Sandbox: Dr.Reddy: Difference between revisions
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**Depression | **Depression | ||
**Insomnia | **Insomnia | ||
*'''Prognosis:''' Prognosis is generally excellent/good/poor, and the 1/5/10-year mortality/survival rate of patients with [disease name] is approximately [#]%. | |||
'''Prognosis:''' Prognosis is generally excellent/good/poor, and the 1/5/10-year mortality/survival rate of patients with [disease name] is approximately [#]%. | |||
==Diagnosis== | ==Diagnosis== | ||
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===Physical Examination=== | ===Physical Examination=== | ||
*Physical examination includes: | *Physical examination includes: | ||
**'''Inspection of the perianal area:''' | **'''Inspection of the perianal area:''' To check for anocutaneous reflex (anal wink sign). Absence of this reflex indicates nerve damage. | ||
**'''Digital rectal examination:''' It is done to evaluate for anal pathology and assess anal resting tone. | **'''Digital rectal examination:''' It is done to evaluate for anal pathology and assess anal resting tone. | ||
*Procedures that may help in determining the underlying cause of fecal incontinence such as: | |||
**Colonoscopy | |||
**Sigmoidoscopy | |||
**Anoscopy | |||
===Laboratory Findings=== | ===Laboratory Findings=== | ||
Stool testing may be helpful in determining the underlying cause of diarrhea. | |||
===Electrocardiogram=== | ===Electrocardiogram=== | ||
There are no ECG findings associated with | There are no ECG findings associated with fecal incontinence. | ||
===X-ray=== | ===X-ray=== | ||
There are no x-ray findings associated with | There are no x-ray findings associated with fecal incontinence. | ||
===Ultrasound/MRI=== | |||
*Ultrasound or magnetic resonance imaging may be helpful in the diagnosis of fecal incontinence. An ultrasound or magnetic resonance imaging may be helpful in determining the underlying abnormalities of the pelvic floor muscles, structural abnormalities of the anal sphincter and abnormalities of the wall of the rectum. | |||
=== | |||
===Other Diagnostic Studies=== | ===Other Diagnostic Studies=== | ||
*Anorectal manometry may be helpful in the diagnosis of fecal incontinence. This procedure helps in determining the anal sphincter tone and also the sensation and reflexes of the rectum. | |||
*Balloon expulsion test may be more helpful in determining defecation disorders in the elderly patients who sufffer from fecal incontinence secondary to fecal impaction. | |||
==Treatment== | ==Treatment== | ||
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**In cases of fecal incontinence related to pregnancy, pelvic floor muscle training may help in prevention and reversal of the condition following the first year of delivery. <ref name="pmid18268289">{{cite journal| author=Landefeld CS, Bowers BJ, Feld AD, Hartmann KE, Hoffman E, Ingber MJ et al.| title=National Institutes of Health state-of-the-science conference statement: prevention of fecal and urinary incontinence in adults. | journal=Ann Intern Med | year= 2008 | volume= 148 | issue= 6 | pages= 449-58 | pmid=18268289 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18268289 }} </ref> <ref name="pmid23076935">{{cite journal| author=Boyle R, Hay-Smith EJ, Cody JD, Mørkved S| title=Pelvic floor muscle training for prevention and treatment of urinary and faecal incontinence in antenatal and postnatal women. | journal=Cochrane Database Syst Rev | year= 2012 | volume= 10 | issue= | pages= CD007471 | pmid=23076935 | doi=10.1002/14651858.CD007471.pub2 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23076935 }} </ref> | **In cases of fecal incontinence related to pregnancy, pelvic floor muscle training may help in prevention and reversal of the condition following the first year of delivery. <ref name="pmid18268289">{{cite journal| author=Landefeld CS, Bowers BJ, Feld AD, Hartmann KE, Hoffman E, Ingber MJ et al.| title=National Institutes of Health state-of-the-science conference statement: prevention of fecal and urinary incontinence in adults. | journal=Ann Intern Med | year= 2008 | volume= 148 | issue= 6 | pages= 449-58 | pmid=18268289 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18268289 }} </ref> <ref name="pmid23076935">{{cite journal| author=Boyle R, Hay-Smith EJ, Cody JD, Mørkved S| title=Pelvic floor muscle training for prevention and treatment of urinary and faecal incontinence in antenatal and postnatal women. | journal=Cochrane Database Syst Rev | year= 2012 | volume= 10 | issue= | pages= CD007471 | pmid=23076935 | doi=10.1002/14651858.CD007471.pub2 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23076935 }} </ref> | ||
**Elimination of interventions such as episiotomy, lateral sphincterotomy, and anal sphincter stretch in women may be helpful in preventing fecal incontinence. <ref name="pmid20025031">{{cite journal| author=Norton C, Whitehead WE, Bliss DZ, Harari D, Lang J, Conservative Management of Fecal Incontinence in Adults Committee of the International Consultation on Incontinence| title=Management of fecal incontinence in adults. | journal=Neurourol Urodyn | year= 2010 | volume= 29 | issue= 1 | pages= 199-206 | pmid=20025031 | doi=10.1002/nau.20803 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20025031 }} </ref> | **Elimination of interventions such as episiotomy, lateral sphincterotomy, and anal sphincter stretch in women may be helpful in preventing fecal incontinence. <ref name="pmid20025031">{{cite journal| author=Norton C, Whitehead WE, Bliss DZ, Harari D, Lang J, Conservative Management of Fecal Incontinence in Adults Committee of the International Consultation on Incontinence| title=Management of fecal incontinence in adults. | journal=Neurourol Urodyn | year= 2010 | volume= 29 | issue= 1 | pages= 199-206 | pmid=20025031 | doi=10.1002/nau.20803 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20025031 }} </ref> | ||
===abcd=== | |||
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==Follow-up== | ==Follow-up== |
Latest revision as of 04:31, 1 February 2018
http://www.aafp.org/afp/2011/0615/p1403.html
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Overview
Historical Perspective
[Disease name] was first discovered by [name of scientist], a [nationality + occupation], in [year]/during/following [event].
The association between [important risk factor/cause] and [disease name] was made in/during [year/event].
In [year], [scientist] was the first to discover the association between [risk factor] and the development of [disease name].
In [year], [gene] mutations were first implicated in the pathogenesis of [disease name].
There have been several outbreaks of [disease name], including -----.
In [year], [diagnostic test/therapy] was developed by [scientist] to treat/diagnose [disease name].
Classification
There is no established system for the classification of [disease name].
OR
[Disease name] may be classified according to [classification method] into [number] subtypes/groups: [group1], [group2], [group3], and [group4].
OR
[Disease name] may be classified into [large number > 6] subtypes based on [classification method 1], [classification method 2], and [classification method 3]. [Disease name] may be classified into several subtypes based on [classification method 1], [classification method 2], and [classification method 3].
OR
Based on the duration of symptoms, [disease name] may be classified as either acute or chronic.
OR
If the staging system involves specific and characteristic findings and features: According to the [staging system + reference], there are [number] stages of [malignancy name] based on the [finding1], [finding2], and [finding3]. Each stage is assigned a [letter/number1] and a [letter/number2] that designate the [feature1] and [feature2].
OR
The staging of [malignancy name] is based on the [staging system].
OR
There is no established system for the staging of [malignancy name].
Pathophysiology
The exact pathogenesis of [disease name] is not fully understood.
OR
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
OR
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
OR
The progression to [disease name] usually involves the [molecular pathway].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.
Causes
- Fecal Incontinence may be caused due to the following: [1] [2] [3]
- Anal sphincter dysfunction/damage
- Rectal prolapse
- Surgical procedures of the rectum and anus may lead to muscle or nerve injuries. Anorectal surgical procedures such as hemorrhoidectomy, fistula surgery and sphincterotomy. [2]
- Impaired rectal sensation
- Rectocele
- Damage to the nerves
- Diarrhea
- Inflammatory bowel disease
- Constipation
- Hemorrhoids
- Neurologic abnormalities such as multiple sclerosis and pudendal neuropathy
- Decreased compliance of the rectum
Differentiating Fecal incontinence from Other Diseases
- Fecal incontinence must be differentiated from other diseases such as:
Epidemiology and Demographics
- The prevalence of fecal Incontinence is approximately 2000-3000 per 100,000 individuals worldwide. [4]
- In the US, the prevalence of fecal Incontinence is similar in women and men and increases with age, with the prevalence of 8900 per 100,000 individuals in women and 7700 per 100,00 individuals in men. [5]
- In the US, fecal Incontinence affects 2600 per 100,000 individuals in the age group of 20 to 29 years and in elderly people up to 15,300 per 100,000 individuals who are over the age of 70 years. [5]
- There is no racial predilection to fecal Incontinence.[5]
Risk Factors
- Common risk factors in the development of Fecal incontinence include: [5] [6] [7] [8] [9]
- Age factor: Mostly seen in middle-age and older adult population.
- Gender: Females are more likely to have fecal incontinence when compared to men. The major risk factor being the complications during childbirth that damage the anal sphincter and injure the pelvic floor muscles and nerves such as:
- Episiotomy
- Forceps delivery
- Prolonged second stage of labor
- Occipitoposterior presentation of the fetus
- Pelvic floor injury resulting in significant tears and higher birth-weight of the infant
- Nerve injury/neuropathy: Damage to the pudendal nerve/pudendal neuropathy
- Alzheimer's disease and Dementia: Fecal incontinence is usually seen in individuals with Alzheimer's disease(advanced stage) and Dementia.
- Multiple sclerosis
- Anorectal congenital abnormalities
- Radiation therapy of the pelvis
- Rectal prolapse
- Hormone therapy: In post-menopausal women, fecal incontinence may be due to hormonal therapy.
Screening
- There is insufficient evidence to recommend routine screening for fecal incontinence.
- However, a physician should rule out the symptoms in conditions which may pose as risk factors for developing fecal incontinence.
Natural History, Complications, and Prognosis
- If left untreated, patients with Fecal incontinence may progress to develop complications such as:
- Pain and itching in the anal region leading to rashes and ulcers
- Social withdrawal
- Emotional distress
- Depression
- Insomnia
- Prognosis: Prognosis is generally excellent/good/poor, and the 1/5/10-year mortality/survival rate of patients with [disease name] is approximately [#]%.
Diagnosis
Diagnostic Study of Choice
- Reliable scoring systems for the assessment of fecal incontinence based on symptoms and the response received as a result of interventions are:[10] [11]
- The American Medical System Score
- The Vaizey Score
- The Wexner Score
History and Symptoms
- A thorough and detailed history is crucial while obtaining a history from a patient experiencing fecal incontinence. [2]
- The history taking should be focused mainly on obstetrical and surgical history apart from medication history and other associated medical conditions if any. [2]
- Symptoms should be categorized based on the onset, duration, severity and the type of incontinence. [2]
- Soiling of undergarments is a common symptom observed in individuals with fecal incontinence wherein stains of stool are observed on the undergarments.
- Symptoms of fecal incontinence vary acoording to the type of incontinence such as the urge fecal incontinence and passive fecal incontinence.
- Symptoms in individuals with urge fecal incontinence, the patient realizes the need to defecate but lacks control over it and may pass the stool even before reaching the restoom. [12] [13]
- Symptoms in individuals with passive fecal incontinence, the patient doesn't realize nor does have control over the passage of stools and hence it happens without their knowledge.[13]
Physical Examination
- Physical examination includes:
- Inspection of the perianal area: To check for anocutaneous reflex (anal wink sign). Absence of this reflex indicates nerve damage.
- Digital rectal examination: It is done to evaluate for anal pathology and assess anal resting tone.
- Procedures that may help in determining the underlying cause of fecal incontinence such as:
- Colonoscopy
- Sigmoidoscopy
- Anoscopy
Laboratory Findings
Stool testing may be helpful in determining the underlying cause of diarrhea.
Electrocardiogram
There are no ECG findings associated with fecal incontinence.
X-ray
There are no x-ray findings associated with fecal incontinence.
Ultrasound/MRI
- Ultrasound or magnetic resonance imaging may be helpful in the diagnosis of fecal incontinence. An ultrasound or magnetic resonance imaging may be helpful in determining the underlying abnormalities of the pelvic floor muscles, structural abnormalities of the anal sphincter and abnormalities of the wall of the rectum.
Other Diagnostic Studies
- Anorectal manometry may be helpful in the diagnosis of fecal incontinence. This procedure helps in determining the anal sphincter tone and also the sensation and reflexes of the rectum.
- Balloon expulsion test may be more helpful in determining defecation disorders in the elderly patients who sufffer from fecal incontinence secondary to fecal impaction.
Treatment
Medical Therapy
- Medical management of fecal incontinence involves medical therapy along with supportive measures that are focused at symptom control and also resolving the underlying conditions such as the stool consistency, rectal prolapse and other underlying associated medical conditions, if any.[2]
- The first-line of management inn case of the affected patients would be the streamlining of conservative measures. Symptom control approach that includes dietary modification along with behavioral modification, usage of pads, skin care and pharmacotherapy. The patients in whom behavioral changes are suggested, should be made aware of the gastrocolic reflex.[2]
- Dietary habits have to be assessed inorder to minimize the negative impacts of the food on stool consistency and volume.[2]
- Inclusion of fiber rich foods or supplements may help in minimizing loose stools but, such foods should be used cautiously in patients with baseline formed stools, because the softer consistency and increased volume of the stools may result in the symptoms getting deteriorated.[2]
- Medical therapy includes the use of drugs such as diphenoxylate/atropine, loperamide, cholestyramine, ondansetron, and/or amitriptyline. In order to reduce diarrhea and slightly increase the internal sphincter tone, diphenoxylate/atropine or loperamide are frequently used.[14] Amitriptyline may also be used as an alternative for treating diarrhea, and it may also be used to reduce rectal urgency.[15]
- In order to reduce episodes of incontinence in patients with fecal impaction and overflow incontinence, enema is suggested to facilitate stool elimination and reduce the stool load. [16]
- Supportive measures such as perianal skin care with barrier creams and restraining from over-the-counter topical creams without prescription.
- Physical therapy and biofeedback may help strengthen pelvic floor and sphincter muscles as they serve as exercises thereby helping the muscles to recordinate. [17]
Surgery
Surgical intervention is not recommended for the management of [disease name].
OR
Surgery is not the first-line treatment option for patients with [disease name]. Surgery is usually reserved for patients with either [indication 1], [indication 2], and [indication 3]
OR
The mainstay of treatment for [disease name] is medical therapy. Surgery is usually reserved for patients with either [indication 1], [indication 2], and/or [indication 3].
OR
The feasibility of surgery depends on the stage of [malignancy] at diagnosis.
OR
Surgery is the mainstay of treatment for [disease or malignancy].
Primary Prevention
- Effective measures for the primary prevention of Fecal incontinence include:
- Avoid constipation by exercising regularly and maintaining healthy food habits by drinking plenty water and including foods rich in fiber in the diet
- Avoiding straining or forceful defecation which may effect the anal sphincter and damage the related muscles and nerves which may lead to fecal incontinence.
- Treating Diarrhea by managing the underlying cause such as the gastrointestinal infection.
- In cases of fecal incontinence related to pregnancy, pelvic floor muscle training may help in prevention and reversal of the condition following the first year of delivery. [18] [19]
- Elimination of interventions such as episiotomy, lateral sphincterotomy, and anal sphincter stretch in women may be helpful in preventing fecal incontinence. [20]
abcd
- American Association for the Surgery of Trauma (AAST) Spleen Trauma Classification: [21]
American Association for the Surgery of Trauma (AAST) Spleen Trauma Classification | ||
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Grade | Injury description | |
I | Hematoma | Subcapsular, < 10% surface area |
Laceration | Capsular tear, < 1 cm parenchymal depth | |
II | Hematoma | Subcapsular, 10–50% surface area |
Intraparenchymal, < 5 cm diameter | ||
Laceration | 1–3 cm parenchymal depth not involving a perenchymal vessel | |
III | Hematoma | Subcapsular, > 50% surface area or expanding |
Ruptured subcapsular or parenchymal hematoma | ||
Intraparenchymal hematoma > 5 cm | ||
Laceration | > 3 cm parenchymal depth or involving trabecular vessels | |
IV | Laceration | Laceration of segmental or hilar vessels producing major devascularization (> 25% of spleen) |
V | Laceration | Completely shatters spleen |
Vascular | Hilar vascular injury which devascularized spleen |
- WSES Spleen Trauma Classification for adult and pediatric patients:[21]
WSES Class | Mechanism of injury | AAST | Hemodynamix Status (a), (b) | CT scan | First-line treatment in adults | First-line treatment in pediatric | |
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Minor | WSES I | Blunt/penetrating | I - II | Stable | Yes + local exploration in SW (d) | NOM (c) + serial clinical/laboratory/radiological evaluation
Consider angiography/angioembolization |
NOM (c) + serial clinical/laboratory/radiological evaluation |
Moderate | WSES II | Blunt/penetrating | III | Stable | Consider angiography/angioembolization | ||
WSES III | Blunt/penetrating | IV - V | Stable | NOM (c) All angiography/angioembolization + serial clinical/laboratory/radiological evaluation | |||
Severe | WSES IV | Blunt/penetrating | I - V | Unstable | No | OM | OM |
SW - Stab wound; GSW - Gunshot wound; OM - Operative management; NOM - Non-Operative management
(b) Hemodynamic stability in pediatric patients is considered systolic blood pressure of 90 mmHg plus twice the child’s age in years (the lower limit is inferior to 70 mmHg plus twice the child’s age in years, or inferior to 50 mmHg in some studies). Stabilized or acceptable hemodynamic status is considered in children with a positive response to fluid resuscitation: 3 boluses of 20 mL/kg of crystalloid replacement should be administered before blood replacement; positive response can be indicated by the heart rate reduction, the sensorium clearing, the return of peripheral pulses and normal skin color, an increase in blood pressure and urinary output, and an increase in warmth of extremity. Clinical judgment is fundamental in evaluating children (c) NOM should only be attempted in centers capable of a precise diagnosis of the severity of spleen injuries and capable of intensive management (close clinical observation and hemodynamic monitoring in a high dependency/intensive care environment, including serial clinical examination and laboratory assay, with immediate access to diagnostics, interventional radiology, and surgery and immediately available access to blood and blood products or alternatively in the presence of a rapid centralization system in those patients amenable to be transferred (d) Wound exploration near the inferior costal margin should be avoided if not strictly necessary because of the high risk to damage the intercostal vessels. |
- Non-operative management: [21]
Non-operative management | ||
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Adults | Pediatrics | |
General indications |
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Blunt/penetrating trauma |
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Penetrating trauma
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The role of angiography/angioembolization (AG/AE) |
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- Operative management: [21]
Operative management (OM) | |
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Adults | Pediatrics |
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Follow-up
Short- and long-term follow-up: [21]
Short- and long-term follow-up | |
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Adults | Pediatrics |
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- Diagnostic procedures: [21]
Diagnostic procedures | |
Adults | Pediatrics |
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Staging and TNM Classification related to Incidence, Treatment, and Prognosis | ||||
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Stage | TNM Classification | Clinical Classification | Incidence at diagnosis (%) | 5-year survival rate (%) |
0 | Tis, N0, M0 | Resectable | 7.5 | 15.2 |
IA | T1, N0, M0 | — | — | — |
IB | T2, N0, M0 | — | — | — |
IIA | T3, N0, M0 | — | — | — |
IIB | T1-3, N1, M0 | Locally advanced | 29.3 | 6.3 |
III | T4, any N, M0 | — | — | — |
IV | Any T, any N, M1 | Metastatic | 47.2 | 1.6 |
1[22]
- Stage grouping of pancreatic cancer:[22]
Stage grouping of pancreatic cancer: | |||
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Primary tumor | |||
Stage | T | N | M |
0 | Tis | N0 | M0 |
IA | T1 | N0 | M0 |
IB | T2 | N0 | M0 |
IIA | T3 | N0 | M0 |
IIB | T1 | N1 | M0 |
T2 | N1 | M0 | |
T3 | N1 | M0 | |
III | T4 | Any N | M0 |
IV | Any T | Any N | M1 |
TNM Classification for Pancreatic Cancer: | |||
---|---|---|---|
Primary tumor | |||
TX | Primary tumor cannot be assessed | ||
T0 | No evidence of primary tumor | ||
Tis | Carcinoma in situ | ||
T1 | Tumor limited to the pancreas, ≤2 cm in greatest dimension | ||
T2 | Tumor limited to the pancreas, >2 cm in greatest dimension | ||
T3 | Tumor extends beyond the pancreas but without involvement of the celiac axis or the superior mesenteric artery | ||
T4 | Tumor involves the celiac axis or the superior mesenteric artery (unresectable primary tumor) | ||
Regional lymph nodes | |||
NX | Regional lymph nodes cannot be assessed | ||
N0 | No regional lymph node metastasis | ||
N1 | Regional lymph node metastasis | ||
Distant metastases | |||
MX | Distant metastasis cannot be assessed | ||
M0 | No distant metastasis | ||
M1 | Distant metastasis |
- Types of Pancreatic Intraepithelial Neoplasia (PanIN):[23]
Types of Pancreatic Intraepithelial Neoplasia (PanIN) |
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PanIN 1 (low grade) |
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PanIN 2 (intermediate grade) |
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PanIN 3 (high grade/carcinoma in situ) |
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- Risk factors for Pancreatic Cancers:[23]
Risk factors for Pancreatic Cancer |
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Risk factors |
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Familial Cancer Syndromes |
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Other medical conditions |
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- Risk Factors and Inherited Syndromes associated with Pancreatic Cancer:[24]
Risk Factors and Inherited Syndromes associated with Pancreatic Cancer | |||
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Risk Factor | Approximate Risk | ||
Smoking | 2-3 % | ||
Long-standing Diabetes mellitus | 2 % | ||
Nonhereditery and Chronic Pancreatitis | 2-6 % | ||
Obesity, Inactivity or both | 2 % | ||
Non O Blood Group | 1-2 % | ||
Genetic SYndrome and Associated Gene or Genes | |||
Hereditary pancreatitis (PRSS1, SPINK1) | 50 % | ||
Familial atypical multiple mole and melanoma syndrome (p16) | 10-20 % | ||
Hereditary breast and ovarian cancer syndromes (BRCA1, BRCA2, PALB2) | 1-2 % | ||
Peutz-Jeghers syndrome (STK11 [LKB1]) | 30-40 % | ||
Hereditary nonpolyposis colon cancer (Lynch syndrome) (MLH1, MSH2, MSH6) | 4 % | ||
Ataxia-telangiectasia (ATM) | Unknown | ||
Li-Fraumeni syndrome (P53) | Unknown |
Aravind | |||
Reddy | Reddy | Reddy | Reddy |
Functional Pancreatic Neuroendocrine Tumors and their Characteristics | |||
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Tumor type and syndrome | Location in pancreas | Signs and symptoms | Circulating biomarkers |
Insulinoma (Whipple’s triad) |
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Gastrinoma (Zollinger–Ellison) |
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VIPoma (Verner– Morrison syndrome, WDHA) |
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Glucagonoma |
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Somatostatinoma |
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Ppoma |
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Gastritis staging in clinical practice: The OLGA staging system | |||||
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Atrophy Score | Corpus | ||||
No Atrophy (Score: 0) | Mild Atrophy (Score: 1) | Moderate Atrophy (Score: 2) | Severe Atrophy (Score: 3) | ||
A N T R U M |
No Atrophy (Score: 0) (including incisura angularis) | STAGE 0 | STAGE I | STAGE II | STAGE II |
Mild Atrophy (Score: 1) (including incisura angularis) | STAGE I | STAGE I | STAGE II | STAGE III | |
Moderate Atrophy (Score: 2) (including incisura angularis) | STAGE II | STAGE II | STAGE III | STAGE IV | |
Severe Atrophy (Score: 3) (including incisura angularis) | STAGE III | STAGE III | STAGE IV | STAGE IV |
Sydney system for grading of chronic gastritis
Sydney system for grading of chronic gastritis | ||
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Feature | Definition | Grading guidelines |
Chronic inflammation |
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Activity |
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Atrophy |
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Helicobacter pylori |
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Intestinal Metaplasia |
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Feature | Non-atrophic
Helicobacter |
Atrophic Helicobacter | Autoimmune |
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Inflammation pattern | Antral or diffuse | Antrum & corpus, mild inflammation | Corpus only |
Atrophy & metaplasia | Nil | Atrophy present, metaplasia at incisura | Corpus only |
Antral predominant gastritis | Corpus predominant gastritis |
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More predominant in antrum in developed countries | Less predominant in developed countries |
High acid output | Low acid output |
Associated with duodenal ulceration |
Classification Gastritis
Classification and grading of Gastritis: Updated Sydney System | |||
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Type of Gastritis | Etiology | Gastritis synonyms | |
Non-atrophic |
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Atrophic | Autoimmune |
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Multifocal atrophic |
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Special forms | Chemical |
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Radiation |
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Lymphocytic |
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Eosinophilic |
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Other infectious gastritides |
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Classification and grading of gastritis: Updated Sydney System | |||
Type of gastritis | Etiologic factors | Gastritis synonyms | |
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Nonatrophic |
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Aravind | |||
Reddy | Reddy | Reddy | Reddy |
The table below differentiates Gastritis from other conditions
Differential Diagnosis | ||||||||||||
Disease | Cause | Symptoms | Diagnosis | Other findings | ||||||||
Pain | Nausea & Vomiting | Heartburn | Belching or Bloating | Weight loss | Loss of Appetite | Stools | Endoscopy findings | |||||
Location | Aggravating Factors | Alleviating Factors | ||||||||||
Acute gastritis |
|
Food | Antacids | ✔ | ✔ | ✔ | - | ✔ | Black stools | - | ||
Chronic gastritis |
|
Food | Antacids | ✔ | ✔ | ✔ | ✔ | ✔ | - | H. pylori gastritis
Lymphocytic gastritis
|
- | |
Atrophic gastritis | Epigastric pain | - | - | ✔ | - | ✔ | ✔ | - | H. pylori
|
| ||
Crohn's disease | - | - | - | - | - | ✔ | ✔ |
|
|
|||
GERD |
|
|
|
✔
(Suspect delayed gastric emptying) |
✔ | - | - | - | - |
|
Other symptoms:
Complications
| |
Peptic ulcer disease |
|
|
|
|
✔ | ✔ | - | - | - | Gastric ulcers
Duodenal ulcers
|
Other diagnostic tests | |
Gastrinoma |
|
- | - | ✔
(suspect gastric outlet obstruction) |
✔ | - | - | - | Useful in collecting the tissue for biopsy |
Diagnostic tests
| ||
Gastric Adenocarcinoma |
|
- | - | ✔ | ✔ | ✔ | ✔ | ✔ |
|
Esophagogastroduodenoscopy
|
Other symptoms | |
Primary gastric lymphoma |
|
- | - | - | - | - | ✔ | - | - | Useful in collecting the tissue for biopsy | Other symptoms
|
Aravind | |||
Reddy | Reddy | Reddy | Reddy |
Aravind | |||
Reddy | Reddy | Reddy | Reddy |
Chronology of Yersinia pestis infection Outbreaks("WHO | Plague".) | |||||
Date | Region Affected | Suspected, Probable & Confirmed Cases | Deaths | Details | |
15 October 2017 | Seychelles - Suspected Plague (Ex- Madagascar) | 1 | 0 |
| |
2 October 2017 | Madagascar | 73 | 17 |
| |
29 September 2017 | Madagascar | 51 | 12 |
| |
9 January 2017 | Madagascar | 62 cases (6 confirmed, 5 probable, 51 suspected) | 26 (case fatality rate of 42%) |
| |
6 September 2015 | Madagascar | 14 | 10 |
| |
21 November 2014 | Madagascar | 119 | 40 |
| |
10 August 2010 | Peru | 17 | - |
| |
11 August 2009 | China | 12 | 3 |
| |
7 November 2006 | Democratic Republic of the Congo | 1174 | 50 |
| |
13 October 2006 | Democratic Republic of the Congo | 626 | 42 |
| |
14 June 2006 | Democratic Republic of the Congo | 100 | 19 |
| |
15 March 2005 | Plague in the Democratic Republic of the Congo - update 4 | 130 | 57 |
| |
9 March 2005 | Plague in the Democratic Republic of the Congo - update 3 | 114 cases (110 suspect cases, 4 probable cases) | 54 |
| |
4 March 2005 | Plague in the Democratic Republic of the Congo - update 2 | 57 cases (54 suspect cases, 3 probable cases) | 16 |
| |
1 March 2005 | Plague in the Democratic Republic of the Congo - update | 4 probable cases and 4 suspect cases | 1 |
| |
18 February 2005 | Plague in the Democratic Republic of the Congo | - | 61 |
| |
10 July 2003 | Plague in Algeria - Update 2 | 10 laboratory confirmed cases and 1 probable case | - |
| |
3 July 2003 | Plague in Algeria - Update | 10 cases of which 8 have been laboratory confirmed | - |
| |
24 June 2003 | Plague in Algeria | 10 cases, 8 cases of bubonic plague and 2 of septicemic plague | one fatal case reported |
| |
5 June 2002 | 2002 - Plague in Malawi | 71 | - |
| |
20 February 2002 | 2002 - Plague in India | 16 cases of pneumonic plague | 4 deaths in Hat Koti village |
| |
26 March 2001 | 2001 - Plague in Zambia | 23 hospitalized cases | 3 deaths in Petauke district, Eastern Province |
|
Years | Country | Apparent or suspected origin | Reported number of human cases | Reported number (%) of deaths among cases | Situation |
---|---|---|---|---|---|
2014 | Uganda | Uganda | 1 | 1 (100%) | Ninety-nine individuals were quarantined after a 30-year-old male health-worker died of Marburg hemorrhagic fever on the 28th of September. |
2012 | Uganda | Kabale | 15 | 4 (27%) | Testing at CDC/UVRI identified a Marburg virus disease outbreak in the districts of Kabale, Ibanda, Mbarara, and Kampala over a 3 week time period[25] |
2008 | Netherlands ex Uganda | Cave in Maramagambo forest in Uganda, at the southern edge of Queen Elizabeth National Park | 1 | 1 (100%) | A 40-year-old Dutch woman with a recent history of travel to Uganda was admitted to hospital in the Netherlands. Three days prior to hospitalization, the first symptoms (fever, chills) occurred, followed by rapid clinical deterioration. The woman died on the 10th day of the illness. |
2007 | Uganda | Lead and gold mine in Kamwenge District, Uganda | 4 | 1 (25%) | Small outbreak, with 4 cases in young males working in a mine. To date, there have been no additional cases identified[26] |
2004-2005 | Angola | Uige Province, Angola | 252 | 227 (90%) | Outbreak believed to have begun in Uige Province in October 2004. Most cases detected in other provinces have been linked directly to the outbreak in Uige[27] |
1998-2000 | Democratic Republic of Congo (DRC) | Durba, DRC | 154 | 128 (83%) | Most cases occurred in young male workers at a gold mine in Durba, in the north-eastern part of the country, which proved to be the epicenter of the outbreak. Cases were subsequently detected in the neighboring village of Watsa.[26] |
1990 | Russia | Russia | 1 | 1 (100%) | Laboratory contamination.[26] |
1987 | Kenya | Kenya | 1 | 1 (100%) | A 15-year-old Danish boy was hospitalized with a 3-day history of headache, malaise, fever, and vomiting. Nine days prior to symptom onset, he had visited Kitum Cave in Mount Elgon National Park. Despite aggressive supportive therapy, the patient died on the 11th day of illness. No further cases were detected[28] |
1980 | Kenya | Kenya | 2 | 1 (50%) | A man with a recent travel history to Kitum Cave in Kenya's Mount Elgon National Park. Despite specialized care in Nairobi, the male patient died. A doctor who attempted resuscitation developed symptoms 9 days later but recovered[29] |
1975 | Johannesburg, South Africa | Zimbabwe | 3 | 1 (33%) | A man with a recent travel history to Zimbabwe was admitted to hospital in South Africa. Infection spread from the man to his traveling companion and a nurse at the hospital. The man died, but both women were given vigorous supportive treatment and eventually recovered.[30] |
1967 | Germany and Yugoslavia | Uganda | 31 | 7 (23%) | Simultaneous outbreaks occurred in laboratory workers handling African green monkeys imported from Uganda. In addition to the 31 reported cases, an additional primary case was retrospectively diagnosed by serology. [31] |
Marburg hemorrhagic fever: Symptoms and Disease Progression | ||
Generalisation Phase (Day 1 to Day 5) |
| |
---|---|---|
Early Organ Phase (Day 6 to Day 13) |
| |
Late Organ or Convalescence Phase (Day 14 to Day 21) |
|
Disease | Gene | Chromosome | Differentiating Features | Components of MEN | Diagnosis | ||
---|---|---|---|---|---|---|---|
Parathyroid | Pitutary | Pancreas | |||||
von Hippel-Lindau syndrome | Von Hippel–Lindau tumor suppressor | 3p25.3 |
|
- | - | + |
|
Carney complex | PRKAR1A | 17q23-q24 |
|
- | - | - |
|
Neurofibromatosis type 1 | RAS | 17 | - | - | - | Prenatal
Postnatal Cardinal Clinical Features" are required for positive diagnosis.
| |
Li-Fraumeni syndrome | TP53 | 17 | Early onset of diverse amount of cancers such as | - | - | - |
Criteria
|
Gardner's syndrome | APC | 5q21 |
|
- | - | - |
|
Multiple endocrine neoplasia type 2 | RET | - |
|
+ | - | - |
Criteria Two or more specific endocrine tumors
|
Cowden syndrome | PTEN | - | Hamartomas | - | - | - |
|
Acromegaly/gigantism | - | - |
|
- | + | - |
|
Pituitary adenoma | - | - |
|
- | + | - |
|
Hyperparathyroidism | - | - | - | + | - | - |
|
Pheochromocytoma/paraganglioma |
VHL RET NF1 SDHB SDHD |
- | Characterized by | - | - | - |
|
Adrenocortical carcinoma |
|
17p, 13q |
|
- | - | - |
|
Adapted from Toledo SP, Lourenço DM, Toledo RA. A differential diagnosis of inherited endocrine tumors and their tumor counterparts, journal=Clinics (Sao Paulo), volume= 68, issue= 7, 07/24/2013[32] |
Disease | Definition |
---|---|
von Hippel-Lindau syndrome | An autosomal dominant genetic disorder causing abnormal growth of blood vessels in different parts of the body. |
Tuberous sclerosis | A rare multi-system genetic disease that causes benign tumors to grow in the brain and on other vital organs such as the kidneys, heart, eyes, lungs, and skin. |
Carney complex | An autosomal dominant condition comprising myxomas of the heart and skin, hyperpigmentation of the skin (lentiginosis), and endocrine overactivity. |
Neurofibromatosis type 1 | An autosomal dominant tumor disorder of central nervous system due to germline mutations in neurofibromin manifesting as scoliosis (curvature of the spine), learning disabilities, vision disorders, cutaneous lesions and epilepsy. |
Li-Fraumeni syndrome | An autosomal dominant rare disorder due to germline mutations of the TP53 tumor suppressor gene characterized by early onset of diverse amount of cancers such as sarcoma, cancers of the breast, brain and adrenal glands. |
Gardner's syndrome | Familial colorectal polyposis is an autosomal dominant form of polyposis characterized by the presence of multiple polyps in the colon together with tumors outside the colon . |
Multiple endocrine neoplasia type 2 | An autosomal dominant disorder characterized by medullary thyroid carcinoma (MTC), pheochromocytoma and primary hyperparathyroidism. |
Cowden syndrome | A rare autosomal dominant disorder due to germline mutation of PTEN, a tumor suppressor gene characterized by multiple tumor-like growths called hamartomas. |
Cushing's syndrome | A disorder due to prolonged exposure to cortisol characterized by hypertension, abdominal obesity but with thin arms and legs, purple abdominal striae, moon facies, buffalo lump, weak muscles, weak bones, acne, and fragile skin that heals poorly. |
Acromegaly/gigantism | A rare syndrome due to excess growth hormone characterized by enlargement of the hands, feet, nose, lips and ears, and a general thickening of the skin, hypertrichosis, hyperpigmentation and hyperhidrosis and carpal tunnel syndrome. |
Hyperaldosteronism | A disorder due to excess production of the aldosterone by the adrenal glands characterized by hypertension, muscular weakness, muscle spasms, tingling sensations and excessive urination. |
Pituitary adenoma | A tumor in pituitary gland characterized by visual field defects, classically bitemporal hemianopsia, increased intracranial pressure, migraine and lateral rectus palsy. |
Hyperparathyroidism | A disorder due to excess production of parathyroid hormone characterized by kidney stones, hypercalcemia, constipation, peptic ulcers and depression. |
Thyroid carcinoma | A tumor of the thyroid gland characterized by signs and symptoms of hyperthryroidism or hypothyroidism. |
Pheochromocytoma/paraganglioma | A neuroendocrine tumor of the medulla of the adrenal glands characterized by episodic hypertension, palpitations, anxiety, diaphoresis and weight loss. |
Adrenocortical carcinoma | An aggressive cancer originating in the cortex of the adrenal gland that may either by non-secretory (asymptomatic) or secretory with signs and symptoms of Cushing syndrome (cortisol hypersecretion), Conn syndrome (aldosterone hypersecretion), virilization (testosterone hypersecretion) |
Adapted from Toledo SP, Lourenço DM, Toledo RA. A differential diagnosis of inherited endocrine tumors and their tumor counterparts, journal=Clinics (Sao Paulo), volume= 68, issue= 7, 07/24/2013[32] |
Risk factors of VTE may be categorized in to modifiable, non-modifiable, temporary and other risk factors.
Modifiable Risk Factors | Non-Modifiable Risk Factors | Temporary Risk Factors | Other Risk Factors |
❑ Modifiable risk factors are reversible based upon lifestyle/behavior modification. |
❑ Advanced age
|
❑ Pregnancy and the peri-partum period |
❑ Other possible factors associated with VTE include:[38]
|
Functional (Nuclear) Imaging for Thyrotoxicosis | |||||
Diagnosis | Degree of Thyrotoxicosis | Radioactive iodine Uptake | Scintigraphy Image | ||
---|---|---|---|---|---|
Toxic multinodular goiter | +/++ | Normal or +/++ | Enlarged gland with multiple "hot" or "cold" nodules | ||
Grave's disease | ++++ | ++++ | Enlarged gland with homogenous uptake | ||
Thyrotoxic phase of subacute thyroiditis | ++++ | <1% at 4 or 24 hr. | Absent isotope uptake | ||
Toxic adenoma | +/++ | Normal or +/++ | Dominant "hot" nodule with low or absent uptake in the surrounding normal gland. |
Multiple Endocrine Neoplasia-1 (MEN-1) Syndrome Tumors | ||
Enteropancreatic tumor |
| |
---|---|---|
Pituitary adenoma |
| |
Associated tumors |
| |
Parathyroid adenoma |
- |
|- ! colspan="1" style="background: #4479BA; padding: 5px 5px;" | Parathyroid adenoma | style="padding: 5px 5px; background: #F5F5F5;" | Parathyroid adenoma
Laboratory Findings of Familial Hypocalciuric Hypercalcemia | |||||
Condition | PTH | Serum Calcium | Serum phosphate | Urine Calcium | Urine Calcium/Serum Creatinine Ratio |
---|---|---|---|---|---|
Familial Hypocalciuric Hypercalcemia | Normal | Normal or ↑ | Normal | ↓ | ↓ |
Primary Hyperparathyroidism | ↑ | ↑ | ↓ | Normal | ↑ |
Cause of dementia | Characteristics and clinical and cognitive features |
---|---|
Alzheimer's disease | Brain disease that encompasses predementia and dementia phases. Memory changes and AD biomarker evidence required for diagnosis of probable AD. Slow cognitive and functional decline with early loss of awareness. Amnestic and nonamnestic phenotypes |
Lewy body dementia | Spectrum of disorders with movement, cognitive, autonomic changes. Includes dementia with Lewy bodies and Parkinson's disease dementia. Early visual hallucinations, muscle rigidity, sleep disturbance. α-synuclein deposits present in neurons |
Frontotemporal lobar degeneration | Focal atrophy of frontal and temporal lobes; knife-edge atrophy noted on MRI. Younger onset, changes in personality and behavior, language impairment, strong familial component. |
Vascular dementia | Stepwise progression and focal neurologic signs (also known as multi-infarct dementia or poststroke dementia). Dysexecutive syndrome, slowed processing speed, retrieval difficulties, depression, mild motor signs in subcortical vascular dementia. Symptoms overlap with alzheimer's disease. |
Causes of Hypergastrinemia | ||
Appropriate hypergastrinemia |
| |
---|---|---|
Inappropriate hypergastrinemia |
| |
Spurious hypergastrinemia |
|
Cause of dementia | Characteristics and clinical and cognitive features |
AD | Brain disease that encompasses predementia and dementia phases. Memory changes and AD biomarker evidence required for diagnosis of probable AD. Slow cognitive and functional decline with early loss of awareness. Amnestic and nonamnestic phenotypes |
| |
Lewy body dementia | Spectrum of disorders with movement, cognitive, autonomic changes. Includes dementia with Lewy bodies and Parkinson's disease dementia. Early visual hallucinations, muscle rigidity, sleep disturbance. α-synuclein deposits present in neurons |
| |
Frontotemporal lobar degeneration | Focal atrophy of frontal and temporal lobes; knife-edge atrophy noted on MRI. Younger onset, changes in personality and behavior, language impairment, strong familial component |
| |
VaD | Stepwise progression and focal neurologic signs (also known as multi-infarct dementia or poststroke dementia). Dysexecutive syndrome, slowed processing speed, retrieval difficulties, depression, mild motor signs in subcortical VaD. Symptoms overlap with AD |
Cause of dementia | Characteristics and clinical and cognitive features |
AD | Brain disease that encompasses predementia and dementia phases. Memory changes and AD biomarker evidence required for diagnosis of probable AD. Slow cognitive and functional decline with early loss of awareness. Amnestic and nonamnestic phenotypes |
| |
Lewy body dementia | Spectrum of disorders with movement, cognitive, autonomic changes. Includes dementia with Lewy bodies and Parkinson's disease dementia. Early visual hallucinations, muscle rigidity, sleep disturbance. α-synuclein deposits present in neurons |
| |
Frontotemporal lobar degeneration | Focal atrophy of frontal and temporal lobes; knife-edge atrophy noted on MRI. Younger onset, changes in personality and behavior, language impairment, strong familial component |
| |
VaD | Stepwise progression and focal neurologic signs (also known as multi-infarct dementia or poststroke dementia). Dysexecutive syndrome, slowed processing speed, retrieval difficulties, depression, mild motor signs in subcortical VaD. Symptoms overlap with AD |
Clinical Dementia Rating | |||||
Based on the severity of Impairment | |||||
Criteria | Minimal | Questionable | Mild | Moderate | Severe |
---|---|---|---|---|---|
Memory | No memory loss or slight inconsistent forgetfulness | Consistent slight forgetfulness; partial recollection of events; “benign” forgetfulness | Moderate memory loss; more marked for recent events; defect interferes with everyday activities | Severe memory loss; only highly learned material retained; new material rapidly lost | Severe memory loss; only fragments remain |
Orientation | Fully oriented | Fully oriented except for slight difficulty with time relationships | Moderate difficulty with time relationships; oriented for place at examination; may have geographic disorientation elsewhere | Severe difficulty with time relationships; usually disoriented to time, often to place | Oriented to person only |
Judgment and problem solving | Solves everyday problems and handles business and financial affairs well; judgment good in relation to past performance | Slight impairment in solving problems, determining similarities and differences | Moderate difficulty in solving problems, determining similarities and differences; social judgment usually maintained | Severely impaired in solving problems, determining similarities and differences; social judgment usually impaired | Unable to make judgments or solve problems |
Community affairs | Independent function at usual level in job, shopping, and volunteer and social groups | Slight impairment in these activities | Unable to function independently at these activities, although may still be engaged in some; appears normal to casual inspection | No pretense of independent function outside of home; appears well enough to be taken to functions outside a family home | No pretense of independent function outside of home; appears too ill to be taken to functions outside a family home |
Home and hobbies | Life at home, hobbies, and intellectual interests well maintained | Life at home, hobbies, and intellectual interests slightly impaired | Mild but definite impairment of function at home; more difficult chores abandoned; more complicated hobbies and interests abandoned | Only simple chores preserved; interests very restricted and poorly maintained | No significant function in home |
Personal care | Fully capable of self-care | Fully capable of self-care | Needs prompting | Requires assistance in dressing, hygiene, keeping of personal effects | Requires much help with personal care; frequent incontinence |
Sandbox: Dr.Reddy | |
xxx |
{| class="wikitable"
!Condition !T3 !T4 !TSH |- |Thyrotoxicosis |Increased |Increased |Supressed |- |T3 Toxicosis |2X (Increased Twice) |Normal |Supressed |- |Hypothyroidism |Low/Normal |Low |Increased |} ↓ β
Differentiating Thyroid adenoma from other Diseases
The table below summarizes the findings that differentiate thyroid adenoma from other conditions that cause neck swelling.[39]
Disease | Findings |
---|---|
Multinodular goiter | Multinodular goiter is the multinodular enlargement of the thyroid gland. They are large nodules of more than 1 cm that produces symptoms of hyperthyroidism. |
Grave's disease | Grave's disease is an autoimmune disease that affects the thyroid. It frequently results in hyperthyroidism and an enlarged thyroid. Pretibial myxedema and ophthalmopathy are some of the findings of grave's disease. |
Hashimoto's disease | Hashimoto's disease is an autoimmune disease in which the thyroid gland is attacked by a variety of cell-mediated and antibody-mediated immune processes, causing primary hypothyroidism. |
Medullary thyroid carcinoma | Medullary thyroid carcinoma is a form of thyroid carcinoma which originates from the parafollicular cells (C cells), which produce the hormone calcitonin. |
Thyroid lymphoma | Thyroid lymphoma is a rare malignant tumor which manifests as rapidly enlarging neck mass causing respiratory difficulty. |
De Quervain's thyroiditis | De Quervain's thyroiditis is a subacute granulomatous thyroiditis preceded by an upper respiratory tract infection. |
Acute suppurative thyroiditis | Acute suppurative thyroiditis is an uncommon thyroid disorder usually caused by bacterial infection. |
Thyroid adenoma must be differentiated from other causes of hyperthyroidism such as Grave's disease and toxic nodular goiter.
Cause of thyrotoxicosis | TSH receptor antibodies | Thyroid US | Color flow Doppler | Radioactive iodine uptake/Scan | Other features |
---|---|---|---|---|---|
Graves' disease | + | Hypoechoic pattern | ? | ? | Ophthalmopathy, dermopathy, acropachy |
Toxic nodular goiter | - | Multiple nodules | - | Hot nodules at thyroid scan | - |
Toxic adenoma | - | Single nodule | - | Hot nodule | - |
Subacute thyroiditis | - | Heterogeneous hypoechoic areas | Reduced/absent flow | ? | Neck pain, fever, and elevated inflammatory index |
Painless thyroiditis | - | Hypoechoic pattern | Reduced/absent flow | ? | - |
Amiodarone induced thyroiditis-Type 1 | - | Diffuse or nodular goiter | ?/Normal/? | ? but higher than in Type 2 | High urinary iodine |
Amiodarone induced thyroiditis-Type 2 | - | Normal | Absent | ?/absent | High urinary iodine |
Central hyperthyroidism | - | Diffuse or nodular goiter | Normal/? | ? | Inappropriately normal or high TSH |
Trophoblastic disease | - | Diffuse or nodular goiter | Normal/? | ? | - |
Factitious thyrotoxicosis | - | Variable | Reduced/absent flow | ? | ? Serum thyroglobulin |
Struma ovarii | - | Variable | Reduced/absent flow | ? | Abdominal RAIU |
Disease | Findings | |
---|---|---|
Thyroiditis | Direct chemical toxicity with inflammation | Amiodarone, sunitinib, pazopanib, axitinib, and other tyrosine kinase inhibitors may also be associated with a destructive thyroiditis.[40][41] |
Radiation thyroiditis | Patients treated with radioiodine may develop thyroid pain and tenderness 5 to 10 days later, due to radiation-induced injury and necrosis of thyroid follicular cells and associated inflammation. | |
Drugs that interfere with the immune system | Interferon-alfa is a well-known cause of thyroid abnormality. It mostly leads to the development of de novo antithyroid antibodies.[42] | |
Lithium | Patients treated with lithium are at a high risk of developing painless thyroiditis and Graves' disease. | |
Palpation thyroiditis | Manipulation of the thyroid gland during thyroid biopsy or neck surgery and vigorous palpation during the physical examination may cause transient hyperthyroidism. | |
Exogenous and ectopic hyperthyroidism | Factitious ingestion of thyroid hormone | The diagnosis is based on the clinical features, laboratory findings, and 24-hour radioiodine uptake.[43] |
Acute hyperthyroidism from a levothyroxine overdose | The diagnosis is based on the clinical features, laboratory findings, and 24-hour radioiodine uptake.[44] | |
Struma ovarii | Functioning thyroid tissue is present in an ovarian neoplasm. | |
Functional thyroid cancer metastases | Large bony metastases from widely metastatic follicular thyroid cancer cause symptomatic hyperthyroidism. | |
Hashitoxicosis | It is an autoimmune thyroid disease that initially presents with hyperthyroidism and a high radioiodine uptake caused by TSH-receptor antibodies similar to Graves' disease. It is then followed by the development of hypothyroidism due to the infiltration of the thyroid gland with lymphocytes and the resultant autoimmune-mediated destruction of thyroid tissue, similar to chronic lymphocytic thyroiditis.[45] | |
Toxic adenoma and toxic multinodular goiter | Toxic adenoma and toxic multinodular goiter are results of focal/diffuse hyperplasia of thyroid follicular cells independent of TSH regulation. Findings of single or multiple nodules are seen on physical examination or thyroid scan.[46] | |
Iodine-induced hyperthyroidism | It is uncommon but can develop after an iodine load, such as administration of contrast agents used for angiography or computed tomography (CT), or iodine-rich drugs such as amiodarone. | |
Trophoblastic disease and germ cell tumors | Thyroid-stimulating hormone and HCG have a common alpha-subunit and a beta-subunit with considerable homology. As a result, HCG has weak thyroid-stimulating activity and high titer HCG may mimic hyperthyroidism.[47] |
Sandbox: Dr.Reddy |
Diagnostic accuracy of imaging for localization of gastrinoma | ||
---|---|---|
CT | 50% | Tumors enhance on early arterial phase because of high vascularity; sensitivity decreases for tumors <2cm |
MRI | ||
Diagnostic accuracy of imaging for localization of gastrinoma | ||
Modality | Sensitivity | Comments |
---|---|---|
|
|
|
Sporadic and MEN-1-associated ZES | ||
Factors | Sopradic ZES | MEN-1 ZES |
---|---|---|
|
|
|
Causes of Hypergastrinemia | ||
Appropriate hypergastrinemia |
| |
---|---|---|
Inappropriate hypergastrinemia |
| |
Spurious hypergastrinemia |
|
Surgical approach to gastrinoma in sporadic ZES and ZES associated with MEN-1 | ||
sporadic ZES | MEN-1 ZES | |
---|---|---|
|
|
|
Surgical approach to gastrinoma in sporadic ZES and ZES associated with MEN-1 | ||
sporadic ZES | MEN-1 ZES | |
---|---|---|
|
|
|
Classification of Androgen Insensitivity Syndrome Phenotypes | ||
Type | External Genitalia | Findings |
---|---|---|
CAIS - (Complete androgen insensitivity syndrome) | Female (“testicular feminization”) |
|
Predominantly female (“incomplete AIS”) |
| |
PAIS - (Partial androgen insensitivity syndrome) | Ambiguous |
|
Predominantly male |
| |
MAIS - (Mild androgen insensitivity syndrome) | Male (“undervirilized male syndrome”) |
|
Template:Topic
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
Topic
References
- ↑ Ness W (2012). "Faecal incontinence: causes, assessment and management". Nurs Stand. 26 (42): 52–4, 56, 58–60. doi:10.7748/ns2012.06.26.42.52.c9162. PMID 22908765.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 Alavi K, Chan S, Wise P, Kaiser AM, Sudan R, Bordeianou L (2015). "Fecal Incontinence: Etiology, Diagnosis, and Management". J Gastrointest Surg. 19 (10): 1910–21. doi:10.1007/s11605-015-2905-1. PMID 26268955.
- ↑ Muñoz-Yagüe T, Solís-Muñoz P, Ciriza de los Ríos C, Muñoz-Garrido F, Vara J, Solís-Herruzo JA (2014). "Fecal incontinence in men: causes and clinical and manometric features". World J Gastroenterol. 20 (24): 7933–40. doi:10.3748/wjg.v20.i24.7933. PMC 4069320. PMID 24976729.
- ↑ Nelson R, Norton N, Cautley E, Furner S (1995). "Community-based prevalence of anal incontinence". JAMA. 274 (7): 559–61. PMID 7629985.
- ↑ 5.0 5.1 5.2 5.3 Whitehead WE, Borrud L, Goode PS, Meikle S, Mueller ER, Tuteja A; et al. (2009). "Fecal incontinence in US adults: epidemiology and risk factors". Gastroenterology. 137 (2): 512–7, 517.e1–2. doi:10.1053/j.gastro.2009.04.054. PMC 2748224. PMID 19410574.
- ↑ Rey E, Choung RS, Schleck CD, Zinsmeister AR, Locke GR, Talley NJ (2010). "Onset and risk factors for fecal incontinence in a US community". Am J Gastroenterol. 105 (2): 412–9. doi:10.1038/ajg.2009.594. PMC 3189687. PMID 19844202.
- ↑ Staller K, Townsend MK, Khalili H, Mehta R, Grodstein F, Whitehead WE; et al. (2017). "Menopausal Hormone Therapy Is Associated With Increased Risk of Fecal Incontinence in Women After Menopause". Gastroenterology. 152 (8): 1915–1921.e1. doi:10.1053/j.gastro.2017.02.005. PMC 5447480. PMID 28209529.
- ↑ Andy UU, Vaughan CP, Burgio KL, Alli FM, Goode PS, Markland AD (2016). "Shared Risk Factors for Constipation, Fecal Incontinence, and Combined Symptoms in Older U.S. Adults". J Am Geriatr Soc. 64 (11): e183–e188. doi:10.1111/jgs.14521. PMID 27783401.
- ↑ Matthews CA (2014). "Risk factors for urinary, fecal, or double incontinence in women". Curr Opin Obstet Gynecol. 26 (5): 393–7. doi:10.1097/GCO.0000000000000094. PMID 25110978.
- ↑ Baxter NN, Rothenberger DA, Lowry AC (2003). "Measuring fecal incontinence". Dis Colon Rectum. 46 (12): 1591–605. doi:10.1097/01.DCR.0000098906.61097.1C. PMID 14668583.
- ↑ Vaizey CJ, Carapeti E, Cahill JA, Kamm MA (1999). "Prospective comparison of faecal incontinence grading systems". Gut. 44 (1): 77–80. PMC 1760067. PMID 9862829.
- ↑ van Meegdenburg MM, Heineman E, Broens PM (2015). "Pudendal Neuropathy Alone Results in Urge Incontinence Rather Than in Complete Fecal Incontinence". Dis Colon Rectum. 58 (12): 1186–93. doi:10.1097/DCR.0000000000000497. PMID 26544817.
- ↑ 13.0 13.1 Buhmann H, Nocito A (2014). "[Update on fecal incontinence]". Praxis (Bern 1994). 103 (22): 1313–21. doi:10.1024/1661-8157/a001831. PMID 25351694.
- ↑ Read M, Read NW, Barber DC, Duthie HL (1982). "Effects of loperamide on anal sphincter function in patients complaining of chronic diarrhea with fecal incontinence and urgency". Dig Dis Sci. 27 (9): 807–14. PMID 7105952.
- ↑ Santoro GA, Eitan BZ, Pryde A, Bartolo DC (2000). "Open study of low-dose amitriptyline in the treatment of patients with idiopathic fecal incontinence". Dis Colon Rectum. 43 (12): 1676–81, discussion 1681-2. PMID 11156450.
- ↑ Chassagne P, Jego A, Gloc P, Capet C, Trivalle C, Doucet J; et al. (2000). "Does treatment of constipation improve faecal incontinence in institutionalized elderly patients?". Age Ageing. 29 (2): 159–64. PMID 10791451.
- ↑ Heymen S, Scarlett Y, Jones K, Ringel Y, Drossman D, Whitehead WE (2009). "Randomized controlled trial shows biofeedback to be superior to pelvic floor exercises for fecal incontinence". Dis Colon Rectum. 52 (10): 1730–7. doi:10.1007/DCR.0b013e3181b55455. PMC 3855426. PMID 19966605.
- ↑ Landefeld CS, Bowers BJ, Feld AD, Hartmann KE, Hoffman E, Ingber MJ; et al. (2008). "National Institutes of Health state-of-the-science conference statement: prevention of fecal and urinary incontinence in adults". Ann Intern Med. 148 (6): 449–58. PMID 18268289.
- ↑ Boyle R, Hay-Smith EJ, Cody JD, Mørkved S (2012). "Pelvic floor muscle training for prevention and treatment of urinary and faecal incontinence in antenatal and postnatal women". Cochrane Database Syst Rev. 10: CD007471. doi:10.1002/14651858.CD007471.pub2. PMID 23076935.
- ↑ Norton C, Whitehead WE, Bliss DZ, Harari D, Lang J, Conservative Management of Fecal Incontinence in Adults Committee of the International Consultation on Incontinence (2010). "Management of fecal incontinence in adults". Neurourol Urodyn. 29 (1): 199–206. doi:10.1002/nau.20803. PMID 20025031.
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- ↑ 26.0 26.1 26.2 "Outbreak of Marburg Hemorrhagic Fever Among Miners in Kamwenge and Ibanda Districts, Uganda, 2007". Missing or empty
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(help) - ↑ Towner JS, Khristova ML, Sealy TK, Vincent MJ, Erickson BR, Bawiec DA; et al. (2006). "Marburgvirus genomics and association with a large hemorrhagic fever outbreak in Angola". J Virol. 80 (13): 6497–516. doi:10.1128/JVI.00069-06. PMC 1488971. PMID 16775337.
- ↑ Mehedi M, Groseth A, Feldmann H, Ebihara H (2011). "Clinical aspects of Marburg hemorrhagic fever". Future Virol. 6 (9): 1091–1106. doi:10.2217/fvl.11.79. PMC 3201746. PMID 22046196.
- ↑ Smith DH, Johnson BK, Isaacson M, Swanapoel R, Johnson KM, Killey M; et al. (1982). "Marburg-virus disease in Kenya". Lancet. 1 (8276): 816–20. PMID 6122054.
- ↑ "WHO". Missing or empty
|url=
(help) - ↑ Feldmann H, Slenczka W, Klenk HD (1996). "Emerging and reemerging of filoviruses". Arch Virol Suppl. 11: 77–100. PMID 8800808.
- ↑ 32.0 32.1 Toledo SP, Lourenço DM, Toledo RA (2013). "A differential diagnosis of inherited endocrine tumors and their tumor counterparts". Clinics (Sao Paulo). 68 (7): 1039–56. doi:10.6061/clinics/2013(07)24. PMC 3715026. PMID 23917672.
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- ↑ Vayá A, Martínez-Triguero ML, España F, Todolí JA, Bonet E, Corella D (2011). "The metabolic syndrome and its individual components: its association with venous thromboembolism in a Mediterranean population". Metab Syndr Relat Disord. 9 (3): 197–201. doi:10.1089/met.2010.0117. PMID 21352080.
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- ↑ Pomp ER, Rosendaal FR, Doggen CJ (2008). "Smoking increases the risk of venous thrombosis and acts synergistically with oral contraceptive use". Am J Hematol. 83 (2): 97–102. doi:10.1002/ajh.21059. PMID 17726684.
- ↑ den Heijer M, Koster T, Blom HJ, Bos GM, Briet E, Reitsma PH; et al. (1996). "Hyperhomocysteinemia as a risk factor for deep-vein thrombosis". N Engl J Med. 334 (12): 759–62. doi:10.1056/NEJM199603213341203. PMID 8592549.
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- ↑ Thyroid adenoma. Wikipedia. https://en.wikipedia.org/wiki/Thyroid_adenoma Accessed on October 11, 2015
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- ↑ Vialettes B, Guillerand MA, Viens P, Stoppa AM, Baume D, Sauvan R, Pasquier J, San Marco M, Olive D, Maraninchi D (1993). "Incidence rate and risk factors for thyroid dysfunction during recombinant interleukin-2 therapy in advanced malignancies". Acta Endocrinol. 129 (1): 31–8. PMID 8351956.
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- ↑ Jha S, Waghdhare S, Reddi R, Bhattacharya P (2012). "Thyroid storm due to inappropriate administration of a compounded thyroid hormone preparation successfully treated with plasmapheresis". Thyroid. 22 (12): 1283–6. doi:10.1089/thy.2011.0353. PMID 23067331.
- ↑ Fatourechi V, McConahey WM, Woolner LB (1971). "Hyperthyroidism associated with histologic Hashimoto's thyroiditis". Mayo Clin. Proc. 46 (10): 682–9. PMID 5171000.
- ↑ Laurberg P, Pedersen KM, Vestergaard H, Sigurdsson G (1991). "High incidence of multinodular toxic goitre in the elderly population in a low iodine intake area vs. high incidence of Graves' disease in the young in a high iodine intake area: comparative surveys of thyrotoxicosis epidemiology in East-Jutland Denmark and Iceland". J. Intern. Med. 229 (5): 415–20. PMID 2040867.
- ↑ Oosting SF, de Haas EC, Links TP, de Bruin D, Sluiter WJ, de Jong IJ, Hoekstra HJ, Sleijfer DT, Gietema JA (2010). "Prevalence of paraneoplastic hyperthyroidism in patients with metastatic non-seminomatous germ-cell tumors". Ann. Oncol. 21 (1): 104–8. doi:10.1093/annonc/mdp265. PMID 19605510.