GI & Nutritional Disorders Flashcards
1
Q
What are the 6 primary risk factors for cholelithiasis?
A
- Fat
- Fair
- Female
- Forty
- Fertile
- Flatus (esp burping)
2
Q
What are the clinical manifestations of cholelithiasis?
A
- Biliary colic- episodic, abrupt RUQ pain that resolves slowly
- Nausea possible
- Precipitated by fatty foods & large meals
3
Q
What is the test of choice for diagnosing cholelithiasis?
A
Ultrasound
4
Q
What is the treatment for cholelithiasis?
A
- Asymptotic- observation
2. Elective cholecystectomy in symptomatic patients (usually laparoscopic)
5
Q
What drains internal hemorrhoids?
A
Superior rectal vein to the portal system
6
Q
What drains external hemorrhoids?
A
Inferior rectal vein to the vena cava
7
Q
What are some risk factors for hemorrhoids?
A
Increase venous pressure Cirrhosis Portal HTN Straining during defecation Pregnancy Obesity Prolonged sitting
8
Q
What are the clinical manifestations of internal hemorrhoids?
A
Intermittent rectal bleeding, hematochezia, purple nodules with prolapse
9
Q
What are the clinical manifestations of external hemorrhoids?
A
Perianal pain (aggravated by defecation), +/- tender/palpable mass
10
Q
Name 3 treatment options for hemorrhoids (from most conservative to least)
A
- Increase fiber in diet, increase fluids, warm sitz baths, and topical rectal corticosteroids for pruritus and discomfort
- If failed #1 or if you have debilitating pain, strangulation, or they are stage 4- rubber band ligation
- Hemorrhoidectomy
11
Q
What are the clinical manifestations of anal fissures?
A
SEVERE rectal pain, especially with BMs- causes pt to withhold
Can lead to constipation and bright red blood per rectum
12
Q
How do you treat anal fissures?
A
- about 80% resolve spontaneously
- supportive measures: warm sitz baths, analgesics, increase fiber, increase water, stool softeners, laxatives, mineral oil
13
Q
What is a perianal abscess? Fistula?
A
- Abscess- bacterial infection of anal ducts/glands and fluid accumulation. If fluid drains to outside of skin you can get…
- Fistula- open tract between 2 epithelium-lined areas, seen especially with deeper abscesses
14
Q
What are the clinical manifestations of perianal abscess?
A
Redness, tenderness, swelling/mass around anus, pain is worse with sitting, coughing, and defecation
15
Q
How do you treat perianal abscess?
A
I&D followed by WASH
W: warm water cleansing
A: analgesics
S: sitz baths
H: high fiber diet
(For fistulas- small tracks: fistulotomy)
16
Q
Where do indirect inguinal hernias occur?
A
LATERAL to inferior epigastric artery
Travel through deep and superficial inguinal rings
17
Q
Where do direct inguinal hernias originate and terminate?
A
Originate- MEDIAL to epigastric vessels within Hesselbach’s triangle (RIP: rectus abdominis, inferior epigastric, pouparts ligament/inguinal ligament)
Terminate- may protrude through superficial inguinal ring, does NOT reach scrotum
18
Q
What are the clinical manifestations of inguinal hernias?
A
- Swelling or fullness, enlarges with increased intra-abdominal pressure and standing (may develop scrotal swelling)
- Incarcerated: painful enlargement of irreducible hernia (+/- N/V)
- Strangulated: ischemic with systemic toxicity, severe/painful BM (EMERGENCY)
19
Q
Who is most likely to get a femoral hernia?
A
Women
20
Q
Who’s most at risk for incisional (ventral) hernias?
A
Patients who have undergone operation with vertical incision
Obese patients
21
Q
What are the main causes of ventral hernias?
A
- Weakness of surgical wounds
- Increased intra-abdominal pressure due to chronic cough, constipation, urinary obstruction (BPH), pregnancy, or ascites
22
Q
What population is most often associated with umbilical hernias? How are they managed?
A
Children, usually resolve by 2
Kids > 5 you will do surgical repair to avoid incarceration/strangulation
23
Q
What is the main cause of LBO?
A
Malignancy
24
Q
Abdominal DDX
Abrupt onset?
A
Acute event
25
Abdominal DDX
Chronic constipation and BM straining?
Diverticulitis or carcinoma
26
Abdominal DDX
Changes in stool caliber?
Carcinoma
27
Abdominal DDX
Recurrent LLQ pain over several years?
Diverticulitis or diverticular stricture
28
Imaging for suspected LBO?
CT is preferred if obstruction suspected- contrast enhanced!
Can also do X-ray (with or without contrast)
29
How do you treat a LBO?
1. Initial- volume resuscitation, pre-op abx, timely surgical consultation, consider NG
2. Surgical emergency- closed loop obstruction, bowel ischemia, volvulus
30
What’s the most common area for diverticula to develop?
Sigmoid colon
31
What’s the likely age of onset for diverticular disease?
>40
32
What is the main cause of lower GI bleeding?
Diverticulosis
33
What is associated with diverticulosis?
Low fiber diet, constipation, obesity
34
How is diverticulitis defined?
Inflamed diverticula secondary to obstruction or infection (fecaliths)
35
Fever, LLQ pain, and N/V/D/constipation/and bloating are commonly associated with what?
Diverticulitis
36
How do you diagnose diverticulitis?
CT scan!
High WBCs
Positive guaic
37
How do you treat diverticulosis?
Diverticulitis?
1. Diverticulosis: increase fiber (+/- supplements)
| 2. Diverticulitis: clear liquid diet, abx (Cipro or Bactrim + Flagyl)
38
What is defined by the twisting of bowel at its mesenteric attachment site?
Volvulus
39
Where is a volvulus most likely to occur?
Sigmoid colon & cecum
40
How is a volvulus treated?
Endoscopic decompression
2nd line- surgical correction
41
Most common etiology of a SBO?
Post-surgical adhesions
42
Other causes of SBOs?
Incarcerated hernias, Crohns, malignancy, and intussuception
43
Different types of SBO include...
1. Closed loop- lumen is occluded at 2 points, which can reduce blood supply (causing strangulation, necrosis, and peritonitis)
2. Open loop
3. Complete v. Partial
4. Distal v. Partial (distal has more distention and less vomiting)
44
What are the clinical manifestations of a SBO (think CAVO)?
1. Cramping abdominal pain
2. Abdominal distention: +/- dehydration and electrolyte imbalance
3. Vomiting: may be bilious if proximal, N/V usually follows pain
4. Obstipation: late finding, diarrhea first!
45
_________ (hypoactive/hyperactive) bowel sounds are heard in the early phases of a SBO and _________(hypoactive/hyperactive) sounds are heard in the late phases.
Hyperactive...Hypoactive
46
How is a SBO diagnosed?
Abdominal X-ray
Will see air-fluid levels in step ladder pattern and dilated bowel loops
47
How is a SBO managed?
1. Nonstrangulated: NPO, IV fluids, bowel decompression (NG suction)
2. Strangulated: surgical intervention
48
What are the RFs for pancreatic carcinoma?
Smoking, >60, chronic pancreatitis, EtOH, DM, male, obesity, A.A.
49
Histology of pancreatic carcinoma...
MC: Ductal Adenocarcinoma
-70% found in head of pancreas
50
What are the clinical manifestations of pancreatic carcinoma?
Usually have mets by time of presentation (regional lymph nodes and liver)
1. Abdominal pain radiating to back- may be relieved by sitting up and leaning forward
2. PAINLESS JAUNDICE (80%)- 2ry to common bile duct obstruction. WEIGHT LOSS in 75% of cases
3. Pruritus due to increased bile salts on skin, anorexia, acholic stools, dark urine
51
What is Courvoisiers sign?
PE finding in Pancreatic Cancer
Palpable, nontender, distended gallbladder associated with jaundice
52
How is pancreatic cancer diagnosed?
CT scan 1st choice!
ERCP is most sensitive
Labs: tumor markers CA 19-9 and CEA
53
What is a Whipple Procedure?
For treating pancreatic cancer-
Radical pancreaticoduodenal resection, done if cancer is confined to head/duodenal area
54
What is Meckel’s Diverticulum?
Persistent portion of embryonic yolk stalk
55
What is the Rule of 2s and what does it apply to?
Applies to Meckel’s Diverticulum
```
2% of population
2 feet from ileocecal valve
2% symptomatic
2 inches in length
2 types of ectopic tissue- gastric or pancreatic
2 years- MC age at presentation
2 times more common in boys
```
56
Clinical manifestations:
1. Usually asymptomatic
2. Painless rectal bleeding/ulceration (peri umbilical and radiates to RLQ)
3. Can cause: intussuception, volvulus, or obstruction. May cause diverticulitis in adults
Of...
Meckel’s Diverticulum
57
How do you diagnose Meckel’s Diverticulum?
Meckel’s scan looks for ectopic gastric tissue in ileal area
Management: surgical excision if symptomatic
58
What lab findings are associated with anorexia nervosa?
Leukocytosis, leukopenia, anemia, hypokalemia, increased BUN (dehydration), hypothyroidism
59
How long does it take the stomach to empty clears? Light meal?
Clears- 2h
| Light meal- at least 6h
60
____ (percentage) amount of total body water is intracellular and _____ (percentage) is extracellular
```
Intracellular= 2/3
Extracellular= 1/3
```
61
Of the extracellular portion of total body water about ____ (fraction) is interstitial and ____ (fraction) is intravascular
```
Interstitial= 3/4
Intravascular= 1/4
```
62
TBW= 0.6 X Body weight (kg)
Do I need to know this???
63
Calculating maintenance fluid requirements...
Hourly: 4-2-1 Rule
4cc/kg/hr for 1st 10kg
2cc/kg/hr for 2nd 10kg
1cc/kg/hr for remaining kgs
For 70kg person that would be 110cc/hr
64
Third-spacing occurs when too much fluid moves from intravascular space to interstitial space. Usually happens around POD __ (number). Can get a very large UOP at this time.
3
65
What are the 5 W's of post-op fever and what POD does each represent?
*early fever is normal, later fever is more concerning for infection
```
Day 1= Wind (Atelectasis)
Day 3= Water (UTI)
Day 5= Wound (Surgical site infection)
Day 7= Walking (DVT)
Day ≥ 9= Wonder (Drugs)
```
66
Atelectasis will most likely be bilateral. A unilateral infiltrate will most likely be _______.
Pneumonia
67
What is Virchow's Triad?
Explains 3 categories thought to contribute to thrombosis:
1. Stasis
2. Hypercoaguability
3. Vessel damage
68
_____ is #1 cause of post-op infection
Wound infection= 40%
| UTI= 29%
69
Normal daily water loss...
```
Urine= 1200-1500cc
Respiratory= 500-700cc
Sweat= 200-400cc
Feces= 100-200cc
```
70
Typical maintenance fluid for an adult is...
D5 1/2 NS with 20 mEq of KCl (5% dextrose solution in 1/2 normal saline solution with 20 mEq of KCl)
71
___% of total body weight= blood volume
Approximately 7%
72
Minimal urine output for an adult on maintenance fluid is ____ cc/kg/hr
0.5cc/kg/hr (for 75kg adult that is about 35cc/hr)
73
Nutritional Requirements:
```
Protein= ____ g/kg/day
Calories= _____ kcal/kg/day
```
Protein= 1 g/kg/day
Calories= 35 kcal/kg/day
* For surgical patient you need to be mindful of Vitamins A, C, and zinc
* *Albumin level is a good indicator of overall nutrition
74
Heartburn that is retrosternal and postprandial (30-60 min after eating) is associated with what condition?
GERD
75
Most common cause of noncardiac chest pain is _____?
GERD
76
How is GERD diagnosed?
Usually clinically based on history.
ENDOSCOPY is used if symptoms persist/with complications
24h pH monitoring used if symptoms persistent
77
What foods should be avoided with GERD dx?
fatty/spicy, citrus, chocolate, caffeinated products, peppermint, alcohol
78
What pharmacological agents can treat GERD?
1. Antacids
2. H2 recetor antagonists
3. PPIs (moderate to severe dz)
4. Nissen fundoplication if refractory
79
2 key electrolyte abnormalities we worry about with persistent vomiting are...?
1. Hypokalemia
| 2. Metabolic alkalosis
80
3 most common causes of N/V are?
1. Gastroenteritis
2. Drugs
3. Toxins
81
Bilious vomiting is often a sign of a ____?
Bowel obstruction
82
Vomiting partially digested food a few hours after eating is a sign of ____?
(HINT: common after abdominal surgery and in diabetics)
Gastroparesis or Ileus
83
Mild to moderate nausea for many days with accompanying: jaundice, anorexia, and malaise may be a sign of ____?
Hepatitis
84
N/V Red Flags include:
1. Signs of hypovolemia
2. HA, stiff neck, mental status change
3. Peritoneal signs
4. Distended, tympanitic abdomen
85
Drugs for vomiting include:
1. Motion sickness: Scopolamine, antihistamines
2. Mild-moderate: Metoclopramide (Reglan), Promethazine (Phenergan)--> Dopamine blockers
3. Severe/Refractory: Odansetron (Zofran)--> 5-HT3 antagonists, serotonin receptor blockers
86
What are the main causes of esophagitis and how is it diagnosed?
MC: GERD, infections in immunocompromised (Candida, CMV, HSV)
Dx: Upper Endoscopy
87
____ is defined by increased LES pressure. MC in 5th decade.
Achalasia
| no inhibitory nitric oxide= increased tone
88
What is the gold standard for diagnosing achalasia?
Esophageal manometry
| esophagram shows the bird's beak appearance of LES
89
Achalasia results in dysphagia to BOTH ___ & ___
Solids and Liquids
90
A corkscrew appearance on an esophagram suggests a diagnosis of ______
Diffuse esophageal spasm
91
Achalasia is treated with what medications?
Botox injections, nitrates, calcium channel blockers
92
A pharyngoesophageal pouch that causes dysphagia, regurgitation of undigested food, feeling as if there is a lump in neck, and halitosis is associated with what diagnosis?
Zenker's Diverticulum
93
How is Zenker's Diverticulum treated?
- Diverticulectomy
| - Cricopharyngeal myotomy
94
Full thickness rupture of the distal esophagus, associated with repeated and forceful vomiting is known as _____ Syndrome?
Boerhaave Syndrome
95
How is Boerhaave Syndrome diagnosed?
1. Chest CT/CXR: pneumomediastinum, left-sided hydropneumothorax
2. Contrast esophagram
96
Vomiting with hematemesis after an EtOH binge with hydrophobia is known as _____ Syndrome?
Mallory-Weiss Syndrome
97
How is Mallory-Weiss Syndrome diagnosed?
Upper Endoscopy (see superficial, longitudinal mucosal erosions)
98
Dilation of gastroesophageal veins as a complication of portal vein HTN is known as ______?
Esophageal varices
99
Main cause of esophageal varices in adults is ____?
Cirrhosis
100
The primary clinical manifestation of esophageal varices is ______?
Upper GI bleeds
101
How are esophageal varices diagnosed?
Upper Endoscopy- enlarged veins
102
How are esophageal varices treated?
1. Endoscopic Intervention- ligation
2. Pharmacologic Vasoconstrictors- Octreotide
3. Surgical Decompression- TIPS
103
What medications are used to prevent rebleeds in patients with esophageal varices?
1. Nonselective beta blockers (NOT used in acute bleeds because it blunts cardiac output)
2. Isosorbide (long acting nitrate)
104
Protrusion of the upper portion of the stomach into the chest cavity due to a diaphragm tear or weakness is known as a ____ hernia?
Hiatal
105
A type 1 hiatal hernia is also known as a _____ hernia and is the _____ (most/least) common type.
Sliding, Most
106
A type 2 hiatal hernia is also known as a _____ hernia.
Rolling
(fundus of stomach protrudes through diaphragm- may lead to strangulation)
Treatment- surgical repair of the defect
107
_____ is the MC cause of esophageal cancer worldwide and occurs in the _____ (portion) of the esophagus.
Squamous cell, upper 1/3
108
RFs for squamous cell esophageal cancer are?
Tobacco/EtOH use, exposure to noxious stimuli, increased incidence in A.A.
109
______ type of esophageal cancer is MC in younger patients, obese, and caucasians. Occurs in the ____ (portion) of the esophagus.
Adenocarcinoma, lower 1/3
| adenocarcinoma can be a complication of GERD, leading to Barrett's esophagus
110
Clinical manifestations of esophageal cancer include:
1. Dysphagia to solid food and eventually fluids, odynophagia
2. Weight loss and chest pain
3. Hypercalcemia in patients with squamous cell
111
How is esophageal cancer diagnosed? Treated?
Upper Endoscopy with biopsy
Treatment- resection, radiation, chemo (depending on stage)
112
What is the primary agent responsible for gastritis?
H. pylori
113
NSAIDs/Aspirin can cause irritation of what organ?
Stomach (Gastritis)
114
How is gastritis diagnosed?
Endoscopy
115
What are the top 2 causes of PUD (peptic ulcer disease)?
1. H. pylori
2. NSAIDs
(Zollinger-Ellison Syndrome- gastrin producing tumor)
116
Dyspepsia that is worse at night is associated with what condition?
PUD
117
Pain that is worse 2-5h after meals along with nocturnal symptoms are classically associated with _____ (gastric, duodenal) ulcers while pain 1-2h after meals and weight loss is associated with _____ ulcers.
1. Duodenal
| 2. Gastric
118
What is the main cause of an UPPER GI bleed?
PUD
119
How is PUD diagnosed?
Endoscopy
| -biopsy to rule out malignancy if GU present
120
What are 3 ways to test for H. pylori?
1. Endoscopy with biopsy
2. Urea breath test- if Endo can't be done, can also confirm eradication after therapy
3. H. pylori stool antigen
121
How is H. pylori eradicated (hint: triple therapy)?
CAP
| Clarithromycin + Amoxicillin + PPI (Flagyl if PCN allergic)
122
______ (drug) is good for preventing NSAID induced ulcers but should be avoided in premenopausal women because it is abortifacent & causes cervical ripening
Misoprostol (Cytotec)
123
_____ (DU/GU) are more common in younger patients: 30-55y and _____ (DU/GU) are more common in older patients: 55-70y.
1. DU
| 2. GU
124
_________ Syndrome is caused by gastrin-secreting neuroendocrine tumors.
Clinical Manifestations?
Zollinger-Ellison
CM- multiple peptic ulcers, refractory ulcers, diarrhea
125
How is ZES diagnosed?
| Treated?
1. Fasting gastrin level
2. Secretin test- increased gastrin levels seen with this test (usually gastrin release is inhibited by secretin)
Treatment-
1. Surgical resection of tumor
2. If metastatic then PPIs and surgical resection (usually liver and abdominal LN are MC sites for METS)
126
_______ is MC cause of gastric carcinoma.
The most important RF is _______.
Adenocarcinoma
RF- H. pylori
127
Clinical manifestations of gastric carcinoma include:
Dyspepsia, weight loss, early satiety, iron deficiency anemia (bleeding)
128
How is gastric carcinoma diagnosed?
Treated?
Upper Endoscopy with Biopsy
Poor prognosis :( Gastrectomy, radiation & chemo
129
Dark urine & light colored stools are only seen with elevated _________.
Direct bilirubin
-Because there is excess direct bilirubin and it gets excreted in urine
130
Some Info...
1. PREHEPATIC PHASE: Bilirubin is produced from heme metabolism. Heme is degraded by macrophages primarily in the liver and spleen. Unconjugated (indirect) bilirubin is not soluble in water and is sent to the liver for conjugation and excretion!
2. INTRAHEPATIC PHASE: Unconjugated bilirubin is conjugated in hepatocytes with a sugar via the enzyme UGT. It is now water soluble (for bile excretion).
3. POSTHEPATIC PHASE: Transported to be stored in the gallbladder or intestine. In the intestine, conjugated bilirubin is converted to urobilinogen which can go through 3 main pathways:
- Oxidation into stercobilin (gives stool brown color)
- Some converted in kidney and excreted (giving urine its color)
- Some is recycled back to the LIVER & BILE for reuse (enterohepatic circulation)
Learning is so fun : x
131
Jaundice is not a disease but a sign of disease. Occurs when bilirubin levels > 2.5mg/dL
Etiologies include:
- increased bilirubin production (ex- hemolysis), decreased hepatic bilirubin uptake, impaired conjugation, biliary obstruction, hepatitis
- increased bilirubin without increased LFTs--> suspect familial bilirubin disorders
132
What are the 3 D's of Dubin-Johnson Syndrome?
Dubin, Direct bilirubinemia, Dark liver
133
What is Crigler-Najjar Syndrome and how is it treated?
Hereditary unconjugated hyperbilirubinemia
Type 1 more severe (no UGT activity)- see neonatal jaundice with severe progression in the 2nd week leading to kernicterus
DX- Isolated indirect hyperbilirubinemia with normal LFTs
Treatment:
1. Type 1- phototherapy and liver transplant (definitive)
2. Type 2- usually not needed. Phenobarbital can increase UGT activity
134
What is Gilbert's Syndrome?
Relatively common, hereditary indirect hyperbilirubinemia (reduced UGT activity)
-May develop transient episodes of jaundice during periods of stress, fasting, ETOH, or illness
NO TREATMENT NEEDED :)
135
____ (ALT/AST) is more sensitive for liver disease.
ALT
136
Cholestasis (when flow of bile from liver stops or slows) is measured by an increase in _____ and ______.
Alkaline phosphatase & GGT
* Also increase in bilirubin is greater than increase in ALT and AST
* *If ALP goes up and NOT GGT then look for sources other than the liver (bone, gut)
137
PT (prothrombin time) depends on synthesis of coagulation factors (vitamin K dependent). It is an early indicator of severe LIVER INJURY/PROGNOSIS
Albumin is a useful marker of overall liver protein synthesis. Levels decrease with liver failure.
138
Would AST or ALT be higher in alcohol hepatitis?
AST (S= Scotch)
139
Gallstones located in the common bile duct is associated with ________.
Choledocholithiasis
140
Acute pancreatitis and acute cholangitis are complications of _______.
Choledocholithiasis
141
What are the 3 elements of Charcot's Triad (associated with acute cholangitis)?
1. RUQ
2. Fever
3. Jaundice
142
How is choledocholithiasis diagnosed?
1. Transabdominal ultrasound
| 2. ERCP- Test of choice!! (diagnostic and therapeutic)
143
Biliary tract infection secondary to obstruction is known as _______.
Acute cholangitis
*E. coli ascending from duodenum is the most common cause!
144
What is Reynold's Pentad (associated with acute cholangitis)?
1. Charcot's Triad PLUS
2. Shock
3. Altered mental status
145
How is acute cholangitis diagnosed?
1. Labs= leukocytosis and cholestasis findings (increase in alk phos, ggt, and bilirubin).
2. US or CT scan may show dilation of the common bile duct.
3. GOLD STANDARD= Cholangiography
146
How is acute cholangitis treated?
1. ABX (monotherapy of ampicillin/sulbactam or Ceftriaxone + Flagyl or Fluoroquinolone + Flagyl)
2. Common bile duct decompression/stone extraction via ERCP
147
What is the primary cause of acute cholecystitis?
E. coli (also Klebsiella and Enterococci)
148
What are the clinical manifestations of acute cholecystitis?
1. CONTINUOUS RUQ/epigastric pain. May be associated with nausea and may be precipitated by fatty foods and large meals
149
What are the PE findings for acute cholecystitis?
1. Fever (often low-grade)
2. Positive Murphy's sign- acute RUQ pain/inspiratory arrest with palpation of the gallbladder
3. Positive Boas sign- referred pain to the right shoulder/subscapular area (phrenic nerve irritation)
150
How is acute cholecystitis diagnosed?
1. US= test of choice! Thickened gallbladder (>3mm) , sludge, gallstones
2. CT scan or AXR
3. Labs= increase in WBCs, bilirubin, alk phos, and LFTs
4. HIDA scan: Gold standard. Positive HIDA scan= nonvisualization of the gallbladder in cholecystitis
151
How is acute cholecystitis managed?
1. NPO, IV fluids, abx (ceftriaxone + flagyl)--> cholecystectomy (usually within 72 hours)
2. Cholecystostomy (percutaneous drainage of gallbladder) if patient is nonoperative
3. Pain control with NSAIDs or narcotics
152
Acute acalculous cholecystitis most commonly occurs in the seriously ill (postop, ICU patients)
Secondary to: dehydration, prolonged fasting, TPN, gallbladder stasis, burns, DM...
Due to gallbladder sludge, not gallstones
153
CHRONIC cholecystitis is associated with gallstones
- Strawberry gallbladder: interior of gallbladder resembles a strawberry, secondary to cholesterol submucosal aggregation
- Porcelain gallbladder: premalignant condition
154
What is the MC cause of fulminant hepatitis (acute hepatic failure)?
Acetaminophen
-Also: drug reactions (rifampin, antiepileptics, abx), viral hep, Reye syndrome
155
What are the clinical manifestations of acute hepatitis?
1. Encephalopathy: vomiting, coma, AMS, seizures, asterixis (flapping tremor of hand with wrist extension)
2. Coagulopathy: due to decreased hepatic production of coagulation factors (proteins)
3. Hepatomegaly, jaundice
156
How is acute hepatitis diagnosed?
Increased ammonia levels, PT/INR ≥ 1.5, increased LFTs, hypoglycemia
157
How is acute hepatitis treated?
1. Encephalopathy: Lactulose (neutralizes ammonia), ABX that decrease bacteria that produce ammonia in GI tract (neomycin), Protein restriction (reduced breakdown of protein into ammonia)
2. Liver transplant- only definitive treatment
158
What are some of the clinical manifestations of viral hepatitis?
1. Prodromal phase: malaise, arthralgia, fatigue, URI sx, N/V, loss of appetite (Hep A assoc. with spiking fever)
2. Icteric phase: jaundice
159
Chronic hepatitis is when the disease lasts longer than _____.
6 months, may lead to end stage liver disease (ESLD) or hepatocellular carcinoma (HCC)
*10% of HBV cases become chronic and 80% of HCV cases become chronic
160
Both AST and ALT are >500 if ____ (acute/chronic) and <500 if _____ (acute/chronic).
Acute, Chronic
161
_______ malignancies are more commonly secondary to metastasis (lung, breast, etc)
Hepatic
162
What are the RFs for hepatocellular carcinoma (HCC)?
Clinical manifestations?
RFs: Chronic viral hepatitis (B,C, & D), cirrhosis, aflatoxin B1 exposure
Clinical Manifestations: Malaise, weight loss, jaundice, abdominal pain, hepatosplenomegaly
163
How is HCC diagnosed?
Treated?
DX:
1. US!! (also CT, MRI, hepatic angiogram)
2. Increase in alpha-fetoprotein
Treatment:
Surgical resection if confined to a lobe & no cirrhosis
164
Irreversible liver fibrosis with nodular regeneration secondary to chronic liver disease is known as _____.
Cirrhosis
165
What causes cirrhosis?
ETOH (MC in US), chronic viral hepatitis, NAFLD (obesity, DM, hypertriglyceridemia), hemochromatosis, drug toxicity, etc.
166
What do you find on a PE in a patient with cirrhosis?
1. Ascites (decrease production of albumin and third spacing of fluid due to decreased oncotic pressure)
2. Gynecomastia (liver can't metabolize estrogen)
3. Caput medusa, spider angioma, muscle wasting, bleeding, palmar erythema, jaundice, Dupuytren's contractures
167
Asterixis (flapping tremor), fetor hepaticus ("breath of the dead"), and increased ammonia levels are associated with _______.
Hepatic encephalopathy
168
How is cirrhosis diagnosed?
US: determines liver size and evaluate for HCC with liver biopsy
169
Management of encephalopathy, ascites, and pruritus includes?
1. Encephalopathy: lactulose or neomycin- lactulose is converted into lactic acid and pulls ammonia into the gut, neomycin decrease the ammonia-producing flora
2. Ascites: Na restriction and diurectics, paracentesis
3. Pruritus: Cholestyramine (bile acid sequestrant that reduces bile salts in the skin leading to less irritation)
4. LIVER TRANSPLANT IS DEFINITIVE
170
What are the 2 primary causes of acute pancreatitis?
Gallstones and ETOH
*Also scorpion bite and mumps in children
171
Constant, boring epigastric pain that radiates to the back and relieved by leaning forward is associated with ______.
Acute pancreatitis
172
Cullen's sign (periumbilical ecchymosis) and Grey Turner (flank ecchymosis) are associated with _____.
Acute pancreatitis
173
What laboratory values are associated with acute pancreatitis?
Leukocytosis, increased glucose & bilirubin & triglycerides
1. Lipase! (more specific than amylase)
2. Increased ALT is highly specific for gallstone pancreatitis
3. Hypocalcemia (necrotic fat binds to calcium)
174
What is the test of choice for acute pancreatitis?
Abdominal CT!!
*Abdominal US is used to rule out gallstones, bile duct dilation, ascites, pseudocysts
175
How is acute pancreatitis managed?
90% recover with supportive measures like NPO, IV fluids, analgesia (abx NOT used routinely)
176
What criteria is used to determine prognosis of acute pancreatitis?
Ransons Criteria (APACHE score also used)
- takes into account glucose, age, LDH, AST, and WBC
- If score is ≥3 then pancreatitis is likely (on a scale of 0-8)
177
Chronic ______ can lead to exocrine and sometimes endocrine dysfunction
Pancreatitis
178
MC of chronic pancreatitis in adults is _______.
MC in children is _______.
Adults- ETOH
Children- CF
179
Triad of calcifications, steatorrhea, and DM is a hallmark of _______.
Chronic pancreatitis
180
How is chronic pancreatitis diagnosed?
AXR- calcified pancreas
| Amylase and lipase usually not elevated
181
How is chronic pancreatitis treated?
1. Oral pancreatic enzyme replacement
2. ETOH abstinence
3. Pain control
182
Acute dilation of the cecum and right hemicolon (mostly in men > 60) is known as _______.
Ogilvie's Syndrome
183
Clinical manifestations of Celiac Disease include:
- Malabsorption- diarrhea
| - Dermatitis Herpetiformis- papulovesicular rash on extensor surfaces, neck, trunk, and scalp
184
How is celiac disease diagnosed?
- positive endomysial IgA Ab & transglutaminase Ab
| - Small bowel biopsy for definitive diagnosis
185
How is lactose intolerance diagnosed?
Hydrogen breath test
186
What is the MC cause of appendicitis?
Fecalith
187
What are the clinical manifestations of appendicitis?
Anorexia, periumbilical/epigastric pain followed by...
-RLQ pain, nausea and vomiting (vomiting usually occurs after the pain)
-MC 10y-30y
188
What do you find on a PE exam with appendicitis?
- Rebound tenderness, rigidity, and guarding
1. Rovsing sign: RLQ pain with LLQ palpation
2. Obturator sign: RLQ pain with internal and external hip rotation with flexed knee
3. Psoas sign: RLQ pain with leg raise against resistance
4. McBurney's point tenderness: point 1/3 the distance from the ASIS & navel
189
How is appendicitis diagnosed?
1. CT scan, US, Leukocytosis
190
What is the hallmark symptom of irritable bowel syndrome?
Abdominal pain with altered defecation/bowel habits (diarrhea, constipation, or alternation between the 2)
- Pain often relieved with defecation
- MC in late teens-early 20s in Women
(Rome IV Criteria for diagnosing- p.158 PPP)
191
How is IBS managed?
1. Lifestyle Changes- smoking cessation, low fat/unprocessed food diet
2. Diarrhea- Anticholinergics/spasm (Dicyclomine), antidiarrheal (Loperamide)
3. Constipation- prokinetics, bulk-forming laxatives (Benefiber), saline (Milk of Mag) or osmotic laxatives (Miralax, Golytely)
192
What are the clinical manifestations of chronic mesenteric ischemia?
Chronic, dull abdominal pain WORSE AFTER MEALS, weight loss
193
How is chronic mesenteric ischemia diagnosed?
Managed?
Dx- Angiogram, Colonoscopy- muscle atrophy with loss of villi
Management- bowel rest. Surgical revascularization
194
What is a common site for acute mesenteric ischemia?
Splenic flexure- less collateral blood perfusion
195
What are the causes of acute mesenteric ischemia?
MC occlusion- embolus (A fib, MI), thrombus (atherosclerosis)
Shock (decreased blood flow) and cocaine (vasospasm) are also causes
196
What are the clinical manifestations of acute mesenteric ischemia?
SEVERE abdominal pain out of proportion to physical findings- usually poorly localized
197
How is acute mesenteric ischemia diagnosed?
Managed?
Dx- Angiogram is definitive
Managed- surgical revascularization or resection if bowel is not salvageable
198
Where is ischemic colitis most likely to occur?
"Watershed" areas with decreased collaterals (splenic flexure & rectosigmoid junction)
199
What are the clinical manifestations of ischemic colitis?
Diagnosed? Managed?
LLQ pain with tenderness, BLOODY DIARRHEA (due to sloughing of the colon)
Dx- Colonoscopy
Management- restore perfusion and observe for signs of perforation
200
Extreme colon dilation > 6cm + signs of systemic toxicity is associate with what condition?
Toxic Megacolon
201
What are some causes of toxic megacolon?
UC, Crohns, Pseudomembranous colitis, infections, radiation, ischemia
202
What are the clinical manifestations of toxic megacolon?
Fever, abdominal pain, diarrhea, nausea, vomiting, rectal bleeding, tenesmus, electrolyte disorders
203
What are PE findings for toxic megacolon?
Abdominal tenderness, rigiditiy, tachycardia, dehydration, hypotension, AMS
204
How is toxic megacolon diagnosed?
Managed?
Dx- AXR, Colon > 6CM!!!
Management- bowel decompression, bowel rest, NG tube, broad spectrum ABX, electrolyte repletion
205
What is the etiology of IBD (UC and Crohns)?
Idiopathic- most likely immune reaction to GI tract flora
MC- Caucasians 15-35y
206
A little about UC...
1. Where--> limited to colon (begins in RECTUM), involves mucosa and submucosa only
2. What--> Abdominal pain: LLQ, colicky, Urgency, BLOODY DIARRHEA (Hematochezia)
3. Dx--> Colonoscopy (UNIFORM INFLAMMATION), pseudopolyps
- Barium studies: "Stovepipe sign" (loss of haustral markings)
- Labs: +P-ANCA
4. Treatment--> Surgery is curative
207
A little about Crohns...
1. Where--> Any segment of GI tract from mouth to anus, MC in TERMINAL ILEUM- RLQ pain, transmural
2. What--> Abdominal pain: RLQ, crampy, weight loss common, diarrhea with NO visible blood
3. Associations--> perianal disease: fistulas, strictures, abscesses, granulomas. Malabsorption- Fe & B12 deficiencies
4. Dx--> Colonoscopy (SKIP LESIONS, cobblestone appearance)
- Barium studies: "String Sign"
5. Treatment--> Surgery is NONCURATIVE
208
How are UC and Crohns diagnosed in acute disease?
UC: flex sigmoidoscopy
Crohn: Upper GI series with small bowel follow through
209
How are UC and Crohns treated?
Aminosalicylates (sulfasalazine, mesalamine), Corticosteroids, Immune modifying agents
210
90% of colon polyps are ______ polyps and are a low risk for malignancy.
Hyperplastic polyps
211
10% of colon polyps are ______ polyps and take 10-20y before becoming cancerous (esp if >1cm)
Adenomatous polyps
212
What are the 3 types of adenomatous colon polyps?
1. Tubular adenoma: nonpedunculated (MC and lowest risk of 3 types)
2. Tubulovillous (mixture): intermediate risk
3. Villous adenoma: tends to be sessile, HIGHEST RISK OF BECOMING CANCEROUS
213
How does colorectal cancer develop?
Progression of adenomatous polyp into malignancy, MC site of metastatic spread is the LIVER
214
RF for colorectal cancer include (3):
1. Familial adenomatous polyposis (100% develop cancer by 40y)
2. Lynch syndrome (40% risk of CRC development)
3. Peutz-Jehgers (hamartomatous polyps, mucocutaneous hyperpigmentation)
215
What are some clinical manifestations of CRC?
- Iron deficiency anemia, rectal bleeding, abdominal pain, change in bowel habits
* CRC MC cause of LBO in adults!
216
How is CRC diagnosed?
1. Colonoscopy with biopsy is test of choice!
2. Barium enema: apple core lesion is classic
3. Increase CEA
217
How is CRC managed?
1. Localized (Stage 1-3): surgical resection
| 2. Stage 3 & Metastatic: chemo is mainstay- 5FU
218
Guidelines for colonoscopies for CRC screening
1. Average risk: start at 50y, q10 years after
2. 1st degree relative > 60y: start at 40, q10 years after
3. 1st degree relative < 60y: start at 40 (or 10y before the age relative was diagnosed), q5 years after
**Colonoscopies done until 75 then individualized after
219
CRC prognosis:
Preop CEA > 5, ulcerative growth patterns are associated with worse prognosis
220
Autosomal recessive disorder of amino acid metabolism is known as _______.
Phenylketonuria- PKU
221
Clinical manifestations of PKU are:
Dx:
Treatment:
Vomiting, mental delays, children often blonde & blue-eyed with fair skin.
Dx: Urine with musty (mousy) odor
Treatment: Lifetime dietary restriction of phenylalanine- milk, cheese, nuts, fish, chicken, meats, eggs, legumes, aspartame
222
Vitamin A is found in kidney, liver, egg yolk, butter, and green leafy veggies. It contributes to vision, immune function, hematopoiesis, skin and cellular health.
Patients at risk for deficiency include:
ETOHics, patients with liver disease, fat free diets
223
Visual changes such as night blindness & SQUAMOUS METAPLASIA/BITOT'S SPOTS (white spots on conjunctiva due to squamous metaplasia of corneal epithelium) are associated with what deficiency?
Vitamin A
224
What populations are at risk for Vitamin C deficiency?
Those with diets lacking raw citrus fruits and green veggies, smokers, alcoholics, malnourished individuals, elderly
225
Vitamin C deficiency is associated with SCURVY. What are the 3 H's?
Hyperkeratosis
Hemorrhage- vascular fragility w/ recurrent hemorrhages in gums, skin, & joints. Impaired wound healing.
Hematologic- anemia, glossitis, malaise, weakness. Increased bleeding time.
226
Fortified milk and sun exposure are great sources of _____.
Vitamin D
227
Vitamin D deficiency can cause ______ in children and ______ in adults.
Rickets- softening of the bones leading to bowing deformities and fractures.
Osteomalacia- diffuse body pains, muscle weakness and fractures. Looser lines on X ray.
228
____ is the mainstay of management of gastroenteritis.
Fluids- IV if needed but PO preferred.
| -sports drinks, broths, IV saline, pedialyte
229
____ diet is good when dealing with diarrhea.
BRAT
230
Pepto-bismol (bismuth subsalicylate) should not be given to children with viral illness because of increased risk of ____ syndrome.
Reye
231
_____ is an opioid agonist and is a good medication for non-invasive diarrhea (absent fever and no blood).
Loperamide (Immodium)
*Anticholinergics are another class of drugs for diarrhea that will inhibit GI motility and relax GI muscles
232
_____ is given for N/V. It blocks serotonin receptors. It may cause diarrhea, constipation, and headache (also has some cardiac S/E).
Ondansetron (Zofran)
233
_____ is given for N/V. It blocks dopamine receptors. It may cause QT prolongation, anticholinergic & antihistamine S/E (drowsiness!).
Promethazine (Phenergan)
| Metoclopramide (Reglan)
234
Extrapyramidal Sx (EPS) that may be brought on by dopamine blockers (for N/V) include:
Rigidity, bradykinesia, tremor, akathisia, dyskinesia (intermittent, sustained involuntary contractions including tongue protrusions, forced jaw opening, and facial grimacing)
235
_____ is the MC overall cause of gastroenteritis in adults in N. America.
Norovirus
236
Common causes of noninvasive (enterotoxin) infectious diarrhea include:
(Think voluminous, small intestine, no fecal WBCs or blood)
1. Staph aureus- food contamination MC source
2. Bacillus cereus- see above
3. Vibrio cholerae & Vibrio parahemolyticus- leads to severe dehydration!
- V.C.- think poor sanitation and overcrowding (esp. abroad)
- V.P.- associated with raw shellfish (esp. Gulf of Mexico)
* See copious watery diarrhea (grey "rice water stools")
* *Treatment: fluids, tetracyclines
4. E. coli- MC cause TRAVELER'S DIARRHEA. Think unsanitary drinking water/ice.
* Treatment: fluid replacement. If severe then fluoroquinolone.
5. C. diff- Nosocomial/iatrogenic. Usually after abx (esp. CLINDAMYCIN) or chemo.
* Presentation: Lymphocytosis, pseudomembranous colitis, & toxic megacolon
* *Treatment: Flagyl 1st line for mild dz, Vancomycin PO 1st line for severe dz!
237
Do not give ______ drugs with invasive diarrhea!
Anti-motility (may cause toxicity)
238
Invasive (infectious) diarrhea is associated with:
High fever, blood and fecal leukocytes, less voluminous (think large intestine), mucus
239
Some examples of invasive diarrhea include:
1. Campylobacter Enteritis- C. jejuni is MC cause of BACTERIAL ENTERITIS in US!
* Sources: undercooked poultry, raw milk
* *Sx: diarrhea--> first watery then bloody
* **Treatment: fluids, Erythromycin if severe
2. Shigella- fecal/oral contamination. Highly virulent!
* Sx: Explosive, watery diarrhea--> mucoid and bloody!
* *Dx: Fecal WBCs/RBCs. CBC--> WBC > 50,000; Sigmoidoscopy--> punctate areas of ulceration
* **Treatment: Fluids; if severe- Bactrim is 1st line
3. Salmonella- greater in summer months. MC source- poultry products, exotic pets (reptiles, turtles)
* High risk groups: immunocompromised, sick cell dz, kids, old
* *Treatment: fluids, if severe fluoroquinolones!
240
______ is a cause of invasive diarrhea that is associated with daycare centers, contaminated water, undercooked ground beef, and unpasteurized milk.
Enterohemorrhagic E. coli
241
Protozoan infections include:
1. Giardia lamblia- contaminated water from remote streams/wells.
* Sx: frothy, greasy, foul diarrhea (no blood or pus)
* *Treatment: fluids and flagyl
2. Amebiasis- MC seen in travelers to developing nations or in the immigrant population.
* Sx: GI colitis, dysentery, amebic liver abscesses
* *Dx: stool ova & parasites
* **Treatment: fluids, Flagyl, Tinidazole
3. Cryptosporidium- MC cause of chronic diarrhea in patients with AIDS (feco-oral transmission)
242
Osmotic v. Secretory Diarrhea
See p. 171/ look up
243
Whipple's Disease is MC in _____ around contaminated soil. Symptoms include:
Farmers
* Sx: malabsorption, weight loss, steatorrhea, rhythmic motion of eye muscles while chewing
* *Dx: Duodenal bx- dilation of lacteals
* **Treatment: Penicillin 1-2 years
244
Some causes of slow colonic transit (constipation) include:
idiopathic, motor disorders (CRC, DM, hypothyroid), S/E of many drugs like opioids, verapamil, outlet delay (Hirschsprung's dz)
245
Medical interventions for constipation
1. Fiber
2. Bulk forming laxatives: Benefiber, Citrucel
3. Osmotic laxatives: Miralax, Lactulose, Sorbitol, Milk of Mag/Mag Citrate
4. Stimulant laxatives: Dulcolax, Senna
246
What is the MC intestinal obstruction in infancy that increases with erythromycin use?
Pyloric Stenosis (rare >6 months!)
- If seen in adults it's associated with chronic ulcer disease
* Sx: non-bilious vomiting/regurgitation- projectile, hypochloremic metabolic alkalosis from vomiting, olive-shaped hard pylorus
* *Dx: US, Upper GI contrast- "string sign"
* **Treatment: IV fluids, potassium repletion, pyloromyotomy is the definitive management.
247
The most common cause of small bowel cancer is ____.
Carcinoid tumors- pretty rare
* MC in 60-68y black males
* *Intestinal obstruction is more common than perforation
* **Dx: CT, AXR
* ***Treatment: Surgical resection +/- chemo if METs
248
Pancreatic pseudocysts are associated with ____ (acute/chronic) pancreatitis and are usually found _____ (within/outside) the pancreas.
Chronic, outside
*Dx: transabdominal US, contrast CT and/or MRI
249
Bariatric surgery is indicated for patients between 21-55y with either a BMI ≥ ____ or a BMI > _____ with life-threatening comorbidities, and for whom supervised weight-reducing programs have failed.
40, 35
250
Examples of restrictive bariatric procedures include:
-Adjustable gastric banding (AGB), sleeve gastrectomy, and vertical banded gastroplasty
251
Examples of malabsorptive bariatric procedures include:
-Jejunal-ileal bypass or biliopancreatic diversion
252
2 most common types of bariatric surgery are ______ and ______.
1. AGB
| 2. Roux-en-Y Gastric Bypass (RYGB)- restrictive and malabsorptive
253
Nutritional complications of gastric bypass include:
Anemia (iron and B12), calcium deficiency, electrolyte deficiencies, dehydration, protein malnutrition
254
Some more about RYGB...
- Creates a gastric pouch with a 30mL holding capacity
- postoperatively patients may experience "dumping syndrome"--> abdominal cramps, N/V, flushing (esp. with sweets)
- associated with 75-80% excess weight loss
- associated with resolution of DM, HTN, OSA
255
Some more about AGB...
- placing a silicone band around upper portion of stomach
- a catheter connects the band to an injection chamber, implanted subcutaneously (band is gradually inflated postoperatively to progressively narrow the gastric inlet)
- NO intestines bypassed- no dumping syndrome
- 30-40% excess weight loss within a year. Long-term weight loss is about 50-55%. DM improvements
256
Which of the following typical findings would be revealed during a sigmoidoscopy on a patient with Crohn's disease of the intestine?
Intermittent, longitudinal mucosal ulcers and fissures- Ulcerations tend to be linear with transverse fissures in Crohn's disease. These skip lesions are common with Crohn's disease.
