GI/Liver Flashcards

1
Q

What are some components of a GI history?

A

Does the patient have :

  • Nutritional deficiency
  • Weight loss greater than 10% in last 6 months
  • Nausea/Vomiting
  • Occult blood loss
  • Overt GI bleeding
  • Abdominal pain
  • Abdominal distention
  • Abdominal masses
  • Dysphagia
  • Gastric hyperacidity with or without reflux
  • Epigastric pain
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2
Q

What is NPO status?

What is the guideline?

A

•Balance risk of fasting against pulmonary aspiration

In “healthy patients” liberal fasting guidelines can be followed

  • No chewing gum or candy after midnight
  • Clear liquids up to 2 hours before OR
  • Breast milk up to 4 hours before OR
  • Light meal, milk, formula up to 6 hours before OR
  • Fatty foods, fried foods, meats 8 hours or more
  • Sip of water or liquid pre-med up to 1 hour before OR
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3
Q

Which patients are at high risk for Aspiration?

A

Patients considered an aspiration risk:

  • Age extremes <1 yr or >70 yr
  • Ascites (ESLD)
  • Collagen vascular disease, metabolic disorders (Diabetes obesity, ESRD, hypothryoid)
  • Hiatal Hernia/GERD/Esophageal disorder
  • Mechanical obstruction (pyloric stenosis, intestinal obstruction)
  • Prematurity
  • Pregnancy
  • Neurologic diseases
  • Morbid obesity
  • Severe pain/ anxiety
  • Eaten food
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4
Q

What are some medications used for aspiration prophylaxis?

A

ASA does not promote the routine use of these medications to decrease aspiration in patients with no apparent risk factors

H2 Antagonists

  • Cimetidine, Ranitidine and Famotidine (best result)
  • Acts as competitive antagonist of histamine binding to H2 receptors on gastric parietal cells
  • Reduces acid secretion
  • Best if given the night before and repeated 45-60 minutes before surgery

Metoclopramide

  • Dopamine antagonist
  • Increases the pressure of the lower esophageal sphincter and enhances GI motility which speeds gastric emptying
  • Prevents or alleviates nausea and vomiting
  • Contraindicated in the presence of an obstruction

Sodium Citrate - Bicitra

  • Non-particulate antacid
  • Customary dose of 30 ml po to raise gastric pH
  • Disadvantage: Increases gastric volume
  • Give 15 minutes before surgery and lasts 1-3 hours

Omeprazole- Prilosec

  • Proton pump inhibitor
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5
Q

What is Mendelson Syndrome?

A
  • Chemical pneumonitis or aspiration pneumonitis
  • Characterized according to
  • pH
  • Volume
  • Gastric material aspirated
  • Risk factors for aspiration sequelae include
  • pH less than 2.5
  • Gastric volume of 0.4ml/kg (25ml/70kg)
  • Manifests as respiratory distress with bronchospasm, cyanosis, tachycardia and dyspnea from irritating action of hydrochloric acid and particulate material which are damaging to the lungs
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6
Q

What is Achalasia?

A
  • Neuromuscular disorder of esophagus leading to failure of LES to relax when swallowing, reduced peristalsis, esophageal dilation
  • Triad is dysphagia, weight loss, regurgitation
  • Risk of aspiration
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7
Q

What is Barrett’s Esophagus?

What are the treatments?

What are the signs and symptoms?

A
  • Metaplastic disorder of the esophagus secondary to reflux
  • Precursor to esophageal cancer

Treatment

  • H2 Blockers
  • Proton Pump Inhibitors
  • Nissen fundoplication

Signs & Symptoms

  • Dysphagia
  • Reflux esophagitis
  • Retrosternal pain or heartburn
  • LES dystonia
  • Weight loss
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8
Q

Whats Schatzki RIng?

A
  • A narrowing of the lower esophagus caused by a ring of mucosal tissue or muscular tissue
  • Causes dysphagia, food obstruction, vomiting
  • Aspiration risk
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9
Q

What is Hiatal Hernia?

What are the signs and symptoms?

A
  • Protrusion of a portion of the stomach through the hiatus of the diaphragm upward into the thoracic cavity
  • Aspiration risk

Signs & Symptoms

  • Retro-sternal discomfort
  • Burning after meals
  • Reflux (+/-)
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10
Q

What is GERD?

S/S?

Tx?

A

•Retrograde movement of gastric contents through the lower esophageal sphincter into esophagus

Signs

  • Heartburn
  • Noncardiac chest pain
  • Dysphagia
  • Pharyngitis, cough, asthma, hoarseness

Treatment:

  • Metoclopramide, H2 blockers, PPIs
  • Aspiration risk
  • High incidence of bronchospasm
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11
Q

What is Gastroparesis?

A
  • Partial paralysis of the stomach
  • Vagus nerve-stomach contraction-injury
  • Autonomic Neuropathy-Diabetes- most common cause
  • Connective tissue diseases-Scleroderma, Ehlers-Danlos
  • Opioids and anticholinergics
  • Leads to prolonged food retention
  • Aspiration risk
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12
Q

Describe Peptic Ulcer Disease

Treatment?

SIgns?

A
  • Ulcerations in the GI mucosa most commonly the duodenal bulb or antrum of stomach
  • H. Pylori –usual cause
  • Men and Women age 45-60
  • Causes: Chronic use of NSAIDS, ETOH, Steroids

Treatment

  • H2 antagonists
  • Proton pump inhibitors
  • Antimicrobial therapy
  • Antacids

Signs:

  • Epigastric pain
  • Anorexia, wt. loss
  • Vomiting
  • Hematemesis or melena (this may be acute hemorrhage)
  • Abdominal tenderness and rigidity
  • Perforation (severe pain)
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13
Q

What is Malaborption Syndromes?

S/S?

A
  • Clinically significance deficits in mineral, vitamins and electrolytes
  • Small bowel perforation or obstruction
  • Small Intestine
  • Celiac Sprue
  • Fat Malabsorption
  • Protein Malabsorption

Signs & Symptoms

  • Unexplained wt. loss
  • Steatorrhea
  • Diarrhea
  • Anemia
  • Fatigue
  • Deficiency in Vitamin K
  • Bleeding dyscrasia
  • Edema/ascites
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14
Q

Discribe the difference between the 2 inflammatory bowel disease

A

Crohn’s Disease

•Inflammation and ulceration to the distal ileum and large colon

  • Deficiency in absorption of magnesium, calcium, vit D, B12, Phosphorus, Folic acid, Zinc, Iron potassium
  • Protein loss, decreased plasma albumin
  • Anemia

•Recurrent right lower quadrant pain, diarrhea, palpable mass, fever, anorexia/wt. loss

Ulcerative Colitis

•Inflammation and loss of colonic mucosa from rectum to distal colon; becomes hemorrhagic, edematous, ulcerated

  • Intermittent bloody diarrhea
  • Fever/ malaise
  • Anorexia/wt. loss
  • Abdominal pain
  • Associated with risk of colon cancer
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15
Q

Where are carinoid tumors?

What can it produce?

What are signs and symptoms of Carcinoid syndrome?

A
  • Site of origin in the GI tract
  • Can produce carcinoid syndrome or crisis
  • produced by the effects of hormones and substances secreted in the GI tract and systemic circulation
    • Bradykinin
    • Histamine
    • Serotonin
    • Dopamine

S&S Carcinoid Syndrome

  • Cutaneous flushing
  • Diarrhea
  • Tachycardia, arrhythmias
  • Dyspnea, wheezing, bronchospasm
  • Hypotension
  • Hypertension
  • Orthostasis
  • Fibrosis of pulmonary and tricuspid valves
  • Right-sided valvular heart dz

•Pre-op test are guided by physical findings

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16
Q

What is Nutritional Deficiency?

What is used as a predictor?

A
  • Malnutrition is associated with
  • prolonged hospital stay
  • wound infection
  • abscess
  • respiratory failure
  • death
  • Serum Albumin level of
  • Less than 3.5 in the general surgical population is accurate predictor of malnutrition
  • Less than 2.1 major predictor of morbidity in veterans undergoing non-cardiac surgery

•Weight loss of greater than 10% in last 6 months

17
Q

What does the GI physical consist of?

A
  • General inspection
  • Weight, vital signs
  • Abdominal examination
  • Auscultate bowel sounds
  • Palpate abdomen
  • Note guarding and pain
  • Note organomegaly
  • Percuss
18
Q

What are some useful labs for a GI patient?

A
  • Hematocrit
  • Serum electrolytes
  • BUN
  • Serum albumin
19
Q

What are some preop considerations for a GI Pt?

A
  • Aspiration risk
    • Prophylaxis and airway management considerations; bronchospasm
  • Bleeding causing anemia
  • Nutritional deficits and/or electrolyte disturbances
  • Pain control
  • Medications: stress-dose steroids,
  • If carcinoid, cardiac workup needed? Hemodynamically stable?
20
Q

What are some functions of the liver?

A

Liver is responsible for an enormous number of complex and interrelated functions.

  • Reservoir of blood (10-15%total blood volume)
  • Maintains normal clotting
  • Mediator of endocrine functions
  • Bilirubin excretion
  • Metabolism
  • Synthesis of proteins
  • Immunologic Function
  • Pharmacokinetics

Liver has large functional reserve

21
Q

What are some components of a liver history?

A
  • Easy bruising?
  • Anorexia or weight changes
  • N&V or pain with fatty meals
  • Pruritus or fatigue
  • Abdominal distention/ascites
  • GI Bleeding
  • Scleral icterus, jaundice
  • Hepatomegaly or splenomegaly
  • Palmer erythema
  • Gynecomastia
  • Spider angiomata, petechiae, and ecchymosis
  • Dark urine and/or pale stools
  • History of jaundice
  • Prior blood transfusions
  • Recreational drugs/Alcohol
  • Current medications including herbals
  • Family history of jaundice and liver disease
  • History of blood transfusions
  • Travel history
  • Occupational history
22
Q

What medications increases liver enzyme levels?

A
  • Antibiotics
  • Antiepileptic drugs
  • Inhibitors of hydroxymethylglutaryl-coenzyme
  • Nonsteroidal anti-inflammatory drugs
  • Sulfonylureas for hyperglycemia
  • Herbals
  • Cocaine, ecstasy, angel dust, glues/solvents
23
Q

What is included in a liver physical?

A
  • General inspection (wt., vital signs, mental status)
  • Exam patient’s hands, looking for:
  • Koilonychia
  • Leukonychia
  • Nail clubbing
  • Palmar erythema
  • Asterixis
  • Dupuytren’s contracture
  • Check sclera for jaundice or pallor
  • Exam chest for gynaecomastia or spider nevi- signs liver dz
  • Skin color (jaundice), scratches (itching)
  • Skin turgor
  • Dependent edema
  • Auscultate breath sounds
  • Pleural effusions
  • Abdominal examination
  • Auscultate bowel sounds
  • Palpate abdomen
  • Note guarding and pain
  • Note organomegaly
  • Percuss
24
Q

What labs would you want to assess?

and what would you want to consider?

A
  • Albumin (normal 3.5-5.0 g/dl)
  • Complete CBC
  • Coagulation studies (esp PT)
  • Serum electrolytes and glucose levels
  • Serum BUN/ Cr
  • Serum liver enzymes (LFTs)
  • Serum ammonia levels
  • Platelet count >100,000
  • Bilirubin
  • ABG
  • Consider a toxicology screen and blood alcohol levels
  • Liver patients often require increased sedatives due to induced enzymes
  • Preoperative degree of liver dysfunction is a major determinant of post-operative outcome
  • Anemia is a common finding
  • CBC, PT/PTT, INR platelet count
25
Q

What are some Normal LFTs?

A
26
Q

Describe the coagulation disorder in liver failure

A
  • Disorders of coagulation rapidly develop in patients with severe liver failure
  • Factors II, V, VII, IX, X all reduced in liver failure
  • PT and INR elevated
  • Thrombocytopenia
  • Abnormal fibrinogen
27
Q

What are platlets? What platelet disorder may you find with liver failure?

A
  • Platelets are derived from the megakaryocytes in the bone marrow in response to thrombopoietin which is synthesized in the liver.
  • This process is abnormal in liver disease and you may find
    • Abnormal platelet function
    • Decreased platelet function
    • Increased bleeding time
28
Q

Why is Vit K important? What are are the results of a Vit K deficiency?

A
  • Vitamin K is fat soluble and requires bile salts for the absorption into the jejunum
  • Vitamin K is necessary for the hepatic synthesis of Factors II, VII, IX, X, and Protein S and Protein C
  • Vitamin K deficiency develops in patients on parenteral nutrition, biliary obstruction, pancreatic insuff, malabsorption, GI obstruction and rapid GI transit
  • Effects of Vitamin K deficiency include prolonged PT, PTT
29
Q

What kind of Preoperative testing would you want with Liver Failure and why?

A

Pre-operative EKG is warranted

CV

  • Increased levels of endogenous vasodilators such as vasoactive intestinal peptide
  • High cardiac output
  • Decreased systemic vascular resistance
  • Hyperdynamic circulatory state
  • Arteriovenous shunting
  • Portal hypertension

CXR

30
Q

What is the Child-Turcotte-Pugh Classification for Severity of Cirrhosis?

A
31
Q

Whats the Meld score?

A
32
Q

What are some Liver Dz?

A
  • Cholestatic Disease
  • Chronic hepatitis
  • Acute hepatitis
  • Non-alcoholic fatty liver disease
  • Alcoholic liver disease
  • Cirrhosis
33
Q

Describe Cholestatic Dz

What are some treatments?

What are some expected findings?

A
  • Cholestatic disease predisposes towards Vitamin K deficiency
  • Biliary obstruction coagulopathy results from a deficiency of factors dependent on Vitamin K (II,VII, IX, X)
  • Absorption of Vitamin K depends on Bile Salt excretion into GI tract
  • Long term biliary obstruction can cause liver dysfunction interfering with protein synthesis
  • Treatment is to correct with parental Vitamin K
  • FFP is necessary if emergent surgery or presence of hepatic injury

Expected findings

  • Increased peripheral vasodilation
  • Increased CO
  • Increased portal venous pressure
  • Decreased portal venous blood flow
34
Q

What is hepatitis?

Treatment?

A
  • Group of liver disorders of varying etiologies that result in hepatic inflammation and necrosis for >6 months
  • Includes etiologies such as HBV HDV, HCV auto-immune, drugs, alcohol
  • Liver is graded based on degree of inflammation, necrosis, progression of disease and degree of fibrosis
  • Treatment may include Interferon, Ribavirin, corticosteroids, AZT
35
Q

What are some preop considerations for Hepatitis?

Labs?

A
  • Aspiration precautions
  • Preoperative evaluation should focus on signs and symptoms of encephalopathy, bleeding, jaundice, ascites, and hemodynamics

Labs:

•Electrolytes, BUN, creatinine, serum glucose, H/H, liver enzymes, bilirubin, coagulation studies, albumin, and abg

36
Q

Describe Non-Alcoholic Fatty Liver Dz

A
  • Most common cause of chronic liver disease
  • Fat accumulation in the liver exceeding 5%
  • Risk factors include NIDDM and obesity
  • Asymptomatic but elevated liver enzymes (AST & ALT) found on physical exam
  • Produces some degree of hepatocyte necrosis which promotes the accumulation of inflammatory cells in liver
  • Leads to cirrhosis
  • Weight loss (even 5 lbs) can reverse the elevated liver enzymes
37
Q

Described Alcoholic Liver Disease

How do diagnosis?

S/S?

A
  • Liver damage results from chronic heavy ETOH use
  • Clinical features do not distinguish from the 3 types
  • Liver biopsy is necessary to give definitive diagnosis
  • Steatosis (fatty liver)
  • Alcoholic hepatitis (precursor Cirrhosis)
  • Cirrhosis

S&S

  • malaise
  • nausea
  • anorexia
  • weakness
  • abdominal discomfort
  • hepatomegaly jaundice
38
Q

Describe Alcoholism and Delirium Tremens

A
  • Heavy ETOH use is associated with acute hepatitis and abrupt cessation is associated with DTs
  • With ETOH withdrawal:
  • 6-8 hours may become tremulous
  • 6-24 hours hallucinations and seizures
  • Within 72 hours, DTs usually appear (can last up to 5 days)

•DTs are hallucinations, profound confusion, tachycardia, hypertension, hyperthermia, agitation, sweating

  • Treatment is with benzodiazepines
  • Consider other co-morbidities
39
Q

What is Cirrhosis due to?

S/S?

A

•Commonly due to hepatitis C and alcoholism

S & S:

  • Gastroesophageal variceal
  • Intrapulmonary shunting
  • Ventilation/perfusion mismatch
  • Arterial hypoxemia due to Intra-pulmonary vascular dilations (IPVD)
  • Ascites and edema
  • Coagulation disorders w/ bleeding
  • Endocrine disorders
  • Encephalopathy
  • Portal hypertension