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Semestre 6: bloque 3 > Partial exam > Flashcards

Partial exam Flashcards

(121 cards)

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1
Q

Esophageal motility disorder with failure of LES to relax and loss of peristalsis

A

Achalasia

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2
Q

Most common etiology of achalasia

A

Idiopathic

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3
Q

Infectious etiology of achalasia

A

Chagas disease: Trypanoma cruzi

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4
Q

Pathophysiology of achalasia

A

Atrophy inhibitory neurons in Auerbach plexus
Absence NO and VIP, presence of Ach and substance P → inability to relax and more pressure of LES → no peristalsis

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5
Q

Clinical features of achalasia

A

Gradual onset
Dysphagia of solids and liquids
Weight loss
Retrosternal pain and cramps
Chest pain and heartburn

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6
Q

Confirmatory test for achalasia

A

Esophageal manometry

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7
Q

What would you expect to find in an esophageal manometry for a px with achalasia

A

Incomplete relaxation of LES
Aperistalsis in distal 2/3 esophagus

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8
Q

Characteristic sign found in the barium swallow for achalasia

A

Bird beak sign → dilation of proximal esophagus and stenosis of gastroesophageal junction

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9
Q

First line treatment of achalasia

A

Mechanical:
Pneumatic dilation of LES with balloon
LES myotomy (Heller)

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10
Q

Pharmacological treatment of achalasia

A

Botulinum toxin
Oral nitrates
Ca channel blockers

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11
Q

Premature and rapidly propagated contractions of distal esophagus

A

Esophageal spasm

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12
Q

Pathophysiology of esophageal spasm

A

Dysfunction of nitrogenous enteric neural innervation of smooth muscle portion of esophagus

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13
Q

Clinical features of esophageal spasm

A

Dysphagia to both solids and liquids
Non cardiac chest pain

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14
Q

What is the main characteristic of esophageal spasm

A

First exclude other conditions associated with symptoms

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15
Q

What would a high resolution esophageal manometry and a barium esophagram show in esophageal spasm

A

High resolution esophageal manometry → aperistalsis
Barium esophagram → corkscrew

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16
Q

First line tx for esophageal spasm

A

Control GERD, calcium channel blockers, nitrates

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17
Q

High amplitude contractions longer in duration than normal

A

Hypercontractile esophagus

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18
Q

Pathophysiology of hypercontractile esophagus

A

Excessive excitatory enteric neural innervation and/or smooth muscle hypertrophy

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19
Q

What would you find in a high resolution esophageal manometry for hypercontractile esophagus

A

Premature contractions in distal esophagus

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20
Q

What would you find in a barium study for hypercontractile esophagus

A

Normal

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21
Q

Dilated collateral veins resulting from increased blood flow due to portal hypertension

A

Esophageal varices

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22
Q

Where are esophageal varices most commonly found

A

Distal esophagus

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23
Q

Etiology of esophageal varices

A

Portal hypertension (cirrhosis)

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24
Q

Clinical features of esophageal varices

A

Non bleeding → asymptomatic
Bleeding → sudden onset of severe symptoms of GI bleeding

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25
Size classification of esophageal varices
Small <5 mm Medium/large >5 mm
26
Treatment of esophageal varices
Band ligation
27
Antibiotic prophylaxis for esophageal varices
Ceftriaxone
28
Acute inflammatory process of pancreas
Acute pancreatitis
29
Most common causes of acute pancreatitis
Biliary pancreatitis Alcohol induced Idiopathic
30
Main pathophysiological events of acute pancreatitis
Intrapancreatic activation of pancreatic enzymes Increased proteolytic and lipolytic enzyme activity Attraction of inflammatory cells
31
What happens to trypsinogen in acute pancreatitis
Premature activation to trypsin within acinar cell instead of duct of lumen
32
What is the role of lipase in acute pancreatitis
Released by damaged cells → breaks down triglycerides in free fatty acids which bind calcium → saponification necrosis
33
Sequelae of acute pancreatitis
Capillary leakage Pancreatic necrosis Hypocalcemia
34
Cardinal manifestation of acute pancreatitis
Epigastric abdominal pain
35
Examination findings in acute pancreatitis
Signs of shock Abdominal tenderness Cullen sign Grey Turner sign
36
Diagnostic criteria for acute pancreatitis
2/3 should be met for a diagnosis to be made: * Characteristic abdominal pain * High serum pancreatic enzymes 3x higher * Characteristic findings in imaging
37
Most indicative pancratic enzyme for diagnosis of acute pancreatitis
Lipase
38
Other diagnostic findings in acute pancreatitis (besides main dx criteria)
Leukocytosis or high hematocrit C-reactive protein and lactate Low ionized calcium levels
39
1st line imaging modality for acute pancreatitis and its findings
Abdomen ultrasound Enlarged hypoechoic pancreas: edema
40
Atlanta grading for acute pancreatitis
Mild acute → no organ failure and no local or systemic complications Moderate acute → transient organ failure (<48 hrs) and/or local or systemic complications Severe acute → persistent organ failure
41
Characteristics of Marshall prognostic score for acute pancreatitis
For organ failure 2< → organ failure
42
Characteristics of Randall prognostic score for acute pancreatitis
To estimate severity and prognosis of biliary and non biliary pancreatitis Full assessment only possible after 48 hrs
43
Characteristics of APACHE prognostic score for acute pancreatitis
ICU to determine severity >8 score indicates severe
44
Characteristics of BISAP prognostic score for acute pancreatitis
To estimate in-hospital mortality >2 severe Characteristics: BUN >8.9, altered mental status, SIRS, >60 years, pleural effusion
45
Balthazar grading for acute pancreatitis
* Mild (interstitial) → Balthazar B or C without pancreatic or extrapancreatic necrosis * Intermediate (exudative): Balthazar D or E without pancreatic necrosis; peripancreatic collections due to extrapancreatic necrosis * Severe (necrotizing): necrosis of pancreas
46
Priority of acute pancreatitis treatment
Goal-directed IV fluid therapy in first 24-48 hrs
47
Treatment for pain control in acute pancreatitis
Analgesics
48
Characteristics of nutritional treatment in acute pancreatitis
Resume food in absence of → pain, nausea, vomiting, ileus
49
Complications of acute pancreatitis
Necrotizing pancreatitis SIRS → systemic inflammatory response syndrome
50
Most common cause of chronic pancreatitis
Heavy alcohol consumption
51
Risk factors for chronic pancreatitis
Hypertriglyceridemia: >1,000 Hereditary pancreatitis: PRSS1 gene mutation
52
2 pathophysiological mechanisms involved in chronic pancreatitis
Autodigestion and inflammation Fibrosis
53
Features of pancreatic insufficiency in chronic pancreatitis
Late manifestation after 90% of pancreas is destroyed Steatorrhea, malabsorption, weight loss, pancreatic diabetes
54
1st line diagnosis for chronic pancreatitis and what would you find
Imaging: tomography Ductal dilations, calcifications, chain of lakes, atrophy
55
What is evaluated in pancreatic function testing in chronic pancreatitis
Fecal elastase-1
56
Gold standard for dx fat malabsorption
72 hrs stool collection
57
Treatment of chronic pancreatitis
Treat pain → NSAIDS
58
Complications of chronic pancreatitis
Exocrine pancreatic insufficiency Splenic vein thrombosis
59
Syndrome of objectively delayed gastric emptying of solids in absence of mechanical obstruction
Gastroparesis
60
Most common etiology of gastroparesis
Idiopathic
61
Most frequent systemic disease associated with gastroparesis
Diabetes mellitus
62
Clinical manifestations of gastroparesis
Early satiety Nausea Vomiting Abdominal pain Weight loss
63
What would you find on a physical examination of a px with gastroparesis
Epigastric distention without guarding or rigidity
64
Diagnostic methods to exclude differentials to gastroparesis
Upper endoscopy, CT, MRE
65
Confirmatory test for gastroparesis
Gastric emptying scintigraphy (GES)
66
Characteristics of gastric emptying scintigraphy (GES)
Give px radioactive meal → scanner → track food Should be done for at least 4 hrs
67
Result values found in a gastric emptying scintigraphy
Mild → 10-15% Moderate → 16-35% Severe → >35%
68
Medications given to treat gastroparesis
Metoclopramide, domperidone, erythromycin
69
Medication that increases antral contractions and decrease gastric fundus relaxation
Metoclopramide
70
Medication with high risk of cardiac arrhythmias
Domeperidone
71
Medication that induces high amplitude gastric contractions
Erythromycin
72
Treatment for functional dyspepsia
1st line → PPIs 2nd line → tricyclic antidepressants
73
Etiology of upper GI bleeding
Source proximal to ligament of Treitz Peptic ulcer disease Esophageal varices Tumors Mallory-Weis syndrome Hiatal hernias
74
Forrest classification of peptic ulcers
Stage I: active hemorrhage * Ia: spurting arterial hemorrhage * Ib: actively oozing hemorrhage Stage II: evidence of recent hemorrhage * IIa: non bleeding ulcer with visible vessel * IIb: ulcer with an adherent clot * IIc: flat ulcer with a dark base (covered with hematin) Stage III: clean-based ulcer * III: flat ulcer base (no active hemorrhage)
75
Most common cause of upper GI bleeding
Duodenal peptic ulcers
76
Clinical features of upper GI bleeding
Anemia Acute hemorrhage Signs of circulatory insufficiency or hypovolemic shock
77
Features of overt GI bleeding
Hematemesis, melena, hematoquezia
78
Diagnostic method for occult bleeding
Fecal occult blood test (FOBT) and complete blood count Non Urgent endoscopy if FOBT is positive
79
Diagnositc method for macroscopically visible GI bleeding
Labs: tests to assess the severity of GI bleeding
80
Treatment for upper GI bleeding
Endoscopic homeostasis Interventional radiology (angiography) Surgery
81
Complications of upper GI bleeding
Hypovolemic shock Hepatic encephalopathy Aspiration pneumonia
82
Presence of abnormal concretions (gallstones) in gallbladder
Cholelithiasis
83
Risk factors for cholelithiasis
5 Fs: female, fat, forty, fertile, family history
84
Etiology of cholelithiasis
* Imbalance in bile salts, lecithin, cholesterol, calcium carbonate, bilirubin * Biliary stasis * Cholestasis
85
Most common type of gallbladder stones
Cholesterol stones
86
Risk factors for black pigment stones
Chronic hemolytic anemia Alcoholic cirrhosis Crohn disease TPN Advanced age
87
Pathophysiology of black pigment stones
High hemolysis → increased circulating unconjugated bilirubin → increased uptake and conjugation → precipitation of bilirubin polymers and stone formation
88
Risk factors for brown/mixed pigment stones
Bacterial infections and parasites in biliary tract Sclerosing cholangitis
89
Pathophysiology of brown/mixed pigment stones
Infection → release of B glucuronidase by injured hepatocytes and bacteria → hydrolyzed conjugated bilirubin and fatty acids → precipitation of calcium carbonate, cholesterol and calcium bilirubinate in bile
90
Clinical features of gallstones
Most are asymptomatic Abdominal pain → biliary colic Murphy sign
91
Best initial test to identify cholelithiasis
Transabdominal RUQ ultrasound
92
What would you find in a transabdominal RUQ ultrasound for cholelithiasis
Acoustic shadow → ultrasound beams cannot get through because stones bounce them off
93
Pharmacological treatment for gallstones
Ursodeoxycholic acid: oral bile acid dissolution therapy
94
Complication of gallstones
Mirizzi syndrome → extrinsic compression of CBD by gallstones impacted in cystic duct
95
Acute inflammation of gallbladder, typically due to cystic duct obstruction by a gallstone
Acute cholecystitis
96
Most common complication of cholelithiasis
Acute cholecystitis
97
Etiology of acute cholecystitis
Acute calculous cholecystitis (obstructing cholelithiasis)
98
Pathophysiology of acute cholecystitis
Cholelithiasis → passage gallstones into cystic duct → obstruction → distention and inflammation of gallbladder
99
Should be suspected in px with history of gallstones who presents RUQ pain, fever and leukocytosis
Acute cholecystitis
100
Initial evaluation of acute cholecystitis
Labs and RUQ ultrasound
101
Preferred initial imaging dx for acute cholecystitis
RUQ transabdominal ultrasound
102
What would you find in an ultrasound for acute cholecystitis
Gallbladder wall thickening Gallbladder distention Gallbladder wall edema: double wall sign Pericholecystic free fluid
103
Preferred confirmatory test for suspected uncomplicated acute cholecystitis if ultrasound findings are inconclusive
Cholescintigraphy
104
Gold standard for definitive management of acute cholecystitis
Laparoscopic cholecystectomy
105
Typically performed for unstable or clinically deteriorating px with acute cholecystitis
Percutaneous cholecystostomy
106
Most common complication of acute cholecystitis
Gangrenous cholecystitis
107
Histologic hallmark of chronic cholecystitis
Rokitansky-Aschoff sinus
108
Diagnositc method for chronic cholecystitis
Ultrasound abdomen or CT abdomen with IV contrast
109
Complications of chronic cholecystitis
* Porcelain gallbladder (calcification of gallbladder wall due to chronic infection) * Gallbladder cancer * Cholecystoenteric fistula and gallstone ileus
110
Only vasoactive treatment associated with lowering esophageal varices mortality
Terlipresine
111
Adverse effect of terlipresine
Hyponatremia
112
Factors evaluated in Child-Pugh evaluation
Total bilirubin Ascitis Albumin
113
Treatment used as secondary prophylaxis to esophageal varices bleeding
Propranolol
114
Syndrome associated with post hepatic portal hypertension
Budd-Chiari syndrome
115
Associated with a poor prognostic factor for chronic pancreatitis
Pain
116
Most common cause of esophageal dysphagia
GERD stenosis
117
Main hormone responsible for gallbladder contraction
Colecistoquinine
118
Charcot´s triad for cholangitis
Jaunice Fever RUQ pain
119
In which cases should you use antibioticotherapy in the setting of acute pancreatitis
Infected pancreatic necrosis
120
Classification of achalasia
Type I: aperistalsis with no increased pressure Type II: apersitalsis with panesophageal pressurization >30 mmHg Type III: spastic contractions with or w/o panesophageal pressurization
121
When is a barium swallow required in case of achalasia
When an esophageal manometry shows equivocal findings

Semestre 6: bloque 3 (2 decks)

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