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GI/Endo/Repro > Assessment 2 > Flashcards

Assessment 2 Flashcards

1
Q

Intestinal reserve: enzymes

A

Brush border AND pancreatic oligosaccharides/proteinases

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2
Q

Intestinal reserve: pancreas

A

Pancreas secretes and excess of enzymes

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3
Q

Intestinal reserve malabsorbed nutrients

A

Transit slowed if malabsorbed nutrients reach distal portion of GI tract

Colon scavenges malabsorbed carbs as SCFA

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4
Q

Malabsorption clinical presentation

A

Weight loss/fatigue

Excess calorie intake with no weight gain

Excess flatulence/distension

Diarrhea: oily or liquid

Vit/mineral deficiency

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5
Q

Watery diarrhea comes from

A

Carbohydrate osmotic effect

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6
Q

Oily diarrhea comes from

A

Fat malabsorption

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7
Q

Diarrhea can come from

A

Osmotically active molecules reach colon

Malabsorbed molecules stimulate colon/ion secretion –> osmotic gradient

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8
Q

Diagnostic confirmation of malabsorption

A

Low beta carotene, cholesterol, TG, Ca

Elevated PT

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9
Q

Evidence of mucosal disease

A

Low albumin, folate, B12, iron

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10
Q

Malabsorption stool tests

A

Quantitative fecal collection

Steatocrit: >31% = abnormal

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11
Q

72 hr fecal fat test

A

100g input, measure output

> 7 = malabsroption

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12
Q

Lactase deficiency

A

Lactase enzyme not in brush border, lactase buildup in lumen –> osmotic diarrhea

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13
Q

Lactose malabsorption and symptoms

A

6-20g malabsorbed = flatus

> 20g malabsorbed = flatus+diarrhea

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14
Q

Cystic Fibrosis and pancreas

A

75% of CF patients have pancreatic exocrine insufficiency by 6 months

60% of remaining patients develop PEI by young adulthood

10% retain pancreatic sufficiency

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15
Q

Chronic pancreatitis

A

Long term alcohol abuse

Destruction of ducts/acini

Reduction of digestive enzymes

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16
Q

ERCP

A

Detect ductal abnormalities

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17
Q

MRCP

A

Detect ductal/parenchymal abnormalities

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18
Q

EUS

A

Detect ductal/parenchymal abnormalities

Tissue sampling

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19
Q

D-xylose test

A

Old test - directly asses mucosal function of sugar absorption

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20
Q

Celiac sprue

A

Immune mediated destruction of enterocytes in response to gluten

Small intestinal villi destroyed

Mature digesting/transporting enterocytes absent

Digestion AND absorption imapired

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21
Q

Celiac sprue antibody

A

IgA to transglutaminase, endomysium, gliadin

Deaminated gliadin petides

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22
Q

Celiac visual presentation

A

Decreased folds, scalloping mosaic pattern

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23
Q

Celiac histology stages

A

Stage 1: inflammation
Stage 2: Deep crypts
Stage 3: Villi/enterocytes destroyed

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24
Q

Clinical manifestation of celiac

A 
Weight loss
Bulky/oily stools
Flatus/frothy stools
Anemia
Bone disease
Edema/hypoproteinemia
Vit B deficiency
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25
Q

Bacterial overgrowth

A

Deconjugation of bile acids by bacterial enzymes

Consumption of nutrients by bacteria

Damage to enterocytes

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26
Q

Bacterial overgrowth diagnosis

A

Small bowel culture
Lactulose/glucose hydrogen breath test
Anitbiotic response

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27
Q

Terminal ileum resection and malabsorption

A

Less than 100cm gone: Excess bile salts in colon = watery diarrhea

100cm gone: Liver cant keep up with bile salt loss = steatorrhea

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28
Q

Fat soluble vitamin absorption

A

Bile salt defecits > mucosal/pancreatic disease

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29
Q

Folate deficiency

A

Proximal small bowel disease, alcohol, drugs, congenital effect

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30
Q

Protective mechanisms in pancreas

A

Synthesis of enzymes as inactive zymogens

Trypsin inhibitor in zymogen granule

Segregation of enzymes

Enterokinase restricted to SI

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31
Q

Acute pancreatitis

A

Acute inflammatroy condition w/ abdominal pain and increase in pancreatic enzymes

Interstitial (mild): Complete recovery

Necrotizing (severe): Permanent damage

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32
Q

Major etiologies of acute pancreatitis

A

Alcoholism
Biliary
Idiopathic
Other

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33
Q

Pancreatic divisum

A

Failure of dorsal and ventral pancreas to fuse

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34
Q

Time course of enzyme elevation - acute pancreatitis

A

Enzymes 3x UL

Lipase increases faster and to higher degree than amylase, takes longer to decrease

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35
Q

Risk factors of severity

A 
Age
Obesity
1st or 2nd episode
Organ failure at admission
Short interval to admission
Pleural effusion
CT scan-grade D/E
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36
Q

Diagnostic indicators of acute pancreatitis

A 
Tachycardia/hypotension
Tachypnea, hypoxemis
Hemoconcentration
Oliguria
Encephalopathy
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37
Q

Local complications of acute pancreatitis

A 
Fluid collection
Necrosis
Ascites
Erosion into adjacent structures
GI obstruction
Hemorrhage
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38
Q

Systemic complications of acute pancreatitis

A

Pulmonary

Renal

CNS

Multiorgan failure

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39
Q

Metabolic complications of acute pancreatitis

A

Hypocalcemia

Hyperglycemia

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40
Q

Chronic pancreatitis

A

Pain

Calcification

Pancreatic insufficiency

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41
Q

Etiologies of chronic pancreatits

A

Alcoholism
Idiopathy
Other - CF, hereditary pancreatitis, hypertriglyceridemia, autoimmune, fibrocalcific

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42
Q

Treatment of chronic pancreatitis

A

Medical therapy: low fat diet, pain control, pancreatic enzyme supplementation

Surgical therapy
-ERCP, Decompression surgery, resective surgery

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43
Q

Pancreatic cancer and pancreatitis

A

Increase risk of neoplasm in chronic pancreatitis

May present as acute pancreatitis

Poor prognosis

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44
Q

Cystic neoplasm

A

No prior pancreatitis

Unexplained pancreatitis with cystic lesion

Fluid analysis, endoscopic US, resection

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45
Q

Inflammatory bowel Disease types

A

Ulcerative Colitis

Crohns

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46
Q

Ulcerative colitis clinical presentation

A 
BLOODY DIARRHEA
Fever
Cramping/abdominal pain
Weight loss
Tenesmus
General malaise
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47
Q

Ulcerative colitis location

A

Mainly distal, 95% rectal involvement

15-25% pan colitis - more likely in children

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48
Q

Crohns disease location

A

Mainly proximal

40% SI

30% Ileocolonic

30% colon only

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49
Q

Endoscopic chrons appearance

A

Cobblestone mucoas
Inflammatory polyps
Skip lesions

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50
Q

Crohns clinical presentation

A 
Diarrhea
Abdominal pain
Bleeding
Pyrexia
Fistulae
Perianal disease
More mucus than ulcerative colitis
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51
Q

Age and incidence of IBD

A

Incidence spike in 20s/30s and again in older age for UC

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52
Q

Differences between UC and Crohns

A

UC: More malaise, diarrhea, and BLOOD

Crohns: More pain, mucus, pus

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53
Q

Etiology of IBD

A 
Genetic
ENVIRONMENT
Smoking
Dietary
Infection/bacteria/gut flora
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54
Q

Indications for surgery (IBD)

A 
Perforation
Toxic dilation
Massive hemorrhage
Chronic ill health
Cancer risk
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55
Q

Pharmacological treatments

A

5ASA

Corticosteroids

Immunosuppressants

Anti TNFa

Anti Adhesion molecules

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56
Q

5ASA targets

A

Leukotrienes and prostaglandins

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57
Q

Corticosteroid immune system target

A

trafficking, proliferation, t cell regulation

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58
Q

Intestinal complications of Crohnss

A 
Fistulae
Abscesses
Adhesions
Strictures
Obstruction
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59
Q

Systemic complications of Crohns

A

Arthritis
gallstones
Malabsorption: Lactase/B12
Renal stone

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60
Q

Intestinal complications of UC

A 
Fibrosis
Shortening of colon
Bleeding 
Stricture
Bowel perforation
Toxic megacolon
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61
Q

Systemic complications of UC

A

Arthritis

Uveitis

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62
Q

Classification of laxatives

A

Hydrophilic
Stimulant
Secretory

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63
Q

Hydrophilic types

A

Bulk forming
Lubricants
Hyperosmotics

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64
Q

Hydrophilic intervention

A

Hydrophilic –> increase water content of stool

Increase stool mass = increase peristalsis

Dietary fiber
Pysllium: Metamucil/konsyl
Methylcellulose

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65
Q

Bulk forming drugs

A

Psyllium: Metamucil/Konsyl
Methylcellulose: Citrucel

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66
Q

Lubricants

A

Stool softeners

Ducosate Sodium: Colace
Ducosate Calcium: Surfak

Mineral oil - highly effective but incontinence

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67
Q

Osmotic laxatives

A

Non absorbable hypertonic ions/agents = increase osmotic gradient

Magnesium salts: milk of magnesia, epsom salt, magnesium citrate

Lactulose - Cephulac

Polyethylene glycol: Golytely, Colyte, Miralax

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68
Q

Stimulant laxatives

A

Stimulate secretion/peristalsis

Rapid onset

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69
Q

Simulant laxative examples

A

Phenolphthalein
Bisacodyl (Dulcolax)
Sodum phosphate
Neostigmine - stimulates peristalsis

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70
Q

Lubiprostone

A

Chloride channel activator

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71
Q

Methylnaltrexone

A

Opioid receptor antagonist

Does not cross BBB

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72
Q

Glycerin suppositories

A

Hyperosmotic laxative - draws water into lumen at end of intestine

Very quick

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73
Q

Diarrhea drugs - opioid agonist

A

Decrease peristalsis
Constipation/dependence

Loperamide

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74
Q

Diarrhea drugs - anti muscarinic

A

Decrease peristalsis

Anti spasmodic

low doses so no atropine like side effects

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75
Q

Diarrhea drugs - aomatostatin analog

A

Octreotide

Inhibits secretion
Inhibits gastrin release
Decrease SM contraction

Short half life = frequent dosing = impractical for long term use

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76
Q

Diarrhea drugs - bulk forming agents

A

Psyllium

Methylcellulose

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77
Q

Aminosalicylates

A

IBD

Administered as pro drugs, digested by gut bacteria to produce active 5ASA

Can result in toxic byproducts: Sulfapyridine

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78
Q

Corticosteroids

A

Rectal: hydrocortisone - rapid onset

Oral: Prednisone, methylprednisolone - first pass metabolic steroids

Limit long term use

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79
Q

Immunosuppressive drugs

A

Azathioprine, 6mercaptopurine

Purine biosynthesis inhibitor
Risk of infection

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80
Q

Methotrexate

A

Immunosuppressive IBD drug

Folate antagonist

Hepatotoxicity, alopecia, myelosuppression, infection

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81
Q

Cyclosporin

A

Cyclic polypeptide immunosuppressant

Many toxicities, infection

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82
Q

IBD Biologicals

A

TNF-1 inhibitor: Infliximab, adalimumab

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83
Q

Natalizumab

A

Humanized MAB that antagonizes integrin heterodimers

Use for UC patients that dont respond ot other treatment

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84
Q

Diverticula

A

Sac like protrusion of colonic wall

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85
Q

Diverticulosis

A

Having diverticulum

80% asymptomatic

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86
Q

Diverticluosis epidemiology

A

Increases with age

Varies geographically

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87
Q

Risk factors

A

Inverse relation with fiber

High fat/red meat

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88
Q

Pathophysiology of diverticulosis

A

Erostion of diverticular wall caused by increased intraluminal pressure

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89
Q

Clinical presentation of diverticulitis

A

LLQ abdominal pain
Change in bowel habits
Urinary symptoms- dysuria/frequency

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90
Q

Diagnostic tests for diverticulitis

A

Check white count/urinalysis

Ab CT is best/most sensitivity

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91
Q

Complicated diverticulitis (3 types)

A

Abscess
Fistula
Obstruction

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92
Q

Abscess diverticulitis

A

Seen on CT

Patients wont be responding to treatment

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93
Q

Fistula diverticulitis

A

5%

Colovesical: Between colon and bladder - air coming from urine

Colovaginal

Require surgical repair

94
Q

Obstruction diverticulitis

A

Acute - partial obstruction due to inflammation or abscess

Chronic - metal stents treat obstruction

95
Q

Colonoscopy and diverticulitis

A

DONT DO RIGHT AWAY

Risk perforation

Do 6 months after recovery to rule out cancer

96
Q

Diverticular bleeding

A

Fresh blood with stool through anus

Tagged RBC scan, angiography, surgery

97
Q

5 I’s of acquisition

A 
Intimacy
Inhalation
Ingestion
Inoculation
Injection
98
Q

Resolution of bacterial infection

A

Immunity and physical factors (abscesses) contribute to clearance –> does not equal resolution

99
Q

Enterotixin vs cytotoxin

A

Enterotoxin: functional alteration

Cytotoxin: Cellular damage

100
Q

Gastroenteritis enterotoxins

A

Cholera

E. Coli Labile toxin

Bacillus cereus toxin

101
Q

Gastroenteritis cytotoxin

A

Shigella

C. Diff

C. Perfringes

102
Q

Exotoxin structure

A

A: Enzymatic activity

B: Binding domain

103
Q

Cholera toxin

A

Increase cAMP –> Increase Cl release into lumen –> diarrhea

104
Q

Shiga like toxins

A

Released by Enterohemorrhagic E. Coli

Esp: E. Coli O157:H7

Attack endothelial cells

105
Q

Hemolytic Uremic syndrome

A

Shiga like toxin attacks endothelial cells –> platelets deposit –> blood cells caught in fibrin deposition –> ischemia –> kidney failure

106
Q

Salmonella

A

G(-) bacilli, ferments sugars, oxidase negative

Contaminated food, fecal oral transmission, reptiles

Enteritidis: Does not survive gastric acid, needs high dose

Typhy/Shigaella are more acid resistant

When reach terminal ileum, pili attach to epithelial cells and M cells –> Type II secretion helps salmonella invade and survive

Inflammation/hemorrhage/epithelial injury

107
Q

Listeria

A

Internalins: Adhere to epithelial cells
Listeriolysin O: Escape from phagosome
ActA - move to adjacent cell

Injury, inflammation, hemorrhage

108
Q

Infectious diarrhea types

A

Intoxication

Non inflammatory

Inflammatory

109
Q

Intoxication infectious diarrhea

A

Pre formed toxins in food

Quick onset

Vomiting and watery diarrhea

24hr recovery

110
Q

Non inflammatory infectious diarrhea

A

Viruses and non invasive bacteria

2-7 day incubation

Watery, large volume stools

No fever or blood in stool

Focus on SI - vomiting

111
Q

Inflammatory infectious diarrhea

A

Invasive or cytotoxin producing bacteria

Fever, tenesmus, blood in stool

Vomiting is less prominent

112
Q

Intoxication organisms (3)

A

Staph aureus

Bacillus cereus

C. Perfringes

113
Q

Staph aureus

A

G(+) cocci, catalase +

Enterotoxins = superantigens

Cytokine release = serotonin = emesis

Short incubation, vomiting, cramping, no diarrhea

114
Q

Bacillus cereus

A

G+ spore forming

Improperly refrigerated food - germinated and toxin produced

115
Q

Types of bacillus cereus

A

Emetic: Cerulide toxin - stimulates serotonin
1-6 hr after ingest food
Rice products/starchy food

Diarrheal: Other toxins
6-15 hr after ingestion

Meat, milk, vegetables, fish

Watery diarrhea

116
Q

C. Perfringes

A

G+ spore forming

Vegetative cells in food –> Bacteria multiple i gut and sporulate

CPE distrupts tight junctions between enterocytes

Watery diarrhea

117
Q

Viruses causing non inflammatory diarrhea

A

Rotavirus

Norovirus

Adenovirus

Astrovirus

118
Q

Non inflammatory diarrhea Enterotoxin producing bacteria

A

Cholera

ETEC

119
Q

Inflammatory diarrheal invasive bacteria

A

Campylobacter

Shigella

Salmonella

Yersinia

120
Q

Inflammatory diarrhea cytotoxin producing bacteria

A

C diff

EHEC

121
Q

Norovirus

A

Most common overall

Food/water borne, fecal oral, aerosolized vomit

Abrupt onset, 72hrs

122
Q

Rotavirus

A

Ubiquitious - almost all children infected by age 3

2 vaccines developed

123
Q

ETEC

A

Enterotoxigenic E coli

Fecal/oral via water

Similar to cholera mechanism

124
Q

EPEC

A

Enteropathogenic E coli

Daycare

Type II secretion

125
Q

Shigella

A

Overt pathogen, not normal flora

Non lactose fermenting

Diarrhea, dystentery

Human is natural reservoir

Acid resistant

126
Q

Campylobacter jejuni

A

Reservoir in GI tract of asymptomatic animals

Undercooked poultry/meats

Mucosal invasion by bacteria and damage

127
Q

Yersinia (2)

A

Enterocolitica: Cattle/pig and pseudotuberculosis: rodents/birds

Intimin and type III secretion = close attachment and invasion of macrophages

Survive in peyers patches

Pseudoappendicitis

128
Q

EHEC

A

Shiga toxin producing

E Coli O157:H7 - sorbitol negative

Damage microvilli/alter fluid transport

129
Q

C diff

A

G+ spore forming

Withstand heat, alcohol, ammonia

On the rise, very effective transmission

Damage to epithelial cells = inflammation

Result from antibiotic use

130
Q

Obesity BMI range

A

Obese: >30
Severe obese: >35
Extreme obese: >40

131
Q

Dieting EWL

A

14-20%

132
Q

Weight loss drugs indication and EWL

A

BMI >30

3-8% EWL

133
Q

Physician directed weight loss indication/EWL

A

BMI >30

4-13% EWL

134
Q

Surgery indications

A

BMI >40 or >35 w/comorbidities

Failed other treatments

135
Q

Types of surgery (3)

A

Restrictive: Smaller stomach

Malabsorbtive: Shorter colon

Combine

136
Q

Gastric bypass

A

Make small pouch to bypass stomach

Laparoscopic better than open surgery

Dumping syndrome, vit def, bleed/obstruction/stricture

137
Q

Sleeve gastrectomy

A

Risk/benefit much better

Mobilize greater curvature to make stomach smaller

GERD, bleed, stricture

138
Q

Gastri band

A

Band around stomach, gastric pouch based on lesser curvature

Need multidisciplinary care and frequent follow up

139
Q

Hyperplastic polyp

A

Most common, asymptomatic

Not precursor for cancer, no dysplasia

140
Q

Inflammatory polyp

A

Inflammatory pseudo polyp

No malignant potential

IBD or infectious colitis

141
Q

Juvenile retention polyp

A

SI, pedunculated, rectal bleeding

142
Q

Juvenile polyposis

A

Autosomal dominant

SMAD4, BMPR1A

Increased risk of colon cancer

143
Q

Peutz-Jeghers syndrome

A

AD, hamartomatous polyps

LBK1/STK11 gene

Increased risk of colon, pancreas, breast, lung cancer

144
Q

Cowden Syndrome

A

AD, hamartomatous polyp

PTEN loss of function mutation

Many extraintestinal manifestations

145
Q

Cronkhite Canada syndrome

A

Nonhereditary

Juvenile polyps in elderly patients

Diarrhea, weight loss, 50% fatal

146
Q

Dysplasia features

A

Hyperchromatic, elongated, stratified nuclei

Reduced goblet cells

147
Q

Sessile serrated adenoma

A

Looks like hyperplastic polyp

No dysplasia but increase cancer risk

148
Q

Intramucosal carcinoma

A

Dysplastic cells reach BM and enter lamina propria

Invasion beyond muscularis mucosa = invasive adenocarcinoma

149
Q

Familial adenomatous polyposis

A

AD, mutated APC or MUTYH

Many polyps

100% risk for colorectal carcinoma

Colectomy

150
Q

FAP extraintestinal manifestations

A

Congenital retinal pigment hypertrophy

Gardner syndrome: FAP + osteomas/cysts/thyroid tumors

Turcot syndrome: FAP + CNS tumors

151
Q

Hereditaroy non polyposis colon cancer

A

AD, fewer polyps

MSH1/MSH2 gene mutations: Mismatch repair genes

152
Q

Right side vs left side adenocarcinomas

A

Right: Iron deficiency, fatigue/weight loss, ab pan/mass

Left: Rectal bleeding, bowel habit change, LLQ pain

153
Q

SI Adenocarcinoma

A

Elderly

Duodenum/ampulla of vater

Biliary obstruction –> jaundice

154
Q

Carcinoid tumors

A

Low grade malignant neoplasm

Secrete many hormones

155
Q

Primary GI lymphoma

A

Stomach and SI

Risk factor: MALT lymphoma
PTLD

156
Q

GIST

A

Gastrointestinal stromal tumor

Arise from ICC

Surgery + anti c-kit

157
Q

Peyers patch

A

APC’s, B-cell region, T cell zone

158
Q

Intestinal epithelial cell immunity (5)

A

Goblet cells: Mucus

Paneth cells: alpha defensins and antibacterial activity

Enterocytes

sIgA transport

159
Q

M cell

A

Specialized epithelial cell usually above Peyers patch

Little to no microvili

Take up particles/molecules and present to Macrophages/DC’s

160
Q

Dendritic cell

A

CD103+: Protection/tolerance

CD103-: Identifies pathogenic - proinflammatory, t cell activation etc

161
Q

Antigen presentation (3)

A

Direct: Pseudopod of DC travels across enterocyte

Indirect: Goblet cell presents antigen

Indirect: M cell presents antigen

162
Q

Intraepithelial cell Lymphocyte

A

Between epithelial cells

Mainly CD8 t cells

Activate due to cellular injury

163
Q

Lamina propria lymphocytes

A

CD4 T cells –> cytokines and host defense

Immune suppression: IL10/TGFB

Parasites/allergens: IL4/IL13

Bacteria/pathogens: IFN-gamma, IL17/IL22

164
Q

B cells and IgA

A

Secretory: J chain, dimeric

pIgR made by enterocyte

IgA + pIgR travel across cell into lumen –> IgA breaks off and does stuff

165
Q

Natural IgA

A

Low affinity

Immunosuppressive, homeostasis, T cell independent

166
Q

High affinity IgA

A

T cell dependent

Invasive pathogenic organisms

167
Q

TLR localizations

A

Cell surface and intracellular

168
Q

C type Lectin receptors

A

Carbohydrate binding domain

Activate inflammation

169
Q

NBD-NLR

A

Cytosolic sensor that activate inflammasome

170
Q

RIG like receptor

A

Recognize viruses

Norovirus/Rotavirus

171
Q

Appendicitis cause

A

Luminal obstruction

Rapid increase in pressure

172
Q

Appendicitis clinical presentation

A

RLQ pain

McBurneys point tenderness

173
Q

Acute Cholecystitis

A

Impacted stone, >6hrs pain

Murphys sign

174
Q

Choledocholithiasis

A

Stone in pancreatic duvt

Bacterial infection

175
Q

True vs pseudo diverticulitis

A

True: All layers of organ pushed out

Psuedo: Not all layers

176
Q

Hinchey staging

A

1: Small or confined abscess
2: Pelvic abscess
3: Gaseous release but sealed by omentum
4: Fecal discharge

177
Q

Hinchey staging and treatment

A

1: Medical management, supportive care and anitibiotics
2: Drainage

3/4: Surgery

178
Q

Mechanical occlusion of bowel (3)

A

Luminal obstruction
Intrinsic bowel lesions
Extrinsic bowel disease

179
Q

Luminal obstruction

A

Intussusception: bowel in itself

Foreign body

Bezoars

180
Q

Intrinsic bowel disease

A

Congenital atresia/stenosis

Stricture

181
Q

Extrinsic bowel disease

A

Adhesion from operation
hernia
Extrinsic mass
Volvulus

182
Q

Paralytic ileum

A

Impaired gut motilit

183
Q

Pseudo obstruction

A

No real blockage

184
Q

Strangulation

A

Impaired circulation to obstructed bowel

Intestinal gangrene

185
Q

Amebiasis: Parasite, location, infective form

A

Entamoeba histolytica

Colon

Cyst is infective

186
Q

Amebiasis life cycle

A

Ingest cyst (survive stomach) –> transform to trophozoite –> invades colonic mucosa –> Cysts/trophozoites passed in feces

187
Q

Trophozoite invasion of mucosa (amebiasis)

A

Proteinases

Surface lectins

Channel forming proteins

188
Q

Amebiasis when enters blood/clinical manifestatiosn

A

Enters liver via blood stream, can go to lungs

Asymptomatic (E. Dispar)

Dysentery

189
Q

Giardiasis: Parasite, location, infective form

A

Giardia lamblia

SI

190
Q

Giardiasis life cycle

A

Ingest cyst –> transform to trophozoite in SI –> Colonization –> cysts passed in feces

191
Q

Giardiasis and mucosa

A

Attach via sucker/lectin

No invasion

192
Q

Giardiasis clinical manifestation

A

Most asymptomatic (endemic areas)

Watery diarrhea

193
Q

Cryptosporidiosis parasite

A

Cryptosporidium parvum

194
Q

Cryptosporidiosis life cycle and pathogenesis

A

Complicated as shit

Lectin binding but unknown diarrhea mechanism

195
Q

Cryptosporidiosis pathogenesis

A

Self limited diarrhea in immunocompetent patients

Chronic diarrhea in immunocompromised patients

196
Q

Cryptosporidiosis diagnostic test

A

Acid fast

O&P doesn’t show it

197
Q

Strongylodiasis parasite, location

A

Helminthic nematode, SI

198
Q

Strongylodiasis life cycle

A

Live in soil and penetrate skin –> travel to lung –> travel up tracheobronchial tree –> cough up and swallow –> mature in SI and lay ova –> hatch and passed in feces (can reinfect in perianal area)

199
Q

Strongylodiasis and immunocompromised patients

A

FUCKED

200
Q

Strongylodiasis pathological manifestation

A

Larve: pneumonitis, eosinophilia

Adult worms: not a big deal

201
Q

Strongylodiasis clinical manifestation

A

HyperinfectionL Diarrhea, GI hemorrhage, meningitis

202
Q

Enterobiasis

A

Pinworm, LI

203
Q

Enterobiasis life cycle

A

Ingest ova –> eggs hatch –> adults live in cecum –> female lays ova in perianal skin

ITCHY

204
Q

Taeniasis

A

Cestode parasitic disease, tapeworm

SI

205
Q

Taeniasis life cycle

A

Cattle/pig eat ova –> Get into muscle –> raw food eaten by human –> tapeworm attaches to SI mucosa and grow

206
Q

Cysticercosis

A

Cestode parasite

Ingest pork tapeworm ova –> eggs hatch and form in tissue –> can go to brain and fuck everything up

207
Q

Schistosomiasis

A

Flatworm helminthic parasite, most significatn worldwide

208
Q

Schistosomiasis life cycle

A

Eggs enter water from humans and hatch –> infect snails –> Cercaria released and penetrate skin –> travel to portal veins and grow –> ova deposited and accumulate in tissue

209
Q

Schistosomiasis pathogenesis adult vs ova

A

Adult hide from immune system

Ova are immunogenic

Liver and urinary effects

210
Q

Schistosomiasis clinical manifestations

A

Bloody diarrhea, hematuria, ascites

211
Q

Travelers Diarrhea management

A

Fluids - rehydration

Loperamide (preferred)

Pepto-Bismol

Antibiotics

212
Q

Antibiotics for TD

A

Fluoroquinolones - large daily dose (3d)

Rifaximin

Azithromycin

213
Q

Fluoroquinolones

A

Broad spectrum

Inhibit DNA gyrase and topoisomerase

214
Q

Fluoroquinolone adverse effects

A

Photosensitivity
CNS symptoms

Boxed warnings: tendonitis/rupture, long QTc, neuropathy

Not in children or pregnant women

215
Q

TD and antiperistaltic agents

A

Only for mild/watery diarrhea

Avoid in patients with high fever/blood diarrhea

216
Q

Rifaximin

A

Mostly excreted - stays in target zone

Bind DNA dependent RNA polymerase - blocks transcription

Only for ETEC, not inflammatory diseases

217
Q

Macrolides

A

50S ribosomal subunit inhibitor

Bacteriostatic, conc dependent killing

Block elongation of/exit of peptide from 50S

218
Q

Macrolide drug interaction

A

P450 inhibitor

219
Q

ETEC/EPEC antibiotics

A

FQ, Azithromycin: 3d

220
Q

EHEC antibiotic

A

NONE

221
Q

Shigella antibiotic

A

FQ

Azithromycin

Ceftriaxone

222
Q

Salmonella antibiotic

A

FQ

Azithromycin

Ceftriaxone

ONLY FOR SEVERE

223
Q

Campylobacter antibiotic

A

Macrolide

SEVERE

224
Q

Listeria antibiotic

A

Ampicillin

225
Q

Vibrio antibiotic

A

Macrolide

FQ

226
Q

Sulfonamide/Trimethoprim

A

Folate inhibitors

Block purine production

Broad spectrum

227
Q

Sulfonamide/Trimethoprim drug interaction

A

CYP 2C8/9 inhibitor

NOT in 3rd trimester

228
Q

C diff treatment

A

Metronidazole: drug of choice for 1st episode

Disrupts DNA of microbial cells

Not in pregnancy

Amebiasis, Giardiasis, BV

229
Q

Vancomycin

A

Inhibit cell wall synthesis

Severe C diff

230
Q

Vancomycin (IV) adverse effects

A

Nephrotoxicity

Ototoxicity

Red-Man syndrome

231
Q

C diff follow up

A

1st relapse: Metronidazole

2nd relapse: Oran vanco, fidaxomicin

232
Q

Fidaxomicin

A

Non absorbed macrolide

Inhibits RNA polymerase

C Diff

Equal to or better than Vancomycin

GI/Endo/Repro (8 decks)

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