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Nausea

MedGen UID:
10196
Concept ID:
C0027497
Sign or Symptom
Synonyms: NAUSEA; nausea; Nauseated; Nauseous; Observation of nausea
SNOMED CT: Nausea (422587007); Observation of nausea (422587007); Nauseous (422587007); Nauseated (422587007)
 
HPO: HP:0002018

Definition

A sensation of unease in the stomach together with an urge to vomit. [from HPO]

Conditions with this feature

Fabry disease
MedGen UID:
8083
Concept ID:
C0002986
Disease or Syndrome
Fabry disease results from deficient activity of the enzyme alpha-galactosidase A (a-Gal A) and progressive lysosomal deposition of globotriaosylceramide (GL-3) in cells throughout the body. The classic form, occurring in males with less than 1% a-Gal A enzyme activity, usually has its onset in childhood or adolescence with periodic crises of severe pain in the extremities (acroparesthesia), the appearance of vascular cutaneous lesions (angiokeratomas), sweating abnormalities (anhidrosis, hypohidrosis, and rarely hyperhidrosis), characteristic corneal and lenticular opacities, and proteinuria. Gradual deterioration of renal function to end-stage renal disease (ESRD) usually occurs in men in the third to fifth decade. In middle age, most males successfully treated for ESRD develop cardiac and/or cerebrovascular disease, a major cause of morbidity and mortality. Heterozygous females typically have milder symptoms at a later age of onset than males. Rarely, they may be relatively asymptomatic throughout a normal life span or may have symptoms as severe as those observed in males with the classic phenotype. In contrast, males with greater than 1% a-Gal A activity may have: (1) a cardiac variant phenotype that usually presents in the sixth to eighth decade with left ventricular hypertrophy, cardiomyopathy and arrhythmia, and proteinuria, but without ESRD; or (2) a renal variant phenotype, associated with ESRD but without the skin lesions or pain; or (3) cerebrovascular disease presenting as stroke or transient ischemic attack.
Chinese restaurant syndrome
MedGen UID:
891
Concept ID:
C0008127
Disease or Syndrome
Hereditary fructosuria
MedGen UID:
42105
Concept ID:
C0016751
Disease or Syndrome
Following dietary exposure to fructose, sucrose, or sorbitol, untreated hereditary fructose intolerance (HFI) is characterized by metabolic disturbances (hypoglycemia, lactic acidemia, hypophosphatemia, hyperuricemia, hypermagnesemia, hyperalaninemia) and clinical findings (nausea, vomiting, and abdominal distress; chronic growth restriction/failure to thrive). Untreated HFI typically first manifests when fructose- and sucrose-containing foods are introduced in the course of weaning young infants from breast milk. If large quantities of fructose are ingested, the infant may acutely develop lethargy, seizures, and/or progressive coma. Untreated HFI may result in renal and hepatic failure. If identified and treated before permanent organ injury occurs, individuals with HFI can experience a normal quality of life and life expectancy.
Hyperlipoproteinemia, type I
MedGen UID:
7352
Concept ID:
C0023817
Disease or Syndrome
Familial lipoprotein lipase (LPL) deficiency usually presents in childhood and is characterized by very severe hypertriglyceridemia with episodes of abdominal pain, recurrent acute pancreatitis, eruptive cutaneous xanthomata, and hepatosplenomegaly. Clearance of chylomicrons from the plasma is impaired, causing triglycerides to accumulate in plasma and the plasma to have a milky ("lactescent" or "lipemic") appearance. Symptoms usually resolve with restriction of total dietary fat to 20 grams/day or less.
Ovarian hyperstimulation syndrome
MedGen UID:
38966
Concept ID:
C0085083
Disease or Syndrome
A complication of OVULATION INDUCTION in infertility treatment. It is graded by the severity of symptoms which include OVARY enlargement, multiple OVARIAN FOLLICLES; OVARIAN CYSTS; ASCITES; and generalized EDEMA. The full-blown syndrome may lead to RENAL FAILURE, respiratory distress, and even DEATH. Increased capillary permeability is caused by the vasoactive substances, such as VASCULAR ENDOTHELIAL GROWTH FACTORS, secreted by the overly-stimulated OVARIES.
Migraine
MedGen UID:
57451
Concept ID:
C0149931
Disease or Syndrome
Migraine is the most common type of chronic, episodic headache, as summarized by Featherstone (1985). One locus for migraine with or without aura (MGR1) has been identified on chromosome 4q24. Other loci for migraine have been identified on 6p21.1-p12.2 (MGR3; 607498), 14q21.2-q22.3 (MGR4; 607501), 19p13 (MGR5; 607508), 1q31 (MGR6; 607516), 15q11-q13 (MGR7; 609179), 5q21 (with or without aura, MGR8, 609570; with aura, MGR9, 609670), 17p13 (MGR10; 610208), 18q12 (MGR11; 610209), 10q22-q23 (MGR12; 611706), and the X chromosome (MGR2; 300125). Mutation in the KCNK18 gene (613655) on chromosome 10q25 causes migraine with aura (MGR13; 613656). A subtype of autosomal dominant migraine with aura (MA), familial hemiplegic migraine (FHM; see 141500), is caused by mutation in the CACNA1A gene (601011) on chromosome 19p13 (FHM1; 141500), by mutation in the ATP1A2 gene (182340) on chromosome 1q21 (FHM2; 602481), or by mutation in the SCN1A gene (182389) on chromosome 2q24 (FHM3; 609634). Another locus for FHM has been mapped to chromosome 1q31 (FHM4; see 607516). There is evidence that a polymorphism in the estrogen receptor gene (ESR1; 133430.0005) and a polymorphism in the TNF gene (191160.0004) may confer susceptibility to migraine. A polymorphism in the endothelin receptor type A gene (EDNRA; 131243.0001) may confer resistance to migraine.
Cyclical vomiting syndrome
MedGen UID:
57509
Concept ID:
C0152164
Disease or Syndrome
Cyclic vomiting syndrome is a disorder that causes recurrent episodes of nausea, vomiting, and tiredness (lethargy). This condition is diagnosed most often in young children, but it can affect people of any age.The episodes of nausea, vomiting, and lethargy last anywhere from an hour to 10 days. An affected person may vomit several times per hour, potentially leading to a dangerous loss of fluids (dehydration). Additional symptoms can include unusually pale skin (pallor), abdominal pain, diarrhea, headache, fever, and an increased sensitivity to light (photophobia) or to sound (phonophobia). In most affected people, the signs and symptoms of each attack are quite similar. These attacks can be debilitating, making it difficult for an affected person to go to work or school.Episodes of nausea, vomiting, and lethargy can occur regularly or apparently at random, or can be triggered by a variety of factors. The most common triggers are emotional excitement and infections. Other triggers can include periods without eating (fasting), temperature extremes, lack of sleep, overexertion, allergies, ingesting certain foods or alcohol, and menstruation.If the condition is not treated, episodes usually occur four to 12 times per year. Between attacks, vomiting is absent, and nausea is either absent or much reduced. However, many affected people experience other symptoms during and between episodes, including pain, lethargy, digestive disorders such as gastroesophageal reflux and irritable bowel syndrome, and fainting spells (syncope). People with cyclic vomiting syndrome are also more likely than people without the disorder to experience depression, anxiety, and panic disorder. It is unclear whether these health conditions are directly related to nausea and vomiting.Cyclic vomiting syndrome is often considered to be a variant of migraines, which are severe headaches often associated with pain, nausea, vomiting, and extreme sensitivity to light and sound. Cyclic vomiting syndrome is likely the same as or closely related to a condition called abdominal migraine, which is characterized by attacks of stomach pain and cramping. Attacks of nausea, vomiting, or abdominal pain in childhood may be replaced by migraine headaches as an affected person gets older. Many people with cyclic vomiting syndrome or abdominal migraine have a family history of migraines.Most people with cyclic vomiting syndrome have normal intelligence, although some affected people have developmental delay or intellectual disability. Autism spectrum disorders, which affect communication and social interaction, have also been associated with cyclic vomiting syndrome. Additionally, muscle weakness (myopathy) and seizures are possible. People with any of these additional features are said to have cyclic vomiting syndrome plus.
Acute intermittent porphyria
MedGen UID:
56452
Concept ID:
C0162565
Disease or Syndrome
Acute intermittent porphyria (referred to as AIP in this GeneReview) results from half-normal activity of the enzyme hydroxymethylbilane synthase (HMBS). It is characterized clinically by life-threatening acute neurovisceral attacks of severe abdominal pain without peritoneal signs, often accompanied by nausea, vomiting, tachycardia, and hypertension. Attacks may be complicated by neurologic findings (mental changes, convulsions, and peripheral neuropathy that may progress to respiratory paralysis), and hyponatremia. Acute attacks, which may be provoked by certain drugs, alcoholic beverages, endocrine factors, calorie restriction, stress, and infections, usually resolve within two weeks. Most individuals with AIP have one or a few attacks; about 5% (mainly women) have recurrent attacks (defined as >4 attacks/year) that may persist for years. Other long-term complications are chronic renal failure, hepatocellular carcinoma (HCC), and hypertension. Attacks, which are very rare before puberty, are more common in women than men. All individuals with a genetic change in the gene HMBS that predisposes to AIP are at risk of developing acute attacks; however, most never have symptoms and are said to have latent (or presymptomatic) AIP.
Choroid plexus papilloma
MedGen UID:
64439
Concept ID:
C0205770
Neoplastic Process
Choroid plexus tumors are of neuroectodermal origin and range from benign choroid plexus papillomas (CPPs) to malignant choroid carcinomas (CPCs). These rare tumors generally occur in childhood, but have also been reported in adults. Patients typically present with signs and symptoms of increased intracranial pressure including headache, hydrocephalus, papilledema, nausea, vomiting, cranial nerve deficits, gait impairment, and seizures (summary by Safaee et al., 2013).
Familial hypokalemic alkalosis, Gullner type
MedGen UID:
78677
Concept ID:
C0268444
Disease or Syndrome
Glutaric aciduria, type 2
MedGen UID:
75696
Concept ID:
C0268596
Disease or Syndrome
Glutaric aciduria II (GA II) is an autosomal recessively inherited disorder of fatty acid, amino acid, and choline metabolism. It differs from GA I (231670) in that multiple acyl-CoA dehydrogenase deficiencies result in large excretion not only of glutaric acid, but also of lactic, ethylmalonic, butyric, isobutyric, 2-methyl-butyric, and isovaleric acids. GA II results from deficiency of any 1 of 3 molecules: the alpha (ETFA) and beta (ETFB) subunits of electron transfer flavoprotein, and electron transfer flavoprotein dehydrogenase (ETFDH). The clinical picture of GA II due to the different defects appears to be indistinguishable; each defect can lead to a range of mild or severe cases, depending presumably on the location and nature of the intragenic lesion, i.e., mutation, in each case (Goodman, 1993; Olsen et al., 2003). The heterogeneous clinical features of patients with MADD fall into 3 classes: a neonatal-onset form with congenital anomalies (type I), a neonatal-onset form without congenital anomalies (type II), and a late-onset form (type III). The neonatal-onset forms are usually fatal and are characterized by severe nonketotic hypoglycemia, metabolic acidosis, multisystem involvement, and excretion of large amounts of fatty acid- and amino acid-derived metabolites. Symptoms and age at presentation of late-onset MADD are highly variable and characterized by recurrent episodes of lethargy, vomiting, hypoglycemia, metabolic acidosis, and hepatomegaly often preceded by metabolic stress. Muscle involvement in the form of pain, weakness, and lipid storage myopathy also occurs. The organic aciduria in patients with the late-onset form of MADD is often intermittent and only evident during periods of illness or catabolic stress (summary by Frerman and Goodman, 2001). Importantly, riboflavin treatment has been shown to ameliorate the symptoms and metabolic profiles in many MADD patients, particularly those with type III, the late-onset and mildest form (Liang et al., 2009).
Lysinuric protein intolerance
MedGen UID:
75704
Concept ID:
C0268647
Disease or Syndrome
Lysinuric protein intolerance (LPI) typically presents after an infant is weaned; variable findings include recurrent vomiting and episodes of diarrhea, episodes of stupor and coma after a protein-rich meal, poor feeding, aversion to protein-rich food, failure to thrive, hepatosplenomegaly, and muscular hypotonia. Over time, findings include: poor growth; osteoporosis; involvement of the lungs (progressive interstitial changes; pulmonary alveolar proteinosis) and of kidneys (progressive glomerular and proximal tubular disease); hematologic abnormalities (normochromic or hypochromic anemia, leukopenia, thrombocytopenia, erythroblastophagocytosis at the bone marrow aspirate) and a clinical presentation resembling the hemophagocytic lymphohistiocytosis/macrophagic activation syndrome. Acute pancreatitis can also be seen.
Hyperthermia, cutaneous, with headaches and nausea
MedGen UID:
374453
Concept ID:
C1840373
Disease or Syndrome
Migraine with or without aura 6
MedGen UID:
334829
Concept ID:
C1843765
Finding
Migraine with or without aura 5
MedGen UID:
334831
Concept ID:
C1843771
Finding
For a phenotypic description and discussion of genetic heterogeneity of migraine headaches, see MGR1 (157300).
Migraine without aura 4
MedGen UID:
336040
Concept ID:
C1843773
Finding
Migraine with or without aura 3
MedGen UID:
375283
Concept ID:
C1843782
Finding
Episodic ataxia, type 3
MedGen UID:
376220
Concept ID:
C1847839
Disease or Syndrome
The hereditary ataxias are a group of genetic disorders characterized by slowly progressive incoordination of gait and often associated with poor coordination of hands, speech, and eye movements. Frequently, atrophy of the cerebellum occurs. In this GeneReview the hereditary ataxias are categorized by mode of inheritance and gene (or chromosome locus) in which pathogenic variants occur.
Episodic ataxia, type 4
MedGen UID:
376222
Concept ID:
C1847843
Disease or Syndrome
The hereditary ataxias are a group of genetic disorders characterized by slowly progressive incoordination of gait and often associated with poor coordination of hands, speech, and eye movements. Frequently, atrophy of the cerebellum occurs. In this GeneReview the hereditary ataxias are categorized by mode of inheritance and gene (or chromosome locus) in which pathogenic variants occur.
Migraine with or without aura, susceptibility to, 2
MedGen UID:
341144
Concept ID:
C1848066
Finding
Hypervitaminosis A
MedGen UID:
343435
Concept ID:
C1855883
Finding
Migraine with or without aura 11
MedGen UID:
387900
Concept ID:
C1857751
Finding
Migraine with or without aura 10
MedGen UID:
341839
Concept ID:
C1857752
Finding
Charcot-Marie-Tooth disease with ptosis and parkinsonism
MedGen UID:
396191
Concept ID:
C1861668
Disease or Syndrome
Charcot-Marie-Tooth disease, Guadalajara neuronal type
MedGen UID:
350075
Concept ID:
C1861673
Disease or Syndrome
Mitochondrial DNA depletion syndrome 11
MedGen UID:
767376
Concept ID:
C3554462
Disease or Syndrome
Mitochondrial DNA depletion syndrome-11 is an autosomal recessive mitochondrial disorder characterized by onset in childhood or adulthood of progressive external ophthalmoplegia (PEO), muscle weakness and atrophy, exercise intolerance, and respiratory insufficiency due to muscle weakness. More variable features include spinal deformity, emaciation, and cardiac abnormalities. Skeletal muscle biopsies show deletion and depletion of mitochondrial DNA (mtDNA) with variable defects in respiratory chain enzyme activities (summary by Kornblum et al., 2013). For a discussion of genetic heterogeneity of autosomal recessive mtDNA depletion syndromes, see MTDPS1 (603041).

Recent clinical studies

Etiology

Shen CH, Yang LY
Biol Res Nurs 2017 Mar;19(2):145-152. Epub 2016 Dec 27 doi: 10.1177/1099800416683801. PMID: 28024410
Vidall C, Sharma S, Amlani B
Br J Nurs 2016 Sep 8;25(16):S4-S11. doi: 10.12968/bjon.2016.25.S4. PMID: 27615540
Hesketh PJ, Schnadig ID, Schwartzberg LS, Modiano MR, Jordan K, Arora S, Powers D, Aapro M
Cancer 2016 Aug 1;122(15):2418-25. Epub 2016 May 13 doi: 10.1002/cncr.30054. PMID: 27176138Free PMC Article
Grant C, Ewart L, Muthas D, Deavall D, Smith SA, Clack G, Newham P
Toxicol Appl Pharmacol 2016 Apr 1;296:10-8. Epub 2016 Feb 11 doi: 10.1016/j.taap.2016.02.007. PMID: 26876616
Kottschade L, Novotny P, Lyss A, Mazurczak M, Loprinzi C, Barton D
Support Care Cancer 2016 Jun;24(6):2661-7. Epub 2016 Jan 15 doi: 10.1007/s00520-016-3080-y. PMID: 26768436Free PMC Article

Diagnosis

Fahlenkamp AV, Stoppe C, Cremer J, Biener IA, Peters D, Leuchter R, Eisert A, Apfel CC, Rossaint R, Coburn M
PLoS One 2016;11(4):e0153807. Epub 2016 Apr 25 doi: 10.1371/journal.pone.0153807. PMID: 27111335Free PMC Article
Grant C, Ewart L, Muthas D, Deavall D, Smith SA, Clack G, Newham P
Toxicol Appl Pharmacol 2016 Apr 1;296:10-8. Epub 2016 Feb 11 doi: 10.1016/j.taap.2016.02.007. PMID: 26876616
Dupuis LL, Lu X, Mitchell HR, Sung L, Devidas M, Mattano LA Jr, Carroll WL, Winick N, Hunger SP, Maloney KW, Kadan-Lottick NS
Cancer 2016 Apr 1;122(7):1116-25. Epub 2016 Jan 15 doi: 10.1002/cncr.29876. PMID: 26773735Free PMC Article
Kovacic K, Di Lorenzo C
J Pediatr Gastroenterol Nutr 2016 Mar;62(3):365-71. doi: 10.1097/MPG.0000000000001076. PMID: 26655943
de Souza CM, Visacri MB, Ferrari GB, Tuan BT, Costa AP, Barbosa CR, Lima CS, Mazzola PG, Moriel P
Int J Pharm Pract 2015 Oct;23(5):357-60. Epub 2015 Jan 9 doi: 10.1111/ijpp.12169. PMID: 25572714

Therapy

Shen CH, Yang LY
Biol Res Nurs 2017 Mar;19(2):145-152. Epub 2016 Dec 27 doi: 10.1177/1099800416683801. PMID: 28024410
Marx W, Ried K, McCarthy AL, Vitetta L, Sali A, McKavanagh D, Isenring L
Crit Rev Food Sci Nutr 2017 Jan 2;57(1):141-146. doi: 10.1080/10408398.2013.865590. PMID: 25848702
Vidall C, Sharma S, Amlani B
Br J Nurs 2016 Sep 8;25(16):S4-S11. doi: 10.12968/bjon.2016.25.S4. PMID: 27615540
Hong K, Herrmann K, Dybala C, Halseth AE, Lam H, Foreyt JP
Clin Obes 2016 Oct;6(5):305-12. Epub 2016 Aug 1 doi: 10.1111/cob.12157. PMID: 27477337Free PMC Article
Hesketh PJ, Schnadig ID, Schwartzberg LS, Modiano MR, Jordan K, Arora S, Powers D, Aapro M
Cancer 2016 Aug 1;122(15):2418-25. Epub 2016 May 13 doi: 10.1002/cncr.30054. PMID: 27176138Free PMC Article

Prognosis

Vidall C, Sharma S, Amlani B
Br J Nurs 2016 Sep 8;25(16):S4-S11. doi: 10.12968/bjon.2016.25.S4. PMID: 27615540
Hong K, Herrmann K, Dybala C, Halseth AE, Lam H, Foreyt JP
Clin Obes 2016 Oct;6(5):305-12. Epub 2016 Aug 1 doi: 10.1111/cob.12157. PMID: 27477337Free PMC Article
Ruhlmann CH, Herrstedt J
Expert Opin Pharmacother 2016 Aug;17(12):1623-9. Epub 2016 Jun 27 doi: 10.1080/14656566.2016.1202923. PMID: 27322893
Grant C, Ewart L, Muthas D, Deavall D, Smith SA, Clack G, Newham P
Toxicol Appl Pharmacol 2016 Apr 1;296:10-8. Epub 2016 Feb 11 doi: 10.1016/j.taap.2016.02.007. PMID: 26876616
Kottschade L, Novotny P, Lyss A, Mazurczak M, Loprinzi C, Barton D
Support Care Cancer 2016 Jun;24(6):2661-7. Epub 2016 Jan 15 doi: 10.1007/s00520-016-3080-y. PMID: 26768436Free PMC Article

Clinical prediction guides

Hesketh PJ, Schnadig ID, Schwartzberg LS, Modiano MR, Jordan K, Arora S, Powers D, Aapro M
Cancer 2016 Aug 1;122(15):2418-25. Epub 2016 May 13 doi: 10.1002/cncr.30054. PMID: 27176138Free PMC Article
Grant C, Ewart L, Muthas D, Deavall D, Smith SA, Clack G, Newham P
Toxicol Appl Pharmacol 2016 Apr 1;296:10-8. Epub 2016 Feb 11 doi: 10.1016/j.taap.2016.02.007. PMID: 26876616
Dupuis LL, Lu X, Mitchell HR, Sung L, Devidas M, Mattano LA Jr, Carroll WL, Winick N, Hunger SP, Maloney KW, Kadan-Lottick NS
Cancer 2016 Apr 1;122(7):1116-25. Epub 2016 Jan 15 doi: 10.1002/cncr.29876. PMID: 26773735Free PMC Article
Kottschade L, Novotny P, Lyss A, Mazurczak M, Loprinzi C, Barton D
Support Care Cancer 2016 Jun;24(6):2661-7. Epub 2016 Jan 15 doi: 10.1007/s00520-016-3080-y. PMID: 26768436Free PMC Article
Poon M, Hwang J, Dennis K, DeAngelis C, Zhang L, Chung H, Stinson J, Wong S, Pulenzas N, Chow E
Support Care Cancer 2016 Apr;24(4):1545-61. Epub 2015 Sep 16 doi: 10.1007/s00520-015-2942-z. PMID: 26377308

Recent systematic reviews

Song HJ, Seo HJ, Son H
Eur J Clin Pharmacol 2016 Nov;72(11):1289-1301. Epub 2016 Aug 15 doi: 10.1007/s00228-016-2100-7. PMID: 27526189
Phillips RS, Friend AJ, Gibson F, Houghton E, Gopaul S, Craig JV, Pizer B
Cochrane Database Syst Rev 2016 Feb 2;2:CD007786. doi: 10.1002/14651858.CD007786.pub3. PMID: 26836199
Chow R, Chiu L, Navari R, Passik S, Chiu N, Popovic M, Lam H, Pasetka M, Chow E, DeAngelis C
Support Care Cancer 2016 Feb;24(2):1001-1008. Epub 2015 Nov 4 doi: 10.1007/s00520-015-3000-6. PMID: 26530228
Jordan K, Warr DG, Hinke A, Sun L, Hesketh PJ
Support Care Cancer 2016 May;24(5):1941-1954. Epub 2015 Oct 17 doi: 10.1007/s00520-015-2990-4. PMID: 26476625
Gonella S, Di Giulio P
Clin J Oncol Nurs 2015 Aug;19(4):438-43. doi: 10.1188/15.CJON.438-443. PMID: 26207708

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