Sandbox:Hamid

Sandbox:Hamid
ICD-10	K42
ICD-9	551-553
DiseasesDB	23647
MedlinePlus	000987
MeSH	D006554

Hamid Qazi, MD, BSc [1]

Salm.. ==Historical Perspective== [1]

Discovery

• Salmonella was first discovered by Daniel E. Salmon, an American veterinarian, who first isolated Salmonella choleraesuis from pigs in 1884 with hog cholera.

• 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].

Outbreaks

• There have been several outbreaks of [disease name], which are summarized below:

Landmark Events in the Development of Treatment Strategies

• In [year], [diagnostic test/therapy] was developed by [scientist] to treat/diagnose [disease name].

Famous Cases

• The following are a few famous cases of disease name:

Classification

• [Disease name] may be classified according to Kaufmann-White typing system into [number] subtypes:
  • Somatic O
  • Surface Vi
  • Flagellar H antigens

Pathophysiology

After ingestion, infection with salmonellae is characterized by attachment of the bacteria by fimbriae or pili to cells lining the intestinal lumen. Salmonellae selectively attach to specialized epithelial cells (M cells) of the Peyer patches. The bacteria are then internalized by receptor-mediated endocytosis and transported within phagosomes to the lamina propria, where they are released. Once there, salmonellae induce an influx of macrophages (typhoidal strains) or neutrophils (nontyphoidal strains).

The Vi antigen of S typhi is important in preventing antibody-mediated opsonization and complement-mediated lysis. Through the induction of cytokine release and via mononuclear cell migration, S typhi organisms spread through the reticuloendothelial system, mainly to the liver, spleen, and bone marrow. Within 14 days, the bacteria appear in the bloodstream, facilitating secondary metastatic foci (eg, splenic abscess, endocarditis). In some patients, gallbladder infection leads to long-term carriage of S typhi or S paratyphi in bile and secretion to the stool. [17] As a rule, infection with nontyphoidal salmonellae generally precipitates a localized response, while S typhi and other especially virulent strains invade deeper tissues via lymphatics and capillaries and elicit a major immune response.

Pathogenesis

• It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
• [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
• Following ingestion, salmonella uses the [entry site] to invade the [cell name] cell.
• [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
• The progression to [disease name] usually involves the [molecular pathway].
• The pathophysiology of [disease/malignancy] depends on the histological subtype.

Genetics

• [Disease name] is transmitted in [mode of genetic transmission] pattern.
• Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
• The development of [disease name] is the result of multiple genetic mutations.

Gross Pathology

• On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].

Microscopic Pathology

• On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].

Overview

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Historical Perspective

===Discovery===

• Peutz-Jeghers syndrome was first discovered by Dr. Connor, a British, in 1895 in identical twin sisters.

• The association between gastrointestinal polyposis with distinctive pigmentation of the skin and Peutz-Jeghers syndrome was made in 1921 by Dr. Johannes Peutz of Holland.
• In 1949, Dr. Harold Jeghers of United States was the first to discover the association between combination of intestinal polyposis and skin pigmentation, and the development of Peutz-Jeghers syndrome.
• In 1954, A. Bruwer used the eponym Peutz-Jeghers syndrome
• In 1998, serine/threonine-protein kinase 11 alias LKB1 (STK11/LKB1) gene mutations were first implicated in the pathogenesis of Peutz-Jeghers syndrome.

Classification

• There is no established system for the classification of Peutz-Jeghers syndrome.

Pathophysiology

Pathogenesis

• It is thought that Peutz-Jeghers syndrome is the result of deletion or partial deletion of STK11 (LBK1) gene, located on chromosome 19p13.3.
• STK11 protein plays an important role in second messenger signal transduction and is found to regulate cellular proliferation, controls cell polarity, and responds to low energy states.
• In Mammalian studies, STK11 is shown in the inhibition of AMP-activated protein kinase (AMPK), and signals downstream to inhibit the mammalian target of rapamycin (mTOR).
  • The mTOR pathway is dysregulated in Peutz-Jeghers syndrome.

Pathology

• Peutz-Jeghers syndrome associated polyps have a unique smooth muscle core that arborizes throughout the polyp.
  • These polyps can only be differentiated from other polyp types by histopathology.

Causes

• Peutz-Jeghers syndrome is caused by STK11 gene mutation
• Variable penetrance

Epidemiology and Demographics

Prevalence

• The prevalence of Peutz-Jeghers syndrome is estimated to be 1 in 8300 to 250000
• Most likely prevalence is 1 in 100000

Age

• Peutz-Jeghers syndrome affects individuals between the ages of 10 to 30 years; average age of diagnosis is 23 years for males and 26 years for females.

Gender

• Males and females are equally affected.

Risk Factors

• There are no established risk factors for Peutz-Jeghers

Screening

• According to the American College of Gastroenterology (ACG) and the National Comprehensive Cancer Network (NCCN), screening for Peutz-Jeghers syndrome by physical exam, complete blood work for iron deficiency anemia, and endoscopy are recommended every year among patients with Peutz-Jeghers Syndrome.

Natural History, Complications, and Prognosis

Natural History

• The symptoms of Peutz-Jeghers syndrome usually develop in the first decade of life, and start with symptoms such as hyperpigmentation, abdominal pain, and rectal bleeding.
• If left untreated, patients with Peutz-Jeghers syndrome may progress to develop colon cancer, breast cancer, and gastrointestinal cancers.
• Extraintestinal manifestation include pancreatic, lung, breast, uterine, ovarian and testicular malignancies.

Complications

• Common complications of Peutz-Jeghers syndrome include:
  • Intussusception
  • Gastric outlet obstruction
  • Extraintestinal polyps

Prognosis

• Prognosis is generally excellent/good/poor, and the 1/5/10-year mortality/survival rate of patients with [disease name] is approximately [#]%.
• Depending on the extent of the [tumor/disease progression/etc.] at the time of diagnosis, the prognosis may vary. However, the prognosis is generally regarded as poor/good/excellent.
• The presence of [characteristic of disease] is associated with a particularly [good/poor] prognosis among patients with [disease/malignancy].
• [Subtype of disease/malignancy] is associated with the most favorable prognosis.
• The prognosis varies with the [characteristic] of tumor; [subtype of disease/malignancy] have the most favorable prognosis.

Signs and Symptoms Differential compared to Peutz-Jeghers Syndrome

"Peutz-Jeghers Syndrome - GeneReviews® - NCBI Bookshelf".

Diseases	History and Symptoms				Physical Examination				Laboratory Findings				Other Findings
	Abdominal Pain	Rectal Bleeding	Hyperpigmentation	Fatigue	Abdominal Pain	Hyperpigmentation	Anemia	Physical Finding 4	Gene(s)	Sertoli Cell Tumors	Gastrointestinal Tumors	Cancers
Juvenile Polyposis Syndrome	+		-	+		-	-		SMAD4 BMPR1A	-	Adenoma+  Hamartoma+++	Colon
Cowden Syndrome	-	-	Axillary+ Inguinal+ Facial+	-		Axillary+ Inguinal+ Facial+	-		PTEN	-	Adenoma+  Hamartoma+++	Breast, Thyroid, Endometrium	Trichilemmoma, skin hamartoma, hyperplastic polyps, macrocephaly, breast fibrosis
Carney Syndrome	-	-	Facial+ Mucosal+	-		Facial+ Mucosal+	-		PRKAR1A	++		Thyroid	Myxomas of skin and heart
Familial Adenomatous Polyposis	+	+	-	+		-	+		APC	-	Adenoma+++	Colon, brain	Desmoid tumors, osteomas
Hereditary Non-Polyposis Colon Cancer	-	+	-	+		-	+		MLH1 MSH2 MSH3 MSH6 PMS1 PMS2	-	Adenoma+	Endometrial, gastric, renal pelvis, ureter, and ovarian	Sebaceous adenoma

Use if the above table can not be made

Differential Diagnosis	Similar Features	Differentiating Features
Juvenile Polyposis Syndrome	On [physical exam; history; diagnostic test; imaging], [Differential 1] {has; demonstrates} [feature 1], [feature 2], [feature 3] also observed in [disease name].	On [physical exam; history; diagnostic test; imaging], [Differential 1] {has; demonstrates} [feature 1], [feature 2], [feature 3] that distinguish it from [disease name].
Cowden Syndrome	On [physical exam; history; diagnostic test; imaging], [Differential 1] {has; demonstrates} [feature 1], [feature 2], [feature 3] also observed in [disease name].	On [physical exam; history; diagnostic test; imaging], [Differential 1] {has; demonstrates} [feature 1], [feature 2], [feature 3] that distinguish it from [disease name].
Carney Syndrome	On [physical exam; history; diagnostic test; imaging], [Differential 1] {has; demonstrates} [feature 1], [feature 2], [feature 3] also observed in [disease name].	On [physical exam; history; diagnostic test; imaging], [Differential 1] {has; demonstrates} [feature 1], [feature 2], [feature 3] that distinguish it from [disease name].
Familial Adenomatous Polyposis	On [physical exam; history; diagnostic test; imaging], [Differential 1] {has; demonstrates} [feature 1], [feature 2], [feature 3] also observed in [disease name].	On [physical exam; history; diagnostic test; imaging], [Differential 1] {has; demonstrates} [feature 1], [feature 2], [feature 3] that distinguish it from [disease name].
Hereditary Non-Polyposis Colon Cancer	On [physical exam; history; diagnostic test; imaging], [Differential 1] {has; demonstrates} [feature 1], [feature 2], [feature 3] also observed in [disease name].	On [physical exam; history; diagnostic test; imaging], [Differential 1] {has; demonstrates} [feature 1], [feature 2], [feature 3] that distinguish it from [disease name].

Differentiating Gastrointestinal Bleeding from other Diseases

Disease Clinical manifestations Diagnosis Comments Symptoms Signs Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo- tension Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging Peutz-Jeghers syndrome Depends on location of polyps it maybe present ± - ± - ± ± ± Rectal bleeding may be present due to polyp - - - + Hamartomatous polyps present on endoscopy Iron deficiency anemia on CBC STK11 mutation Intra-operative enteroscopy (laparatomy with endoscopy Double balloon eneteroscopy Colonoscopy Barium Swallow Can lead to colon cancer, breast cancer, ovarian cancer, cervical cancer, and testicular cancer Peptic ulcer disease Diffuse ± − + − − − + Gastric ulcer- melena and hematemesis Duodenal ulcer- melena and hematochezia Positive if perforated Positive if perforated Positive if perforated N Ascitic fluid LDH > serum LDH Glucose < 50mg/dl Total protein > 1g/dl Air under diaphragm in upright CXR Upper GI endoscopy for diagnosis Gastritis Epigastric ± − + − − − Positive in chronic gastritis + − − − N H.pylori infection diagnostic tests Endoscopy H.pylori gastritis guideline recommendation Gastrointestinal perforation Diffuse + ± - ± − − − + + + ± Hyperactive/hypoactive WBC> 10,000 Air under diaphragm in upright CXR Hamman's sign Acute diverticulitis LLQ + ± + − + ± − + Positive in perforated diverticulitis + + Hypoactive Leukocytosis CT scan Ultrasound History of constipation Inflammatory bowel disease Diffuse ± − − ± − + + + − − − Normal or hyperactive Anti-neutrophil cytoplasmic antibody (P-ANCA) in Ulcerative colitis Anti saccharomyces cerevisiae antibodies (ASCA) in Crohn's disease String sign on abdominal x-ray in Crohn's disease Extra intestinal findings: Uveitis Arthritis Infective colitis Diffuse + − ± − − + − + Positive in fulminant colitis ± ± Hyperactive Stool culture and studies Shiga toxin in bloody diarrhea PCR CT scan Bowel wall thickening Edema Colon carcinoma Diffuse/localized − − − − ± ± + + ± − − Normal or hyperactive if obstruction present CBC Carcinoembryonic antigen (CEA) Colonoscopy Flexible sigmoidoscopy Barium enema CT colonography  PILLCAM 2: A colon capsule for CRC screening may be used in patients with an incomplete colonoscopy who lacks obstruction Budd-Chiari syndrome RUQ ± − − ± − − − Positive in liver failure leading to varices − − − N Elevated serum aspartate aminotransferase and alanine aminotransferase levels may be more than five times the upper limit of the normal range. Elevated serum alkaline phosphatase and bilirubin levels, decreased serum albumin level. Findings on CT scan suggestive of Budd-Chiari syndrome include: Early enhancement of the caudate lobe and central liver around the inferior vena cava Delayed enhancement of the peripheral liver with accompanying central low density (flip-flop appearance) Peripheral zones of the liver show reversed portal venous blood flow In the chronic phase, there is caudate lobe enlargement and atrophy of the peripheral liver in affected areas Ascitic fluid examination shows: Total protein more than 2.5 g per deciliter White blood cells are usually less than 500/μL. Hemochromatosis RUQ − − − − − − − Positive in cirrhotic patients − − − N >60% TS >240 μg/L SF Raised LFT Hyperglycemia Ultrasound shows evidence of cirrhosis Extra intestinal findings: Hyperpigmentation Diabetes mellitus Arthralgia Impotence in males Cardiomyopathy Atherosclerosis Hypopituitarism Hypothyroidism Extrahepatic cancer Prone to specific infections Cirrhosis RUQ − − − + − − + + + − − N Hypoalbuminemia Prolonged PT Abnormal LFTs Hyponatremia Thrombocytopenia US Nodular, shrunken liver Ascites Stigmata of liver disease Cruveilhier- Baumgarten murmur Mesenteric ischemia Periumbilical Positive if bowel becomes gangrenous − + − − + + + Positive if bowel becomes gangrenous Positive if bowel becomes gangrenous − Hyperactive to absent Leukocytosis and lactic acidosis Amylase levels D-dimer CT angiography SMA or SMV thrombosis Also known as abdominal angina that worsens with eating Acute ischemic colitis Diffuse + ± + − − + + + + + + Hyperactive then absent Leukocytosis Abdominal x-ray Distension and pneumatosis CT scan Double halo appearance, thumbprinting Thickening of bowel May lead to shock Ruptured abdominal aortic aneurysm Diffuse ± − + − − − + + + − − N Fibrinogen D-dimer Focused Assessment with Sonography in Trauma (FAST)  Unstable hemodynamics Intra-abdominal or retroperitoneal hemorrhage Diffuse ± − ± − − − − + + − − N ↓ Hb ↓ Hct CT scan History of trauma

Overview

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Diagnostic Study of Choice

Gold standard/Study of choice:

• [Name of the investigation] is the gold standard test for the diagnosis of [disease name].
• The following result of [gold standard test] is confirmatory of [disease name]:
  • Result 1
  • Result 2
• The [name of investigation] should be performed when:
  • The patient presented with symptoms/signs 1. 2, 3.
  • A positive [test] is detected in the patient.
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The comparison table for diagnostic studies of choice for [disease name]

	Sensitivity	Specificity
Test 1	✔	...%
Test 2	...%	✔

✔= The best test based on the feature

Diagnostic results

The following result of [investigation name] is confirmatory of [disease name]:

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• Result 2

Sequence of Diagnostic Studies

The [name of investigation] should be performed when:

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Diagnostic Criteria

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• [Disease name] is mainly diagnosed based on clinical presentation. There are no established criteria for the diagnosis of [disease name].
• There is no single diagnostic study of choice for [disease name], though [disease name] may be diagnosed based on [name of criteria] established by [...].

• The diagnosis of [disease name] is made when at least [number] of the following [number] diagnostic criteria are met: [criterion 1], [criterion 2], [criterion 3], and [criterion 4].
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  • Criteria 1
  • Criteria 2
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IF there are clear, established diagnostic criteria:

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• The diagnosis of [disease name] is based on the [criteria name] criteria, which include [criterion 1], [criterion 2], and [criterion 3].
• The diagnosis of [disease name] is based on the [definition name] definition, which includes [criterion 1], [criterion 2], and [criterion 3].

IF there are no established diagnostic criteria: 

• There are no established criteria for the diagnosis of [disease name].

References

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Associate Editor(s)-in-Chief:

Overview

The majority of patients with [disease name] are asymptomatic.

OR

The hallmark of [disease name] is [finding]. A positive history of [finding 1] and [finding 2] is suggestive of [disease name]. The most common symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3]. Common symptoms of [disease] include [symptom 1], [symptom 2], and [symptom 3]. Less common symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3].

History and Symptoms

• Symptoms of Peutz-Jegher syndrome include abnormal pigmentation of the oral mucosa, abdominal pain, blood in stool, and extrusion of anal polyp. 

History

Patients with Peutz-Jegher syndrome may have a positive history of:

• Intussesception at a young age

References

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [3]; Associate Editor(s)-in-Chief:

Overview

Patients with [disease name] usually appear [general appearance]. Physical examination of patients with [disease name] is usually remarkable for [finding 1], [finding 2], and [finding 3].

OR

Common physical examination findings of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

The presence of [finding(s)] on physical examination is diagnostic of [disease name].

OR

The presence of [finding(s)] on physical examination is highly suggestive of [disease name].

Physical Examination

• Physical examination of patients with [disease name] is usually remarkable for:[finding 1], [finding 2], and [finding 3].
• The presence of [finding(s)] on physical examination is diagnostic of [disease name].
• The presence of [finding(s)] on physical examination is highly suggestive of [disease name].

Appearance of the Patient

• Patients with [disease name] usually appear [general appearance].

Vital Signs

• High-grade / low-grade fever
• Hypothermia / hyperthermia may be present
• Tachycardia with regular pulse or (ir)regularly irregular pulse
• Bradycardia with regular pulse or (ir)regularly irregular pulse
• Tachypnea / bradypnea
• Kussmal respirations may be present in _____ (advanced disease state)
• Weak/bounding pulse / pulsus alternans / paradoxical pulse / asymmetric pulse
• High/low blood pressure with normal pulse pressure / wide pulse pressure / narrow pulse pressure

Skin

• Cyanosis
• Jaundice
• Pallor
• Bruises

• Description (Adapted from Dermatology Atlas)

  Description (Adapted from Dermatology Atlas)

• 

  Description (Adapted from Dermatology Atlas)

HEENT

• Abnormalities of the head/hair may include ___
• Evidence of trauma
• Icteric sclera
• Nystagmus
• Extra-ocular movements may be abnormal
• Pupils non-reactive to light / non-reactive to accomodation / non-reactive to neither light nor accomodation
• Ophthalmoscopic exam may be abnormal with findings of ___
• Hearing acuity may be reduced
• Weber test may be abnormal (Note: A positive Weber test is considered a normal finding / A negative Weber test is considered an abnormal finding. To avoid confusion, you may write "abnormal Weber test".)
• Rinne test may be positive (Note: A positive Rinne test is considered a normal finding / A negative Rinne test is considered an abnormal finding. To avoid confusion, you may write "abnormal Rinne test".)
• Exudate from the ear canal
• Tenderness upon palpation of the ear pinnae / tragus (anterior to ear canal)
• Inflamed nares / congested nares
• Purulent exudate from the nares
• Facial tenderness
• Erythematous throat with/without tonsillar swelling, exudates, and/or petechiae

Neck

• Jugular venous distension
• Carotid bruits may be auscultated unilaterally/bilaterally using the bell/diaphragm of the otoscope
• Lymphadenopathy (describe location, size, tenderness, mobility, and symmetry)
• Thyromegaly / thyroid nodules
• Hepatojugular reflux

Lungs

• Asymmetric chest expansion / Decreased chest expansion
• Lungs are hypo/hyperresonant
• Fine/coarse crackles upon auscultation of the lung bases/apices unilaterally/bilaterally
• Rhonchi
• Vesicular breath sounds / Distant breath sounds
• Expiratory/inspiratory wheezing with normal / delayed expiratory phase
• Wheezing may be present
• Egophony present/absent
• Bronchophony present/absent
• Normal/reduced tactile fremitus

Heart

• Chest tenderness upon palpation
• PMI within 2 cm of the sternum (PMI) / Displaced point of maximal impulse (PMI) suggestive of ____
• Heave / thrill
• Friction rub
• S1
• S2
• S3
• S4
• Gallops
• A high/low grade early/late systolic murmur / diastolic murmur best heard at the base/apex/(specific valve region) may be heard using the bell/diaphgram of the otoscope

Abdomen

• Abdominal distention
• Abdominal tenderness in the right/left upper/lower abdominal quadrant
• Rebound tenderness (positive Blumberg sign)
• A palpable abdominal mass in the right/left upper/lower abdominal quadrant
• Guarding may be present
• Hepatomegaly / splenomegaly / hepatosplenomegaly
• Additional findings, such as obturator test, psoas test, McBurney point test, Murphy test

Back

• Point tenderness over __ vertebrae (e.g. L3-L4)
• Sacral edema
• Costovertebral angle tenderness bilaterally/unilaterally
• Buffalo hump

Genitourinary

• A pelvic/adnexal mass may be palpated
• Inflamed mucosa
• Clear/(color), foul-smelling/odorless penile/vaginal discharge

Neuromuscular

• Patient is usually oriented to persons, place, and time
• Altered mental status
• Glasgow coma scale is ___ / 15
• Clonus may be present
• Hyperreflexia / hyporeflexia / areflexia
• Positive (abnormal) Babinski / plantar reflex unilaterally/bilaterally
• Muscle rigidity
• Proximal/distal muscle weakness unilaterally/bilaterally
• ____ (finding) suggestive of cranial nerve ___ (roman numerical) deficit (e.g. Dilated pupils suggestive of CN III deficit)
• Unilateral/bilateral upper/lower extremity weakness
• Unilateral/bilateral sensory loss in the upper/lower extremity
• Positive straight leg raise test
• Abnormal gait (describe gait: e.g. ataxic (cerebellar) gait / steppage gait / waddling gait / choeiform gait / Parkinsonian gait / sensory gait)
• Positive/negative Trendelenburg sign
• Unilateral/bilateral tremor (describe tremor, e.g. at rest, pill-rolling)
• Normal finger-to-nose test / Dysmetria
• Absent/present dysdiadochokinesia (palm tapping test)

Extremities

• Clubbing
• Cyanosis
• Pitting/non-pitting edema of the upper/lower extremities
• Muscle atrophy
• Fasciculations in the upper/lower extremity

References

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [4]; Associate Editor(s)-in-Chief:

Overview

An elevated/reduced concentration of serum/blood/urinary/CSF/other [lab test] is diagnostic of [disease name].

OR

Laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].

OR

[Test] is usually normal among patients with [disease name].

OR

Some patients with [disease name] may have elevated/reduced concentration of [test], which is usually suggestive of [progression/complication].

OR

There are no diagnostic laboratory findings associated with [disease name].

Laboratory Findings

• There are no diagnostic laboratory findings associated with [disease name].

OR

• An elevated/reduced concentration of serum/blood/urinary/CSF/other [lab test] is diagnostic of [disease name].
• [Test] is usually normal among patients with [disease name].
• Laboratory findings consistent with the diagnosis of [disease name] include:
  • [Abnormal test 1]
  • [Abnormal test 2]
  • [Abnormal test 3]

• Some patients with [disease name] may have elevated/reduced concentration of [test], which is usually suggestive of [progression/complication].

References

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [5]; Associate Editor(s)-in-Chief:

Overview

There are no ECG findings associated with [disease name].

OR

An ECG may be helpful in the diagnosis of [disease name]. Findings on an ECG suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

Electrocardiogram

• There are no ECG findings associated with [disease name].

OR

• An ECG may be helpful in the diagnosis of [disease name]. Findings on an ECG suggestive of/diagnostic of [disease name] include
  • [Finding 1]
  • [Finding 2]
  • [Finding 3]