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M&R > Quiz 2 > Flashcards

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

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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

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3
Q

An AST:ALT value of over 2 is most likely to be due to what pathology?

A

Alcoholic fatty liver disease

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4
Q

Is a hepatic or non-hepatic cause most likely for isolated hyperbilirubinemia?

A

Hepatic

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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)

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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

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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)

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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%)

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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

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10
Q

What is the respiratory quotient (RQ)?

A

The ratio of CO2 released to O2 absorbed during respiration

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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

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12
Q

How can protein oxidation be calculated in an inpatient setting?

A

Measuring urinary nitrogen excretion

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13
Q

What effect does fever have on BMR with a 1 degree C increase in temperature?

A

10-12% increase/degree C

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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

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15
Q

How is enteral nutrition provided?

A

Directly into the stomach/small intestine

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16
Q

How is parenteral nutrition provided?

A

Into a central/peripheral vein

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17
Q

In cases where the GI tract is non-functional, should parenteral or enteral nutrition begin immediately?

A

Parenteral nutrition

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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)

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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

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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

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21
Q

Who might work with a dietician to establish a macro and micro nutrient prescription?

A

A pharmacist

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22
Q

What peptide hormone is triggered by food in the stomach and precipitates acid secretion into the stomach?

A

Gastrin

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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

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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

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25
Q

What are three complications that can occur from long-term parenteral feeding?

A

1) Micronutrient deficiencies
2) Liver/gallbladder disease (from overfeeding)
3) Catheter-related infection

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26
Q

What are three complications of underfeeding?

A
  • Poor wound healing
  • Weakness
  • Malnutrition
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27
Q

What are three complications of overfeeding?

A
  • Hyperglycemia
  • CO2 retention
  • Fatty liver
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28
Q

T/F: A child who loses 70% of their small bowel can fully recover absorption and digestion?

A

True

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29
Q

What is the pathophysiology of refeeding syndrome?

A

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

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30
Q

What are three potential complications of refeeding syndrome?

A
  • Cardiac arrest
  • Neuromuscular complications
  • Respiratory dysfunction
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31
Q

What practices can be avoided and implemented inorder to prevent refeeding syndrome (2 of each)?

A

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

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32
Q

One of what two HLA mutations is carried by nearly all celiac patients?

A

HLA-DQ2
HLA-DQ8

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33
Q

What are classic symptoms of celiac disease? Are they common or uncommon?

A

Chronic diarrhea, weight loss, failure to thrive

Uncommon

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34
Q

What are 5 common non-classical symptoms of celiac disease?

A

1) Iron deficiency (also hypocalcemia)
2) Abdominal discomfort and bloating
3) Altered bowel habits mimicking IBS
4)Peripheral/central neurologic disorders
5) Osteoporosis

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35
Q

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?

A

Dermatitis herpetiformis

Around 1 in 6 patients

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36
Q

What deficiency could affect the results of an anti-TTG IgA screening test for celiac disease?

A

IgA deficiency

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37
Q

Following a positive anti-TTG IgA screen in adults, what are the next steps for confirming a diagnosis of celiac disease?

A

Endoscopy, followed by duodenal biopsy if necessary

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38
Q

Between celiac disease, gluten sensitivity, and wheat allergy; which presents with enteropathy? Which presents with detectable autoantibodies?

A

Celiac disease (both)

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39
Q

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?

A

Celiac disease

Absolutely, they are common mutations in gluten sensitivity and wheat allergy

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40
Q

What are three major risks of untreated celiac disease?

A

1) Lymphoma (other small bowel cancers as well)
2) Osteoporosis
3) Nutritional deficiencies (most types, especially Iron)

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41
Q

What percentage of US adults have IBD (ulcerative colitis or Crohn’s disease)?

A

1.3%

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42
Q

What is the peak age of onset for IBD?

A

15-25 years old

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43
Q

What are 5 risk factors for IBD?

A

1) Infections
2) Antibiotics
3) Low fiber, high refined-sugar diet
4) NSAID use
5) Stress

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44
Q

When is celiac disease likely to present?

A

In childhood or adulthood

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45
Q

Should a patient refrain from ingesting gluten before serologic testing for anti-IgA TTG?

A

No, the exact opposite

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46
Q

Is smoking a risk factor for UC or CD?

A

it is a risk for CD, somewhat protective against UC

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47
Q

Where can Crohn’s disease affect the GI tract?

A
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48
Q

Where can Ulcerative colitis affect the GI tract?

A
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49
Q

Between Ulcerative colitis and Crohn’s disease, which is more likely to present with abdominal pain, and abdominal mass, and intestinal obstruction?

A

Crohn’s disease

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50
Q

Between Ulcerative colitis and Crohn’s disease, which is more likely to present with bloody diarrhea?

A

Ulcerative colitis

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51
Q

Between Ulcerative colitis and Crohn’s disease, which is more likely to present with perianal disease and/or fistulae?

A

Crohn’s disease

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52
Q

Between Ulcerative colitis and Crohn’s disease, which is more likely to present with systemic symptoms?

A

Crohn’s disease

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53
Q

In the diagnosis of IBD, what is another likely cause of similar symptoms to rule out?

A

Infection

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54
Q

What are the three pillars of diagnosis for IBD?

A

1) Endoscopy
2) Histology (biopsy)
3) Radiological criteria

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55
Q

What blood work and serologic markers can be used to diagnose IBD?

A

CBC, ESR, CRP

ASCA
anti-OmpC
anti-CBir1
pANCA

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56
Q

What is the signifiance of testing for calprotectin and lactoferrin in the diagnosis of IBD?

A

They will be elevated in inflammation (such as IBD) but NOT in IBS

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57
Q

What are 3 kinds of quick onset medications for treating IBD?

A

1) Corticosteroids
2) Anti-TNF agnets
3) JAK inhibitors

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58
Q

What are 2 kinds of longer onset medications for treating IBD?

A

1) Azathioprine/6MP
2) Methotrexate

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59
Q

Is IBD curable? Why is there an emphasis on balance in treatment?

A

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

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60
Q

Which lab values are positioned in which spot on these templates?

A
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61
Q

What two situations can create a false positive result on a urea breath test?

A

1) PPI use
2) GI bleed

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62
Q

Is AST or ALT more specific for hepatic injury?

A

ALT (AST is found also in heart, brain, kidney, and skeletal muscle)

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63
Q

Alkaline phosphatase (Alk phos/ALP) is derived mostly from what two organs/structures?

A

Liver and bones

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64
Q

What other lab value can be used in tandem with ALP in order to determine hepatic or extrahepatic injury?

A

GGT

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65
Q

T/F: Albumin levels will be normal in in acute liver injury and high in advanced liver disease?

A

False; albumin will be normal in acute liver injury, but will be LOW in advanced liver disease

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66
Q

Where are nearly all coagulation factors produced?

A

the liver

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67
Q

While platelets are not precise to liver function, they can help gauge what?

A

Severity of liver disease

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68
Q

How is absolute risk reduction (aRR) calculated?

A

aRR = CER - EER

CER- control event rate
EER- experimental event rate

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69
Q

What is selection bias?

A

A distortion in the integrity of the data due to a sample selection that does not accurately reflect the target population

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70
Q

What is a complication of advanced GERD?

A

Barrett esophagus

*Note transition between stratified squamous to simple columnar with abundant goblet cells

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71
Q

How is Barrett esophagus characterized?

A

Intestinal metaplasia within squamous mucosa of distal esophagus

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72
Q

How is Barrett esophagus distinct from esophageal adenocarcinoma?

A

Barrett esophagus is characterized by an increased risk for adenocarcinoma

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73
Q

In what part of the esophagus is adenocarcinoma most likely to be found? What are the major risk factors?

A

Typically found at the distal end

RF
-GERD/Barrett esophagus
-Tobacco use

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74
Q

In what part of the esophagus is squamous cell carcinoma most likely to be found? What are 7 risk factors?

A

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

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75
Q

Over 90% of all gastric cancers are what type?

A

Adenocarcinoma

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76
Q

What is the majory difference between intestinal type and diffuse type gastric adenocarcinomas?

A

Intestinal type
-tends to form bulky masses

Diffuse type
-Infiltrates and thickens gastric wall

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77
Q

What is the most common mesenchymal tumor of the abdomen?

A

Gastrointestinal stromal tumors (GIST)

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78
Q

Why is identifying a KIT or PDGFRA gene mutation in cases of GIST important?

A

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

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79
Q

What is the most common inducer of gastric MALT?

A

H. pylori

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80
Q

How does H. pylori contribute to inducation of gastric MALT, and eventually to MALTomas?

A

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

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81
Q

What pathophysiologic changes to the stomach can lead to pernicious anemia?

A

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
Q

What is a notable cause of damage to or loss of parietal cells in the stomach?

A

Autoimmune atrophic gastritis

83
Q

What is peptic ulcer disease (PUD)?

A

Chronic mucosal ulceration affecting the duodenum or stomach

84
Q

What are the three main causes of PUD?

A

1) H. pylori
2) NSAID use
3) Cigarette smoking

85
Q

What are common symptoms for PUD?

A

Symptoms usually coincide with chronic gastritis, most notably epigastric burning or aching pain

Other symptoms:
-iron deficiency anemia
-hemorrhage
-perforation

86
Q

What are two complications associated with PUD?

A

1) Mucosal atrophy (especially oxyntic cells)
2) Intestinal metaplasia -> increased risk for adenocarcinoma

87
Q

How are hypertrophic gastropathies characterized?

A

Uncommon diseases characterized by giant “cerebriform” enlargement of rugal folds (due to epithelial hyperplasia) WITHOUT inflammation

88
Q

What is Zollinger-Ellison syndrome?

A

A subtype of hypertrophic gastropathies

89
Q

What is Menetrier’s disease?

A

A subtype of hypertrophic gastropathies associated with giant mucosal fold development as well as decreased acid secretion leading to hyperproteinemia

90
Q

Menetrier’s disease is more likely to present with what types of cells as inflammatory infiltrates? What about for Zollinger-Ellison syndrome?

A

MD: lymphocytes (limited infiltration)

Z-ES: neutrophils

91
Q

Of Menetrier’s disease and Zollinger-Ellison syndrome, which of the two is associated with adenocarcinoma?

A

Menetrier’s disease

92
Q

What is the most common cause of acute cholecystitis? What are common symptoms?

A
93
Q

How does chronic cholecystitis develop? What is the most common cause? What is a unique feature of the gallbladder mucosa in chronic cholecystitis?

A
94
Q

What are 3 complications of acute/chronic cholecystitis?

A

1) Bacterial superinfection with cholangitis or sepsis
2) Gallbladder perforation with local abscess formation
3) Gallbladder rupture with diffuse peritonitis

95
Q

Identify all of the functional parts of the liver lobule
be able to explain how blood and nutrients are moved through the lobule

A

Hepatocytes
Endothelial cells
Kupffer cells
Hepatic stellate cells (?)
Sinusoids
Portal triads
-hepatic arteriole
-hepatic portal branch
-bile duct
-lymphatic duct
Central veins

96
Q

Loss of fenestrations of hepatic sinusoidal endothelial cells can occur during what notable pathologies?

A

Liver cirrhosis or fibrosis

97
Q

Which hepatic functions are carried out in the periportal zone of the liver acinus?

A
98
Q

Which hepatic functions are carried out in the pericentral or perivenular zone?

A
99
Q

What is the pathway of blood after entering the central vein?

A

Central vein -> Interlobular vein -> Hepatic veins -> IVC

100
Q

What is the pathway of bile after it is produced by hepatocytes?

A

Hepatocytes -> bile canaliculi -> intrahepatic bile ductules -> intrahepatic bile ducts -> common hepatic duct -> combines with cystic duct to form common bile duct

101
Q

What are potential complications of portal hypertension? What about for hepatic insufficiency?

A
102
Q

Which liver cirrhosis complications are most heavily associated with spontaneous bacterial peritonitis and hepatorenal failure?

A
103
Q

What is the median survival between compensated and decompensted cirrhosis?

A

Compensated: about 12 years
Decompensated: about 1.6 years

104
Q

What are common symptoms of decompenated cirrhosis?

A

Fatigue
Weight loss
Decreased muscle mass/weakness

105
Q

What notable abnormality pictured here is suggestive of liver cirrhosis?

A

Ascites

106
Q

What notable abnormality pictured here is suggestive of liver cirrhosis?

A

Caput medusa

107
Q

What notable abnormality pictured here is suggestive of liver cirrhosis?

A

Digital clubbing (many pathologies besides cirrohsis as well)

108
Q

What notable abnormality pictured here is suggestive of liver cirrhosis?

A

Esophageal varices

109
Q

What notable abnormality pictured here is suggestive of liver cirrhosis?

A

Gynecomastia (a sign of estrogen imbalance in men)

110
Q

What notable abnormality pictured here is suggestive of liver cirrhosis?

A

Palmar erythema

111
Q

What notable abnormality pictured here is suggestive of liver cirrhosis?

A

Spider angiomata (low platelets)

112
Q

What notable abnormality pictured here is suggestive of liver cirrhosis?

A

Telangectasia (low platelets)

113
Q

What abnormalities in the left and right image are characteristic of alcoholic liver disease?

A

Left: Mallory hyaline (tangled skeins of intermediate filaments)

Right: Ballooned hepatocytes

114
Q

This prussian blue stain displays what abnormality? What disease is it characteristic of?

A

Iron deposition in the liver

Hemochromatosis

115
Q

What is Virchow’s node and what pathology does it suggest?

A

An enlarged left supraclavicular lymph node, which is indicative of metastasis from the stomach

116
Q

What is the purpose of a schilling test?

A

To determine the cause of vitamin B12 deficiency

117
Q

What is the purpose of a stool elastase test?

A

To test for exocrine pancreatic insufficiency

118
Q

What are two major types of cells that make up the exocrine pancreas?

A

Acinar and ductal cells

119
Q

What is the main purpose of pancreatic acinar cells? What are the 2 molecules are principally responsibly for signaling the pathway for zymogen release?

A
120
Q

What is the main purpose of pancreatic ductal cells? What two inputs are reponsible for triggering secretion?

A

Ion secretion; a bicarbonate-rich fluid to transport acinar zymogens

Secretin and Acetylcholine (they are semi-redundant)

121
Q

What are the different phases of pancreatic stimulation? Roughly what percentage of total secretions accompanies each phase?

A
122
Q

What are the most common causes of acute pancreatitis?

A

Additionally: Idiopthatic causes represent 15-20% of all cases (I GET SMASHED)

123
Q

What is the main risk factor for chronic pancreatitis?

A

Heavy alcohol use (70% of cases)

124
Q

What are the approximate incidence rates annually for acute pancreatitis, chronic pancreatits, and pancreatic cancer?

A
125
Q

What are the common sx, dx tools, and tx for acute pancreatitis?

A

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
Q

Why are trypsin and protease inhibitors not used to treat pancreatitis?

A

Minimal impact on morbidity/mortality when tried

*Theorized that treatment is too late by time of pancreatitis dx

127
Q

What are common sx, dx tools, and tx for chronic pancreatitis?

A

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
Q

What percentage of the population experiences congenital pancreatic variation? What should be done?

A
129
Q

What are complications of annular pancreas in infants versus adults?

A
130
Q

What are three genetic mutations affecting pancreatic acinar cells that are associated with pancreatitis?

A

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
Q

What is one notable genetic mutation affecting pancreatic ducts that is associated with pancreatitis?

A

CFTR- Chloride (possibly bicarbonate as well) channel
-LOF: Backup, acidification of pancreatic secretions

132
Q

Which genetic mutations associated with pancreatitis are also associated with increased risk of pancreatic cancer?

A

PRSS1 and CFTR

133
Q

What would be the best treatment for autoimmune pancreatitis?

A

Corticosteroid treatment

134
Q

What is deglutitive inhibition?

A

The stoppiing of a peristaltic wave when another swallow is initiated

135
Q

Peristaltic contractions of the esophagus are always preceded by what?

A

Inhibition

136
Q

Does the lower esophageal sphincter (LES) have tone? What does this help prevent?

A

Yes

Reflux of gastric contents

137
Q

GERD represents a failure of what structure? What is the pathology?

A

LES (lower esophageal sphincter)

Decreased tone resulting in reflux of gastric contents

138
Q

What are 3 main functions of hepatocytes?

A

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
Q

Where is the space of Disse found?

A

Between endothelial cells (lining hepatic sinusoidal capillaries) and hepatocytes

140
Q

Where are Kupffer cells found? What is their function?

A

Between endothelial cells in the liver

They help neutralize bacteria during liver processing

*They represent 90% of the macrophages in the body

141
Q

What is the normal activity of Hepatic stellate cells (Ito cells)? What role do they play in fibrosis?

A

-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
Q

How does blood travel through hepatic sinusoids?

A

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
Q

What does the portal triad consist of?

A

Portal vein branch
Hepatic artery branch (arteriole)
Bile duct
(also lymphatic duct but it is not usually included)

144
Q

How much of the body’s lymph is produced by the liver?

A

50%

145
Q

What are alternative names for the 3 hepatic acinar zones?

A

Zone 1- periportal
Zone 2- transitional
Zone 3- pericentral

146
Q

In what zone of the liver does detoxification of lipophilic compounds occur? What are the two phases of detoxification?

A
147
Q

What notable coagulation factors or associated molecules are not produced by the liver?

A

Factor VIII
von Willebrand factor

148
Q

What organ is responsible for production of thrombopoeitin?

A

the liver

149
Q

What organ in the body is most responsbile for iron and copper storeage?

A

the liver

150
Q

What is the proportion of cardiac output that is dedicated to splanchnic circulation?

A

35% of CO (1200-1800mL/min)

151
Q

What percentage of blood does the liver receive from the hepatic artery versus the portal vein? What is the oxygen distribution?

A

70% from portal vein
30% from hepatic artery
Oxygen distribution is 50/50

152
Q

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?

A

Around a 20-fold increase in hepatic lymphatic flow

Edema and ascites

153
Q

What is a definition of cirrhosis?

A

Fibrotic damage characterized by chronic scarring that is no longer reversible (late-stage liver damage)

154
Q

What are potential physical exam findings in cirrhosis? What are two common patient- reported symptoms?

A

Jaundice
Scleral icterus
Spider angiomata
Gynecomastia (if male)
Palmar erythema
Terry’s nails (white)
Digital clubbing
Caput medua
Ascites

Pruritus
Fatigue

155
Q

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?

A

They lose stored vitamin A, and secrete TGF-B

156
Q

What are the 3 main causes of cirrhosis in the United States?

A

Alcohol
NAFLD (MASLD)
Chronic hepatitis C

157
Q

What are likely lab findings associated with cirrhosis? What is done to confirm a diagnosis in suspected cases?

A

-Elevated billirubin, AST, ALT, ALP, GGT, thrombocytopenia
*AST&raquo_space; ALT especially in ALD
-Liver biopsy

158
Q

When does portal hypertension occur? What is the most common cause of intrahepatic portal hypertension?

A

When blood flow from the portal vein to the IVC meets resistance

Cirrhosis

159
Q

What are two less common metabolic causes of cirrhosis besides NAFLD (MASLD)?

A

Hemochromatosis
Wilson’s disease

160
Q

What are the three major complications of portal hypertension?

A

1) Variceal rupture
2) Hepatic encephalopathy
3) Ascites (can progress to spontaneous bacterial peritonitis)

161
Q

What is the most common decompensating even for cirrhosis? What percentage of patients develop this event within 10 years of diagnosis?

A
162
Q

What is the pathophysiology of ascites in cirrhosis? (Just know important steps)

A
163
Q

What are three treatments (or preventions) commonly used to help cirrhotic patients with ascites?

A
  • Salt-restricted diet
  • Avoidance of NSAID use
  • Diuretics
164
Q

What are the major differences between Spironolactone and Furosemide?

A
165
Q

What percentage of patients with compensated cirrhosis present with esophageal varices? In decompensated cirrhosis?

A
166
Q

The risk of variceal hemorrhage is related most strongly to what three variables?

A

1) Size of varices (large > small)
2) Presence of red wale signs on varix wall
3) Severity (Child-Pugh classes A-C)

167
Q

What are primary/secondary prophylactic treatments for variceal bleeding?

A

Non-selective beta blockers

168
Q

What are acute treatments for variceal bleeding?

A

-Octreotide
-Antibiotics
-Blood transfusion to hemoglobin > 7g/dL
-Endoscopic band placement to seal bleeding varix

169
Q

What is the MoA and ADR for Octreotide?

A
170
Q

How does the MoA of non-selective beta blockers (i.e. nadolol, propanolol, carvedilol) reduce the risk of variceal rupture?

A
171
Q

What is the median survival in decompensated cirrhosis?

A

Less than 2 years

172
Q

What is the difference between covert hepatic encephalopathy and overt hepatic encephalopathy?

A
173
Q

What is the first line pharmacologic treatment used in cases of hepatic encephalopathy?

A

Lactulose (Rifaximan is added if necessary or used if lactulose is not well tolerated)

174
Q

What is the MoA/ADR for lactulose?

A
175
Q

What is the MoA/ADR for rifaximin?

A
176
Q

Does the attached picture depict early or late stage liver fibrosis? What are nodules surrounded by fibrous tissue often called?

A

Late stage fibrosis or cirrhosis

Parenchymal or regenerative nodules

177
Q

Would this liver biopsy be more indicative of ALD or NAFLD/MASLD?

A

Not currently possible to differentiate based on histology

178
Q

Does ALD or NAFLD/MASLD tend to appear more acutely?

A

ALD

179
Q

What kind of liver disease is strongly associated with obesity, T2DM, hyperlipidemia, and metabolic syndrome components?

A

NAFLD/MASLD

180
Q

What are common symptoms of NAFLD/MASLD? How is it diagnosed?

A

Sx
-often asymptomatic
-fatigue
-abdominal discomfort
-insulin resistance (high BG)

Dx
-lab values (AST, ALT, ALP, billirubin, etc)
-liver biopsy

181
Q

What three findings present most commonly in a patient with hemochromatosis?

A

1) Micronodular cirrhosis (100%)
2) DM (80%)
3) Abnormal skin pigmentation (75%)

182
Q

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?

A
183
Q

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

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
Q

What can cause a B-Catenin-activated hepatocellular adenoma?

A

An activating mutation in CTNNB1 (B-catenin gene) or in other areas of Wnt pathway (like APC)

185
Q

What drug use is associated with a B-catenin-activated hepatocellular adenoma? What is the risk for transformation into a hepatcellular carcinoma?

A

Oral contraceptive and anabolic steroid use

High risk for transformation to hepatocellular carcinoma

186
Q

What are some of the main causes of ileus?

A
187
Q

What is ileus?

A

An obstruction in the flow of bowel contents usually due to dysfunctional peristalsis

188
Q

What is a small bowel obstruction? What are common causes?

A

Obstruction of intestinal flow due to intraluminal or extraluminal mechanical compression
- adhesion
- hernias
- malignancies
- various other pathologies

189
Q

What is the main difference between NALFD/MASLD and NASH?

A
190
Q

What percentage of patients with NAFLD progress to NASH? What percentage of patients with NASH progress to cirrhosis?

A

10-30% NAFLD progression to NASH -> 20-30% NASH progression to cirrhosis

191
Q

What are the VACTERL associated anomalies?

A

Vertebral (tethered cord and bony spine
Anorectal malformation
Cardiac
TEF/EA
Renal and genitourinary
radial Limb deformities

192
Q

Why can removing the antrum of the stomach help to treat hundreds of small neoplastic growths in the fundus of the stomach?

A

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
Q

What is the TMNT cell on the right diagnostic of in this esophageal biopsy sample?

A

HSV

194
Q

In what layer of the gut is Meissner’s plexi normally found?

A

the Submucosa

195
Q

In what layer of the gut are Auerbach’s/Myenteric plexi normally found?

A

the Mucularis propria (mucularis externa)

196
Q

What is the function of the Interstitial Cells of Cajal (ICC)?

A

To act as pacemaker cells, creating a spontaneous slow AP to cause smooth muscle contraction

197
Q

What is the intrinsic slow wave activity for the stomach, small intestine, and colon?

A
198
Q

What are the two types of motility (phasic waves)?

A

1) Segmental- mixing contractions of circular muscles
2) Peristaltic- propulsive contractions involving circular and longitudinal muscles

199
Q

What substances stimulate or reduce the migrating motor complex in the GI?

A

Stimulate
-IV erythromycin
-ghrelin
Reduce
-Narcotics
-Stress

200
Q
A

M&R (8 decks)

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