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== <big>Gastrointestinal Bleeding</big> ==
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{|
<references />{{WikiDoc CMG}}{{AE}}{{MWH}}
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! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Subtypes
 
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! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Explanation
'''''Synonyms and Keywords:''''' Blood loss from GI tract; bloody stool; blood in feces; PR bleeding; gastrointestinal hemorrhage; gastrointestinal hemorrhage; GI bleeding; bright red blood per rectum; BRBPR.
 
 
 
== Overview ==
 
Gastrointestinal (GI) bleeding is defined as bleeding from any part of GI tract starting from mouth to anus. It can also be called as gastrointestinal hemorrhage. Based on the origin of bleeding it can be classified into upper gastrointestinal bleeding and lower gastrointestinal bleeding. Upper gastrointestinal bleeding (UGIB) is defined as bleeding from the gastrointestinal tract that originates proximal to the ligament of Treitz. Lower gastrointestinal bleeding is defined as blood loss originating distal to the ligament of Treitz. The most common causes of UGIB are peptic ulcer disease and esophageal varices while diverticulosis is the most commonly responsible for lower gastrointestinal bleeding. Clinical presentation includes overt bleeding from the gastrointestinal tract, rapid or slow, either manifested by hematemesis of fresh (blood-streaked to frankly bloody), old ('coffee ground') vomitus, melena and or as frank blood per rectum.
 
 
 
Common risk factors in the development of GI bleeding include advancing age, previous history of gastrointestinal bleeding, chronic constipation, hematologic disorders, anticoagulants medications, NSAIDs. It is essential to distinguish between lower gastrointestinal bleeding and brisk upper gastrointestinal bleeding as they can present with similar symptoms. Patients with severe bleeding or hemodynamic disturbance require hospitalization and urgent investigation. Treatment depends on the cause and the severity of the bleeding.
 
 
 
== Types of bleeding ==
 
Bleeding from the gastrointestinal tract can be of the following types:
 
 
 
* '''Hematemesis''': Vomiting fresh red blood.
 
* '''Coffee ground emesis''': Vomiting of altered black blood.
 
* '''Melena''': Passage of black tarry stools.
 
* '''Hematochezia''': Passage of red blood per rectum (usually due to bleeding from the lower gastrointestinal tract but occasionally can be due to massive upper gastrointestinal bleeding).
 
* '''Rebleeding''': Defined as fresh hematochezia and/or melena associated with the development of shock (pulse greater than 100 beats/min, systolic pressure less than 100 mm Hg), a fall in CVP greater than 5 mm Hg, or a reduction in hemoglobin concentration greater than 20 g/l over 24 hours. Rebleeding should always be confirmed by endoscopy.
 
 
 
== Causes ==
 
{| class="wikitable"
 
|+
 
!Gastrointestinal Bleeding
 
!Lethal Causes
 
!Common causes
 
!Less Common causes
 
 
|-
 
|-
|Upper gastrointestinal bleeding
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! style="background: #DCDCDC; text-align: center;" |'''Relapsing remitting'''
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| style="background: #F5F5F5;" |
* Anthrax
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* Relapsing-remitting multiple sclerosis (RRMS) is defined by acute attacks of [[neurological]] [[dysfunction]] followed by full or partial [[recovery]]. Patient [[History and Physical examination|clinical symptoms]] are stable between the attacks
* Ebola virus
 
|
 
* Duodenal ulcer
 
* Esophagitis
 
* Esophageal varices
 
* Gastric tumors
 
* Gastric ulcer
 
* Gastritis
 
* Mallory-Weiss Syndrome
 
* Peptic ulcer
 
|
 
* Gastric cancer
 
* Esophageal Tumors
 
* Esophagitis
 
* Gastric erosions/gastropathy
 
* Dieulafoy lesions
 
* Gastric antral vascular ectasia
 
 
|-
 
|-
|Lower gastrointestinal bleeding
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! style="background: #DCDCDC; text-align: center;" |'''Secondary progressive'''
|
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| style="background: #F5F5F5;" |
|
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* Patient with long term RRMS can switch to secondary relapsing multiple sclerosis (SPMS) when the [[neurological]] [[symptoms]] progressively worsen between the attacks
* Diverticulosis
 
* Vascular ectasias
 
* Ischemic colitis
 
* Colorectal malignancy
 
* Hemorrhoids
 
* Anal fissures
 
* Crohn's disease
 
* Ulcerative colitis
 
* Infectious colitis
 
* Colonic polyps
 
* Radiation proctitis
 
* Rectal varices
 
* Stercoral ulceration
 
* Meckel diverticulum
 
* Intussusception
 
* Henoch-Scholein Purpura (HSP)
 
|}
 
 
 
== Classification ==
 
The following flow chart elobarates the classification of gastrointestinal bleeding:
 
 
 
{{Family tree/start}}
 
{{Family tree||||||||||||||||||||A01||||||||||A01= '''Gastointestinal'''<br> '''bleeding'''}}
 
{{Family tree|||||||||||||||||||||!|||||||||||}}
 
{{Family tree|||||||||||||,|-|-|-|-|-|-|-|^|-|-|-|-|-|-|-|-|-|-|.||||||}}
 
{{Family tree|||||||||||||!|||||||||||||||||||!||||||}}
 
{{Family tree|||||||||||||!|||||||||||||||||||!||||||}}
 
{{Family tree||||||||||||B01|||||||||||||||||B02|||||||B01= '''Upper GI bleeding'''|B02= '''Lower GI bleeding'''}}
 
{{Family tree|||||||||||||!|||||||||||||||||||!||||||}}
 
{{Family tree||||||||||||C01|||||||||||||||||C02|||||C01= Based on blood loss|C02= Based on severity of blood loss}}
 
{{Family tree|||||||,|-|-|-|-|-|+|-|-|-|-|-|.|||||||,|-|-|-|-|-|+|-|-|-|-|-|.||}}
 
{{Family tree|||||D01|||||D02||||D03|||||D04||||D05|||||D06|||||||D01= Overt|D02= Occult|D03= Obscure|D04= Severe|D05= Moderate|D06= Occult}}
 
{{Family tree|||||||!||||||!||||||!|||||||!||||||!||||||!|}}
 
{{Family tree|||||E01|||||E02||||E03|||||E04||||E05|||||E06|||||||||||E01= Hematemesis Coffee-ground emesis Melena|E02= Microscopic Hemorrhage Heme-Occult positive stools|E03= Source is not identified|E04= Hematochezia|E05= Hematochezia|E06= Microscopic Hemorrhage Heme-Occult positive stools}}
 
{{Family tree||||||||||||||||||||||||||||||}}
 
{{Family tree||||||||||||||||||||||||||||||}}
 
{{Family tree||||||||||||||||||||||||||||||}}
 
{{Family tree||||||||||||||||||||||||||||||}}
 
{{Family tree||||||||||||||||||||||||||||||}}
 
{{Family tree/end}}<br />
 
 
 
== Syndrome of Inappropriate antidiuretic hormone classification ==
 
SIADH may be classified into several sub-types based on the pattern of arginine vasopressin (AVP) secretion in response to a range of plasma osmolalities into type A, type B, type C, and type D.
 
<br />
 
 
 
{| class="wikitable"
 
! style="background: #4479BA; width: 100px;" | {{fontcolor|White|'''Classification'''}}
 
! style="background: #4479BA; width: 500px;" | {{fontcolor|White|'''Features'''}}
 
 
|-
 
|-
| style="background: #DCDCDC; text-align:center;" |'''Type A'''
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! style="background: #DCDCDC; text-align: center;" |'''Primary progressive'''
 
| style="background: #F5F5F5;" |
 
| style="background: #F5F5F5;" |
* Accounts for about 60-70% of SIADH
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* Primary progressive multiple sclerosis (PPMS) is defined by continuously worsening of [[neurological]] [[dysfunction]] with no distinct attacks and [[remission]]<nowiki/>s
*Excessive secretion of arginine vasopressin (AVP) is noted
 
*Associated with lung cancer and nasopharyngeal tumors
 
* Patients are more susceptible to development of severe hypo<nowiki/>natremia
 
|-
 
| style="padding: 5px 5px; background: #DCDCDC; text-align:center;" |'''Type B'''
 
| style="padding: 5px 5px; background: #F5F5F5;" |
 
* Accounts for (20–40%) of the cases
 
* Secretion of AVP occurs at lower than normal plasma osmolalities
 
|-
 
| style="background: #DCDCDC; text-align:center;" |'''Type C'''
 
| style="background: #F5F5F5;" |
 
* Failure to suppress AVP secretion at plasma osmolalities below the osmotic threshold
 
* Occurs due to dysfunction of inhibitory neurons in the hypothalamus, leading to persistent low-grade basal AVP secretion
 
 
|-
 
|-
| style="background: #DCDCDC; text-align:center;" |'''Type D'''
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! style="background: #DCDCDC; text-align: center;" |'''Progressive relapsing'''
 
| style="background: #F5F5F5;" |
 
| style="background: #F5F5F5;" |
* Low or undetectable AVP levels and circulating AVP response is not defective 
 
*Nephrogenic SIADH (NSIAD) may be attributed to this condition
 
*Associated with gain-of-function mutations in the vasopressin-2 (V2 receptor) receptor leading to a clinical picture of SIADH, with undetectable AVP levels
 
*The condition is inherited in an X-linked manner, although heterozygous females may have inappropriate anti-diuresis of varying degrees.
 
 
|}
 
|}
  
==Classification of Constipation==
 
Constipation may be classified according to etiology into five subtypes:
 
* '''Gastrointestinal'''
 
* '''Neurologic'''
 
* '''Metabolic'''
 
* '''Endocrine'''
 
* '''Psychiatric'''
 
 
<br />
 
 
{{Family tree/start}}
 
{{Family tree|||||||||||||||||||||||||||||||||||||||||||||||||||A01|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||A01='''Contipation''' <br> Classification}}
 
{{Family tree||||||||||||||||||||||||||||||||||||||||||||||||||||!|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||}}
 
{{Family tree|||||||||||||||||||||||||||||||||||||||||||||||||||B01|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||B01='''Etiology'''}}
 
{{Family tree|||||||||||||||||||||||||||||||||,|-|-|-|-|-|v|-|-|-|-|-|v|-|-|-|-|-|-|+|-|-|-|-|-|v|-|-|-|-|-|v|-|-|-|.||||||||||||||||||||||||||||||||||||||||||||||||||}}
 
{{Family tree|||||||||||||||||||||||||||||||C01|||||C02||||C03|||||C04||||C05||||C06|||C07||||||||||||||||||||||C01= '''Neurologic'''|C02= '''Metabolic'''|C03= '''Endocrine'''|C04= '''Gastrointestinal'''|C05= '''Psychiatric'''|C06= '''Drugs'''|C07= '''Idiopathic'''}}
 
{{Family tree|||||||||||||||||||||||||||||||||!||||||!||||||!|||,|-|-|-|+|-|-|-|.||!||||||!||||!||||||||||||||||||||||||||||||}}
 
{{Family tree|||||||||||||||||||||||||||||||||!||||||!||||||!||D01||D02||D03|!||||||!||||!|||||||||||||||||||||||||||||||||D01= Obstruction|D02= Agangliosis|D03= Idiopathic megacolon}}
 
{{Family tree|||||||||||||||||||||||||||||||||!||||||!||||||!||||,|-|-|^|-|-|.|||!||||||!||||!|||||||||||||||||||||||||||||||||}}
 
{{Family tree|||||||||||||||||||||||||||||||||!||||||!||||||!|||E01||||E02||!||||||!||||!|||||||||||||||||||||||||||||||E01= Hirschprung disease|E02= Chagas disease}}
 
{{Family tree|||||||||||||||||||||||||||||||||!||||||!||||||!|||||||||||||!||||||!||||!||||||||||||||||||||||||||||||||||||||||||}}
 
{{Family tree|||||||||||||||||||||||||||||||||!||||||!||||||!|||||||||||||!||||||!||||!||||||||||||||||||||||||||||||||||||||||||}}
 
{{Family tree|||||||||||||||||||||||||||||||||!||||||!||||||!|||||||||||||!||||||!||||!||||||||||||||||||||||||||||||||||||||||||}}
 
{{Family tree|||||||||||||||||||||||||||||||||!||||||!||||||!|||||||||||||!||||||!||||!||||||||||||||||||||||||||||||||||||||||||}}
 
{{Family tree|||||||||||||||||||||||||||||||F01|||||F02||||F03|||||||||||F04||||F05||F06||||||||||||||||||||||||||||||||||||||||||||||||||||F01= Multiple sclerosis Parkinson's disease Spinal cord Injury|F02= Hypercalcemia Hypermagnesemia Porphyria Hypokalemia|F03= Hypothroidism Diabetes mellitus Panhypopituitarism|F04= Depression Eating disorder|F05= Analgesics Anticholinergics Cation containing agents Neuron targeting agents|F06= Normal colonic transit Sloww colonic transit Dyssynergic defecation}}
 
{{Family tree|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||}}
 
{{Family tree|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||}}
 
{{Family tree|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||}}
 
{{Family tree/end}}<br />
 
 
= Colorectal cancer pathophysiology =
 
The pathogenesis of colorectal carcinoma (CRC) involves the molecular pathways for both sporadic and colitis-associated CRC. Sporadic instability originates from the epithelial cells that line the colon or rectum. Colitis-associated CRC includes genetic instability, epigenetic alteration, chronic inflammation, oxidative stress, and intestinal microbiota. According to the World Health Organization (WHO) histological classification, most colorectal tumors are carcinomas of which almost 90% are adenocarcinomas.
 
 
=== Sporadic colorectal cancers ===
 
The picture below depicts the molecular pathogenesis of sporadic colon cancer:
 
[[Image:Sporadic Colon Cancer3.jpg|center|1000x1000px|frame|Molecular pathogenesis of sporadic colon cancer]]
 
 
*'''APC gene'''
 
:*Produces the APC protein, which prevents the accumulation of β-catenin protein (responsible for stem cell renewal)
 
  
:* Mutation of the APC protein leads to the accumulation of β-catenin protein and causes inappropriately high levels of stem cell renewal.
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Table 1: A few milestones in narcolepsy research and therapy
*'''TP53|TP53 gene'''
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1877 First description in the medical literature (100)
:*Produces the P53 (protein)|p53 protein, which monitors cell division and promotes apoptosis if there are cell defects
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1880 Gelineau called the disorder “narcolepsy” (28)
:*mutation|Mutation <nowiki/> mutation|s result in loss of control over cell division or apoptosis
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1902 Loewenfeld coined the term “cataplexy” (53)
*'''TGF beta|TGF-β and DCC (Deleted in Colorectal Cancer)'''
+
1935 First use of amphetamines in the treatment of narcolepsy (87)
:*Usually responsible for apoptosis, but deactivated in colorectal cancer
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1960 Description of Sleep Onset REM periods in a narcoleptic subject (99)
*'''Oncogenes'''
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1970 Description of the Multiple Latency Test (15, 90)
:*Stimulate cellular division
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1973 First report of a narcoleptic dog (47, 72)
:*Mutations lead to over-activation of cell proliferation
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1983 Association of narcolepsy with HLA-DR2 (37)
 +
1985 Monoaminergic and cholinergic imbalance in narcolepsy (7, 80)
 +
1992 Association of narcolepsy with HLA-DQB1*0602 (56, 63)
 +
1998 Identification of hypocretins/orexins and their receptors (18, 93)
 +
1999 Hypocretin mutations cause narcolepsy in mice and dogs (16, 51)
 +
2000 Human narcolepsy is also associated with an hypocretin deficiency (81)

Revision as of 15:08, 2 August 2020


Subtypes Explanation
Relapsing remitting
Secondary progressive
  • Patient with long term RRMS can switch to secondary relapsing multiple sclerosis (SPMS) when the neurological symptoms progressively worsen between the attacks
Primary progressive
Progressive relapsing


Table 1: A few milestones in narcolepsy research and therapy 1877 First description in the medical literature (100) 1880 Gelineau called the disorder “narcolepsy” (28) 1902 Loewenfeld coined the term “cataplexy” (53) 1935 First use of amphetamines in the treatment of narcolepsy (87) 1960 Description of Sleep Onset REM periods in a narcoleptic subject (99) 1970 Description of the Multiple Latency Test (15, 90) 1973 First report of a narcoleptic dog (47, 72) 1983 Association of narcolepsy with HLA-DR2 (37) 1985 Monoaminergic and cholinergic imbalance in narcolepsy (7, 80) 1992 Association of narcolepsy with HLA-DQB1*0602 (56, 63) 1998 Identification of hypocretins/orexins and their receptors (18, 93) 1999 Hypocretin mutations cause narcolepsy in mice and dogs (16, 51) 2000 Human narcolepsy is also associated with an hypocretin deficiency (81)