discoid lupus is a chronic skin condition that manifests as erythematous, round, scaly lesions 5-10mm in diameter that are common on the cheeks, ears, scalp, and the bridge of the nose. the etiology is unclear, though sunlight seems to be a trigger. it is more common in females 3:1, and usually appears in the third decade. other symptoms may appear such as atrophy and telangiectasias, as well as mouth ulcers in some. ddx's might include SLE, seborrheic dermatitis, rosacea, lichen planus, most of which can be ruled in or out via atrophic features or distribution of lesions on the body.
systemic lupus erythematosus (SLE) is an autoimmune disease that affects many systems of the body that is thought to involve antinuclear antibodies and a type III hypersensitivity response. it has a predilection for females and african americans and affects 1 in 2000 people. etiology is unclear, although genetic factors are presumed, and some environmental triggers have been identified, such as certain medications (procainamide, hydralazine, quinidine), sunlight, infection, silicone implants.
the most characterizing symptom for SLE is the butterfly rash across the face, although this might be absent in some patients. because SLE is a systemic disease, it can manifest in many different ways- ulcerations in the mouth / nasal cavity, xerostomia, polyserositis (inflammation of the serous membranes, leading to pleuritis / peritonitis / etc), recurrent respiratory infections, kidney failure, and very commonly, polyarthralgia that are symmetric and non deforming. diagnosis is by presence of characterizing symptoms as well as ANA tests.
scleroderma is a condition that results from abnormal fibrosis and collagen deposition. it can come in different variants; the diffuse type is more severe, rapid onset, with more internal organ involvement and widespread skin thickening. on the other hand, the CREST variant is more common and less severe-- CREST stands for calcification, raynaud's, esophageal dysfunction, sclerodactyly, and telangiectasias. patients with scleroderma might have hard, taut, shiny skin and faces that resemble mask-like textures, as well as subcutaneous calcifications. joints might have a friction rub, especially the knees. esophageal issues resulting from LES dysfunction might result in dysphagia, acid reflux, and barrett's esophagus. cardiovascular changes might include arrhythmias and pericarditis, while respiratory changes might include pleurisy, pulmonary hypertension, and dyspnea. diagnosis is made by presence of characteristic major and minor symptoms: the one major symptom is sclerotamous skin changes proximal to the MCP joints, and the minor symptoms are sclerodactyly, pulmonary fibrosis, and digital pitting scars. lab tests commonly reveal positive antibodies- ANA and anti-centromere in most cases, and anti-Scl-70 might be present in 30%, indicating pulmonary fibrosis.
polymyalgia rheumatica is a seronegative musculoskeletal condition that mainly presents as muscle pain in the neck, shoulders, or pelvic girdle muscles (as opposed to the joints). it might also result in weight loss, profound morning stiffness, fever, malaise. lab findings would be seronegative, with an increased ESR, and possibly normochromic / normocytic anemia. it is often treated with a 5 day burst of steroids, which may alleviate symptoms greatly. a severe complication is temporal arteritis, which will cause a severe headache and could ultimately lead to blindness.
polyarteritis nodosa is a vasculitis of the small and medium sized artery, with secondary ischemia of the affected tissues. it is an autoimmune condition that affects middle aged males most commonly. this condition affects the whole body and therefore has a presentation that is difficult to diagnose because it mimics many other conditions. the most common symptoms are fever, headache, weight loss, asthma, chest / abdomen pain, renal issues (hypertension, edema, failure), peripheral neuropathy. labs would reveal high WBC count, proteinuria and hematuria.
mixed connective tissue disorder (MCTD) is a combination of scleroderma, lupus, and polymyositis that mostly affects females in the 4th decade of life. it can cause: sausage digits and lupus like rashes, non deforming arthritis, muscle weakness / pain, decreased peristalsis in the esophagus, dyspnea, pulmonary hypertension, pericarditis. diagnosis is by ANA and anti-U1RNP.
ankylosing spondylitis is an inflammatory arthritis that preferentially affects males 15-30 and is fairly well localized to the lower spine, SI joints, ribcage, and eyes. it is usually made worse by prolonged rest and better by motion-- thus morning activities are particularly difficult for AS patients, who present with severe heel pain. ribcage pain might prevent full respirations and cause asthma like symptoms. uveitis might occur as well, resulting in ciliary injection and photophobia. a patient with AS will have a loss of lumbar lordosis and compensatory thoracic accentuation, stooped posture, and abnormal gait. lab findings are seronegative, elevated ESR, and positive HLA-B27. diagnosis is made by xray of the SI joints. ddx's include herniated disc and DISH syndrome.
psoriatic arthritis is a type of arthritis that affects 20% of sufferers of psoriasis, resulting in inflammation of the DIP joints, sausage digits, and nail discoloration / pitting. there are different types that vary in distribution and severity; the most common (50% of cases) are symmetrical, presenting similarly to RA. next is asymmetrical, which is milder and affects less than 3 joints at a time. lab findings are seronegative, increased ESR / CRP, may have positive HLA B27.
reiter's syndrome, aka reactive arthritis, is an arthritis that is secondary to infection such as GU infection or gastroenteritis. it affects males preferentially and seems to have the HLA B27 connection as well. main symptoms are captured by the phrase "can't see, can't pee, can't dance with me"- uveitis, urethritis (milder than that of an STD), and arthritis which is generally an asymmetric polyarthralgia of the lower extremities. severe cases will also develop back pain. RS patients may also develop mucocutaneous, painless lesions in the mouth, tongue, glans penis, and bottom of the feet, as well as hyperkeratosis on the soles of the feet and palms.
osteoarthritis is the most common connective tissue disease that is degenerative in nature: meaning RF-seronegative, non-inflammatory. if under 45, OA is associated with males and if over 55 OA is associated with females. etiological factors are varied and can include microtrauma, infection, malabsorption, genetic factors, endocrine imbalances. the cartilage of an OA patient undergoes erosion via fissuring and pitting, causing osteophytes / bone spurs to form (as adaptive physiology to prevent movement of the affected joint). common locations are the knee, hip, fingers (PIP=bouchard's nodes, DIP=heberden's nodes), spine (C5-7 and L4-5 in particular). some features distinguish OA from RA: the morning stiffness is not as bad, and OA is more of a deep, poorly localized pain. PE findings might include joint swelling / effusion / crepitus, abnormal gait / ROM / deformation, and tenderness to palpation. OA diagnosis is made definitively by xray.
infectious arthritis is arthritis secondary to an infection: in young children this is commonly caused by staph, h. flu, and in adults it is commonly caused by staph, strep, pneumonia, or gonococci. the typical presentation is rapid onset of swelling / tenderness / decreased ROM / redness of a single joint with fever and leukocytosis. the most common location is the knee, but IA often affects the hip, shoulder, wrist, and phalanges. it is diagnosed by a CBC w/ differential and a synovial fluid biopsy.
lyme disease is an infectious condition caused by borelia burgdorferi carried by deer ticks, largely in the northeast. the characteristic symptom is the bullseye lesion: erythema chronicum migrans, which appears 3-30 days after exposure. lyme disease might also affect other systems, causing neurological symptoms (meningitis or encephalitis, chorea, ataxia, peripheral neuropathy), cardiovascular symptoms (AV blocks, pericarditis, cardiomegaly), and myalgias/arthalgias (sudden swelling of a single large joint). CDC recommends a two step diagnosis process: antibody titer test, then western blot.
the last condition of this week was osteomyelitis: infection of the bone via a longstanding condition such as prostatitis, UTI, or open wound. osteomyelitis develops slowly over the course of several months and presents as severe back pain and perivertebral spasm. it is not accompanied by fever or leukocytosis, and is diagnosed by elevated ESR and xray, which would show spotty demineralization of bone.
questions
discoid lupus...
1. what etiological factor commonly precedes the initial lesions of DL?
2. what is the most common age and gender that DL affects?
3. describe the skin lesions in DL.
4. where are the body areas commonly affected in DL?
5. what is a concomitant symptom in DL?
6. are anti-DNA antibodies present or absent?
7. what are some ddx's for DL?
8. how can most of the ddx's be ruled out?
SLE overview...
9. what is SLE?
10. what are the demographic / gender groups most likely to have SLE?
11. what are three etiological categories for SLE?
12. what are some environmental triggers for SLE?
13. what are the most common drugs that are associated with SLE?
14. what is the most characterizing symptom for SLE?
SLE symptom presentation and diagnosis...
15. 40% of SLE patients have...
16. SLE patients might have ulcerations in which locations?
17. what symptoms might cause a SLE patient to be confused with sjogren's?
18. what is the most common symptom of SLE? what condition presents in a similar way?
19. how might SLE manifest in the respiratory system?
20. what are common UA findings for SLE patients?
21. which serous membranes might be affected in SLE? what is this condition called?
22. how common is raynaud's in SLE patients?
23. what is the screening test for SLE?
scleroderma overview...
24. what is scleroderma?
25. how common is scleroderma in the US? which gender is more affected?
26. how does the age of onset for scleroderma compare to SLE?
27. what is the more severe variant of scleroderma? what is it characterized by?
28. what are the hallmarks of CREST syndrome?
scleroderma presentation...
29. describe the distribution of skin changes in scleroderma.
30. describe the morphology of skin changes in scleroderma.
31. what are some other skin changes that might accompany a scleroderma patient?
32. what is a PE sign that might be picked up in the joints of a scleroderma patient?
33. what are the typical GI manifestations of scleroderma?
34. what are the cardiovascular changes in scleroderma?
35. what are the respiratory manifestations of scleroderma?
scleroderma diagnosis...
36. which lab markers are present in over 90% of scleroderma patients?
37. how common is a positive anti Scl-70 antibody and what is it associated with?
38. what is the major diagnostic criteria for scleroderma?
39. what are the three minor diagnostic criteria for scleroderma?
polymyalgia rheumatica...
40. which gender and age is more prone to developing polymyalgia rheumatica?
41. describe the distribution of pain in PR.
42. what are some concomitant symptoms in PR?
43. in the shoulder girdle, are proximal or distal muscles more likely to be affected?
44. what are the lab findings associated with polymyalgia rheumatica?
45. what is a treatment that can serve as a diagnosis for PR?
46. what is an important, severe concomitant that might result from PR?
47. what are the diagnostic criteria for [46]?
48. [46] might lead to...
49. what is the prognosis for PR?
polyarteritis nodosa...
50. what is polyarteritis nodosa?
51. which gender and age is most commonly affected by PN?
52. what is the etiology of PN?
53. why is PN so difficult to diagnose?
54. what are the most common symptoms of PN?
55. what would labs for PN reveal?
mixed connective tissue disease...
56. MCTD is a combination of...
57. which age and gender is most commonly affected by MCTD?
58. what are the dermatological manifestations of MCTD?
59. how does MCTD manifest in the joints?
60. and the muscles?
61. and the esophagus?
62. pulmonary stuff?
63. heart?
64. what are the lab findings for MCTD?
ankylosing spondylitis...
65. what is AS?
66. which gender and age is most commonly affected by AS?
67. what is a genetic marker that is often positive in AS?
68. what are the body areas commonly affected by AS?
69. describe the severity of the morning symptoms of AS.
70. how does movement / rest affect AS patients?
71. why does AS present with asthma?
72. what are the eye symptoms that AS patients present with?
73. what are the PE findings for AS?
74. what are the lab findings for AS?
75. how is diagnosis of AS confirmed?
76. what are the ddx'es for AS?
77. what are the treatment goals for AS?
psoriatic arthritis...
78. what percentage of chronic psoriasis patients develop PA?
79. what percentage of PA patients develop ankylosing spondylitis?
80. describe the distribution and morphology of PA.
81. what are the different types of PA? which is most common?
82. what are the lab findings for PA?
reiter's syndrome...
83. what is reiter's syndrome? what is it also called?
84. what are the etiological agents identified for RS?
85. what is the difference between the people prone to developing sexually transmitted vs. dysenteric RS?
86. what are the signs / symptoms of RS?
87. how does the urethritis differ from that of an STD?
88. describe the arthritis in RS.
89. what are the dermatological manifestations of RS?
osteoarthritis...
90. how common is osteoarthritis?
91. what age and gender is most commonly affected by OA?
92. what are some etiological factors for OA?
93. describe what happens to the bones and joints in OA.
94. which vertebral junctions are particularly prone to developing [93]?
95. what are the most common locations for osteoarthritis?
96. what are Heberden's and Bouchard's nodes?
97. what are the symptoms/signs that differentiate OA from RA?
98. what are some PE findings for OA?
99. how is OA diagnosed?
100. what are the ddx's for OA?
101. what are the treatment strategies for OA?
infectious arthritis...
102. what are the most likely microorganisms responsible for IA in young children?
103. what are the most likely microorganisms responsible for IA in adults?
104. what is the typical presentation of IA?
105. what are the most common locations for IA?
106. how is IA diagnosed?
lyme disease...
107. what are the infectious agents in lyme disease?
108. what is the characteristic symptom of lyme disease? when does it appear?
109. what are the neurological signs of lyme disease?
110. what are the CV symptoms of lymedisease?
111. 50% of patients with lyme disease have...
112. what is the two step diagnostic method advocated for identification of lyme disease by the CDC?
113. what are some ddx's for lyme disease?
osteomyelitis...
114. what is the etiology of osteomyelitis?
115. describe the time course of osteomyelitis.
116. what are the signs and symptoms of osteomyelitis?
117. is osteomyelitis accompanied by fever? what about leukocytosis?
118. what labs are used to diagnose osteomyelitis?
answers
1. sunlight.
2. females in 30's.
3. erythematous, round, scaly papules with follicular plugging. 5-10mm.
4. cheeks, bridge of nose, scalp, ears.
5. many mouth ulcers.
6. absent.
7. SLE
rosacea
seborrheic dermatitis
photosensitivity
lichen planus
8. via lack of atrophic features or a different distribution pattern.
9. an type III hypersensitivity response which results in immune complex deposition and antinuclear antibody formation affecting many systems of the body.
10. young females, african americans.
11. genetic predisposition (not clarified), environmental triggers, drug reactions.
12. medications
stress
sunlight
infection
silicone implants
13. procainamide, hydralazine, quinidine.
14. butterfly rash.
15. photosensitive skin eruptions.
16. oral and nasal.
17. parotid enlargement and xerostomia.
18. polyarthralgia and arthritis, similar to rheumatoid arthritis presentation.
19. recurrent respiratory infections.
20. proteinuria, hematuria, cellular elements.
21. polyserositis: pleuritis, pericarditis (and myocarditis), peritonitis.
22. 1/3.
23. ANA test, UA.
24. rare chronic disease characterized by excess collagen deposition in various tissues.
25. 300,000 in US, 4 times more likely females.
26. slightly older; 30's to 40's.
27. diffuse scleroderma, a rare variant that develops rapidly and has widespread skin thickening and greater lung / GI damage.
28. calcinosis
raynaud's
esophageal dysfunction
sclerodactyly
telangiectasia
29. most commonly on the distal portions of upper extremities, but may be all over the body.
30. taut, shiny, hyperpigmented. face becomes mask like.
31. subcutaneous calcifications and telangiectasias.
32. friction rubs over joints, especially knees.
33. esophageal dysfunction which leads to dysphagia, acid reflux, and may progress to barrett's esophagus (1/3 of patients)
34. arrythmias, abnormal EKG, pericarditis.
35. fibrosis, pulmonary hypertension, pleurisy.
36. ANA, anti centromere antibodies,
37. 30%, pulmonary fibrosis.
38. scleromatous skin changes proximal to the MCP joint.
39. digital pitting scars, sclerodactyly, bibasilar pulmonary fibrosis.
40. females (2:1) over 50.
41. symmetric distribution in neck, shoulder, and pelvic girdle muscles.
42. morning stiffness
weight loss
fever, malaise
43. proximal.
44. seronegative, ESR over 40, may have normochromic/normocytic anemia.
45. if a 5 day burst of steroids helps, it is likely PR.
46. temporal arteritis.
47. age over 50, new onset, temporal artery abnormality (tenderness or diminished pulse), elevated ESR, biopsy.
48. blindness.
49. 90% recover within 2 years.
50. vasculitis of the small and medium arteries and secondary ischemia of the affected tissues.
51. middle aged males.
52. autoimmune/hyperimmune response.
53. because it mimics many other diseases and has a insidious onset.
54. fever
abdominal pain
peripheral neuropathy
renal hypertension / edema / failure
angina / MI / CV issues
weight loss
headache
asthma
55. high WBC's, proteinuria, hematuria.
56. scleroderma, lupus, polymyositis.
57. 80% females in 4th decade.
58. sausage fingers, lupus like rashes.
59. non deforming arthritis.
60. weakness, maybe tenderness.
61. decreased peristalsis.
62. dyspnea, hypertension.
63. pericarditis.
64. high ANA and high titers of anti-U1RNP.
65. an inflammatory arthritis primarily affecting spine and SI joints.
66. males 3:1, 15-30 years old.
67. HLA-B27.
68. heels, spine, rib cage, eyes.
69. prolonged morning stiffness, and heel pain that causes most AS patients to not want to walk.
70. prolonged rest makes worse, movement makes stiffness better.
71. because the rib pain makes breathing difficult.
72. uveitis: ciliary injection, photophobia.
73. reduced lumber range of motion, accentuated thoracic curve, loss of lumbar lordosis, stooped posture, abnormal gait, shallow breathing.
74. seronegative, increased ESR, positive HLA-B27.
75. xray of SI joints.
76. herniated disk, DISH syndrome.
77. prevent joint fusion via regular movement and stretching.
78. 20%.
79. 1/3.
80. DIP's, sausage digits, nail pitting and discoloration.
81. symmetric, asymmetric, arthritis mutilans, spondylitis, DIP predominant. symmetric accounts for 50%.
82. seronegative, increased ESR, CRP, may have positive HLA B-27.
83. reactive arthritis; arthritis that develops secondary to an infection elsewhere in the body such as a GU infection or gastroenteritis.
84. HLA-B27, male gender, white race (connected to HLA-B27)
85. sexually transmitted: young men, chlamydia trachomatis. dysenteric: women, children, elderly. shigella, salmonella, campylobacter, yersinia.
86. uveitis, urethritis, arthritis. [can't see, can't pee, can't dance with me]
87. less painful / more mild.
88. asymmetric polyarthritis that affects larger joints of lower extremities and toes.
89. mucocutaneous lesions- small, painless ulcers in the mouth, tongue, glans penis, bottom of feet. may also develop hyperkeratotic lesions on soles of feet and palms.
90. most common connective tissue disease.
91. under 45: males more affected. over 55: females more affected.
92. genetic, autointoxication, malabsorption, endocrine imbalance, microtrauma, surgery.
93. pitting/fissuring erosions of articular cartilage, formation of osteophytes / bone spurs.
94. C6-C7, L4-L5.
95. knee, hip, fingers.
96. H: DIP involvement. B: PIP involvement.
97. morning stiffness not as bad
deep, poorly localized pain
better with rest, worse with use
might have night time pain
98. tenderness to palpation
joint swelling / effusion / crepitus
ROM limitation / abnormal gait
valgus / varus deformities
99. lab tests are largely uninformative (may have increased ESR). diagnosis by xray.
100. psoriatic arthritis
ankylosing spondylitis
reiter's
RA
101. largely palliation of pain, although glucosamine sulfate can help if taken for a long time. exercise is the most helpful.
102. staph, h influenza, gram- bacilli. [staff, flu, negative]
103. staph, strep, pneumonia, gonococci. [staff, strip, new, gone]
104. rapid onset, unilateral, single hot / swollen / painful joint with fever and decreased ROM.
105. knee, shoulder, wrist, hip, phalanges.
106. CBC with diff: leukocytosis. biopsy of synovial fluid.
107. borelia burgdorferi carried through the deer tick.
108. erythema chronicum migricans, 3-32 days after tick bite.
109. lymphocytic meningitis, encephalitis, chorea, ataxia, cranial neuritis, peripheral neuropathy.
110. AV block, pericarditis, cardiomegaly
111. myalgias/arthralgias that present as sudden swelling of a single large joint.
112. test for antibody titers, then do western blot.
113. juvenile RA
hepatitis
herpes zoster
infectious arthritis
reiter's syndrome
114. an underlying condition that makes the patient more prone to chronic infection such as an open wound, chronic prostatitis or chronic UTI's.
115. slow onset over several months.
116. severe back pain and paravertebral spasm.
117. no.
118. increased ESR and xray would show cloudy/spotty demineralization of bone.
Showing posts with label scleroderma. Show all posts
Showing posts with label scleroderma. Show all posts
Monday, May 24, 2010
Saturday, January 30, 2010
CPD II: esophageal disorders
this is the first lecture for diagnosis of gastrointestinal disorders in CPD II. we started with a discussion on the importance of "food hygiene"-- the manner in which one eats (not only the type of food, but when, how, how fast, etc.). the section that followed was a review of normal esophageal function, in particular the three phases of swallowing: oral, pharyngeal, and esophageal. the oral phase involves the formation of the bolus via mechanical and chemical breakdown of food, and propelling of food into the oropharynx. this phase can take anywhere from 1-2 seconds for liquid to 20 seconds for food (depending on the food hygiene of the chewer) and is mediated by cranial nerves V (trigeminal), VII (facial), and XII (hypoglossal). the next phase is the pharyngeal phase, a reflexive phase mediated by CN IX (glossopharyngeal) and X (vagus) in which the UES relaxes and is pulled open by the forward motion of the hyoid and larynx, letting the bolus into the esophagus. the final phase is the esophageal phase, in which the bolus is moved via peristalsis to the lower esophageal sphincter and released into the stomach upon relaxation of the LES. this phase is controlled by the medulla and may take 8-20 seconds.
dysphagia is the phenomenon of having difficulty swallowing and can occur either in the pharynx or the esophagus, with a variety of etiologies. the pre-esophageal dysphagias are generally neurological or involving skeletal muscle dysfunction, such as stroke, motor neuron disease (ALS, MS), myopathy, myasthenia gravis. esophageal dysphagias are categorized as obstructive (carcinoma, lower esophageal ring) or due to a motor disorder-- motor disorders are generally more severe and restrict passage of both liquid and food while obstructive might let liquid through. symptoms are somewhat similar for both esophageal and pre-esophageal dysphagia and center around difficulty swallowing, coughing, choking, drooling, regurgitation, change in dietary habits / weight loss, but the esophageal dysphagia will result in an obstructive sensation lower down in the chest as compared to the upper throat for pre-esophageal dysphagia.
achalasia is a debilitating disorder of the esophagus that results from neuronal damage of the inhibitory neurons that innervate the esophagus (more commonly afflicting the lower esophagus and LES), resulting in constriction and decreased peristalsis. severe cases can result in a near complete constriction of the LES, prohibiting passage of most solids and resulting in buildup of a fermenting bolus. besides the dysphagia, symptoms are regurgitation of food, chest pain, and possible recurrent bronchopneumonia. a chest xray would show the esophageal beak dilation and esophageal manometry would show decreased relaxation and reduced peristalsis.
DES is a rarer esophageal dysfunction with symptoms just as severe, if not more severe than achalasia. in fact, patients with DES are difficult to manage because their symptoms might be mistaken for a myocardial infarction, the treatment of which (vasodilators for occluded coronary artery) might relieve DES symptoms as well. patients with DES might suffer from acute, substernal chest pain radiating to the back that may be triggered by swallowing, which may be accompanied by paleness or perspiration. chest xray might show a "corkscrew" shape to the esophagus and manometry will reveal an abnormal pressure distribution as well as uncoordinated contractions.
the symptoms of DES are somewhat similar to nutcracker esophagus, another esophageal disorder which contrasts with achalasia and DES in that the peristaltic waves are orderly but simply high in amplitude. nutcracker esophagus can result in prolonged chest pain and intermittent nocturnal dysphagia, but less so than DES.
the last esophageal disorder covered in this lecture is scleroderma, which is a widespread connective tissue and smooth muscle disorder that can manifest in fibrosis of esophageal tissue, leading to decreased motility and a weakened LES. dysphagia, regurgitation, barrett's esophagus, and extreme pain upon pressure can result, along with acid reflux so severe that patients might refuse to pick things up off the ground or lie down while sleeping.
questions
normal esophageal function...
1. what are the three phases of swallowing?
2. what is involved in the oral phase of swallowing?
3. which cranial nerves are involved in the oral phase of swallowing?
4. in the pharyngeal phase, the UES is pulled forward by...
5. which cranial nerves are involved in the pharyngeal phase of swallowing?
6. what is involved in the esophageal phase of swallowing?
7. what part of the brain is involved in the esophageal phase of swallowing?
8. describe the general timescale for each of the three phases of swallowing.
dysphagia...
9. what is dysphagia?
10. dysphagia is often seen in patients with what condition?
11. what are the signs and symptoms of oral dysphagia?
12. what are the signs and symptoms of esophageal dysphagia?
13. what are some pre-esophageal etiologies of dysphagia?
14. what are some esophageal etiologies of dysphagia?
15. what is the difference in severity of dysfunction between dysphagia with a motor vs. obstructive etiology?
16. what is involved in the physical exam for dysphagia?
17. differential diagnoses for oropharyngeal dysphagia include...
18. differential diagnoses for esophageal dysphagia include...
GI related chest pain...
19. what is heart burn?
20. what are some differential diagnoses for heart burn?
21. what is odynophagia and what is the most common cause?
achalasia...
22. what is achalasia?
23. what are the symptoms of achalasia?
24. what might one find in a PE of a patient with achalasia?
25. what would a chest xray of a patient with achalasia show?
26. what is the standard imaging technique of a patient with achalasia and what would it show?
diffuse esophageal spasm...
27. what is DES?
28. what is a DDX that might interfere with the diagnosis of DES?
29. what are the signs and symptoms of patients with DES?
30. the EKG of a patient with DES will look like...
31. barium swallow of a patient with DES will look like...
32. esophageal manometry of DES patients might reveal...
33. what is the classic definition of DES according to esophageal manometry?
nutcracker esophagus...
34. what is nutcracker esophagus?
35. symptoms of nutcracker esophagus can be distinguished from DES by...
36. what are the symptoms of nutcracker esophagus?
37. manometry of nutcracker esophagus reveals...
scleroderma...
38. what is scleroderma and how does it manifest in the esophagus?
39. in scleroderma patients, where is motility preserved in the esophagus?
40. what are the signs and symptoms of scleroderma?
41. describe the severity of acid reflux in patients with scleroderma.
42. what are some PE findings of patients with scleroderma?
43. xray of scleroderma patients shows...
answers
1. oral phase, pharyngeal phase, esophageal.
2. mechanical breakdown, mixing with saliva and enzymes, propelling of food into the oropharynx.
3. V (trigeminal), VII (facial), XII (hypoglossal).
4. hyoid bone and larynx.
5. IX (glossopharyngeal) and X (vagus).
6. propelling of bolus down esophagus and relaxation of LES.
7. the medulla.
8. oral: 1 second liquid, 5-10 seconds solid. pharyngeal: 1 second. esophageal: 8-20 seconds.
9. difficulty swallowing.
10. myasthenia gravis.
11. coughing, choking, difficulty initiating swallowing, drooling, weight loss, nasal regurgitation.
12. sensation of food sticking in chest/throat, regurgitation, change in dietary habits.
13. usually neurological, involving skeletal muscle: stroke, motor neuron disease such as ALS, MS, myopathy, laryngectomy, pharyngectomy, myasthenia gravis, cerebral palsy.
14. either obstructive (carcinoma, lower esophageal ring), or motor disorder.
15. obstructive can still allow liquids but motor disorder oftentimes does not allow either solid or liquid.
16. examining the soft palate / tongue / teeth, testing cranial nerves (V / VII / XII), watching for dysphonia or dysarthria, examining while swallowing, and assessing respiratory function, among other things. [exam test dys swallow breathe] [test dis exam: swallow! breathe!]
17. cerebrovascular accident, parkinson's, brainstem tumor, degenerative diseases, poliomyelitis, peripheral neuropathy, myasthenia gravis. [CV, park, stem, DJ, pole, neuron, gravity] [DJ went to the park to do a CV workout but due to gravity crashed into a pole that was the huge stem of a neuron]
18. achalasia, DES, nutcracker esophagus, scleroderma, obstructive lesions. [des achy nuts are obstructing my skin]
19. substernal burning pain that usually occurs after meals from reflux of acid into esophagus.
20. panic attack, costochondritis, skin conditions (such as herpes zoster, shingles), pulmonary disorders, MI.
21. pain upon swallowing, from sore throat.
22. nerve degeneration of inhibitory neurons of esophagus causes increased esophageal tone and constriction.
23. progressive dysphagia of solids and foods, regurgitation (especially at night), chest pain, possible recurrent bronchopneumonia.
24. normal findings, or halitosis, or weight loss.
25. esophageal "beak" dilation.
26. esophageal manometry, would show incomplete esophageal relaxation, high resting pressure, reduced peristalsis.
27. uncommon disorder that results in abnormal, non functional peristalsis.
28. an MI, because symptom are similar and the vasodilators given to treat MI might also relieve DES symptoms.
29. substernal chest pain upon swallowing that radiates to back or scapulas, maybe paleness or perspiration.
30. NI.
31. corkscrew esophagus.
32. abnormal pressure distribution, uncoordinated contractions.
33. at least 2 uncoordinated contractions for 10 wet swallows.
34. an esophageal disorder with normal LES function but twice the amplitude of contraction and an abnormally long peristaltic wave.
35. motility study.
36. prolonged chest pain, nocturnal intermittent dysphagia (less than DES),
37. orderly contractions with abnormally high amplitude.
38. widespread disorder of smooth muscle and connective tissue, fibrosis of esophageal tissue leads to dysmotility and weakened LES.
39. in the proximal striated portion.
40. dysphagia, regurgitation, acid reflux, barrett's esophagus, extreme pain upon pressure.
41. so severe that patients often can not bend down or lie down.
42. thickening of skin, joint structures, internal organs.
43. loss of peristalsis.
dysphagia is the phenomenon of having difficulty swallowing and can occur either in the pharynx or the esophagus, with a variety of etiologies. the pre-esophageal dysphagias are generally neurological or involving skeletal muscle dysfunction, such as stroke, motor neuron disease (ALS, MS), myopathy, myasthenia gravis. esophageal dysphagias are categorized as obstructive (carcinoma, lower esophageal ring) or due to a motor disorder-- motor disorders are generally more severe and restrict passage of both liquid and food while obstructive might let liquid through. symptoms are somewhat similar for both esophageal and pre-esophageal dysphagia and center around difficulty swallowing, coughing, choking, drooling, regurgitation, change in dietary habits / weight loss, but the esophageal dysphagia will result in an obstructive sensation lower down in the chest as compared to the upper throat for pre-esophageal dysphagia.
achalasia is a debilitating disorder of the esophagus that results from neuronal damage of the inhibitory neurons that innervate the esophagus (more commonly afflicting the lower esophagus and LES), resulting in constriction and decreased peristalsis. severe cases can result in a near complete constriction of the LES, prohibiting passage of most solids and resulting in buildup of a fermenting bolus. besides the dysphagia, symptoms are regurgitation of food, chest pain, and possible recurrent bronchopneumonia. a chest xray would show the esophageal beak dilation and esophageal manometry would show decreased relaxation and reduced peristalsis.
DES is a rarer esophageal dysfunction with symptoms just as severe, if not more severe than achalasia. in fact, patients with DES are difficult to manage because their symptoms might be mistaken for a myocardial infarction, the treatment of which (vasodilators for occluded coronary artery) might relieve DES symptoms as well. patients with DES might suffer from acute, substernal chest pain radiating to the back that may be triggered by swallowing, which may be accompanied by paleness or perspiration. chest xray might show a "corkscrew" shape to the esophagus and manometry will reveal an abnormal pressure distribution as well as uncoordinated contractions.
the symptoms of DES are somewhat similar to nutcracker esophagus, another esophageal disorder which contrasts with achalasia and DES in that the peristaltic waves are orderly but simply high in amplitude. nutcracker esophagus can result in prolonged chest pain and intermittent nocturnal dysphagia, but less so than DES.
the last esophageal disorder covered in this lecture is scleroderma, which is a widespread connective tissue and smooth muscle disorder that can manifest in fibrosis of esophageal tissue, leading to decreased motility and a weakened LES. dysphagia, regurgitation, barrett's esophagus, and extreme pain upon pressure can result, along with acid reflux so severe that patients might refuse to pick things up off the ground or lie down while sleeping.
questions
normal esophageal function...
1. what are the three phases of swallowing?
2. what is involved in the oral phase of swallowing?
3. which cranial nerves are involved in the oral phase of swallowing?
4. in the pharyngeal phase, the UES is pulled forward by...
5. which cranial nerves are involved in the pharyngeal phase of swallowing?
6. what is involved in the esophageal phase of swallowing?
7. what part of the brain is involved in the esophageal phase of swallowing?
8. describe the general timescale for each of the three phases of swallowing.
dysphagia...
9. what is dysphagia?
10. dysphagia is often seen in patients with what condition?
11. what are the signs and symptoms of oral dysphagia?
12. what are the signs and symptoms of esophageal dysphagia?
13. what are some pre-esophageal etiologies of dysphagia?
14. what are some esophageal etiologies of dysphagia?
15. what is the difference in severity of dysfunction between dysphagia with a motor vs. obstructive etiology?
16. what is involved in the physical exam for dysphagia?
17. differential diagnoses for oropharyngeal dysphagia include...
18. differential diagnoses for esophageal dysphagia include...
GI related chest pain...
19. what is heart burn?
20. what are some differential diagnoses for heart burn?
21. what is odynophagia and what is the most common cause?
achalasia...
22. what is achalasia?
23. what are the symptoms of achalasia?
24. what might one find in a PE of a patient with achalasia?
25. what would a chest xray of a patient with achalasia show?
26. what is the standard imaging technique of a patient with achalasia and what would it show?
diffuse esophageal spasm...
27. what is DES?
28. what is a DDX that might interfere with the diagnosis of DES?
29. what are the signs and symptoms of patients with DES?
30. the EKG of a patient with DES will look like...
31. barium swallow of a patient with DES will look like...
32. esophageal manometry of DES patients might reveal...
33. what is the classic definition of DES according to esophageal manometry?
nutcracker esophagus...
34. what is nutcracker esophagus?
35. symptoms of nutcracker esophagus can be distinguished from DES by...
36. what are the symptoms of nutcracker esophagus?
37. manometry of nutcracker esophagus reveals...
scleroderma...
38. what is scleroderma and how does it manifest in the esophagus?
39. in scleroderma patients, where is motility preserved in the esophagus?
40. what are the signs and symptoms of scleroderma?
41. describe the severity of acid reflux in patients with scleroderma.
42. what are some PE findings of patients with scleroderma?
43. xray of scleroderma patients shows...
answers
1. oral phase, pharyngeal phase, esophageal.
2. mechanical breakdown, mixing with saliva and enzymes, propelling of food into the oropharynx.
3. V (trigeminal), VII (facial), XII (hypoglossal).
4. hyoid bone and larynx.
5. IX (glossopharyngeal) and X (vagus).
6. propelling of bolus down esophagus and relaxation of LES.
7. the medulla.
8. oral: 1 second liquid, 5-10 seconds solid. pharyngeal: 1 second. esophageal: 8-20 seconds.
9. difficulty swallowing.
10. myasthenia gravis.
11. coughing, choking, difficulty initiating swallowing, drooling, weight loss, nasal regurgitation.
12. sensation of food sticking in chest/throat, regurgitation, change in dietary habits.
13. usually neurological, involving skeletal muscle: stroke, motor neuron disease such as ALS, MS, myopathy, laryngectomy, pharyngectomy, myasthenia gravis, cerebral palsy.
14. either obstructive (carcinoma, lower esophageal ring), or motor disorder.
15. obstructive can still allow liquids but motor disorder oftentimes does not allow either solid or liquid.
16. examining the soft palate / tongue / teeth, testing cranial nerves (V / VII / XII), watching for dysphonia or dysarthria, examining while swallowing, and assessing respiratory function, among other things. [exam test dys swallow breathe] [test dis exam: swallow! breathe!]
17. cerebrovascular accident, parkinson's, brainstem tumor, degenerative diseases, poliomyelitis, peripheral neuropathy, myasthenia gravis. [CV, park, stem, DJ, pole, neuron, gravity] [DJ went to the park to do a CV workout but due to gravity crashed into a pole that was the huge stem of a neuron]
18. achalasia, DES, nutcracker esophagus, scleroderma, obstructive lesions. [des achy nuts are obstructing my skin]
19. substernal burning pain that usually occurs after meals from reflux of acid into esophagus.
20. panic attack, costochondritis, skin conditions (such as herpes zoster, shingles), pulmonary disorders, MI.
21. pain upon swallowing, from sore throat.
22. nerve degeneration of inhibitory neurons of esophagus causes increased esophageal tone and constriction.
23. progressive dysphagia of solids and foods, regurgitation (especially at night), chest pain, possible recurrent bronchopneumonia.
24. normal findings, or halitosis, or weight loss.
25. esophageal "beak" dilation.
26. esophageal manometry, would show incomplete esophageal relaxation, high resting pressure, reduced peristalsis.
27. uncommon disorder that results in abnormal, non functional peristalsis.
28. an MI, because symptom are similar and the vasodilators given to treat MI might also relieve DES symptoms.
29. substernal chest pain upon swallowing that radiates to back or scapulas, maybe paleness or perspiration.
30. NI.
31. corkscrew esophagus.
32. abnormal pressure distribution, uncoordinated contractions.
33. at least 2 uncoordinated contractions for 10 wet swallows.
34. an esophageal disorder with normal LES function but twice the amplitude of contraction and an abnormally long peristaltic wave.
35. motility study.
36. prolonged chest pain, nocturnal intermittent dysphagia (less than DES),
37. orderly contractions with abnormally high amplitude.
38. widespread disorder of smooth muscle and connective tissue, fibrosis of esophageal tissue leads to dysmotility and weakened LES.
39. in the proximal striated portion.
40. dysphagia, regurgitation, acid reflux, barrett's esophagus, extreme pain upon pressure.
41. so severe that patients often can not bend down or lie down.
42. thickening of skin, joint structures, internal organs.
43. loss of peristalsis.
Labels:
achalasia,
CPD II,
DES,
dysphagia,
nutcracker esophagus,
scleroderma
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