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{{SI}}                                                                  
|-
{{CMG}}
| <figure-inline><figure-inline>[[File:Siren.gif|link=Hypokalemia resident survival guide|41x41px]]</figure-inline></figure-inline>|| <br> || <br>
==Overview==
| [[Hypokalemia resident survival guide|'''Resident'''<br>'''Survival'''<br>'''Guide''']]
|}
{{Hypokalemia}}


'''For patient information on this page, click [[Hypokalemia (patient information)|here]]'''
==Historical Perspective==
 
*[Disease name] was first discovered by [scientist name], a [nationality + occupation], in [year] during/following [event].
{{CMG}}'''; Associate Editor-In-Chief:''' {{CZ}}; {{AIDA}} [[User:Aditya Govindavarjhulla|Aditya Govindavarjhulla, M.B.B.S.]] [mailto:agovi@wikidoc.org] ; '''Assistant Editor(s)-In-Chief:''' [[User:Jack Khouri|Jack Khouri]]
*In [year], [gene] mutations were first identified in the pathogenesis of [disease name].
 
*In [year], the first [discovery] was developed by [scientist] to treat/diagnose [disease name].
{{SK}} Hypokalaemia; potassium levels low (plasma or serum); potassium - low; low blood potassium; potassium depletion
 
==Classification==
==[[Hypokalemia overview|Overview]]==
*[Disease name] may be classified according to [classification method] into [number] subtypes/groups:
:*[group1]
:*[group2]
:*[group3]
*Other variants of [disease name] include [disease subtype 1], [disease subtype 2], and [disease subtype 3].
==Pathophysiology==
==Pathophysiology==
*


==Clinical Features== 


 
==Differentiating [disease name] from other Diseases==
*[Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as:
:*[Differential dx1]
:*[Differential dx2]
:*[Differential dx3]
==Epidemiology and Demographics==
* The prevalence of [disease name] is approximately [number or range] per 100,000 individuals worldwide.
* In [year], the incidence of [disease name] was estimated to be [number or range] cases per 100,000 individuals in [location].
===Age===
*Patients of all age groups may develop [disease name].
*[Disease name] is more commonly observed among patients aged [age range] years old.
*[Disease name] is more commonly observed among [elderly patients/young patients/children].
===Gender===
*[Disease name] affects men and women equally.
*[Gender 1] are more commonly affected with [disease name] than [gender 2].
* The [gender 1] to [Gender 2] ratio is approximately [number > 1] to 1.
===Race===
*There is no racial predilection for [disease name].
   
   
*[Disease name] usually affects individuals of the [race 1] race.
*[Race 2] individuals are less likely to develop [disease name].


*Potassium is the most common intracellular cation. Approximately 98% of total potassium exists in the intracellular fluid (ICF), which has a normal range of  140–150 mEq/l. Merely 2% of this cation is placed in the extracellular fluids (ECF), where it ranges from 3.5 to 5 mEq/l. Potassium is essential during numerous body functions, particularly for excitable cells such as muscle and nerve cells. Any disorder of potassium serum levels can disturb the transmembrane [[potential]] and renders excitable cells ([[nerve]] and [[muscle]]) [[Hyperpolarization (biology)|hyperpolariz]]<nowiki/>ed and less sensitive. However, [[Cardiac|cardiac cells]] don't obey this rule and become hyperexcitable. [[Potassium]] regulation is essential to maintain a normal activity in cells. Any impairment in potassium serum levels will have severe consequences on several organs especially the [[heart]] and the [[nervous system]]. Typically, total potassium excretion in the stool is low and most ingested potassium is absorbed. The [[Kidney|kidne]]<nowiki/>y is the primary regulator of potassium balance through excretion (the kidney excretes 90-95% of dietary potassium); the gut excretes a minimal amount of dietary potassium (approximately 10%).
==Risk Factors==
*Common risk factors in the development of [disease name] are [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].


==[[Hypokalemia historical perspective|Historical Perspective]]==
== Natural History, Complications and Prognosis==
*The majority of patients with [disease name] remain asymptomatic for [duration/years].
*Early clinical features include [manifestation 1], [manifestation 2], and [manifestation 3].
*If left untreated, [#%] of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].
*Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].
*Prognosis is generally [excellent/good/poor], and the [1/5/10­year mortality/survival rate] of patients with [disease name] is approximately [#%].


== Pathophysiology ==
== Diagnosis ==
Hypokalemia can result from several conditions:
===Diagnostic Criteria===
* Trans-cellular shifts of potassium inside the cells (most common)
*The diagnosis of [disease name] is made when at least [number] of the following [number] diagnostic criteria are met:
* [[Renal]] loss of [[potassium]]
:*[criterion 1]
** Increased distal Na delivery
:*[criterion 2]
** Increased urine flow
:*[criterion 3]
** [[Metabolic alkalosis]]
:*[criterion 4]
** Increased [[aldosterone]] level
* Gastrointestinal (GI) loss of potassium
=== Symptoms ===
* Increased [[hematopoiesis]] (increased cellular use of potassium)
*[Disease name] is usually asymptomatic.
* Decreased intake of potassium (least common)
*Symptoms of [disease name] may include the following:
:*[symptom 1]
:*[symptom 2]
:*[symptom 3]
:*[symptom 4]
:*[symptom 5]
:*[symptom 6]
=== Physical Examination ===
*Patients with [disease name] usually appear [general appearance].
*Physical examination may be remarkable for:
:*[finding 1]
:*[finding 2]
:*[finding 3]
:*[finding 4]
:*[finding 5]
:*[finding 6]


Shown below is a table summarizing the different pathophysiological processes that can lead to hypokalemia.<ref name="pmid24139581">{{cite journal |vauthors=Daly K, Farrington E |title=Hypokalemia and hyperkalemia in infants and children: pathophysiology and treatment |journal=J Pediatr Health Care |volume=27 |issue=6 |pages=486–96; quiz 497–8 |date=2013 |pmid=24139581 |doi=10.1016/j.pedhc.2013.08.003 |url=}}</ref> <ref name="pmid21278718">{{cite journal |vauthors=Unwin RJ, Luft FC, Shirley DG |title=Pathophysiology and management of hypokalemia: a clinical perspective |journal=Nat Rev Nephrol |volume=7 |issue=2 |pages=75–84 |date=February 2011 |pmid=21278718 |doi=10.1038/nrneph.2010.175 |url=}}</ref> <ref name="pmid22169581">{{cite journal |vauthors=Cheungpasitporn W, Suksaranjit P, Chanprasert S |title=Pathophysiology of vomiting-induced hypokalemia and diagnostic approach |journal=Am J Emerg Med |volume=30 |issue=2 |pages=384 |date=February 2012 |pmid=22169581 |doi=10.1016/j.ajem.2011.10.005 |url=}}</ref> <ref name="pmid24053336">{{cite journal |vauthors=Bisogni V, Rossi GP, Calò LA |title=Apparent mineralcorticoid excess syndrome, an often forgotten or unrecognized cause of hypokalemia and hypertension: case report and appraisal of the pathophysiology |journal=Blood Press. |volume=23 |issue=3 |pages=189–92 |date=June 2014 |pmid=24053336 |doi=10.3109/08037051.2013.832967 |url=}}</ref>   
=== Laboratory Findings ===
*There are no specific laboratory findings associated with [disease name].


*A  [positive/negative] [test name] is diagnostic of [disease name].
*An [elevated/reduced] concentration of [serum/blood/urinary/CSF/other] [lab test] is diagnostic of [disease name].
*Other laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].
===Imaging Findings===
*There are no [imaging study] findings associated with [disease name].
*[Imaging study 1] is the imaging modality of choice for [disease name].
*On [imaging study 1], [disease name] is characterized by [finding 1], [finding 2], and [finding 3].
*[Imaging study 2] may demonstrate [finding 1], [finding 2], and [finding 3].
=== Other Diagnostic Studies ===
*[Disease name] may also be diagnosed using [diagnostic study name].
*Findings on [diagnostic study name] include [finding 1], [finding 2], and [finding 3].


{| style="cellpadding=0; cellspacing= 0; width: 900px;"
== Treatment ==
|-
=== Medical Therapy ===
| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align="center" |'''Trans-cellular shifts''' || colspan="2" style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align="center" |'''Renal loss''' || style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align="center" |'''GI loss'''|| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align="center" |'''Increased hematopoiesis''' || style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align="center" |'''Decreased intake of potassium'''
*There is no treatment for [disease name]; the mainstay of therapy is supportive care.
|-
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |
*The mainstay of therapy for [disease name] is [medical therapy 1] and [medical therapy 2].
* [[Metabolic alkalosis]] (K+/H+ exchanger)
*[Medical therapy 1] acts by [mechanism of action 1].
* [[Insulin]] (activates Na+/K+ ATPase)
*Response to [medical therapy 1] can be monitored with [test/physical finding/imaging] every [frequency/duration].
* [[Catecholamine]] (activates Na+/K+ ATPase)
* [[Hypokalemic thyrotoxic periodic paralysis]]
=== Surgery ===
* [[Hypothermia]]
*Surgery is the mainstay of therapy for [disease name].
* [[Chloroquine]]
*[Surgical procedure] in conjunction with [chemotherapy/radiation] is the most common approach to the treatment of [disease name].
* [[Barium]] intoxication
*[Surgical procedure] can only be performed for patients with [disease stage] [disease name].
* [[Cesium]] intoxication
* [[Antipsychotic]] overdose
=== Prevention ===
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |
*There are no primary preventive measures available for [disease name].
'''''Subject is normo or hypotensive'''''<br>
''Associated with acidosis''
*Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].
* [[Diabetic ketoacidosis]]
* [[Renal tubular acidosis type 1]]
* [[Renal tubular acidosis type 2]]
''Associated with alkalosis''
* [[Diuretics]]
* [[Vomiting]] (increase in [[aldosterone]])
* [[Bartter's syndrome]] (dysfunction of in loop of Henle)
* [[Gitelman's syndrome]] (dysfunction in distal convoluted tubules)
''Variable acid/base status''
* [[Hypomagnesemia]]
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |
'''''Subject is hypertensive'''''<br>
''Primary hyperaldosteronism''
* Conn's syndrome
''Secondary hyperaldosteronism''
* Renovascular disease
* Renin secreting tumor
''Non aldosterone increase in mineralcorticoid''
* [[Cushing's disease]]
* [[Congenital adrenal hyperplasia]]
* Increased [[mineralcorticoid]]s
* Licorice ingestion
* [[Liddle's syndrome]]
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |
''Associated with metabolic acidosis''
* [[Diarrhea]]
* [[Laxative abuse]]
* [[Villous adenoma]]
''Associated with metabolic alkalosis''
* [[Vomiting]]
* [[Nasogastric tube]] drainage
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |
* [[Megaloblastic anemia]]
* Treatment of [[anemia]]
* Crisis of [[AML]]
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |
* Tea and toast diet
* [[Anorexia nervosa]]
* [[Alcoholism]]
|}


=== The Role of the Kidney ===
*Once diagnosed and successfully treated, patients with [disease name] are followed-up every [duration]. Follow-up testing includes [test 1], [test 2], and [test 3].
* The [[Kidneys]] play a vital role in keeping the balance of [[potassium]].
* At the [[glomerulus]], potassium is freely filtered and reabsorbed mainly in the [[proximal tubule]] and thick ascending [[loop of Henle]] (>60 % of filtered potassium).
* The cortical [[collecting duct]] receives 10–15% of filtered potassium and constitutes the kidney’s primary site of potassium excretion.
* Potassium excretion at the cortical collecting duct depends on the amount of sodium delivered there and the activity of [[aldosterone]].
* The absorption of sodium by the principal cells of the cortical collecting ducts is mediated by the apical epithelial [[sodium channels]] (ENaC); when the amount of [[sodium]] delivered to the cortical [[collecting duct]] is very high, the absorption of sodium increases without concomitant absorption of the accompanying anions (e.g., [[Bicarbonates|bicarbonate]]<nowiki/>s and chloride ions) which are not easy to absorb. This physiologic process causes the formation of a negative charge within the cortical collecting duct lumen, causing potassium and proton secretion.
* [[Aldosterone]] increases sodium absorption at the cortical collecting duct by means of enhancing the activity of Na-K-ATPase pumps and augmenting the number of the ENaC channels.
 
 
 
{{#ev:youtube|gQ39BX-NXsc}}
 
=== Factors Increasing Kidney Potassium Excretion ===
*Increased [[aldosterone]]
*High urine flow rate
*High distal sodium delivery
*[[Metabolic alkalosis]]
*High extracellular fluid K+ concentration
 
=== Some Factors Affecting Potassium Distribution Between the Cells and the Extracellular Fluid ===
*Na/K ATPase
*[[Insulin]]
*[[Catecholamines]]
*Plasma potassium concentration
*Extracellular pH
*[[Hyperosmolarity]] <ref>{{cite book | last = Hall | first = John | title = Guyton and Hall textbook of medical physiology | publisher = Elsevier | location = Philadelphia, PA | year = 2016 | isbn = 978-1-4557-7005-2 }} </ref>
 
=== The Physiologic Role of Potassium ===
*Potassium is the most common intracellular cation. Approximately 98% of total potassium exists in the intracellular fluid (ICF), which has a normal range of  140–150 mEq/l. Merely 2% of this cation is placed in the extracellular fluids (ECF), where it ranges from 3.5 to 5 mEq/l.
* Potassium is essential during numerous body functions, particularly for excitable cells such as muscle and nerve cells. 
* Diet, mostly fruits and vegetables, is the major source of potassium for the body.<ref name="pmid23674806">{{cite journal| author=Weaver CM| title=Potassium and health. | journal=Adv Nutr | year= 2013 | volume= 4 | issue= 3 | pages= 368S-77S | pmid=23674806 | doi=10.3945/an.112.003533 | pmc=3650509 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23674806  }} </ref> <ref>{{cite journal|doi=10.1159/000446268 Received:}}</ref>
 
=== The Cellular Effect of Hypokalemia ===
The normal ratio of intracellular to extracellular potassium in the body is vital for the generation of action potential and results in appropriate cardiac and neuromuscular cells performance. By decreasing the potassium concentration in extracellular space, the amount of the potassium gradient across the cell membrane is risen and results in hyperpolarization. This alteration moves the resting membrane potential from the threshold to a higher level; hence, a bigger than standard stimulus is necessary to generate an action potential. Consequently, reduced excitability in the neurons and muscle cells would appear and cause flaccid muscle paralysis, [[rhabdomyolysis]] (in severe hypokalemia), and paralytic ileus.<ref name="PalmerClegg2016">{{cite journal|last1=Palmer|first1=Biff F.|last2=Clegg|first2=Deborah J.|title=Physiology and pathophysiology of potassium homeostasis|journal=Advances in Physiology Education|volume=40|issue=4|year=2016|pages=480–490|issn=1043-4046|doi=10.1152/advan.00121.2016}}</ref>
 
 
[[Image:Hypokalemia .png|right|400px]]
 
=== Pathophysiology of Hypokalemic Heart Arrhythmias ===
* Hypokalemia in neurons and muscle cells reduces the membrane responsiveness and causes hyperpolarization. But in cardiac cells, specifically in the conducting system, depolarization is observed. The main reason is the alteration of ion selectivity of TWIK-1 K+ channels, which in standard situation leak potassium. During pathological hypokalemia, these channels transport sodium inward the cells, leading to paradoxical depolarization and may result in cardiac arrhythmias.
 
* Decreased extracellular potassium also suppresses the activity of some potassium channels conductance, and in turn, it delays ventricular repolarization. Prolonged repolarization could also predispose re-entrant arrhythmias.
 
* Moreover, Hypokalemia can inhibit Na+-K+ ATPase activity, leading to intracellular Na+ And Ca2+ increase. The accumulation of intracellular ca2+ activates calmodulin kinase and, in turn, induces late Na+ and Ca2+ currents and causes a further reduction in repolarization reserve. This would result in early after-depolarization (EAD)–mediated arrhythmias.<ref name="MaZhang2011">{{cite journal|last1=Ma|first1=L.|last2=Zhang|first2=X.|last3=Chen|first3=H.|title=TWIK-1 Two-Pore Domain Potassium Channels Change Ion Selectivity and Conduct Inward Leak Sodium Currents in Hypokalemia|journal=Science Signaling|volume=4|issue=176|year=2011|pages=ra37–ra37|issn=1945-0877|doi=10.1126/scisignal.2001726}}</ref> <ref name="WeissQu2017">{{cite journal|last1=Weiss|first1=James N.|last2=Qu|first2=Zhilin|last3=Shivkumar|first3=Kalyanam|title=Electrophysiology of Hypokalemia and Hyperkalemia|journal=Circulation: Arrhythmia and Electrophysiology|volume=10|issue=3|year=2017|issn=1941-3149|doi=10.1161/CIRCEP.116.004667}}</ref>
 
=== Pathophysiology of Hypokalemic in GI system: ===
* A low level of potassium  [[Category:Electrophysiology]] [[Category:Cardiology]] [[Category:Endocrinology]] [[Category:Emergency medicine]] [[Category:Nephrology]] [[Category:Electrolyte disturbance]] [[Category:Blood tests]] [[Category:Intensive care medicine]]   causes dysfunctional gastrointestinal smooth muscle performance, the slow movement of the GI system, constipation, and  paralytic ileus. The primary rationale behind them is the impairment of normal action potential in the muscle cell membrane, which disturbs favorable contraction and cellular depolarization. <ref name="StreetenWilliams1952">{{cite journal|last1=Streeten|first1=D. H. P.|last2=Williams|first2=E. M. Vaughan|title=Loss of cellular potassium as a cause of intestinal paralysis in dogs|journal=The Journal of Physiology|volume=118|issue=2|year=1952|pages=149–170|issn=00223751|doi=10.1113/jphysiol.1952.sp004782}}</ref> <ref name="PalmerClegg2016">{{cite journal|last1=Palmer|first1=Biff F.|last2=Clegg|first2=Deborah J.|title=Physiology and pathophysiology of potassium homeostasis|journal=Advances in Physiology Education|volume=40|issue=4|year=2016|pages=480–490|issn=1043-4046|doi=10.1152/advan.00121.2016}}</ref>
 
==[[Hypokalemia causes|Causes]]==
 
==[[Hypokalemia differential diagnosis|Differentiating Hypokalemia from other Diseases]]==
 
==[[Hypokalemia epidemiology and demographics|Epidemiology and Demographics]]==
 
==[[Hypokalemia risk factors|Risk Factors]]==
 
==[[Hypokalemia natural history|Natural History, Complications and Prognosis]]==
 
==[[Hypokalemia Diagnosis|Diagnosis]]==
[[Hypokalemia laboratory findings#Diagnostic Algorithm|Diagnostic Algorithm]] | [[Hypokalemia history and symptoms | History and Symptoms]] | [[Hypokalemia physical examination|Physical Examination]] | [[Hypokalemia laboratory findings | Laboratory Findings]] | [[Hypokalemia electrocardiogram | Electrocardiogram]] | [[Hypokalemia other diagnostic studies|Other Diagnostic Studies]]
 
==[[Hypokalemia treatment|Treatment]]==
[[Hypokalemia medical therapy| Medical Therapy]] | [[Hypokalemia primary prevention|Primary Prevention]] | [[Hypokalemia secondary prevention|Secondary Prevention]] | [[Hypokalemia cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Hypokalemia future or investigational therapies|Future or Investigational Therapies]]
 
==Case Studies==
[[Hypokalemia case study one|Case #1]]
 
==Related Chapters==
* [[Hypomagnesemia]]
* [[Hyperkalemia]]
 
[[Category:Electrophysiology]]
[[Category:Cardiology]]
[[Category:Endocrinology]]
[[Category:Emergency medicine]]
[[Category:Nephrology]]
[[Category:Electrolyte disturbance]]
[[Category:Blood tests]]
[[Category:Intensive care medicine]]


==References==
{{Reflist|2}}
[[Category:Pick One of 28 Approved]]


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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Historical Perspective

  • [Disease name] was first discovered by [scientist name], a [nationality + occupation], in [year] during/following [event].
  • In [year], [gene] mutations were first identified in the pathogenesis of [disease name].
  • In [year], the first [discovery] was developed by [scientist] to treat/diagnose [disease name].

Classification

  • [Disease name] may be classified according to [classification method] into [number] subtypes/groups:
  • [group1]
  • [group2]
  • [group3]
  • Other variants of [disease name] include [disease subtype 1], [disease subtype 2], and [disease subtype 3].

Pathophysiology

Clinical Features

Differentiating [disease name] from other Diseases

  • [Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as:
  • [Differential dx1]
  • [Differential dx2]
  • [Differential dx3]

Epidemiology and Demographics

  • The prevalence of [disease name] is approximately [number or range] per 100,000 individuals worldwide.
  • In [year], the incidence of [disease name] was estimated to be [number or range] cases per 100,000 individuals in [location].

Age

  • Patients of all age groups may develop [disease name].
  • [Disease name] is more commonly observed among patients aged [age range] years old.
  • [Disease name] is more commonly observed among [elderly patients/young patients/children].

Gender

  • [Disease name] affects men and women equally.
  • [Gender 1] are more commonly affected with [disease name] than [gender 2].
  • The [gender 1] to [Gender 2] ratio is approximately [number > 1] to 1.

Race

  • There is no racial predilection for [disease name].
  • [Disease name] usually affects individuals of the [race 1] race.
  • [Race 2] individuals are less likely to develop [disease name].

Risk Factors

  • Common risk factors in the development of [disease name] are [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].

Natural History, Complications and Prognosis

  • The majority of patients with [disease name] remain asymptomatic for [duration/years].
  • Early clinical features include [manifestation 1], [manifestation 2], and [manifestation 3].
  • If left untreated, [#%] of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].
  • Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].
  • Prognosis is generally [excellent/good/poor], and the [1/5/10­year mortality/survival rate] of patients with [disease name] is approximately [#%].

Diagnosis

Diagnostic Criteria

  • 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]
  • [criterion 4]

Symptoms

  • [Disease name] is usually asymptomatic.
  • Symptoms of [disease name] may include the following:
  • [symptom 1]
  • [symptom 2]
  • [symptom 3]
  • [symptom 4]
  • [symptom 5]
  • [symptom 6]

Physical Examination

  • Patients with [disease name] usually appear [general appearance].
  • Physical examination may be remarkable for:
  • [finding 1]
  • [finding 2]
  • [finding 3]
  • [finding 4]
  • [finding 5]
  • [finding 6]

Laboratory Findings

  • There are no specific laboratory findings associated with [disease name].
  • A [positive/negative] [test name] is diagnostic of [disease name].
  • An [elevated/reduced] concentration of [serum/blood/urinary/CSF/other] [lab test] is diagnostic of [disease name].
  • Other laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].

Imaging Findings

  • There are no [imaging study] findings associated with [disease name].
  • [Imaging study 1] is the imaging modality of choice for [disease name].
  • On [imaging study 1], [disease name] is characterized by [finding 1], [finding 2], and [finding 3].
  • [Imaging study 2] may demonstrate [finding 1], [finding 2], and [finding 3].

Other Diagnostic Studies

  • [Disease name] may also be diagnosed using [diagnostic study name].
  • Findings on [diagnostic study name] include [finding 1], [finding 2], and [finding 3].

Treatment

Medical Therapy

  • There is no treatment for [disease name]; the mainstay of therapy is supportive care.
  • The mainstay of therapy for [disease name] is [medical therapy 1] and [medical therapy 2].
  • [Medical therapy 1] acts by [mechanism of action 1].
  • Response to [medical therapy 1] can be monitored with [test/physical finding/imaging] every [frequency/duration].

Surgery

  • Surgery is the mainstay of therapy for [disease name].
  • [Surgical procedure] in conjunction with [chemotherapy/radiation] is the most common approach to the treatment of [disease name].
  • [Surgical procedure] can only be performed for patients with [disease stage] [disease name].

Prevention

  • There are no primary preventive measures available for [disease name].
  • Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].
  • Once diagnosed and successfully treated, patients with [disease name] are followed-up every [duration]. Follow-up testing includes [test 1], [test 2], and [test 3].

References

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