Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clin Med 3 > IBD, Celiac, Lactose Intolerance > Flashcards

IBD, Celiac, Lactose Intolerance Flashcards

1
Q

what is the etiology of IBD?

A

dysregulated mucosal immune response to host gut flora in genetically susceptible individuals

AUTOIMMUNE RESPONSE TO OWN GUT FLORA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the 2 types of IBD?

A

Ulcerative Colitis and Crohn’s Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

in terms of where UC and Crohn’s affect the GIT, what are there differences?

A

UC is limited to colon and rectum

Crohn’s is entire GI tract (mouth to anus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what type of lesions does Crohn’s have?

A

skip lesions

-areas of inflammation, then normal tissue, then area of inflammation, then normal tissue, etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what type of inflammation does UC have?

A

diffuse inflammation, friability, erosions, and bleeding of mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is Crohn’s disease associated with?

A

abscesses, fistulae, sinus tracts (incomplete fistulae ending in a cul-de-sac), strictures, and adhesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the pathophysiology of IBD?

A

A COMBO OF FACTORS IN GUT:

  • Damage to epithelial mucin proteins and tight junctions
  • Breakdown of homeostatic balance b/w host’s mucosal immunity and enteric microflora (host immune response to own gut flora)
  • Genetic polymorphisms in toll-like receptors (TLRs) - body can’t recognize itself
  • Disrupted homeostatic balance b/w regulatory and effector T-cells (more attack T-cels vs regulatory T-cells)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

IBD Global incidence

A

Developing more in industrialized countries -> means something to do with environment, diet, etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what has a higher incidence, UC or CD?

A

UC - more commonly seen in North America and Europe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

UC epidemiology ages

A

Bimodal incidence pattern

-Onset at 15-30 years or 50-70 year olds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what people have high risk of UC?

A

Ashkenazi Jews have 3-5x higher risk

fam hx very important

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

smoking and UC

A

Smoking associated with paradoxically lower risk/incidence, milder disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

environmental factors and UC

A

Smoking has lower risk, milder disease

Hx of prior GI infections (ex: Shigella, Salmonella, Campylobacter) during adulthood double risk of developing UC - 2/2 change in gut flora triggering chronic inflammatory process

Weak associations b/w NSAIDs, OCPs and increased risk of UC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the common presenting sx’s of someone with UC?

A

Rectal bleeding

Diarrhea (HALLMARK BLOODY MUCOID DIARRHEA)

Abdominal pain in LLQ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the HALLMARK sx of UC?

A

Bloody mucoid diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

where is the abdominal pain in UC located?

A

LLQ - b/c usually in sigmoid colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

mild to moderate UC disease presentation

A
  • Gradual onset diarrhea (<4/day) and intermittent blood mucoid stool mild disease
  • Moderate disease is 4-6 bloody stools/day and more abdominal pain
  • Urgency and tenesmus
  • No significant abdominal pain, but LLQ cramping normal and often relieved by BM
  • Mild fever, anemia, hypoalbuminemia possible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

severe UC disease presentation

A

> 6 bloody diarrhea stools/day

Severe anemia (anemia of chronic disease), hypovolemia (d/t diarrhea), hypoalbuminemia w/ nutritional deficit

Abd pain/tenderness

Fulminant colitis = subset of severe UC disease w/systemic sx’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is fulminant colitis?

A

subset of UC severe disease which is rapidly worsening sx’s with toxicity

SURGICAL EMERGENCY

Look septic - systemic six’s - fever, leukocytosis, tachycardia, severe and pain/diarrhea, may develop toxic megacolon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what manifestations are more common in UC than CD?

A

extraintestinal manifestations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what extraintestinal manifestations occur in UC?

A
  • Aphthous oral ulcers
  • Iritis/uveitis/episcleritis (present with extremely red/painful eye b/c inflammation of uveal tissue)
  • Seronegative arthritis, ankylosing spondylitis, sacroilitis (have back pain, stiff joints; Need to watch for 20 y/o that has abd pain and also knee pain/swollen knee - may be UC)
  • Erythema nodosum - Nodular, erythematous discrete lesions that are very painful – develop on lower extremities extensor surfaces anterior tibialis (anterior lesions)
  • Pyoderma gangrenosum
  • Autoimmune hemolytic anemias
  • Primary sclerosing cholangitis - chronic long-term disease of your biliary tree
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

UC PE

A

LLQ abdominal tenderness; peritonitis

DRE = bright red blood and mucoid appearance to it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what extraintestinal manifestations of UC IMPROVE after colectomy?

A

Arthritis (20%)

  • Knees, ankles, hips, shoulders
  • Joints become inflamed and irritated when disease is flaring
Ankylosing spondylitis (3-5%)
-HLA-B27+ or Fam Hx of AS
Erythema nodosum (10-15%)
-Often in conjunction with arthropathy

Pyoderma gangrenosum (rare)

  • Ulcerative cutaneous lesion, dx by biopsy
  • PG is associated with IBD in 50% of cases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what extraintestinal manifestation is associated with IBD in 50% of cases?

A

Pyoderma gangrenosum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what extraintestinal manifestations DON’T improve after colectomy?

A

Primary Sclerosing Cholangitis

  • in men <40 y/o
  • colitis not as severe (vs pts that don’t have PSC colitis more severe)
  • risk of colon cancer increased 5x compared to UC alone
  • LIVER TRANSPLANT = CURE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Classification system of UC

A

Montreal classification

  • used to categorize extent and severity of disease
  • classified by severity and where in the colon it is
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

3 components of diagnosing UC

A

(1) Clinical sx’s and presentations
(2) Sigmoidoscopy/colonoscopy - six’s confirmed by their findings
(3) Biopsy results/Histologic examinations – have infiltration of lamina propia (basement layer) with WBCs and inflammatory cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what must the initial work-up of UC do?

A

r/o infectious and non-infectious causes of the patients’ diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

possible infectious and non-infectious causes of UC pts diarrhea that must be ruled out

A

Infectious colitis

  • Fecal leukocytes (WBCs in stool)
  • Stool cultures, Ova, & Parasites
  • Campylobacter, Salmonella, Shigella, C. diff, Amebiasis, E. Coli - NEED TO RUN LABS FOR THESE

Radiation proctitis

Ischemic colitis (low blood flow to particular part of colon  ischemia -> it bleeds)
-Very common in elderly patients and patients that are dehydrated (ex: run a marathon)

CMV colitis (immunocompromised) - UNCOMMON

STI proctitis – DON’T MISS THIS!!!***

  • Gonorrhea, chlamydia, herpes, syphilis all cause proctitis
  • NEED TO DO SEXUAL HX – ASK ABOUT ANAL INTERCOURSE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is something you should NOT miss when doing initial work-up for UC pt?

A

STI proctitis – DON’T MISS THIS!!!***

  • Gonorrhea, chlamydia, herpes, syphilis all cause proctitis
  • NEED TO DO SEXUAL HX – ASK ABOUT ANAL INTERCOURSE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

UC lab values

A

ESR is high (inflammatory marker)

CRP is high (inflammatory marker)

H/H is low

Albumin is low d/t malnutrition

-These patients will have anemia of chronic disease, microcytic hypochromic type of anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

UC radiography

A

Plain films not much value

CT abd/pelvis (shows colitis/wall thickening, bowel obstruction, perforation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

is imaging part of the core dx of UC or CD?

A

NO!!! b/c you need to see what the tissue actually looks like -> DO TISSUE BX

imaging won’t tell you what type of colitis it is

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is the cornerstone tx of UC mild disease?

A

Aminosalicylates (5-ASA) drugs
-NSAID for colon

Meds:

  • Mesalazine PR suppository for mild proctitis
  • Rectal (suppository) and oral 5-ASA (ex: PO sulfasalazine and PR mesalazine) for distal colon inflammation (COMMON TO GIVE BOTH ORAL AND SUPPOSITORY)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what medication is recommended for maintenance (after remission) for UC?

A

5-ASA - RECOMMENDED FOR ALL MAINTENANCE THERAPY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

medications for UC mild-moderate disease/failure of 5-ASA

A

Budesonide PO - targets colon with minimal systemic effects (can use prednisone, but budesonide is preferred)

MUST TAPER OVER 60 DAYS ONCE GAIN CONTROL OF SX’S

***NOT FOR MAINTENANCE THERAPY -> SWITCH TO 5-ASA AFTER TAPER FOR MAINTENANCE!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

is Budesonide for maintenance therapy of UC?

A

NO!!!! Must taper over 60 days once gain control of six’s and then put on 5-ASA for maintenance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

medications for UC severe disease

A

Hospitalization and IV steroids w/IVF
-Methylprednisolone (if doesn’t work use TNF-alpha blockers)

TNF-alpha blockers (used if IV steroids don’t work) - infliximab, adalimumab, golimumab

VGEF blocker - use if TNF-alpha blockers fail
-Vedolizumab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what medication do you use for UC if 5-ASA failed?

A

Budesonide PO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what is a last resort medication for severe UC?

A

cyclosporine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

if methylprednisolone (IV steroids) doesn’t work for severe UC, what do you use?

A

TNF-alpha blockers

-infliximab, adalimumab, golimumab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

if TNF-alpha blockers don’t work for severe UC, what do you use?

A

VGEF blocker

-vedolizumab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

UC maintenance therapy meds

A

5-ASA

Immunosuppressants (azathioprine or 6-MP) if 5-ASA not working

If TNF-alpha blocker induction works, then continue with agent for maintenance or azathioprine (same for Golimumab)

***Probiotics help with maintaining remission - maintains gut flora

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what meds help with maintaining remission in UC?

A

probiotics - maintains normal gut flora

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what is the surgical treatment for UC?

A

Colectomy

-generally curative in UC and most common rationale is failure of medical management

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

when would a UC pt get an EMERGENCY colectomy?

A

Life-threatening complications related to fulminant disease such as toxic megacolon unresponsive to medical treatment

-Toxic megacolon = dilation of colon and develop ileus unresponsive to meds and need surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

when would a UC pt get an URGENT colectomy?

A

Severe disease admitted to hospital and not responding to intensive medical treatment

48
Q

what type of surgery for UC is the most common and who is it for?

A

Elective surgery (most common)

  • Refractory disease intolerant to long-term maintenance treatments (ex: long-term steroid dependence)
  • Colorectal dysplasia or adenocarcinoma found on screening bx
  • Long-term disease 7-10 years
49
Q

when is surgery recommended for UC

A

failure of medical management

50
Q

what are UC patients at an increased risk of?

A

colorectal cancer

-increasing the longer they have disease

51
Q

what must UC pts be screened for and starting when?

A

must be screened for colorectal cancer beginning at 8 years after disease onset (even if well-maintained disease)

52
Q

after initial screening colonoscopy for UC pts, what does further screening depend on? when do you screen for proctitis/proctosigmoiditis, left-sided colitis/pancolitis, UC w/PSC?

A

extent of disease

Proctitis/proctosigmoiditis
-usually screened every year

Left-sided colitis/pancolitis: Screened every 1-2 years

UC w/PSC: Annually from time of dx of PSC

53
Q

UC risk factors for colorectal cancer

A

Duration and extent of disease (how poorly controlled is the disease)

Colonoscopic and histologic severity of inflammation

54
Q

what is Crohn’s disease characterized as?

A

Intermittent bouts of low grade fever, diarrhea and RLQ pain (flares and remission cycle)

Also have perianal disease (abscess, tissue, fistula)

55
Q

what type of inflammation is in Crohn’s disease, what’s it’s distribution and what does it cause?

A

Transmural inflammation in skip lesion distribution causes strictures, fistulas, ulcerations, abscess

56
Q

where does Crohn’s affect?

A

COMMONLY AFFECTS SMALL BOWEL AND COLON - USUALLY TERMINAL ILEUM AND ASCENDING COLON

-small bowel (usually terminal) can only be affected and colon can only be affected

57
Q

what other disease is associated with having Crohn’s disease?

A

perianal disease (abscesses, fistulas, fissures)

58
Q

can extra intestinal manifestations occur in CD?

A

Yes, but not as common as they are in UC

Includes:

  • arthalgia
  • iritis/uveitis
  • Pyoderma gangrenous or erythema nodosum
59
Q

Crohn’s disease Risk Factors

A

Genetic factors: Need good fam hx (strongest risk factor)

Environmental factors:

  • **Smoking – significantly exacerbates Crohn’s disease
  • Sedentary lifestyle, exposure to air pollution, and consumption of western diet

Infectious factors:
-CD often occurs after infectious gastroenteritis

60
Q

smoking and Crohn’s disease vs smoking and UC

A

smoking exacerbates Crohn’s disease

smoking lowers risk/milder disease in Ulcerative colitis

61
Q

Crohn’s disease clinical presentation

A

MUCH BROADER SX’S VS UC B/C AFFECTS ANY PART OF GIT

  • abdominal pain (intermittent and is RLQ)
  • diarrhea (watery/NONBLOODY!!!)
  • constitutional six’s (low grade fevers, weight loss/anorexia/malnutrition, weakness/fatigue/mailase - anemia, bone loss (d/t malnutrition w/ CD)
  • small bowel obstruction presentation (N/V w/abd pain)
  • anal fissure/skin tag/abscess/fistula (perianal presentation)
62
Q

what types of sx’s are more common in CD vs UC?

A

Constitutional sx’s

  • Low grade fevers
  • Weight loss/anorexia/malnutrition
  • Weakness/fatigue/malaise (anemia)
  • Bone loss – d/t malnutrition associated with CD
63
Q

what are Complications of Crohn’s?

A

Abscess, Small bowel obstruction, Fistulas (and and rectovaginal), Perianal disease, Carcinoma, Malabsorption, possible hx of other autoimmune d/o’s

64
Q

how do you treat abscess in Crohn’s?

A

Broad spectrum abx s/p CT diagnosis and surgery or

Percutaneous drainage (done by interventional radiologist)

65
Q

what is occurring in small bowel of obstruction in CD? how do you treat it?

A

SBO chronic structuring or severe inflammation -> closes off part of gut

If have strictures then need low fiber diet - high fiber diet can
cause bowel obstruction

Tx:
-IVF, NGT decompression and IV steroid but if refractory possible partial resection or stricturoplasty

66
Q

how do you treat fistulas in CD?

A

If symptomatic - TPN (parenteral diet)/oral elemental diet may close fistula temporarily (tried initially)

Antibiologics 10 weeks (1/2 recur)

Surgical resection if medical management fails

67
Q

how do you treat perianal disease in CD?

A

abx (flagyl or Cipro) but recurrence is common

Mesalamine (5-ASA) suppository or tacrolimus ointment for refractory fissure

Antibiologics

***Medical management of Crohn’s first line with surgical intervention last resort

68
Q

how do you treat Carcinoma in CD?

A

• Increased risk of colon cancer (same time interval as UC), thus screening with colonoscopy required for early identification of dysplasia/malignancy

***Screen at 8 years of disease

69
Q

how do you treat Malabsorption in CD?

A

s/p multiple resection or bacterial overgrowth w/fistulas, strictures or stasis

70
Q

CD Classification

A

Montreal classification used to categorize CD

  • L-classification: Defines extent of disease (where in the GIT it is)
  • B-classification: Defines phenotype (structuring, penetrating)
71
Q

3 components of CD diagnosis?

A

Same 3 diagnosing components as UC:

(1) Clinical sx’s and presentations
(2) Sigmoidoscopy/colonoscopy
(3) Biopsy results/Histologic examinations

72
Q

what must you r/o in CD?

A

As with UC, must r/o important non-infectious causes (IBS – dx of exclusion, Behcet’s syndrome) and infectious causes (Yersinia – terminal ileum inflamed like in CD – looks like CD, enteroviruses, etc.) that mimic CD

73
Q

what is the GOLD STANDARD FOR DX in CD?

A

Colonoscopy and mucosal bx is GOLD STANDARD FOR DX (colon & terminal ileum)

  • Really bx from any area w/disease
  • Aphthoid, stellate, linear ulcers
  • Strictures

-***Segmental involvement w/ skip lesions

74
Q

CD radiologic tests for dx

A
  • CT/MRI enterography or enteroclysis
  • Show inflammation (just like in UC), but doesn’t change tx or labs
  • ***LINEAR ULCERS ARE CLASSIC
75
Q

Labs in CD

A

CRP is high, ESR is high, fecal calprotectin (inflammatory marker good for trending flares & remissions), H/H is low (present with anemia of chronic disease), albumin is low, WBC is high

76
Q

what is the first thing pts with CD should be counseled on?

A

All patients with CD should be counseled to QUIT SMOKING (#1)

77
Q

CD diarrhea tx’s

A

Loperamide (Immodium) - if sure no infectious cause of the diarrhea

Terminal ileal disease or resection = bile acid sequestrant

Short gut = low fat diet

78
Q

Mild Crohn’s disease tx?

A

Colon and small bowel disease = mesalamine (can’t be maintained on 5-ASA)

5-ASA derivatives, which are mainstay of UC, have shown to be less useful in treatment of CD b/c mesalamine releases only in the terminal ileum and colon

79
Q

Moderate-Severe Crohn’s disease tx?

A

Steroid therapy (BUDESONIDE)

Immunosuppressant’s (AZATHIOPRINE - 6-MP; METHOTREXATE - induces remission)

TNF-alpha blockers (infliximab, adalimumab, certolizumab pegol)

Anti-integrins (VEDOLIZUMAB) - used after TNF-alpha blockers

Fistula disease (METRO OR CIPRO, SURGERY IF MEDS FAILS)

80
Q

what does Methotrexate do in CD?

A

it’s a tx for moderate-severe Crohn’s disease

IT CAN INDUCE REMISSION AND CAN HOLD PTS IN REMISSION

81
Q

what do the TNF-alpha blockers in CD treat?

A

Fistulas - that aren’t responding to abx and conventional therapy

50% refractory cases respond well to TNF-alpha blockade

Use induction dosage until remission and then maintenance dosage

82
Q

is surgery curative in CD like in UC?

A

NO!!! SURGERY IS NOT CURATIVE IN CD

-high rate of disease recurrence after segmental bowel resection so try to preserve as much bowel as possible

83
Q

what are the indications of surgery in CD?

A

Abscess that you can’t drain percutaneously, intractable fistula, toxic megacolon, fibrotic strictures w/ obstruction, refractory sx’s despite high dose steroids, perforation, intractable hemorrhage, cancer

84
Q

when do you admit a pt for CD?

A
  • Bowel obstruction
  • Abscess (intra-abdominal or perirectal)
  • Severe symptoms of diarrhea/dehydration, weight loss/weakness, abdominal pain and can’t control it
  • Serious infection complication in immunocompromised population (steroids, TNF-alpha blockers, imunomodulators)
85
Q

what must you regularly screen for in CD?

A

Regularly screen for active infection

-Tuberculosis, hepatitis, CMV, HIV, and C. diff

86
Q

CD Colorectal cancer screening

A

In patients with more than a third of colon affected (Montreal classification L3), first screening colonoscopy should occur 8 years after onset, repeated every 1-2 years and then every 1-3 years once normal

Patients with PSC should undergo annual screenings
-Risk of cholangiocarcinoma – need to be evaluated for this (high morality; cancer of biliary tree)

87
Q

what is celiac sprue?

A

***Allergic reaction to gluten

Immunologic/inflammatory response to ingested gluten (gliadin = alcohol-soluble fraction of gluten) affecting mucosa of GI tract

88
Q

what is gluten?

A

Gluten = wheat, rye, barley

89
Q

what does Celiac Sprue affect?

A

mucosa of proximal small bowel

90
Q

celiac sprue is a disease of what?

A

Disease of significant malabsorption b/c nutrients absorbed in small bowel, so if small bowel not working -> malnutrition, electrolyte abnormalities

91
Q

at what ages do most people present with celiac sprue?

A

childhood-adulthood

92
Q

what are the 2 types of sx’s for Celiac Sprue?

A

GI sx’s and extraintestinal symptoms

CAN HAVE ONLY EXTRAINTESTINAL SX’S (NO GI SX’S)

93
Q

what does the severity of GI sx’s of Celiac Sprue depend on?

A

Severity depends on how much of small intestine is involved & age @ presentation

  • < 2 years old malabsorption presentation
    (Much sicker, not hitting growth milestones, have weight loss, abd distention)

-Older age +/- GI sx’s, less weight loss, more atypical sx’s, “silent” sprue (no GI sx’s)

94
Q

Celiac Sprue GI sx’s

A
  • Diarrhea
  • Borborygmus, Flatulence
  • Weight loss

In infants and young children with untreated celiac disease, failure to thrive and growth retardation are common (classic malabsorption)

  • Weakness and fatigue MOST COMMON (usually related to general poor nutrition)
  • Severe abdominal pain
95
Q

Extraintestinal sx’s of Celiac Sprue

A
  • Fatigue, depression, Fe-deficiency anemia
  • Anemia
  • Osteopenia and osteoporosis d/t malnutrition
  • Neurologic symptoms (includes motor weakness, paresthesia’s with sensory loss, and ataxia; Seizures may develop)

Skin disorders
-Dermatitis herpetiformis
Hormonal disorders – Amenorrhea, delayed puberty, and infertility in women and impotence and infertility in men

96
Q

what skin disorders do celiac pts develop?

A

Dermatitis herpetiformis

-a condition with pruritic, papulovesicular skin lesions involving the extensor surfaces of the extremities, trunk, buttocks, scalp, and neck

97
Q

Celiac Sprue Physical Exam

A

LOOKING FOR SIGNS OF MALABSORPTION

  • A protuberant and tympanic abdomen
  • Evidence of weight loss (loss of muscle mass or subcutaneous fat)
  • Orthostatic hypotension (could be d/t diarrhea)
  • Peripheral edema (protein malabsorption)
  • Ecchymoses (vit K deficiency)
  • Hyperkeratosis (vit A deficiency) or dermatitis herpetiformis
  • Cheilosis and glossitis (Fe-deficiency)
  • Evidence of peripheral neuropathy or ataxia (vit B12 or E deficiency) – has to do with vibratory sense would be decreased

-Chvostek or Trousseau sign, tetany (Hypocalcemia) -Can induce tetany w/BP cuff or twitching w/ tap on face

Dermatitis herpetiformis

98
Q

Celiac Lab Dx

A

CBC – anemia (Fe, folate, B12)

CMP – malnutrition, electrolyte imbalance

Coags – PT prolonged d/t malabsorption of vitamin K

Stool – fat malabsorption (72hr fecal fat collection to detect steaorrhea)

Oral tolerance tests – lactose intolerance (often associated with celiac) -> Hydrogen breath test

99
Q

what serologic test do you use to dx Celiac?

A

IgA TTG - 95% sensitive and specific

100
Q

what other Serologic testing can you do for Celiac dx?

A

IgA level

  • If negative IgA TTG, but strong clinical suspicion
  • 3% w/ IgA deficiency

If <2 years or IgA deficiency
-IgA TTG combined with testing for IgG-deamidated gliadin peptide (high sp/sens)

-All levels antibodies become undetectable s/p 3-12 months gluten avoidance so can monitor for compliance

101
Q

when do IgA antibodies become undetectable in Celiac?

A

All levels antibodies become undetectable s/p 3-12 months gluten avoidance so can monitor for compliance

102
Q

what is the GOLD STANDARD DX for Celiac Sprue?

A

Endoscopy and mucosal biopsy prox + distal duodenum

103
Q

what will you see on Endoscopy and mucosal biopsy of pros + distal duodenum in Celiac Sprue?

A

Atrophy or scalloping of duodenal folds

Histology
-Villi are atrophic or absent
-Hypertrophy of crypts
(Celluarlity of the lamina propria is increased with a proliferation of plasma cells and lymphocytes)

104
Q

what is the best dx for Celiac?

A

BEST DX IS TO TAKE PT OFF OF GLUTEN B/C THEN SX’S GO AWAY TO MAKE SURE IT’S NOT SOMETHING OTHER THAN GLUTEN; ALSO BEST TX!!!

105
Q

Celiac Sprue tx

A

Diet, Supplements, Steroids

106
Q

Celiac Sprue diet tx

A
  • Essential therapy = removal of ALL gluten (wheat, rye, barley, oats may be contaminated during processing)
  • improvement in 2 weeks on diet
  • associated w/lactose intolerance -> avoid diary until sx resolution
107
Q

Celiac Sprue supplements tx

A
  • B/c Celiac is a malabsorptive disease
  • Will have electrolyte imbalances, low K, low Mg, etc.

Use: Vit A, B12, D, E

  • Initial stages only required usually not long-term
  • Once villi improve then won’t have to supplement with vitamins as much b/c malabsorption goes away
108
Q

Celiac Sprue steroids tx

A
  • Prednisone or budesonide 2 or more weeks for severe sx’s

- Unintentional or intentional gluten ingestion may trigger severe diarrhea, hypovolemia, electrolyte imbalance

109
Q

what is lactose intolerance?

A

Common disorder d/t inability to digest lactose

All of our lactase we will ever get is when we are very young (breast milk when a baby), but then declines steadily with aging especially in people of non-european descent

110
Q

what is Lactase?

A

Lactase is a brush border enzyme that digests lactose into galactose and glucose

111
Q

Lactose intolerance most common in?

A
  • Asian Americans – 90%
  • Native Americans – 95%
  • African Americans – 70%
112
Q

what disorders can lactose intolerance develop secondarily to?

A
  • Celiac sprue
  • Crohns
  • Giardia
  • Viral gastroenteritis
  • Malnutrition
  • Short bowel syndrome
113
Q

if you don’t have lactase, then how does the gut breakdown lactose?

A

by fermenting it which is done by producing a lot of gas

114
Q

DDx of lactose intolerance

A

IBD, IBS, pancreatic insufficiency, mucosal malabsorptive disorders

115
Q

Lactose intolerance clinical presentation

A
  • Sx’s occur when ingested a raw milk product (ex: milk, cheese)
  • Abdominal bloating
  • Abdominal cramping
  • Flatulence
  • Diarrhea/loose stool (with higher intake of lactose)
  • Nausea
  • Borborygmi
  • Severity of sx’s depends on quantity ingested and severity of deficiency

***EXCLUDE LACTOSE AND SX’S RESOLVE!!!

116
Q

Lactose intolerance labs

A

Hydrogen breath test

After ingestion of 50g lactose a rise in breath H+ of greater than 20ppm w/in 90 min

117
Q

Lactose intolerance tx

A

Goal of therapy is patient comfort and determining “threshold” of intake when symptoms occur

Spread lactose intake throughout the day in quantity <12 g (1 cup of milk) and most pts tolerate this w/o lactase

Lactase enzyme replacement

  • Lactaid, Lactrase, Dairy Ease
  • Quantity taken with lactose or number of capsules = degree of intolerance
  • Some foods are pretreated with lactase (ex: Milk which = 70-100% lactose free)

Calcium supplementation if exclude dairy (prevent osteoporosis)

Clin Med 3 (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions