GI Flashcards

1
Q

Diverticular disease: etiology/risks

A

Lack of fibre in diet
Inactivity
Poor bowel patterns
Aging (80% > 85yo)

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

Diverticulitis

A

Inflammation of diverticula

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

Diverticular Disease Dx?

A

CT scan

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

Diverticulosis

A

Formation of Diverticula
Asymptomatic
Usually found during imaging for other purposes or screening/occult blood

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

Diverticular Disease: Tx?

A

Depending on severity and intended to prevent complications;
Tx of symptoms;
Sx if perforated or obstructed

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

Irritable Bowel Syndrome: Et? (Theories)

A

Unclear;
1- Malabsorption of polyols and fermented CHO
2-Alteration in regulation of motor and sensory GI functions
3-Molecular signalling defective for serotonin

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

IBS: Tx?

A

Antispasmodics
Antidiarrheals (if diarrhea)
Laxative (if constipation)
Antibiotics (with caution)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Diverticular Disease: manifestations?

A

LLQ local dull pain
Abdominal discomfort
Fever (usually indication of infection)
Nausea + vomiting (d/t pain when severe)

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

IBS: manifestations?

A
Diarrhea / Constipation
Abdominal discomfort/pain (relieves with defecating and at night)
Mucoid stools
Flatulence
Bloating
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Peritonitis: Etiology?

A

Bacterial invasion/infection
(acute inflm ruptured appendix/ perforated peptic ulcer/trauma/PID/ruptured diverticulum)
Chemical irritation (bile)

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

Peritonitis: Patho?

A

Causative agent impacts peritoneum > Inflammation

Disadvantage:
Highly vascularized + inflammatory vasodilation > rapid absoption & spread of bacteria/toxins

Well adapted for inflammation/Advantage:

1) Production of thick and sticky exudate > seals off perforated viscus & aids localization of inflammation
2) Localization stimulates a sympathetic response that limits intestinal motility > decreased peristalsis

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

Peritonitis: Manifestations?

A

cardinal signs of inflammation (erythema, swelling, heat, pain, loss of fx)
severe:
> fluid shift into bowel & abdominal cavity > 3rd spacing
> blood shunt to site of inflammation > hyperemia
> Pain > vomiting
> Dyspnea d/t fluid buildup exerting pressure on thoracic cavity > Ascites

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

Peritonitis: Tx?

A
NPO
Antibiotics IV
NG suction
Fluids & electrolytes
Pain meds (narcotics)
Sx > if perf ulcer/inflm appendix
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Appendicitis: Et?

A

Idiopathic
Theories:
1) Intraluminal obstruction by Fecalith (hard piece of stool)
2) Twisting of appendix or bowel

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

Appendicitis: Patho?

A

Lumen becomes obstructed
Drainage from cecum increases luminal pressure in the appendix
Excess venous pressure leads to venous stasis and impedes perfusion > ischemia and necrosis
Bacteria invade appendix’s wall & perforate?

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

Appendicitis: manifestations?

A

abrupt onset
acute epigastric & periumbilical pain at first - referred pain
nausea & vomiting - severe pain
increasing pain - colicky & localized on RLQ over 12h
Fever
WBC

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

Appendicitis: Dx?

A

Hx & Px
Ultrasound
CT (if US not adequate to dx)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Appendicitis: Tx?

A

NPO
Antibiotics
IV Fluids & electrolytes
Sx

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

IBD

A

Inflammatory Bowel Disease
> Crohn’s Disease
> Ulcerative Colitis

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

IBD: Etiology?

A

Complex trait
> genetic susceptibility
> environmental - infective trigger

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

IBD: Patho

A

Mucosal immune system responds against ingested pathogens, but is unresponsive to the normal intestinal microflora

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Crohn’s Disease: Patho?

A

Affects submucosal layer in terminal ileum - other areas can be affected;
Granulomatous, skip lesions (cobblestone pattern)
Slower Progression compared to Ulcerative Colitis
Chronic

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

Crohn’s: Manifestations?

A

periods of exacerbation & remission
symptoms related t the location of the lesions
- intermittent diarrhea
- abdominal pain (colicky usually RLQ)
Weight loss d/t absorptive layer is compromised
Fluid & electrolyte disorders imbalance d/t water loss
low grade fever

Complications:

  • fistulas
  • abdominal abscesses
  • bowel obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Ulcerative Colitis

A

Non-specific inflammatory condition of the colon
Confined to rectum & colon - begins in the rectum & spreads proximately affecting the mucosal layer - can extend to submucosa
Continuous lesions

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

Ulcerative Colitis: Patho?

A
  • bleeding occurs d/t ulceration & inflammation
  • thickened, inflamed areas > scarring tissue
  • edema & congestion of gut content & exudate in the gut
  • crypt abscesses
  • pseudopolyps
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Ulcerative Colitis: manifestations?

A

bloody diarrhea

abdominal cramping

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Ulcerative Colitis: Dx?

A

Hx & Px (exclude other conditions)
Sigmoidoscopy, colonoscopy, biopsy
Labs to exclude GI infection

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

Ulcerative Colitis: Tx?

A

Address inflammatory symptoms
- anti-inflammatories (sulfasalazine)
- steroids (if non responsive or flareups)
- immunomodulator (methotrexate)
? antibiotics (with caution to control overgrowth of normal flora)
? Sx (necrotic bowel sections if required)
Diet Alteration

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

Herniation

A
  • Organ protrusion through retaining structure

- Usually in abdominal cavity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Herniation Patho?

A

-Weakened retaining structure (eg: muscles)

Etiology:

  • Acquired or Congenital
  • Increased intra-abdominal pressure (pregnancy, obesity)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Hernias: Types?

A

1) Hiatal:
- axial/sliding (95%)
- parasophageal/nonaxial (rolling)

2) Inguinal
- direct (through the abdominal wall)
- indirect (through the inguinal canal)

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

Hiatal Hernia: Patho?

A
  • Hiatus enlarges

- part of stomach protrudes into thoracic cavity

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

Axial/Sliding (95%): description + manifestations?

A
  • GEJ and upper part of stomach protrude into TC
  • 50% asymptomatic,
    of symptomatic:
  • reflux (d/t increased gastric acid in esophagus)
  • heartburn pain (d/t being adjacent to heart)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Paraesophageal/Nonaxial (rolling): description + manifestations?

A
  • non-upper part of stomach enters TC
  • GEJ remains below diaphragm
  • pain
  • dyspnea (limited lung expansion d/t hernia)
  • fullness (reduced stomach volume)
  • no reflux (gastric content is pushed into the pouch, therefore no acid in esophagus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Hiatal Hernia: Tx?

A
  • modify lifestyle (avoid caffeine, alcohol & smoking)
  • behavioural changes (avoid bending, drinking fluids @HS, raise HOB)
  • drugs (reflux): antacids, H2RA, PPIs
  • Sx (~15%) fundoplication for hiatal hernia - if affecting breathing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Inguinal Hernia: Types + Tx?

A
  • direct (through body structure - abdominal wall)
  • indirect (through inguinal canal)

Peritoneum forms hernial sac > contains intestine & omentum
Sx required to avoid complications (strangulation of bowel)

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

Direct Hernia

A

projection through abdm wall

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

Indirect Hernia

A

projection through inguinal canal

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

Peptic Ulcer Disease: describe?

A
  • Ulcerative disorder of the lining of the stomach (20%) or duodenum (80%)
  • Affects mucosa (can penetrate) > can lead to peritonitis
  • Spontaneous remissions and exacerbations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Peptic Ulcer: Et/Risk Factors?

Aggressive components that facilitate the formation of ulcers or compromises the protection of the lining

A
  • Aspirin & NSAIDs use
  • Helicobacter pylori
  • HCl & biliary acid
  • Chronic gastritis
  • Smoking, alcohol & caffeine
41
Q

Peptic Ulcer: Patho?

A

Unclear:
H pylori > not part of the normal flora, but survives low pH.
- ability to colonize stomach *& duodenum lining
- adhesion ability with the production of urease which converts urea into CO2 + NH3 > creating a microniche that neutralizes gastric acid and promotes growth

> H pylori induce inflammation & stimulate the release of cytokines and other inflammatory mediators that contribute to the damage of the mucosa.
Hypergastrinemia - increase release of gastrin by the G cells which promotes the secretion of HCl by the parietal cells
Risk factors impede protection and defence of the lining

INFECTION > INFLAMMATION > INCR. ACID > COMPROMISED PROTECTION > TISSUE DAMAGE > ULCER > PERFORATION?

42
Q

Peptic Ulcer: manifestations?

A
  • abdominal pain
  • burning
  • cramping
  • N+V

Complications:
Perforation > Peritonitis > Life Threatening!
Hemorrhage
Obstruction d/t edema, spasm & scar tissue contraction

43
Q

Peptic Ulcer: Dx?

A
  • Hx
  • Serology
  • Stool sample
  • UBT (Urea Breath Test)
  • Barium Swallow (contrast)
  • Endoscopy
44
Q

Peptic Ulcer: Tx?

Aim to eradicate bacteria

A
  • Antiacids to manage manifestations
  • Triple regimen
    >PPI (H2RA) + Amoxyl + Biaxin
    >PPI (H2RA) + Flagyl + Biaxin
    > continued PPI to assist ulcer healing
  • Sx if complications
45
Q

Hepatitis

A

Inflammation of the Liver

46
Q

Hepatitis: Etiology?

A
  • Microbes (viruses mostly; fungi, bacteria, parasites)
  • Autoimmunity
  • Drugs (hepatotoxicity)
47
Q

Viral Hepatitis

A

ABC - most common forms
DE
FG (not severe)

48
Q

Viral Hepatitis: differences?

A

Virus & transmission mode
Incubation period
Severity
Carrier state

49
Q

Hepatitis A

A

mild, acute form
orofecal transmission route
HAV antibodies measured & IgM
28 days - 1 month incubation period

50
Q

Hepatitis B

A
more severe
10-15% chronic or acute state
carrier state?
cirrhosis?? > complication
transmission mode is broad: 
> oral
> blood
> body fluids
> sexual

3 antibodies: anti-HBs, anti-HBc, anti-HBe

51
Q

Hepatitis C

worst form

A
80% chronic > cirrhosis & hepatocellular CA?
via infected blood
- IV use
- high risk sex practices
antibodies & viral testes for Dx
52
Q

Hepatitis: Patho?

A

2 mechanisms cause decrease liver fx:
> IR: inflammation & necrosis
> viral injury > necrosis

Damage to vasculature & ducts
~4 months to heal

53
Q

Hepatitis: Manifestations?

A

Prodromal

  • lethargy, myalgia
  • fever, abdominal pain
  • anorexia, N+V

Clinical

  • manifestations worsen
  • hepatomegaly, tender liver on palpation
  • jaundice, pruritus

Full recovery in ~16 weeks > when lab values are normal

54
Q

Viral Hepatitis Tx

A

Bed Rest to decrease metabolic demand and workload on Liver
Modify diet - small meals
Refrain from alcohol and hepatotoxic drugs
Symptom management ~pruritus
Vaccines for Hep A and B
New direct acting antiviral DAA for Hep C
Adjunct drug ~interferon

55
Q

Autoimmune Hepatitis Et

A

Complex trait
~Environmental triggers viral & chemical agents
~HLA genes and MHC on Chr. 6

56
Q

Autoimmune Hepatitis Type 1

A

More common
~80% in women
ANA & anti smooth muscle antibodies
Usually have other autoimmune conditions associated

57
Q

Autoimmune Hepatitis Type 2

A

2-14 yo

Antibodies against cytosol & microsomes

58
Q

Autoimmune Hepatitis Manifestations and Dx

A

Mnfts vary, usually asymptomatic to those of Liver Failure

Dx
Exclude other liver disease - viral hepatitis
Increase of gamma globulins
ANA tests
Biopsy
59
Q

Autoimmune Hepatitis Tx

A

Immunosuppressants

Transplant if non responsive to immunotherapy

60
Q

Cirrhosis

A

Cirr - yellow- jaundice

Final stage of chronic liver disease
Life threatening 
Leading cause of death
Aka Liver Failure
Complication
61
Q

Cirrhosis Et

A
Alcoholism 60-70%
Hepatitis
Biliary disease - low prevalence when compared to ETOH
Metabolic disorders - Wilson disease
Drugs
Cryptogenic Etiology - aka unknown
62
Q

Cirrhosis Patho

A

Hepatocytes necrosis
Cells regenerate bound by fibrous tissue - nodular appearance
Vessel Constriction
Impeded perfusion leads to Portal HTN - fluids shifts resulting in ascites
Biliary duct constriction leads to bile stasis
Increased waste d/t decreased metabolic waste clearance
Liver Failure —— GAME OVER!! LOL!

63
Q

Cirrhosis Manifestations

A

Vary, based on stage & underlying cause
Anorexia, weakness, Wt loss are common
Hepatomegaly
Jaundice - depending on what is causing liver failure

Complications

  • Portal HTN
  • Ascites
  • Varices -rupture could result in hemorrhage - usually esophageal & hemorrhoidal veins
  • Splenomegaly - vessels become congested
64
Q

Cirrhosis Tx

Think- Goal is to facilitate regeneration and reduce liver workload

A
  • diet modification - smaller meals
  • refrain from ETOH
  • prevent complications
65
Q

Portal HTN

A

Increased pressure in Hepatic Portal System HPS
Greater than 12mmHg
Normal P - 5-10mmHg

Et
Pre- Post - Intra- Et depending on what is causing it
Mostly caused by Cirrhosis & Ascites
Ruptured Varix - major complication
Portosystemic shunts - colaterization of vessels to decrease pressure from Liver resulting in shunting of blood to other vessels

66
Q

Ascites

A

Fluid accumulation in Peritoneal Cavity

Et+patho

  • Cirrhosis
  • Portal HTN
  • Fluid retention d/t increased hydrostatic pressure
67
Q

Ascites Mnfts

A

Dyspnea

Abdominal distension

68
Q

Ascites Tx

A

Small Volume

  • diuretics
  • Na Restriction
  • Fluids and lytes

Large Volume exceeds 5L

  • paracentesis
  • volume expander - albumin - to prevent further fluid leaving vasculature
69
Q

Liver Failure

A

Acute or Chronic
Loss of Functional capacity - 80%
~50% mortality

70
Q

Liver Failure Et

A

Several

  • toxic liver damage
  • fulminant hepatitis
  • cirrhosis
71
Q

Colorectal CA: Et

A

Unknown
Incidence increases with:
-age
-family hx (crohn’s or ulcerative colitis)
-diet (fat intake, refined sugar intake, fibre intake)

72
Q

Colorectal CA: Mnfts

A

Usually present for a long time before producing s+s
Bleeding
Change of bowel patterns (diarrhea or constipation); sense of urgency or incomplete emptying

73
Q

Colorectal CA: Stages

A

Stage 1: limited to invasion of mucosal and submucosal layers
Stage 2: tumour infiltrates into, but not through the muscularis externa
Stage 3: invasion of the serosal layer and lymph node involvement
Stage 4: metastatic tumour penetrates serosa or adjacent organs - poor prognosis!

74
Q

Colorectal CA: screening and Dx

A

Early Dx improves prognosis

Detection methods:
-digital rectal examination
-fecal occult blood test
X-Ray
Colonoscopy and sigmoidoscopy
75
Q

Colorectal CA: Tx

A

Sx - removal
Preoperatively radiation therapy
Postoperative adjuvant chemotherapy

76
Q

Liver Failure

A

Acute or chronic
Loss of functional capacity - greater than 80% to present failure s+s
~50%

77
Q

Liver Failure: Et

A

Several
~toxic liver damage
~Fulminant hepatitis
~Cirrhosis

78
Q

Liver Failure: Patho

A
Hepatic Insufficiency - multiorgan failure
1-Hematology
2-Metabolism
3-Hepatorenal syndrome
4-Encephalopathy
79
Q

Liver Failure: Tx

A

Address underlying cause and reverse cause
Purgative - potent laxative to clear toxins eg. Ammonia
Non absorbable Antibiotics - replace normal flora
Transplant if non responsive

80
Q

Cholelithiasis: Et

A

Bile stasis
Altered bile composition ~Eg high cholesterol dec bile salts
Genetics

81
Q

Cholelithiasis: Patho

A

Debris - nuclei for stone formation

Precipitation of bile content - stone

82
Q

Cholelithiasis: Types

A

Cholesterol stones 80%
Pigment stones 20%
Mixed - bilirubin, Ca salts, Phosp

83
Q

Cholelithiasis: manifestations

A

Colic - intermittent and radiating pain

Nausea and vomitting

84
Q

Cholelithiasis: Dx

A

Hx
Px
US
Nuclear scans

85
Q

Cholelithiasis: Tx

A
Pain management
Dissolving agents - Actigal drug - less invasive
Sx if required
US to blast the stones
Retrograde endoscopy
Tx complications such as Pancreatitis
86
Q

Acute Pancreatitis:

A

inflammation of the Pancreas due to Auto Digestion

87
Q

Acute Pancreatitis: Et

A

Alcohol abuse
Cholelithiasis
Idiopathic
Other: trauma, drugs…

88
Q

Liver CA: Primary?

A
  • Hepatocarcinoma
    (most common >80%);
    mnfts often masked by underlying liver damage;
    poor prognosis
  • Cholangiocarcinoma
    arises from epithelial of bile duct
89
Q

Liver CA: Secondary?

A

Metastasis from colon, lung and breast

90
Q

Liver CA: Primary > Et?

A
  • Chronic Liver disease > eg. Hep C

- Toxins (arsenic)

91
Q

Liver CA: Tx

A

Very poor prognosis
Supportive & palliative
If Tx fails > 2-3 months prognosis & cause of death is liver failure
Debulking Sx- to remove malignancy as much as possible

92
Q

Pancreatic CA: Et?

A

Unclear

Risk Factors:

  • Smoking
  • Age (>50yo)
  • DM, Chronic Pancreatitis, Poor diet
93
Q

Pancreatic CA: mnfts?

A
Very aggressive
Very fast
Jaundice (unclear why?)
Wt loss
Abdominal pain
94
Q

Pancreatic CA: Dx

A

US
CT
Mets at Dx- usually too late when found

95
Q

Pancreatic CA: Tx

A

Pain management

Primary approach -Sx resection then palliative care

96
Q

Cleft Lip

A

Genetic Congenital
~ 1 in 700 live births
Structural anomaly
Incomplete fusion of maxilla and nasal structures
- uni or bilateral
d/t TERATOGENS - smoking during pregnancy, viral infection, folic acid deficiency

97
Q

Cleft palate

A

Incomplete fusion of palatine structures
- malformed nasal structures
Linked to smoking during pregnancy - Teratogens
~1 in 2000 live births
- Problems with speech, swallowing, nutrition and breathing

98
Q

Hirschsprung disease

A

~1 in 5000 live births
RET gene in Chr 10- genetics problem
Areas of colon lack parasympathetic ganglia - NO PERISTALSIS

Tx: Resection Sx

99
Q

Intussusception

A

Intestine invaginates in adjoining part - ileocecal valve region
mechanical problem & increased pressure
Can cause Obstruction and inflammation

Invagination > Obstr > inflamm & edema > ischemia

Complications: necrosis, perforation, peritonitis