population
70
What is a complication of advanced GERD?
Barrett esophagus
*Note transition between stratified squamous to simple columnar with abundant goblet cells
71
How is Barrett esophagus characterized?
Intestinal metaplasia within squamous mucosa of distal esophagus
72
How is Barrett esophagus distinct from esophageal adenocarcinoma?
Barrett esophagus is characterized by an increased risk for adenocarcinoma
73
In what part of the esophagus is adenocarcinoma most likely to be found? What are the major risk factors?
Typically found at the distal end
RF
-GERD/Barrett esophagus
-Tobacco use
74
In what part of the esophagus is squamous cell carcinoma most likely to be found? What are 7 risk factors?
Typically found at the proximal end
RF
-Alcohol use
-Tobacco use
- Frequent consumption of very hot beverages
-Achalasia
-Caustic esophageal injury
-Plummer-Vinson syndrome
-Dietary deficiency in fruits/vegetables
75
Over 90% of all gastric cancers are what type?
Adenocarcinoma
76
What is the majory difference between intestinal type and diffuse type gastric adenocarcinomas?
Intestinal type
-tends to form bulky masses
Diffuse type
-Infiltrates and thickens gastric wall
77
What is the most common mesenchymal tumor of the abdomen?
Gastrointestinal stromal tumors (GIST)
78
Why is identifying a KIT or PDGFRA gene mutation in cases of GIST important?
KIT mutations (75% of cases) and PDGFRA (8% of mutations) respond best to imatinib (TKI), while cases of GIST without either of these two mutatiosn are generally resistant to imatinib, though other TKIs may function
79
What is the most common inducer of gastric MALT?
H. pylori
80
How does H. pylori contribute to inducation of gastric MALT, and eventually to MALTomas?
H. pylori infection antigen presentation to T and B cells causes inflammatory reactions of B cells that can lead to lymphoid tissue deposition (gastric MALT) and in some cases can lead to lymphoma arising from constant overstimulation of B cells in MALT tissue
81
What pathophysiologic changes to the stomach can lead to pernicious anemia?
Damage to or loss of parietal (oxyntic) cells can lead to decreased acid production and loss of instrinsic factor (IF). Loss of IF leads to an inability to bind B12 and absorb it, leading to pernicious anemia
82
What is a notable cause of damage to or loss of parietal cells in the stomach?
Autoimmune atrophic gastritis
83
What is peptic ulcer disease (PUD)?
Chronic mucosal ulceration affecting the duodenum or stomach
84
What are the three main causes of PUD?
1) H. pylori
2) NSAID use
3) Cigarette smoking
85
What are common symptoms for PUD?
Symptoms usually coincide with chronic gastritis, most notably epigastric burning or aching pain
Other symptoms:
-iron deficiency anemia
-hemorrhage
-perforation
86
What are two complications associated with PUD?
1) Mucosal atrophy (especially oxyntic cells)
2) Intestinal metaplasia -> increased risk for adenocarcinoma
87
How are hypertrophic gastropathies characterized?
Uncommon diseases characterized by giant "cerebriform" enlargement of rugal folds (due to epithelial hyperplasia) WITHOUT inflammation
88
What is Zollinger-Ellison syndrome?
A subtype of hypertrophic gastropathies
89
What is Menetrier's disease?
A subtype of hypertrophic gastropathies associated with giant mucosal fold development as well as decreased acid secretion leading to hyperproteinemia
90
Menetrier's disease is more likely to present with what types of cells as inflammatory infiltrates? What about for Zollinger-Ellison syndrome?
MD: lymphocytes (limited infiltration)
Z-ES: neutrophils
91
Of Menetrier's disease and Zollinger-Ellison syndrome, which of the two is associated with adenocarcinoma?
Menetrier's disease
92
What is the most common cause of acute cholecystitis? What are common symptoms?
93
How does chronic cholecystitis develop? What is the most common cause? What is a unique feature of the gallbladder mucosa in chronic cholecystitis?
94
What are 3 complications of acute/chronic cholecystitis?
1) Bacterial superinfection with cholangitis or sepsis
2) Gallbladder perforation with local abscess formation
3) Gallbladder rupture with diffuse peritonitis
95
Identify all of the functional parts of the liver lobule
*be able to explain how blood and nutrients are moved through the lobule*
Hepatocytes
Endothelial cells
Kupffer cells
Hepatic stellate cells (?)
Sinusoids
Portal triads
-hepatic arteriole
-hepatic portal branch
-bile duct
-lymphatic duct
Central veins
96
Loss of fenestrations of hepatic sinusoidal endothelial cells can occur during what notable pathologies?
Liver cirrhosis or fibrosis
97
Which hepatic functions are carried out in the periportal zone of the liver acinus?
98
Which hepatic functions are carried out in the pericentral or perivenular zone?
99
What is the pathway of blood after entering the central vein?
Central vein -> Interlobular vein -> Hepatic veins -> IVC
100
What is the pathway of bile after it is produced by hepatocytes?
Hepatocytes -> bile canaliculi -> intrahepatic bile ductules -> intrahepatic bile ducts -> common hepatic duct -> combines with cystic duct to form common bile duct
101
What are potential complications of portal hypertension? What about for hepatic insufficiency?
102
Which liver cirrhosis complications are most heavily associated with spontaneous bacterial peritonitis and hepatorenal failure?
103
What is the median survival between compensated and decompensted cirrhosis?
Compensated: about 12 years
Decompensated: about 1.6 years
104
What are common symptoms of decompenated cirrhosis?
Fatigue
Weight loss
Decreased muscle mass/weakness
105
What notable abnormality pictured here is suggestive of liver cirrhosis?
Ascites
106
What notable abnormality pictured here is suggestive of liver cirrhosis?
Caput medusa
107
What notable abnormality pictured here is suggestive of liver cirrhosis?
Digital clubbing (many pathologies besides cirrohsis as well)
108
What notable abnormality pictured here is suggestive of liver cirrhosis?
Esophageal varices
109
What notable abnormality pictured here is suggestive of liver cirrhosis?
Gynecomastia (a sign of estrogen imbalance in men)
110
What notable abnormality pictured here is suggestive of liver cirrhosis?
Palmar erythema
111
What notable abnormality pictured here is suggestive of liver cirrhosis?
Spider angiomata (low platelets)
112
What notable abnormality pictured here is suggestive of liver cirrhosis?
Telangectasia (low platelets)
113
What abnormalities in the left and right image are characteristic of alcoholic liver disease?
Left: Mallory hyaline (tangled skeins of intermediate filaments)
Right: Ballooned hepatocytes
114
This prussian blue stain displays what abnormality? What disease is it characteristic of?
Iron deposition in the liver
Hemochromatosis
115
What is Virchow's node and what pathology does it suggest?
An enlarged left supraclavicular lymph node, which is indicative of metastasis from the stomach
116
What is the purpose of a schilling test?
To determine the cause of vitamin B12 deficiency
117
What is the purpose of a stool elastase test?
To test for exocrine pancreatic insufficiency
118
What are two major types of cells that make up the exocrine pancreas?
Acinar and ductal cells
119
What is the main purpose of pancreatic acinar cells? What are the 2 molecules are principally responsibly for signaling the pathway for zymogen release?
120
What is the main purpose of pancreatic ductal cells? What two inputs are reponsible for triggering secretion?
Ion secretion; a bicarbonate-rich fluid to transport acinar zymogens
Secretin and Acetylcholine (they are semi-redundant)
121
What are the different phases of pancreatic stimulation? Roughly what percentage of total secretions accompanies each phase?
122
What are the most common causes of acute pancreatitis?
Additionally: Idiopthatic causes represent 15-20% of all cases (I GET SMASHED)
123
What is the main risk factor for chronic pancreatitis?
Heavy alcohol use (70% of cases)
124
What are the approximate incidence rates annually for acute pancreatitis, chronic pancreatits, and pancreatic cancer?
125
What are the common sx, dx tools, and tx for acute pancreatitis?
Sx
- severe epigastric pain (frequently radiating to back), N/V, tenderness, tachycardia, fever
-If severe pancreatitis: ARDS, renal failure, sepsis, cytokine storm
Dx
-elevated serum lipase & amylase
-Imaging (CT, maybe US for gallstones)
Tx
-mild: aggressive rehydration, pain relief (supportive care)
-severe: aggressive rehydration, antibiotics, surgical debridement if necessary
126
Why are trypsin and protease inhibitors not used to treat pancreatitis?
Minimal impact on morbidity/mortality when tried
*Theorized that treatment is too late by time of pancreatitis dx
127
What are common sx, dx tools, and tx for chronic pancreatitis?
Sx
- smoldering epigastric pain, weight loss, fatty stools, diabetes, ADEK vitamin deficiencies
Dx
- elevated serum lipase and low secretin
- imaging
Tx
- Pain management, cessation of smoking & alcohol use, pancreatic enzyme supplementation
*last resort can do stent, nerve block, or pancreatectomy
128
What percentage of the population experiences congenital pancreatic variation? What should be done?
129
What are complications of annular pancreas in infants versus adults?
130
What are three genetic mutations affecting pancreatic acinar cells that are associated with pancreatitis?
PRSS1- Cationic trypsin
-GOF: hyperactive and/or hyperstable enzyme
SPINK1- Allosteric trypsin inhibitor
-LOF: loss of normal trypsin regulation
CTRC- Protease responsible for cleaving & inactivating trypsin
-LOF: loss of normal trypsin regulation
131
What is one notable genetic mutation affecting pancreatic ducts that is associated with pancreatitis?
CFTR- Chloride (possibly bicarbonate as well) channel
-LOF: Backup, acidification of pancreatic secretions
132
Which genetic mutations associated with pancreatitis are also associated with increased risk of pancreatic cancer?
PRSS1 and CFTR
133
What would be the best treatment for autoimmune pancreatitis?
Corticosteroid treatment
134
What is deglutitive inhibition?
The stoppiing of a peristaltic wave when another swallow is initiated
135
Peristaltic contractions of the esophagus are always preceded by what?
Inhibition
136
Does the lower esophageal sphincter (LES) have tone? What does this help prevent?
Yes
Reflux of gastric contents
137
GERD represents a failure of what structure? What is the pathology?
LES (lower esophageal sphincter)
Decreased tone resulting in reflux of gastric contents
138
What are 3 main functions of hepatocytes?
1) Detoxification of blood
2) Producing proteins (i.e. albumin)
3) Producing bile
*They also store 1/2 to 2/3 of blood nutrients and make up 80% of the liver mass
139
Where is the space of Disse found?
Between endothelial cells (lining hepatic sinusoidal capillaries) and hepatocytes
140
Where are Kupffer cells found? What is their function?
Between endothelial cells in the liver
They help neutralize bacteria during liver processing
*They represent 90% of the macrophages in the body
141
What is the normal activity of Hepatic stellate cells (Ito cells)? What role do they play in fibrosis?
-Normally quiescent, and store vitamin A and fat
-They are activated in liver injury and transform into myofibroblasts, which deposit collagen in the space of Disse
142
How does blood travel through hepatic sinusoids?
1) Blood from the protal vein branch and the hepatic artery branch mixes, and 2) drains through the sinusoidal capillary wall to be processed by hepatocytes, then 3) back into the sinusoid toward the central vein
143
What does the portal triad consist of?
Portal vein branch
Hepatic artery branch (arteriole)
Bile duct
(also lymphatic duct but it is not usually included)
144
How much of the body's lymph is produced by the liver?
50%
145
What are alternative names for the 3 hepatic acinar zones?
Zone 1- periportal
Zone 2- transitional
Zone 3- pericentral
146
In what zone of the liver does detoxification of lipophilic compounds occur? What are the two phases of detoxification?
147
What notable coagulation factors or associated molecules are not produced by the liver?
Factor VIII
von Willebrand factor
148
What organ is responsible for production of thrombopoeitin?
the liver
149
What organ in the body is most responsbile for iron and copper storeage?
the liver
150
What is the proportion of cardiac output that is dedicated to splanchnic circulation?
35% of CO (1200-1800mL/min)
151
What percentage of blood does the liver receive from the hepatic artery versus the portal vein? What is the oxygen distribution?
70% from portal vein
30% from hepatic artery
Oxygen distribution is 50/50
152
Given that the hepatic portal system is very sensitive to pressure increases, what effect may a 10-15mmHg increase in IVC pressure have on hepatic lymphatic flow? What are visible symptoms?
Around a 20-fold increase in hepatic lymphatic flow
Edema and ascites
153
What is a definition of cirrhosis?
Fibrotic damage characterized by chronic scarring that is no longer reversible (late-stage liver damage)
154
What are potential physical exam findings in cirrhosis? What are two common patient- reported symptoms?
Jaundice
Scleral icterus
Spider angiomata
Gynecomastia (if male)
Palmar erythema
Terry's nails (white)
Digital clubbing
Caput medua
Ascites
Pruritus
Fatigue
155
In cases of liver injury, HSCs (Ito cells) lose what stored molecule and concurrently secrete what cytokine in order to produce collagen used in fibrotic scar tissue?
They lose stored vitamin A, and secrete TGF-B
156
What are the 3 main causes of cirrhosis in the United States?
Alcohol
NAFLD (MASLD)
Chronic hepatitis C
157
What are likely lab findings associated with cirrhosis? What is done to confirm a diagnosis in suspected cases?
-Elevated billirubin, AST, ALT, ALP, GGT, thrombocytopenia
*AST >> ALT especially in ALD
-Liver biopsy
158
When does portal hypertension occur? What is the most common cause of intrahepatic portal hypertension?
When blood flow from the portal vein to the IVC meets resistance
Cirrhosis
159
What are two less common metabolic causes of cirrhosis besides NAFLD (MASLD)?
Hemochromatosis
Wilson's disease
160
What are the three major complications of portal hypertension?
1) Variceal rupture
2) Hepatic encephalopathy
3) Ascites (can progress to spontaneous bacterial peritonitis)
161
What is the most common decompensating even for cirrhosis? What percentage of patients develop this event within 10 years of diagnosis?
162
What is the pathophysiology of ascites in cirrhosis? (Just know important steps)
163
What are three treatments (or preventions) commonly used to help cirrhotic patients with ascites?
- Salt-restricted diet
- Avoidance of NSAID use
- Diuretics
164
What are the major differences between Spironolactone and Furosemide?
165
What percentage of patients with compensated cirrhosis present with esophageal varices? In decompensated cirrhosis?
166
The risk of variceal hemorrhage is related most strongly to what three variables?
1) Size of varices (large > small)
2) Presence of red wale signs on varix wall
3) Severity (Child-Pugh classes A-C)
167
What are primary/secondary prophylactic treatments for variceal bleeding?
Non-selective beta blockers
168
What are acute treatments for variceal bleeding?
-Octreotide
-Antibiotics
-Blood transfusion to hemoglobin > 7g/dL
-Endoscopic band placement to seal bleeding varix
169
What is the MoA and ADR for Octreotide?
170
How does the MoA of non-selective beta blockers (i.e. nadolol, propanolol, carvedilol) reduce the risk of variceal rupture?
171
What is the median survival in decompensated cirrhosis?
Less than 2 years
172
What is the difference between covert hepatic encephalopathy and overt hepatic encephalopathy?
173
What is the first line pharmacologic treatment used in cases of hepatic encephalopathy?
Lactulose (Rifaximan is added if necessary or used if lactulose is not well tolerated)
174
What is the MoA/ADR for lactulose?
175
What is the MoA/ADR for rifaximin?
176
Does the attached picture depict early or late stage liver fibrosis? What are nodules surrounded by fibrous tissue often called?
Late stage fibrosis or cirrhosis
Parenchymal or regenerative nodules
177
Would this liver biopsy be more indicative of ALD or NAFLD/MASLD?
Not currently possible to differentiate based on histology
178
Does ALD or NAFLD/MASLD tend to appear more acutely?
ALD
179
What kind of liver disease is strongly associated with obesity, T2DM, hyperlipidemia, and metabolic syndrome components?
NAFLD/MASLD
180
What are common symptoms of NAFLD/MASLD? How is it diagnosed?
Sx
-often asymptomatic
-fatigue
-abdominal discomfort
-insulin resistance (high BG)
Dx
-lab values (AST, ALT, ALP, billirubin, etc)
-liver biopsy
181
What three findings present most commonly in a patient with hemochromatosis?
1) Micronodular cirrhosis (100%)
2) DM (80%)
3) Abnormal skin pigmentation (75%)
182
What is the average age of onset for Wilson disease? What mutation is commonly associated with it, and what is the pathology that follows? How is it treated?
183
What inherited metabolic liver disease is most consistant with this histology slide? What mutation is it associated with? What is the significant histology finding, and clinical presentation?
a-1 antitrypsin deficiency
autosomal recessive disorder of protein folding with low levels of 1-AT
PIZZ protein
Cytoplasmic globular inclusions appear magenta on PAS stain
Major presentation:
-children: rapid progression to cirrhosis
-adults- chronic hepatitis
184
What can cause a B-Catenin-activated hepatocellular adenoma?
An activating mutation in CTNNB1 (B-catenin gene) or in other areas of Wnt pathway (like APC)
185
What drug use is associated with a B-catenin-activated hepatocellular adenoma? What is the risk for transformation into a hepatcellular carcinoma?
Oral contraceptive and anabolic steroid use
High risk for transformation to hepatocellular carcinoma
186
What are some of the main causes of ileus?
187
What is ileus?
An obstruction in the flow of bowel contents usually due to dysfunctional peristalsis
188
What is a small bowel obstruction? What are common causes?
Obstruction of intestinal flow due to intraluminal or extraluminal mechanical compression
- adhesion
- hernias
- malignancies
- various other pathologies
189
What is the main difference between NALFD/MASLD and NASH?
190
What percentage of patients with NAFLD progress to NASH? What percentage of patients with NASH progress to cirrhosis?
10-30% NAFLD progression to NASH -> 20-30% NASH progression to cirrhosis
191
What are the VACTERL associated anomalies?
Vertebral (tethered cord and bony spine
Anorectal malformation
Cardiac
TEF/EA
Renal and genitourinary
radial Limb deformities
192
Why can removing the antrum of the stomach help to treat hundreds of small neoplastic growths in the fundus of the stomach?
If lab results indicate an excessive level of gastrin, the growths are likely gastrinomas. As G cells are found princiaplly in the antrum, removing that area of the stomach can help to normalize the amount of gastrin, reducing the amount of gastric acid production
Zollinger-Ellison syndrome is often a result of the gastrinomas
193
What is the TMNT cell on the right diagnostic of in this esophageal biopsy sample?
HSV
194
In what layer of the gut is Meissner's plexi normally found?
the Submucosa
195
In what layer of the gut are Auerbach's/Myenteric plexi normally found?
the Mucularis propria (mucularis externa)
196
What is the function of the Interstitial Cells of Cajal (ICC)?
To act as pacemaker cells, creating a spontaneous slow AP to cause smooth muscle contraction
197
What is the intrinsic slow wave activity for the stomach, small intestine, and colon?
198
What are the two types of motility (phasic waves)?
1) Segmental- mixing contractions of circular muscles
2) Peristaltic- propulsive contractions involving circular and longitudinal muscles
199
What substances stimulate or reduce the migrating motor complex in the GI?
Stimulate
-IV erythromycin
-ghrelin
Reduce
-Narcotics
-Stress
200
