Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI and Liver > GI Deck 2 > Flashcards

GI Deck 2 Flashcards

1
Q

What is the target of Ghrelin?

A

Hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where is ghrelin produced?

A

Stomach/ proximal small bowel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What ist he action of ghrelin?

A

Increases food intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where is GLP1 produced?

A

Distal small bowel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the target of GLP 1?

A

Stomach, pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the funciton of GLP 1?

A

Decrease gastric emptying, decrease food intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the target of PYY?

A

Stomach, Pancreas, CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where is PYY produced?

A

Distal small bowel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the action of PYY?

A

Decrease gastric emptying

Decrease food intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the target of CCK?

A

Stomach, CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

WHere is CCK produced?

A

Proximal small bowel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is teh action of CCK?

A

Decreases gastric emptying

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What peptide correlates with fat/energy stores and is important in obesity?

A

Leptin - obese humans have high leptin levels so obesity is a state of leptin resistance

Leptin deficient mice are morbidly obese

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are risk stratification measures for obesity (i.e. what defines Metabolic Syndrome)?

A

3 or more abnormal:

Central obesity
Blood pressure

Triglycerides

HDL cholesterol

Fasting Blood Glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What diabetes medications promote weight gain?

A

Insulin

Sulfonylureas

Pioglitazone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What depression medications increase weight?

A

Paroxetine
Amitriptyline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What psychosis medicatiosn increase weight?

A

Olanzapine

Quietapine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What antihypertensives increase weight?

A

β-blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What contraceptives increase weight?

A

Depo-Provera

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What migraine medications increase weight?

A

Amitriptyline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What Diabetic medicaitons are weight neutral?

A

Metformin

Exenatide

Liraglutide

Pramlintide

Canagliflozin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What antidepressants are weight neutral?

A

Buproprion

Fluoxetine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What antipsychotics are weight neutral?

A

Ziprasidone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What antihypertensives are weight neutral?

A

Thiazide diuretics

ACE inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What contraceptives are weight neutral?

A

Ortho Evra

Ortho Tri Cyclen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What antimigraine meds are weight neutral?

A

Nortriptyline

Topiramate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Which patients do we recommend bariatric surgery?

A

BMI >35 with comorbid conditions OR BMI > 40

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

For which patients is medication recommended to treat obesity?

A

BMI >27.5 with comorbid conditions OR >30

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are tips for successful weight loss?

A

Exercise, modify caloric intake

(Watch less TV, weigh yourself, eat breakfast)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is a very low calorie diet defined as?

A

400-800 calories per day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is a low calorie die defined as?

A

800-1500 calories per day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is a balanced diet defined as?

A

>1500 calories per day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What defines starvation diet?

A

0-400 calories per day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Does exercise cause weight loss?

A

Not in and of itself, unless you exercise 2.5+ hours per day

Energy expenditure of physical activity is only 20%, remember

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is orlistat?

A

Lipase inhibitor that prevents lipid digestion - causes steatorrhea

Obesity treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are phentermine and diethylpropion used for in nutrition?

A

For obesity/weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Are bariatric surgeries effective?

A

YES, very much so

And weight loss is maintained

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What factors regulate GI motility?

A

CNS and ANS

ANS - Sympathetic, Parasympathetic, and Enteric NS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What ANS factors regulate GI motility?

A

Sympathetic - fight or flight - inhibit digestion

Parasympathetic - stimulate digestion via vagus nerve

Enteric Nervous System

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are voluntary responses iof the Brain-Gut axis (CNS)?

A

Control of swallowing

Contraction of the external anal sphincter

(skeletal muscle based)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are involuntary muscle responses of the Brain-Gut axis (CNS)?

A

Emotion

Stress associations

Conditioned responses

(Smooth muscle mediated)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are parasympathetic inputs to the GI?

A

Vagus up until distal 2/3 of colon (via ACh)

Sacral plexus for the last 1/3 of colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are sympathetic inputs ot the GI?

A

Superior cervical gangion

Thoracolumbar - Prevertebral ganglion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Where is Myenteric Plexus (Auerbach’s) located?

A

Between longitudinal and circular muscle layers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Where is the Mucosal (Meissner’s) Plexus located?

A

Between circular muscle layer and submucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Where is skeletal muscle located in the GI?

A

Pharynx

Upper esophageal sphincter

Upper 1/3 of esophageal body

External anal sphincter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Where is smooth muscle located in the GI tract?

A

Lower 2/3 of esophagus

Stomach

Small and large intestine

Internal Anal sphincter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What can go wrong in the GI system that can cause defects in motility?

A

Muscle

Nerve

Brain-gut axis

Structural vs functional issues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are symptoms of problems with GI motility?

A

Nausea/Vomiting

Pain

Early satiety

Diarrhea

Constipation

Diarrhea alternating with constipation
Gas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the origin of the motility of the GI tract?

A

Electrical activity - Slow waves with spike activity

Slow waves provide constant background rhythm that is propagated down GI tract and control phasic contractions (each organ has characteristic slow wave frequency)

Spike activity occurs when threshold for action potential is reached, causing rapid depolarization that results in contractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are the pacemaker cells of the gut?

A

Interstitial cells of Cajal (ICC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What are GISTs?

A

GI stromal tumors - tumors of the interstitial cells of Cajal - may lead ot GI motility issues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are interstitial cells of Cajal (ICC) cells?

A

Pacemakers of the gut

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Which part of the gut has the highest frequency of electircal activity?

A

Small intestine - more going on

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Which segmetn of the GI tract has the slowest frequency electrical activity?

A

Stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What are the two major type of contractions in the small intestine?

A

Peristalsis - slow proximal to distal movement

Segmentation - major contractile acitivity - contraction of circular smooth muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is segmentation?

A

Major contractile activity of the small intestine - circular smooth muscle contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is the major contractile activity of the small intestine?

A

Segmentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What controls Peristalsis?

A

5HT, Substance P, Nitric oxide, ACh

Controled by a switch or gate that commands neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How do the motor functions of the stomach differ between fundus/body and antrum?

A

Fundus/body is more receptive relaxation and acts as a reservoir

The antrum mixes and grinds food which is vagally mediated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What area of the stomach regulates the emptying of liquids?

A

Fundus and body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What area of the stomach regulates the emptying of solids?

A

Antrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are some causes of gastroparesis (slow gastric emptying)?

A

Diabetes

Thyroid disease

Connective tissue disorders

Pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is a motility issue commonly seen in diabetes?

A

Gastroparesis (slow gastric emptying)

Exacerbated by elevated blood sugar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What causes accelerated gastric emptying?

A

Dumping syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

How does the small bowel motility change between fed and fasting states?

A

Fed - segmental, promotes mixing and absorption of food

Fasting - cyclic, keeps intestine swept clean of bacteria and other tissue - Migrating Motor Complex (MMC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is the migrating motor complex?

A

“Housekeeper of the GI tract)

Turned off during a meal - so that segmentation can occur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are neurologic factors that can cause small bowel dysmotility?

A

Parkinson’s

Post-viral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What are smooth muscle issues that can cause small bowel dysmotility?

A

Collagen vascular disease

Systemic sclerosis

Polymyositis

Amyloidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are endocrine issues that can cause small bowel dysmotility?

A

Diabetes

Hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are drugs that can cause small bowel dysmotility?

A

Opiates

Anticholinergics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What are myenteric plexus disorders that can cause small bowel dysmotility?

A

Visceral neuropathies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is chronic intestinal pseudoobstruction (CIIP)?

A

Diffuse problem that can affect the small bowel in its entirety

Myopathy (familial, collagen vascular, amyloid) or enteric neuropathy (Hirschsprungs, Chagas, Paraneoplastic, Idiopathic)

Abdominal pain, N/V, anorexia, diarrhea, malnutrition, weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What are the two patterns of motor activity of the colon?

A

HAPC (High amplitude propagating contraction)

LAPC (Low amplitude propagating contraction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What are LAPCs?

A

Low amplitude propagating contractions

Amplitude < 50 mmHg

Occur frequently to transport fluid contents of the large intestine

Associated with distension and flatus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What are HAPCs?

A

High amplitude propagating contractions

Amplitude > 100 mmHg

Occur infrequently and function to move masses

Strongly associated with defecation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

When can you see constipation/

A

Normal

Irritable Bowel Syndrome

Metabolic
Colonic inertia

Pelvic floor dysfunction (megarectum, structural/funcitonal, dyssynergia/anismus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is functional constipation?

A

Chronic constipation that includes at least 2 of :

Straining for >25% of defecations

Lumpy/hard stools

Incomplete evacuation

Anorectal obstruction/blockage

Manual maneuvers needed

< 3 defecations per week

Rarely include loos stools

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is Ogilvie’s Syndrome?

A

Acute pseudoobstruction

Non-obstructive colonic dilatation due to drugs, post-op state, immobility, electrolyte imbalances

Treat the underlying condition, and perhaps decompress the colon if necessary

Neostigmine can be used to stimulate parasympathetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is irritable bowel syndrome?

A

Recurrent abdominal pain or discomfort at least 3 days/month associated with 2+ of:

Improvement with defecation

Change in stool frequency

Change in stool appearance/form

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What is the difference between irritable bowel syndrome and functional constipation?

A

Pain = IBS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What causes the pain in Irritable bowel syndrome?

A

Visceral hyperalgesia

Increased motor reactivity, altered visceral sensation, involves small and large intestine, CNS-ENS dysregulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is the pathophysiology of irritable bowel syndrome?

A

Hyperalgesia of the bowels - increased sensitivity to pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

How do enterochromaffin cells help motility?

A

Stimulate interneurons (increased transit) and epithelium cells (secretion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

How is serotonin involved in dysmotility?

A

5-HT is important in motility and in secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

How do you approach irritable bowel syndrome patients?

A

Reassurance and education

Dietary and behavior modification

Pharm = laxatives, antidiarrheals, antidepressants, 5-HT receptor agents

Psychological treatments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What is defecation?

A

Propagation of intraluminal contents to rectum followed by sensation of fullness

Internal anal sphincter relaxation and external anal sphincter contraction

Anorectal angle straightens, with straining, puborectalis muscle and EAS relax, pelvic floor descends and anorectal angle straightens further

After elimination, tonic activity returns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

During defacation does the internal anal sphincter relax or contract? What about external anal sphincter?

A

Internal = relax

External = contract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What muscles maintain continence?

A

Internal anal sphincter (70%) - continuation of colon

External anal sphincter (30%)

Levator ani muscles

Rectal curvature and transverse rectal folds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Does the internal anal sphincter contain smooth or striated muscle?

A

Smooth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Does the external anal sphincter contain smooth or striated muscle?

A

Both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What is fecal incontinence?

A

Release of rectal contents against one’s wishes (7.9% of population)

More common in women, elderly and institutionalized individuals

Not often volunteered

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What are things that can factor into incontinence?

A

Functional abnormalities

Structural abnormalities
Other

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

How do you treat fecal incontinence?

A

Anti-diarrheals

Bowel training/biofeedback

Surgery (last resort)

Depends on cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

How do you evaluate motility disorders?

A

Contrast radiography

Scintigraphy

Electrogastropathy

Hydrogen Breath Test

Sitz Marker Studies

Manometry

Defecography

MR Defecography

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

How does visceral abdominal pain present?

A

Vague, poorly localized

Dull, aching, burning, gnawing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What type of pain is vague, poorly localized and can be identified as dull, aching, burning, gnawing?

A

Visceral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

How does somatic or parietal pain present?

A

Pinpoint, well localized

Sharp or stabbing pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What type of pain presents as pinpoint, well localized, with sharp or stabbing quality?

A

Somatic or parietal pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Why is visceral pain dull and poorly localized?

A

Visceral afferent nerves are few in number and are bilaterally represented

They diverge over several (up to 8) spinal segments when they enter the spine

They converge in dorsal roots with afferents from different locations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What can stimulate visceral nerves?

A

Distention

Traction

Pressure

Smooth muscle contraction

Ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What can lower the pain threshold in visceral and somatic afferents?

A

Local ischemia and inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What is the effect of local ischemia and inflammation on the pain threshold in visceral and somatic afferents?

A

Lowers the threshold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Why is somatic pain well-localized and sharp in nature?

A

There are numerous afferents that are unilaterally represented

They are highly segmental (travel at somatic levels)

Present in abdomina lwall, diaphragm, mesenteric roots, and superior hepatic ligaments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What can epigastric pain be indicative of?

A

Somtach, duodenum, gallbladder, pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What does right upper quadrant pain indicate?

A

Duodenum, gallbladder, pancreas, right kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

What does left upper quadrant pain indicate?

A

Pancreas, left kidney, stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What does central abdominal pain indicate?

A

Pancreas, small bowel, appendix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What does lower right quadrant pain indicate?

A

Right colon, appendix, terminal ileum, right ureter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What does left lower quadrant pain indicate?

A

Left colon, ureter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What does lower abdominal pain indicate?

A

Colon, bladder, uterus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What does left shoulder pain indicate?

A

Central left diaphragm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What does right back shoulder pain indicate?

A

Liver, hepatic ligaments, central right diaphragm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What does middle back pain indicate?

A

Pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What does mid/upper right back pain indicate?

A

Gall bladder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What does lower back pain indicate?

A

rectal pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

What is the visceral pain reflex phenomena?

A

Visceral pain by peripheral and autonomic nerves at the level of entry into the spinal cord that leads to:

Decreased bowel motility (reflex sympathetic ileus)

Reflex contraction of skeletal muscle and adjacent spinal segments (involuntary guarding)

Changes in local blood flow and sweating

Lowering of cutaneous nerve endings’ pain threshould (cutaneous hyperesthesia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

What does appendicitis feel like at first?

A

Periumbilical diffuse pain

Can also feel generally sick, or not well (poorly described)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What is the pathophysiological cause of appendicitis?

A

Luminal obstruction (fecalith may be present) causes increased intraluminal pressure that causes increased wall tension and distension (visceral pain and local inflammatory response)

Venous pressure is then exceeded, which causes a vicious cycle of increasing pressure -> distension -> …

This leads to ulceration of mucosa, bacterial translocation, peritoneal inflammation with ischemia, followed by gangrene and/or perforation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

What is the most common site of diverticulosis?

A

Colon - not small bowel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What are causes of diverticular disease?

A

Low fiber “western” diet

“western” sedentary lifestyle

Leads to slow colonic transit and increased intraluminal pressures

This combination leads to hard, dry stools that requires increased work to propel feces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

What happens to the colon in the pathophysiology of diverticular disease?

A

Muscular hypertrophy (chicken or egg?)

Segmentation of the sigmoid colon

Increased intraluminal pressure that is transmitted to the colonic wall

Resulting in herniation of the mucosa and submucosa at points of weakness (pseudo-diverticula)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Where are weak points in the colon that are susceptible to diverticula?

A

The places where the blood vessel invades the muscularis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

What are sequellae of diverticular disease?

A

Similar to appendicitis (can engorge, swell, perforate, infect, etc)

Can ulcerate, bleed, etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

What are symptoms of diverticular disease?

A

Majority are asymptomatic, but:

Crampy abdominal pain

Left lower quadrant pain (commonly in sigmoid colon)

Constipation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

What area of the colon is diverticulosis more common?

A

Sigmoid colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

What are some symptoms of diverticular disease?

A

Pain, fever, leukocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

What is needed for a diagnosis of diverticulosis?

A

History, physical, CT scan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

What are treatment options for diverticulosis (diverticular disease)?

A

Antibiotics

Increased fiber in diet

Avoid constipation

Surgery for multiple recurrences or fistulae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

What is diverticular bleeding?

A

Erosion of arteriole at the mouth of the diverticulum

Painless, but typically presents with brisk rectal bleeding (not occult)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

How do you diagnose diverticular bleeding?

A

Colonoscopy or CT/MRI Angiography (may be hard to localize which diverticulum is bleeding)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

How do you treat diverticular bleedign?

A

Most will stop on their own (caution against aspirin or anti-platelet agents)

Colonoscopic cauterization

Angiographic embolization

Surgery if refractory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

What is the goal of the history and physical exam in GI bleeds?

A

To distinguish upper vs lower bleeds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

What does hematemesis indicate?

A

Upper GI bleed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

What does coffee-ground emesis indicate?

A

Upper GI bleed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

What does melena indicate?

A

Upper more often than lower GI bleed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

What is hematochezia indicative of?

A

Lower or massive upper GI bleed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

What are vital sign abnormalities in GI bleed patients?

A

Hypotension, tachycardia - hypovolemia from blood loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

What do you see on CBC in acute bleeds?

A

May have delay in hematocrit drop (since you lose whole blood

INitial hematocrit may not reflect degree of blood loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

Why do you get elevated BUN in GI bleeds?

A

From hypovolemia and absorbed blood protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

What does an elevated BUN indicate?

A

Upper GI bleed - absorbed blood protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

Why is NG tube lavage not reliable?

A

False negatives - tube coiled in stomach, but bleed is from duodenum

False positives - blood from trauma of passing the tube

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

What are some hints for the source of an Upper GI Bleed?

A

Aspirin or NSAID use

Hx of peptic ulcer disease

Presence of liver disease (varices, gastropathy)

Preceding retching (Mallory-Weiss tear)

GERD symptoms (esophagitis)

Prior Aortic aneurysm surgery (aorto-enteric fistula)

Weight loss (neoplasm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

What is hematochezia?

A

Red/maroon blood, sometimes with clots, usually associated with frequen BM or passage of pure blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

What is overt bleedign?

A

Actually see blood in stool

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

What is occult bleedign?

A

Microscopic blood in stool over weeks to months produces anemia and iron deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

What anatomical structure differentiates upper from lower GI bleed?

A

Upper - proximal to ligament of Trietz

Lower - Ileocolonic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

Why do you perform endoscopy for GI bleeds?

A

Locate the bleed

Endoscopially treat the bleed

Prognostically evaluate patient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

What is the most commoon source of upper GI bleeds?

A

Peptic ulcer disease (gastric or duodenal)

Majority due to H pylori and/or NSAIDs/aspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

How many GI bleeds do not spontaneously stop?

A

20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

What are some danger signs of upper GI bleeds?

A

Shock

Number of units of packed RBCs transfused

age > 60

Comorbidities

Melena and hematochezia (big vessel)

Active bleeding or large ulcer seen on EGD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

How do you treat GI bleeds due to peptic ulcer disease?

A

Fluid resuscitation, IV PPI, urgent/emergent endoscopy

Surgery is reserved for failure of medical therapy

Stop NSAIDs, look for H. Pylori

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

What is this?

A

Erosive Gastritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

What is this?

A

Hemorrhagic Gastritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

What type of GI bleed do neoplasias typically cause?

A

Chronic bleeds - less comonly present with melena or hematemesis

Therapy is surgical, Chemo/RT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

What is a Mallory-Weiss tear?

A

Retching leads to mucosal tear at E-G junction.

Usually self-limited

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

Why do bleeding varices carry high mortality rate?

A

Lots of blood, also, you have the underlying causes that led to them too

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

What is this?

A

Mallory-Weiss Tear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

What is this?

A

Esophageal Varices

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

What is a Dieulafoy lesion?

A

Large caliber artery, usually present with significant bleeding that can start and stop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

What is GAVE?

A

Gastric Antral Vascular Ectasia (Watermelon stomach)

Dilated mucosal vessals, more commonly seen in renal patients, elderly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

What is Aorto-Enteric fistula?

A

Massive bleedign in patient with prior aortic graft (aneurysm, etc) that erodes into duodenum

Can have Herald bleed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

What is a herald bleed?

A

Initial significant bleed that stops, only to recur massively

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

What are Cameron Lesions?

A

Erosions or ulcerations that occur within a hiatal hernia

Can lead to iron deficiency anemia

Rare cause of hematemasis or melena

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

What is this?

A

Watermelon stomach (GAVE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

What are endoscopic therapies for GI bleeds?

A

Injection therapy (epinephrine, sclerosing agents)

Hemostatic therapy (cauterizing shut the bleed)

Band ligation

Clips

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

How does Lower GI bleed present?

A

Usually with hematochezia, frequently stops spontaneously or bleeds intermittently

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

What are most common causes of lower GI bleeds?

A

Chronic:
Hemorrhoid - painless blood on tissue or in bowl
Fissure - tearing/ripping as BM passes anal canal

Colitis - urgency, tenesmus, diarrhea, mucus

Polyp - blood mixed with stool

Acute:

Diverticulosis

Arteriovenous malformations (AVMs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

Are hemorrhoids or anal fissures more painful?

A

Anal fissures - hemorrhoids are typically painless

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

How do you diagnose anal fissure?

A

Physical exam - spread buttocks, valsalva makes dentate line visible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

What is the first line diagnostic evaluation of lower GI bleeds?

A

Colonoscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

How do nuclear scans work for diagnosing lower GI bleeds?

A

Technetium labeled RBC scan

20 mL of blood drawn, tagged with Tc-99m, reinjected and scanned at intervals

Can be repeated within 24 hours if the patient rebleeds

Can detect bleeding at low levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

What is the difference between angiography and nuclear scans?

A

Angiography requires greater blood volume bleeds to be seen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

What is a benefit of angiography?

A

Can allow for intervention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

What are drawbacks of angiography?

A

Require high bleeds

Has up to 10% rate of complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

What is “Obscure” GI bleedign?

A

Not upper or lower endoscopically visualized

Typically Small Intestinal:

Vascular (AVM)

Neoplastic

Inflammatory

Meckel’s Diverticulum

Biliary

Pancreatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

What is significant about Meckel’s diverticulum wrt bleeds?

A

Most common cause of bleeds in patients < 3 years old and in small bowel bleed cases in men < 30 years old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

What is a Meckel’s Scan?

A

Tc-99m injected, accumulates in gastric mucosa

Can be considered early in workup of obscure GI bleed in younge otherwise healthy patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

How do you visualize the small bowel?

A

Push enteroscopy - can’t visualize most of it

Intra-operative endoscopy - high rate of complications

Capsule endoscopy - camera in a pill

Double-balloon method

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

What are TLESRs?

A

Transient lower esophageal sphincter relaxations - major cause of GERD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

What is the effect of cholinergic/anticholinergic drugs on the LES pressure?

A

Cholinergics increase LESp, Anti-cholinergics decrease LESp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

What is the effect of progesterone on the LES pressure?

A

Decreases LESp

Significant in pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

What is the role of gastrin on parietal cell acid secretion?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

What is the role of histmaine on parietal cell acid secretion?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

What is the role of acetylcholine on parietal cell acid secretion?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

What is the role of somatostatin on parietal cell acid secretion?

A

Feedback inhibition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

What is the primary acid producing cell in the stomach?

A

Parietal cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

What is the basal stomach pH?

A

2-Jan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

What is post-prandial stomach pH?

A

4-5 (around 1 hour after eating)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
190
Q

What are defense mechanisms that allow the stomach to not eat itself?

A

Tight junctions b/w gastric epithelial cells

Mucin layer overlying cells

Bicarb ions secreted into mucin layer

Prostaglandins (stimulate mucus production, epithelial cell repair, bicarb, and mucosal blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
191
Q

What are drugs that control gastric acidity?

A

Antacids

Cytoprotectants

H2 receptor antagonists

PPIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
192
Q

How do antacids work?

A

Local neutralization of acid

Aluminum hydroxide, magnesium hydroxide, calcium carbonate, sodium bicarbonate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
193
Q

What is aluminum hydroxide?

A

Antacid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
194
Q

What is magnesium hydroxide?

A

antacid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
195
Q

What is calcium carbonate?

A

antacid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
196
Q

What is sodium bicarbonate?

A

Antacid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
197
Q

What are the cytoprotectants?

A

Sucralfate

Misoprostol

Bismuth compounds

198
Q

How do cytoprotectants work?

A

Bind to base of ulcer

Promote mucin and bicarbonate production

Has some antibacterial effects

May produce melena - tell patients its ok

199
Q

What is misoprostol?

A

Prostaglandin E analog

Stimulates secretion of mucin and bicarb

Increases mucosal blood flow

Can have diarrhea nad abdominal cramps due to smooth muscle contraction; increased uterine contraction (contraindic. in pregnancy); used in combination for medical termination with MTX or mifepristone

200
Q

What is a non-indicated use of misoprostol?

A

Abortion, when used in combination with methotrexate or mifepristone

201
Q

How do H2 receptor antagonists work?

A

Competes with histmaine for receptors on parietal cells

(Cimetidine, Ranitidine, Famotidine, Nizatidine)

202
Q

What is cimetidine?

A

H2 receptor antagonist

203
Q

What is ranitidine?

A

H2 receptor antagonist

204
Q

What is famotidine?

A

H2 receptor antagonist

205
Q

What is Nizatidine?

A

H2 receptor antagonist

206
Q

When are H2 receptor antagonists indicated?

A

Gastric and duodenal ulcers

Uncomplicated GERD

Stress ulcer prophylaxis

207
Q

What are drug interactions of H2 receptor antagonists?

A

Interfere with absorption of drugs that require acidic environment

Cimetidine inhibits CYP450

208
Q

What is omeprazole?

A

PPI

209
Q

What is lansoprazole?

A

PPI

210
Q

What is rabeprazole?

A

PPI

211
Q

What is pantoprazole?

A

PPI

212
Q

What is esomeprazole?

A

PPI

213
Q

What are drugs that end in -prazole?

A

PPIs

214
Q

How do PPIs work?

A

Pro-drug that requires protonation in acidic environment

Must be enteric coated since parent compound is unstable

Irreversibly binds to and inactivates H/K ATPase in parietal cell (doesn’t “kill” parietal cell)

IF release not affected

215
Q

Do PPIs affect Intrinsic Factor release?

A

NO

216
Q

What conditions are PPIs used for?

A

Gastric and Duodenal ulcers

GERD

Zollinger-Ellison Syndrome

IV for upepr GI bleeding

217
Q

What are adverse effects of PPIs?

A

Hypergastrinemia - ECL hyperplasia - rare risk of gastric carcinoid

Increase C diff and other infections

Interaction with clopidogrel via CYP450

Increased risk of osteopnia and osteoporosis

218
Q

What is Celecoxib used for in GI ?

A

COX1 is predominant in gastric cells leading to produciton of PGs that enhacne mucous production

COX 2 is important in mediating systemic inflammation

COX2 is less likely to cause gastro-duodenal injury

Celecoxib is COX 2 selective inhibitor

219
Q

What is the location of the panreas?

A

Retroperitoneal, 4-5th lumbar spine

220
Q

Wqhat ist he arterial supply of the pancreas?

A

Gastroduodenal

SMA

Splenic artery

221
Q

What is the venous drainage of the pancreas?

A

Portal Vein

Splenic Vein

222
Q

What are the nerves that innervagte the pancrease?

A

Vagal (stimulatory)

Sympathetic (inhibitory)

223
Q

How does the pancreas devlelop?

A

5 weeks - two buds

6-7 weeks, twisting

8 weeks - joining of buds

224
Q

Where does the main pancreatic duct drain?

A

Major papilla

225
Q

Where does the accessory pancreatic duct drain?

A

minor papilla

226
Q

What structures join at the major papilla?

A

Bile duct, pancreatic duct

Each has sphincter. Sphincter of Oddi does both

Papilla of Vater is another name for this area

227
Q

What percentage of the function of the pancreas is endocrine vs exocrine?

A

Endocrine 2%

Exocrine = rest

228
Q

How is pancreatic bicarb secretion regulated?

A

Acid to S cells in duodenum release secretin which activates pancreatic duct cells to produce bicarb

229
Q

How does CCK regulate pancreatic enzyme release?

A

Amino acids and peptides activate endocrien cells of duodenum which release CCK

These act on the acinar cells of pancreas, which release enzymes

230
Q

What pancreatic cells does CCK act on?

A

Acinar cells

231
Q

What pancreatic cells does secretin act on?

A

Ductal cells

232
Q

What is the major enzyme output of the pancreas

A

Proteases

To lesser degree lipases, glycosidases, nucleases

233
Q

How do pancreatic zymogens get activated?

A

Enterokinases activate trypsinogen to trypsin, which can in turn catalyze reactions from other zymogens to active enzymes

Enterokinase only in duodenal brush border

234
Q

What are mechanisms by which the pancreas protects itself from its own degradation?

A

Synthesis of enzymes as zymogens

Trypsin inhibitor packaged into zymogen granule

Segregation of enzymes in membrane-boudn compartments

Enterokinase restricted to small intestine

235
Q

What are mechanisms of acute pancreatitis?

A

Insult causes ischemia whcih causes inflammation, zymogen activation, systemic inflammation, death. etc..

236
Q

What is teh pathologic activation cascade?

A

When you get trypsinogens converted to trypsin not in the duodenum… This causes cascade of zymogen activation that can be disastrous

237
Q

What causes pancreatitis?

A

Gallstones (45%) - older patients, more common in females

Alcohol (35%) - younger patients, more common in men

238
Q

What are etiologies of acute pancreatitis?

A

Drugs

Trauma

Metabolic

Obstruction (stones, etc.)

Pregnancy

Infection

ESRD

Scorpion bite

Idiopathic

Miscellaneous (autoimmune, other)

239
Q

How can gallstones cause acute pancreatitis?

A

Common bile duct stone that obstructs both ducts

240
Q

How can alcohol cause acute pancreatitis?

A

Intracellular accumulation of pancreatic enzymes

Increased permeability of ductules

Increased tendency to form protein plugs causing obstruction

241
Q

What is a condition where you have a mismatch between pancreatic duct and the papilla that is supposed to drain it?

A

Divisum - ducts are not fused; man pancreatic duct drains through minor papilla

Can cause pancreatitis

242
Q

What is ERCP?

A

Endoscopic Retrograde Cholangio-pancreatography

Scope that gives you view of papilla. Can inject dye and see how it drains

243
Q

What are clinical features of acute pancreatitis?

A

Pain is ALWAYS present; may radiate to back

N/V common, fever

Peritoneal signs are generally absent (not really guarding)

Ileus may arise due to extenison into small intestinal and colonic mesentery

244
Q

What are lab values that you can see in pancreatitis?

A

Leukocytosis

Hyperamylasemia

Hyperlipasemia

245
Q

What are things on the differential for pancreatitis?

A

Choledocholithiasis

Perforated ulcer

Mesenteric ischemia

Intestinal obstruction

Ectopic pregnancy

246
Q

What forms of pancreatitis are more likely to cause organ failure?

A

Necrotizing pancreatitis (54%)

247
Q

What is systemic inflammatory response syndrome?

A

SIRS

2+ of:

Pulse > 90

RR > 20 or PCO2 <32 mmHg

Rectal Temp <36 or >38

WBC < 4000 or >12000

248
Q

How do you diagnose acute pancreatitis?

A

Clinical picture + lab values +/- imaging

Increased amylase and lipase 3x normal

Lipase is more specific

Check renal clearnace

249
Q

How do you predict who does well vs poorly in pancreatitis?

A

Ranson’s criteria
APACHE II score

Serum hematocrit

and others

Gold standard = Ranson’s

250
Q

What imaging modalities are useful for pancreatitis?

A

CT w/ contrast (edema and stranding)

Ultrasound for detection of stones

MRCP - MRI equivalent of ERCP - non-invasive

ERCP - invasive - sedated

251
Q

What do you see here?

A

Gallstone pancreatitis

252
Q

What can you look for to ensure gallstone pancreatitis diagnosis?

A

Transient elevation in liver chemistries

Ultrasound

Bile aspiration analysis - check for crystals

MRCP

ERCP

253
Q

How do you treat interstitial pancreatitis?

A

Resuscitate fluids (lots of fluids)

Rest the pancreas (NPO)

Pain control

Maintain nutrition

Address underlying cause (stones, drinking, offending agent if drug)

254
Q

What is short-term treatment for stone disease as root of pancreatitis?

A

ERCP

255
Q

What is a long-term treatment for stone releated pancreatitis?

A

Cholecystectomy

ERCP is for short term

256
Q

What is a concern with necrotizing pancreatitis?

A

Organ failure

Infection - do gram stain, etc

257
Q

What are local complications of pancreatitis?

A

Pseudocyst - no epithelial lining so not a true cyst; mostly asymptomatic, causes early satiety if it compresses stomach/duodenum. Drain it by endoscopy

Abscess

HEmorrhage

258
Q

How do you identify/treat pseudocyst as a result of pancreatitis?

A

>4 weeks after actue pancreatitis

Mostly asymptomatic

But can have early satiety if it infringes on duodenum or stomach

Drain it by endoscopy interventional radiology or surgery

259
Q

What are systemic complications of acute pancreatitis?

A

ARDS - Acute Respiratory Distress Syndrome

DIC

Renal Failure (part of multi-organ failure)

Treat with broad spectrum Abx

Intubate

Supportive care

260
Q

What is chronic pancreatitis?

A

Chronic inflammation with irreversible morphologic changes that can lead to lsos of exocrine and endocrine function

261
Q

What is the #1 cause of chronic pancreatitis?

A

Alcohol

262
Q

What are causes of chronic pancreatitis?

A

1 - alcohol

Otehrs: Tropical; pancreas divisum; autoimmuen; neoplastic; etc.

263
Q

What is the abnormal secretion theory for the pathogenesis of alcoholic pancreatitis?

A

Protein plugs cause decreased lithostatine (pancreatic stone protein), leads to progressive blockage of ducts

264
Q

What ist he necrosis-fibrosis theory of alcoholic pancreatitis pathogenesis?

A

Acute attacks of pancreatitis lead to necrosis -fibrosis of the duts results with obstruction

265
Q

How do you diagnose chronic pnacreatitis?

A

Severe pain radiating to back - daily pain with exacerbations or painfree intervals between exacerbations

Steatorrhea and weight loss and FLAT PLATE X-RAY to check for calcifications

MRCP/ERCP and ultrasound can help

Secretin stimulation test - rarely done

266
Q

What do you see here?

A

Chronic pancreatitis

Calcifications

267
Q

How do you treat pain in chronic pancreatitis?

A

Stop alcohol!

Analgesics (non narcotics or narcotics)

Pancreatic enzymes to reduce CCK secretion (non-enteric coated - give w/ PPI)

Invasive procedures (nerve block, endoscopic decompression, surgical drainage)

268
Q

How do you treat malabsorption of chronic pancreatitis?

A

Pancreatic enzyme

Decrease dietary fat

Substitute medium chain triglycerides

269
Q

What are complications of chronic pancreatitis?

A

Pseuydocyst

Diabetes

Steatorrhea

Obstruciton of bile duct

Duodenal obstruction

Pancreatic ascites or adenocarcinoma

270
Q

What is the most common pancreatic neoplasm?

A

Adenocarcinoma

271
Q

Who gets pancreatic neoplasms?

A

Men in 60s, smokers

272
Q

Where in the pancreas do neoplasmsm typically present?

A

2/3 of head of gland

1/3 body/tail of it

273
Q

What are clinical features of pancreatic neoplasms?

A

Painless jaundice

Nonspecific symptoms (abdominal pain, anorexia, N/V, depression, new onset diabetes)

Phys exam - jaudnice - Courvoisier’s sign (palpable gallbladder)

274
Q

How do you diagnose pancreatic carcinoma?

A

CT/MRI

275
Q

How do you treat pancreatic carcinoma?

A

Surgery, chemotherapy

ERCP with stent to palliate pruritus

276
Q

What are nonpancreatic carcinoma pancreatic neoplasms?

A

Pancreatic Neuroendocrine tumors (PNETs)

Functioning - gastrinoma, insulinoma, glucagonoma, VIPoma

Diagnosis with EUS, octreotide scan

Treat with octreotide, surgical resection, chemoembolization

277
Q

What are unique features of the biliary tract?

A

Tri-section of hepatic, pancreatic, and intestinal tracts

Repercussions of all three systems

Biliary tract - except for gallbladder, it is essential for life

278
Q

What are components of bile?

A

Mostly water

Bile salts, phospholipids, cholesterol and other components make up the rest

279
Q

Where is bile made?

A

Liver

280
Q

What does bile do?

A

Secretory - carries stuff body needs to function - micelle-forming bile acids, phospholipids, IgA

Excretory - produces stuff body gets rid of - cholesterol, bile pigments, trance minerals, plant sterols, etc etc

281
Q

What factors affect bile flow?

A

Liver function

Concentration of bile acids in bile

Other ATP dependent pumps

The gall-bladder (can sequester bile in fasting state)

Biliary tree patency, sphincters, motility

Small intestinal patency and motility

282
Q

What is the effect of bile acids on bile flow?

A

Induces further flow of bile - greater concentraiton of bile acids, greater flow of bile

283
Q

What is the role of bile acids in the liver?

A

Induces bile flow (bile acid-dependent role)

Transports cholesterol and phospholipids - micelles

284
Q

What is the role of Bile acids in the intestines?

A

Fat digestion

Catharsis - move bowels

285
Q

What is the chemical feature of bile salts that is important in its funciton?

A

Ampiphilic - works as detergent (polar and non-polar portions)

286
Q

What is an important precursor in the formation of bile salts?

A

Cholesterol

287
Q

What are the primary bile acids?

A

Chenodeoxycholic acid and Cholic acid

288
Q

What are the secondary bile acids?

A

Deoxycholic

Lithocholic

289
Q

What is the enterohepatic circulation of bile salts?

A

Secreted into bowels, reabsorbed

Only <5% is made again, so need to absorb 95% of it

290
Q

Where are bile salts absorbed?

A

Predominantly in ileum - some in jejunum and colon

291
Q

What is the function of hepatocyte canaliculus in biliary tract?

A

bile formation

292
Q

What is the funciton of ductules and ducts in the biliary tract?

A

Modificaiton of bile (absorption and secretion

293
Q

What is the fucntion of the gallbladder in the biliary tract?

A

Concentration

Storage

Controlled delivery (CCK)

294
Q

What is the funciton of the sphincter of Oddi in the bililary tract?

A

Regulated delivery of bile to duodenum

Prevention of reflux

295
Q

What is the role of CCK in biliary tract?

A

Causes gallbladder to contract

296
Q

What is cholelithiasis?

A

Gallstones - obstruciton of gall bladder

297
Q

What is cholecystitis?

A

Gall bladder infection

298
Q

What are abnormalities of bile acid metabolism?

A

Defective bile acid synthesis

Abnormalities of delivery to intestine

Interruption of enterohepatic circulation

Bile acid malabsorption

Bacterial overgrowth syndrome

Cholestasis - stand still in tree

Liver disease

299
Q

What is cholestasis?

A

Decerased bile flow

300
Q

What can cause cholestasis?

A

Cholestatic drugs, pregnancy and other processes that affect canaliculus, biliary ductules, that can be detected by lab tests and liver biopsy

Congenital biliary atresia - affects intrahepatic bile ducts that can be detected by imaging, ERCP, PTC

Common duct stone, cancer of pancreas or bile duct - that affects extrahepatic bile ducts, can be diagnosed by imaging, ultrasound, ERCP, PTC

301
Q

What are consequences of cholestasis?

A

Hepatic retention of biliary solutes and intestinal deficiency of digestive detergents (bile acids)

Retain bile acids, bilirubin, cholesterol

Malabsorption of fats, vitamins, etc

302
Q

What are causes of interruption of the enterohepatic circulation of bile acids?

A

External biliary fistula

Ileojejunal exclusion for obesity

Binding exchange resins

Small bowel disease

303
Q

What is the effect of bile acids on GI organs?

A

Esophagus - damage, esophagitis

Stomach - damage, gastritis

Pancreas - pancreatitis

Colon

304
Q

What is choledocholithiasis?

A

Stones in the bile ducts

305
Q

What do we see here via laproscopy?

A

Gall stones (cholelithiasis)

306
Q

What are two types of gall stones?

A

Cholesterol stones

Pigmented stones

307
Q

What are mixed stones of the gall bladder?

A

Both cholesterol and pigment stones

308
Q

What are cholesterol stones?

A

Crystals of cholesterol

309
Q

What are pigment stones?

A

Precipitates - not crystals

310
Q

What are pigmented gallstones?

A

Composed of bilirubin and/or calcium precipitates (not crystals)

Can form whenever there are high concentrations of unconjugated iblirubin in bile

Can arise in either gallbladder or bile ducts

Can be seen in liver disease, hemolysis, ifnected bile, prolonged starvation or total perenteral nutrition

311
Q

What is the basis for pigmented gallstones?

A

High concentrations of unconjugated bilirubin in bile

312
Q

Where do you find pigmetned gallsotnes?

A

Gallbladder and biliary ducts

313
Q

What is the relationship between bile acidity and ability to form precipitates?

A

More acidic - more solubility - less acidic = more chance to form precipitates

314
Q

What are cholesterol gallstones?

A

Most common form

Crystallization form lithogenic bile

Arises in gallbladder, NOT DUCTS

Female, fat, fertile, forty

315
Q

Where do cholesterol gallstones form?

A

Gallbladder, NOT ducts

316
Q

What type of gallstones can form in the bile ducts?

A

Pigmented; cholesterol only form in gallbladder (pigmented can too)

317
Q

What are causes of cholesterol gallstone fomration/

A

Too much cholesterol or too few bile salts

318
Q

What is the relationship between bile salt secretion rate (flow) and the risk of developing precipitates?

A

Slower teh secretory rate, the more likely you are to be in the supersaturated state (more likely to form precipitates)

319
Q

What is the natural history of gallstones?

A

Typically asymptomatic - just because they exist, doesn’t mean they are making the patient sick

320
Q

How can gallstones make you sick?

A

Biliary colic - stone temporarily stuck in cystic duct

Acute cholecystitis - cystic duct obstruction and infectoin

Bile duct obstruction - cholestasis + cholangitis? (cholangitis - inflammation of biliary tree)

Acute pancreatitis

321
Q

How do you get rid of gallstones?

A

Surgically - cholecystetomy = typically laprascopically

Non-surgical - lithotripsy (shock waves); gallstone dissolution (ursodeoxycholic acid)

322
Q

Does cholecystectomy prevent patients from developing gallstones?

A

NO - cholecystectomy does not prevent bile from being supersaturated still (might have had crystals in gallbladder before removal that stayed behind)

323
Q

what is the effect of ursodeoxycholic acid?

A

Secondary bile acid - decreases cholesterol secretion and cholesterol/phospholipid raito in bile

Main constituent of bear bile

ONly modestly effective and must be taken for a long time/indefinitely

Side effects include diarrhea, cost; but can be used to liquefy bile in other diseases

324
Q

How do you diagnose gallstones?

A

Sonography (radar)

X-rays (plain or contrast)

Nuclear scan (HIDA scan)

Bile analysis (for cholesterol crystals)

Endscopy (ERCP)

325
Q

What gallstones can be seen on x-ray without contrast?

A

Pigmented

326
Q

What gallstones can be seen on xray with contrast?

A

cholesterol

327
Q

What are diseases of the gallbladder?

A

Colic

Acute/chronic cholecystitis

Cancer

328
Q

What are diseases of the biliary ducts?

A

Acute cholangitis

Sclerosing cholangitis

Biliary cirrhosis

Cancer

Dysmotility

329
Q

Identify the Islets of Langerhancs, Acinar cells, and ductal epithelium

A
330
Q

Which pancreatic cells are exocrine and which are endocrine?

A

Exocrine - acinar

Endocrine - Islet cells (α, β, etc )

331
Q

What is the malformation of pancreas divisum?

A

Dorsal and Ventral pancreatic ducts fail to fuse together

Common bile duct and pancreatic duct do not drain together

Main duct goes to minor papilla

332
Q

Where can you often find heterotopic/ectopic pancreas?

A

Stomach, duodenum

333
Q

When do you typically find congenital/developmental anomalies of the pancreas?

A

Asypmtomatic, and can cause problems during surgery/endoscopy

Maybe secondarily involved by pancreas pathology

334
Q

What are causes of acute pancreatitis?

A

Duct obstruction, acinar cell injury, defective intracellular transport

335
Q

What do you see here?

A

Interstitial edema

Fat necrosis

Acute interstitial pancreatitis

336
Q

What do you see here?

A

Acute necrotizing pancreatitis

337
Q

What do you see here?

A

Acute hemorrhagic pancreatitis

338
Q

Is acute panreatitis reversible?

A

YES

339
Q

What is the main cause of acute pancreatitis in men?

A

Alcohol

340
Q

What is the main cause of acute pancreatitis in females?

A

Gallstones

341
Q

What are signs/symptoms of acute pancreatitis in acute pancreatitis?

A

Pain (radiating to the back), anorexia/nausea, increased serum amylase (later lipase)

Complications include infection, abscess, pseudocyst

342
Q

What is the difference between acute and chronic pancreatitis?

A

Risk factors are the same

Acute - acinar cell injury followed by inflammation

Oxidative stress injury causes growth factor and pro-inflammatory molecule production

Production of stellate cells and resulting pancreatic fibrosis

343
Q

What do you see here?

A

Chronic pancreatitis - duct dilation, fibrosis, and atrophy

344
Q

Is chronic pancreatitis reversible?

A

NO - Irreversible destruction with fibrosis

345
Q

What are histological findings of chronic pancreatitis?

A

Fibrosis

Atrophy of acini (reduced number/size)

Relative sparing of islet cells (initially)

Duct dilation with protein concretions

346
Q

What are the most common cystic lesions of the pancreas?

A

Pancreatic pseudocyst

347
Q

What are pancreatic pseudocysts?

A

Walled off hemorrhagic/necrotic debris

Lined by capsule/granulation tissue, NOT epithelium (diagnostic)

348
Q

Why are pseudocysts not true cysts?

A

Lined by granulation tissue, notably NOT epithelium

349
Q

What is the most common malignancy of the pancreas?

A

Pancreatic ductal adenocarcinoma

350
Q

What are the most common gene mutations in pancreatic ductal adenocarcinoma?

A

KRAS

p16/CDKN2A

TP53

SMAD4/DPC4

351
Q

What is a hereditary disease that associated with pancreatic ductal adenocarcinoma?

A

Hereditary pancreatitis

Peutz-Jeghers Syndrome

352
Q

What do we see here?

A

Pancreatic ductal adenocarcinoma

353
Q

What are physical exam findings of pancreatic ductal carcinoma?

A

Migratory thrombophlebitis (Trousseau sign)

Acute, painless jaundice and dilated gallbladder (Courvoisier sign/law)

Nontender firm, fixed, left supraclavicular lymph node (Virchow’s or Troisier’s node)

354
Q

What is Trousseau sign?

A

Migratory thrombophlebitis

Seen in pancreatic ductal adenocarcinoma

355
Q

What is Courvoisier sign/law?

A

Acute, painless jaundice and dilated gallbladder

Seen in pancreatic ductal adenocarcinoma

356
Q

What is Virchow’s node?

A

Nontender, firm, fixed, left supraclavicular lymph node

Seen in Pancreatic ductal adenocarcinoma and gastric adenocarcinoma

357
Q

What do you see here?

A

Pancreatic neuroendocrine tumor

358
Q

How are pancreatic neuroendocrine tumors classified?

A

Functional - insuloma, gastrinoma, glucagonoma, somatostatinoma, VIPoma

Nonfunctional - typically malignant

359
Q

What is the most common functional pancreatic neuroendocrine tumor?

A

insuloma - causes hyperinsulinism (mild hypoglycemia)

360
Q

What is the most common cause of acute cholecystitis?

A

Stones - Acute calculous cholecystitis

361
Q

What do you find histologically in acute cholecystitis?

A

Lumen - fibrin, blood, neutrophils=empyema

Wall - edematous, thick, necrosis=gangrenous

Serosa - exudate, gas bacteria=emphysematous

362
Q

What do you see histologically in chronic cholecystitis?

A

Fibrosis, Rokitansky-Aschoff sinuses

calcification (porcelain), atrophy (hydrops)

363
Q

What do you see here?

A

Adenocarcinoma of the Gallbladder

364
Q

What do you typically see with adenocarcinoma of the gallbladder?

A

Stones

More commonly seen in females

365
Q

What are broad funcitons of the liver?

A

Synthesis of protein (albumin, clotting factors)

Substrate metabolism, storage (Carbs, lipids, vitamins, metals)

Metabolizes drugs, biotransformation

Excretes (bilirubin, bile acids, drugs)

Immune funciton

Growth Factor, hormone production

Hematopoiesis

366
Q

What are broad types of liver disease?

A

Injury (acute/chronic: viral, toxic, metabolic)

Genetic (overload of metabolites, defective protein funciton or secretion)

Developmental (biliary atresia, cysts)

Neoplastic (benign tumors, adenmoas, pre-malignant and malignant tumors)

367
Q

What liver dysfunction does a coagulopathy indicate?

A

Loss of clotting factor production

368
Q

What liver function is impaired when you see jaundice, scleral icterus?

A

Bilirubin clearance

369
Q

What liver function is dysfunctional when you see hypoglycemia?

A

Glucose mobilization

370
Q

What liver function is dysfunctional when you see encephalopathy?

A

Metabolite clearance and drug detoxification

371
Q

What liver function is dysfunctional when you see renal failure?

A

Blood flow regulation

372
Q

What liver function is dysfunctional when you see sepsis and bacterial peritonitis?

A

Clearance of bacteria from portal blood

Immune function

373
Q

What liver function is dysfunctional when you see anemia and reduced oncotic pressure leading to edema

A

Production of growth factors and albumin

374
Q

What liver function is dysfunctional when you see feminization with gynecomastia in men?

A

Metabolism of hormones

375
Q

What liver function is dysfunctional when you see portal HTN wiht varices and ascites?

A

Blood flow (can be obstructed due to increased scarring)

376
Q

What cell type of the liver mediates the liver’s immune system?

A

Kupffer cells - macrophages

377
Q

What is unique about the blood supply of the liver?

A

Dual blood supply - portal vein and hepatic artery

378
Q

What is unique about the endothelium of the liver?

A

Fenestrated

379
Q

What organs drain into the liver?

A

Gut and spleen

380
Q

What are features of the blood flow of the liver?

A

Low pressure

High capacitance

381
Q

What is a unique feature of the organ important for transplantation?

A

Ability to regenerate

382
Q

What are acute sources of liver injury?

A

Tylenol or toxins (alcohol)

Viral infection

Unknown (idiopathic)

May require transplant when severe, but if it resolves it can return to normal

383
Q

What are chronic sources of liver injury?

A

Viral infection
Alcohol

Obesity-related

Autoimmune

Metabolic overload

Biliary obstruction

Can be progressive over decades but relatively asymptomatic

384
Q

How does the liver respond to chronic injury?

A

Scarring (fibrosis) - acutely will typically regenerate, so it requires a chronic insult before it will scar

385
Q

What is the endstage result of chronic liver disease?

A

Cirrhosis

386
Q

What is seen on the right?

A

Cirrhosis

387
Q

What do you see on the right?

A

Cirrhosis (normal on left)

388
Q

What are complications of cirrhosis?

A

Hepatic encephalopathy

Ascities/Spontaneous Bacterial Peritonitis

Portal hypertension (varices)

Hepatorenal syndrome

389
Q

What happens during cirrhotic liver blood flow?

A

Blood clogs up - see splenomegaly, varices, ascites, etc

390
Q

What are histories of risk fators or exposures for liver disease?

A

Needle use, transfusions, prescribed or illicit drugs

391
Q

What are signs/symptoms of liver disease?

A

Enlarged liver - acute injury or tumor

“Stigmata of chronic liver disease” - possible cirrhosis

392
Q

What do elevated AST, ALT, bilirubin suggest?

A

Injury to hepatocytes

393
Q

What do increased alkaline phosphatase γGT, bilirubin indicate?

A

Injury to bile ducts

394
Q

What are diagnostic tests for liver disease?

A

Enzymes - AST, ALT, Alkaline Phosphatase, bilirubin

Function - albumin, prothrombin time, platelets

Systemic - CBC, renal function

Imaging

395
Q

What do you see here?

A

Scleral icterus

Spider angioma

Glossitis

Liver disease possible

396
Q

What do you see here?

A

Spider angioma

Seen in chronic liver disease and in pregnancy

397
Q

What do you see here?

A

Palmar erythema

Can be sign of chronic liver disease

398
Q

What do you see here?

A

Digital clubbing

Sign of chronic liver disease (not usually this severe)

399
Q

What do you see here?

A

Signs of gynecomastia in a man

Can be a sign of liver disease

400
Q

What do you see here?

A

Excoriations can indicate biliary obstuction (itchiness)

401
Q

What do you see here?

A

Xanthelasma in cholestatic liver disease

Especially primary biliary cirrhosis

402
Q

What do you see here?

A

Massive ascites

Large umbilical hernia

Collateral vessels on abdominal wall

Sign of chronic liver disease

403
Q

How do you typically treat liver disease?

A

treat underlyign disease - antivirals, remove metabolites, reduce inflammation

Treat complications of liver disease (antibiotics, diuretics, reduce encephalopathy

Transplant

404
Q

How many hepatits viruses are there?

A

5 - A-E

405
Q

What is hepatitis?

A

Indicates biochemical hepatic dysfunction, not necessarily due to virus

406
Q

What is acute viral hepatitis?

A

Can be any of 5 major viruses

Malaise, nausea, abdominal discomfort, jaundice are typical but not necessary

Recovery is usual

407
Q

What is chronic hepatitis?

A

Persistence of hepatitis > 6 months

Occurs with B, C, D

Risk of cirrhosis and hepatocellular carcinoma

Not in Hep. A

408
Q

Which hepatitis viruses can cause chronic hepatitis?

A

B, C, D, maybe E

409
Q

How do you diagnose viral hepatitis?

A

Serologically

Biopsy doesn’t differentiate

ALT, and AST reflect hepatic necrosis

410
Q

What is the incubation period of hepatitis A?

A

4 weeks

411
Q

How do you diagnose hepatitis A?

A

IgM anti HAV during acute phase

IgG anti HAV persists indefinitely

412
Q

How is hepatitis A transmitted?

A

Fecal-oral

Commonly affects children

413
Q

How do you manage hepatitis A patients?

A

Self-limited

Follow older patients carefully because of risk of liver failure

No role for antiviral therapy - immune globulin post exposure

(there is vaccine)

414
Q

How do you prevent hepatitis A?

A

Active immunization (inactivated/killed virus)

Recommended for travel to endemic areas, military, employees of daycare, people handling hep A specimens, people with chronic disease

415
Q

What is the incubation period of hepatitis B?

A

60-90 days (2-3 months)

416
Q

What is unique about the virus of hepatitis B virus?

A

Only DNA virus

417
Q

What is a marker of hepatitis B replication?

A

HBV DNA

418
Q

What is a marker of HBV replication and infectivity?

A

Hepatitis B E antigen

419
Q

What is the first detectable virologic marker of Hep B infection?

A

HBsAg

Precedes rise in AST/ALT nad symptoms

Antibody appears after, and is detectable indefinitely

420
Q

What is the only antibody detectable upon receiving HBV vaccination?

A

Anti-HBs (surface) antibody

Protective

421
Q
A
422
Q

How is Hepatitis B acquired?

A

Percutaneous (blood transfusion, needle stick)

Perinatal

Sexual

Most common cause of chronic hepatitis in Asia and Africa

(any age)

423
Q

What are differences between childhood and adult hepatitis B infection?

A

Childhood = perinatal or preschool; infection is typically subclinical

Adult = sexual contact, IV drug use, exposure to blood; infection is typically sypmtomatic

424
Q

Who are populations at risk of Hep B?

A

Hemodialysis

IV drug use

Spouses of acutely infected individuals

Promiscuous people (MSM)

Healthcare workers

Transfusion pts

Nursing home residents/staff

Prisoners

425
Q

How many people progress to chronic hepatitis?

A

1-10% of patients - risk of developing cirrhosis, HCC

Fulminant (acute) liver failure is rare (0.1-0.5%)

426
Q

What is the natural history of Hepatitis B?

A
427
Q

What are forms of prophylaxis for Hepatitis B?

A

Active: plasma or recombinant vaccines

Passive: Hepatitis B immune globulin (HBIG) - not proven

428
Q

What are clinical features of chronic Hep B?

A

Range of no symptoms to end stage liver disease

(ALT, Jaundice, hypoalbuminemia, coagulopathy, etc.)

429
Q

What are goals of Hep B treatment?

A

Prevent cirrhosis and HCC

430
Q

What are first-line agents for Hep B infection?

A

Lamivudine

Adefovir

Entecavir

Peg-IFNα2a

Telbivudine

Tenofovir +/- emtricitabine

431
Q

What is the most common cause of chronic viral hepatitis in Asia and Africa?

A

Hepatitis B

432
Q

What can diagonse Hepatitis B infection?

A

HBsAg

433
Q

What is the incubation period of hepatitis C?

A

50 days (1-2 months)

434
Q

What is the most sensitive indicator of Hepatitis C infection?

A

HCV RNA

435
Q

Where does Hepatitis C replicate?

A

Hepatocytes

436
Q

What is the most common genotype of hepatitis C in the US?

A

genotype 1

437
Q

How is hepatitis C acquired?

A

percutaneous (perinatal and sexual

Transfusions

438
Q

What is the most common cause of chronic viral hepatitis in the USA and Europe?

A

Hepatitis C

439
Q

What is more effective at establishing infection, IV drug use with Hepatitis C or HIV?

A

Hepatitis C - it is highly efficient (1:75 vs 1:300 of HIV)

440
Q

What is the natural history of hepatitis C?

A
441
Q

What are clinical features of chronic hepatitis C?

A

Similar to hepatitis B

Extrahepatic manifestations are seen more in hepatitis C - cryoglobulinemia, non-immune mediated

Antibody is present once exposure occurs (doesn’t always mean chronic infection though = look at RNA level for that)

442
Q

What laboratory value can help evaluate the presence of chronic hepatitis C infection and of response to treatment?

A

HCV RNA level

443
Q

What is treatment for Chronic Hepatitis C?

A

Interferon monotherapy

Combination interferon + ribavirin (or pegylated interferon)

Protease inhibitors (telaprevir, boceprivir, simeprivir)

Polymerase inhibitors ( sofosubuvir)

444
Q

What avenues of prophylaxis exist for hepatitis C?

A

No vaccine

Immune globulins aren’t useful

(nothing, essentially)

445
Q

What is the incubation period of hepatitis D?

A

60-90 days (2-3 months)

446
Q

What is a requirement of hepatitis D virus for replication and expression?

A

Presence of Hepatitis B Virus

447
Q

How can you be infected with hepatitis D?

A

Co-infeciton (simultaneously wiht HBV acutely)

Superinfectino (acute HDV in chronic HBV)

448
Q

What is a serological marker of acute HDV infection?

A

IgM anti-HDV

449
Q

What prophylaxis measures are available for hepatitis D?

A

Immunization against HBV

No known prophylaxis for those already with HBsAg

450
Q

How do you treat Hepatitis D?

A

Interferon

451
Q

What is the incubation period of hepatitis E?

A

40 days (~1 month)

452
Q

What serologic markers do you see in acute hepatitis E infection?

A

IgM anti-HEV

(not routinely available though)

453
Q

How is hepatitis E transmitted?

A

Fecal-oral

In india, asia, africa, central america - after contamination of water supply

Mostly in young adults

454
Q

What are clinical sequellae of hepatitis E?

A

Fulminant hepatitis particularly in pregnant women

455
Q

What population is particularly susceptible to negative consequences of Hepatitis E?

A

Pregnant women

456
Q

When do you see chronic hepatitis E infection?

A

In immunosuppressed patients (post organ transplant, HIV, chemo)

457
Q

How do you treat chronic hepatitis E?

A

Reduce immunosuppressive agent (remember, it is typically only seen in immunosuppressed)

Pegylated interferon, ribavirin

458
Q

How do you manage hepatitis E?

A

good higene

459
Q

How do you prevent hepatitis E spread?

A

No antiviral therapy available, vaccines are recently tested, but nothing yet

460
Q

What is jaundice?

A

Physical sign noted when bilirubin level is elevated (>2.5 mg/dL)

461
Q

What can cause jaundice?

A

Increased bilirubin production

Impaired hepatic handling

Benign laboratory finding

462
Q

What is bilirubin?

A

End-product of metabolic degradation of heme

463
Q

What are sources of bilirubin?

A

70-90% comes from erythrocytes (senescent, injured, ineffective erythropoiesis, hematomas)

Remainder comes from turnover of non hemoglobin hemoproteins (myoglobin, cytochromes, catalases)

464
Q

How is bilirubin found in plasma?

A

bound to albumin - unconjugated is insoluble in plasma

Total bilirubin - 1-1.5 mg/dl (90% unconjugated, 10% conjugated)

465
Q

What are the four steps of bilirubin transfer from blood to bile?

A

Hepatocellular uptake

Intracelular binding

Conjugation

Excretion of conjugates into bile canaliculus

466
Q

What happens to bilirubin in the intestines?

A

No absorption in gallbladder/intestine

Terminal ileum/colon - hydrolysis to unconjugated bilirubin and reduction to complex tetarpyrroles (urobilinogen) by colonic bacteria; this is either excreted in feces (most), or re-enters enterohepatic circulation; small amount is excreted in urine

467
Q

How is bilirubin processed in the kidneys?

A

Unconjugated bilirubin is not excreted into urine

Conjugated bilirubin is filtered at glomerulus

Bilirubinuria indicates presence of conjugated bilirubin in plasma, thus hepatobiliary dysfunction

468
Q

What is dark urine a sign of?

A

Conjugated bilirubinuria (bilirubinemia)

469
Q

What is direct bilirubin?

A

Conjugated

470
Q

What is indirect bilirubin?

A

Unconjugated

471
Q

What are causes of unconjugated hyperbilirubinemias?

A

Increased production

Reduced hepatic clearance

Inherited disroders of metabolism

472
Q

What can cause an increase of production of bilirubin?

A

hemolysis, hematomas, ineffective erythropoiesis

473
Q

What are causes of reduced hepatic clearance?

A

Neonatal jaundice

Breast milk jaundice
Drugs (rifampicin, chloramphenicol, gentamicin)

474
Q

What are common inherited disorders of bilirubin conjugation?

A

Gilbert’s syndrome

Crigler Najjar syndrome (type I and type II)

475
Q

What is Gibert’s syndrome?

A

MOst common hereditary hyperbilirubinemia

UGT1A1 Mutation - 10-33% of normal enzyme activity

Males>females

Mild chronic or recurrent unconjugated hyperbilirubinemia

Typically can be benign

476
Q

What is Crigler-Najjar Syndrome Type I?

A

Mutation in common exon of UGT1 complex

no functional enzyme activity

Appears neonatally, with severe neurological impairment - often fatal

(Rare disorder affecting the metabolism of bilirubin, a chemical formed from the breakdown of red blood cells. The disorder results in an inherited form of non-hemolytic jaundice, which results in high levels of unconjugated bilirubin and often leads to brain damage in infants.)

477
Q

What is Crigler-Najjar Syndroem Type II?

A

Mutations of UGT1A1

Markedly reduced but detectable enzyme activity

treated with phenobarbital to induce UGT enzyme activity

478
Q

What differentiates Crigler-Najjar Type I and type II?

A

No enzyme UGT activity = Type I; Some activity = Type II

479
Q

What is kernicterus?

A

Bilirubin staining of basal ganglia, pons, and cerebellum resulting in neuronal toxicity

480
Q

What is Dubin-Johnson syndrome?

A

Mutations in gene encoding for canalicular transporter - have global defect in organic anion transport

Chronic intermittent jaundice with grossly pigmented liver

See scleral icterus, moderately enlarged/tender liver

Plasma bilirubin is 2-5 mg/dl (normal liver enzymes)

CONJUGATED hyperbilirubinemia

481
Q

What is Rotor’s Syndrome?

A

Unknown mutation
total bilirubin < 10 mg/dl

Benign course with normal life expectancy

Only difference from Dubin-Johnson is the lack of pigmented liver that is seen in Dubin-Johnson

482
Q

How does chronic liver injury result in hyperbilirubinemia?

A

Injury causes less efficient capacity to tranpsort bilirubin

End up with conjugated hyperbilirubinemia

483
Q

How does intrahepatic cholestasis of pregnancy cause conjugated hyperbilirubinemia?

A

Occurs during 2nd or 3rd trimester

Elevated ALT in addition to bilirubin, as well as bile acids

Disappears after delivery, but may recur with subsequent pregnancies and with oral contraceptives

Unclear mechanism of action

484
Q

What type of hyperbilirubinemia does biliary obstruction cause?

A

Conjugated

Choledocholithiasis

Neoplasms

Extrinsic compression
Inflammation/infection

485
Q

How do you approach hyperbilirubinemia?

A
486
Q

What lab tests are markers of hepatocyte integrity?

A

AST- Aspartate aminotransferase

ALT - Alanine aminotransferase

487
Q

What are lab test markers for cholestasis?

A

Bilirubin

Alkaline phosphatase

Gamma glutamyl transpetidase (GGT)

5’ Nucleotidase (not used anymore)

488
Q

what are tru markers of liver function?

A

Albumin

prothrombin time or INR

489
Q

What does acute hepatocellular injury look like on labs?

A

Elevated ALT/AST

Normal-to-elevated alkaline phosphatase, GGTP

Elevated total bilirubin

Normal PT and Albumin

490
Q

What lab tests are useful for diagnosis cirrhosis?

A

Elevated prothormbin time

Decreased albumin

491
Q

What is the classic lab finding in alcoholic hepatitis?

A

2 to 1 ratio of AST over ALT

GI and Liver (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions