GI Flashcards
Diverticular disease: etiology/risks
Lack of fibre in diet
Inactivity
Poor bowel patterns
Aging (80% > 85yo)
Diverticulitis
Inflammation of diverticula
Diverticular Disease Dx?
CT scan
Diverticulosis
Formation of Diverticula
Asymptomatic
Usually found during imaging for other purposes or screening/occult blood
Diverticular Disease: Tx?
Depending on severity and intended to prevent complications;
Tx of symptoms;
Sx if perforated or obstructed
Irritable Bowel Syndrome: Et? (Theories)
Unclear;
1- Malabsorption of polyols and fermented CHO
2-Alteration in regulation of motor and sensory GI functions
3-Molecular signalling defective for serotonin
IBS: Tx?
Antispasmodics
Antidiarrheals (if diarrhea)
Laxative (if constipation)
Antibiotics (with caution)
Diverticular Disease: manifestations?
LLQ local dull pain
Abdominal discomfort
Fever (usually indication of infection)
Nausea + vomiting (d/t pain when severe)
IBS: manifestations?
Diarrhea / Constipation Abdominal discomfort/pain (relieves with defecating and at night) Mucoid stools Flatulence Bloating
Peritonitis: Etiology?
Bacterial invasion/infection
(acute inflm ruptured appendix/ perforated peptic ulcer/trauma/PID/ruptured diverticulum)
Chemical irritation (bile)
Peritonitis: Patho?
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
Peritonitis: Manifestations?
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
Peritonitis: Tx?
NPO Antibiotics IV NG suction Fluids & electrolytes Pain meds (narcotics) Sx > if perf ulcer/inflm appendix
Appendicitis: Et?
Idiopathic
Theories:
1) Intraluminal obstruction by Fecalith (hard piece of stool)
2) Twisting of appendix or bowel
Appendicitis: Patho?
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?
Appendicitis: manifestations?
abrupt onset
acute epigastric & periumbilical pain at first - referred pain
nausea & vomiting - severe pain
increasing pain - colicky & localized on RLQ over 12h
Fever
WBC
Appendicitis: Dx?
Hx & Px
Ultrasound
CT (if US not adequate to dx)
Appendicitis: Tx?
NPO
Antibiotics
IV Fluids & electrolytes
Sx
IBD
Inflammatory Bowel Disease
> Crohn’s Disease
> Ulcerative Colitis
IBD: Etiology?
Complex trait
> genetic susceptibility
> environmental - infective trigger
IBD: Patho
Mucosal immune system responds against ingested pathogens, but is unresponsive to the normal intestinal microflora
Crohn’s Disease: Patho?
Affects submucosal layer in terminal ileum - other areas can be affected;
Granulomatous, skip lesions (cobblestone pattern)
Slower Progression compared to Ulcerative Colitis
Chronic
Crohn’s: Manifestations?
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
Ulcerative Colitis
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
Ulcerative Colitis: Patho?
- bleeding occurs d/t ulceration & inflammation
- thickened, inflamed areas > scarring tissue
- edema & congestion of gut content & exudate in the gut
- crypt abscesses
- pseudopolyps
Ulcerative Colitis: manifestations?
bloody diarrhea
abdominal cramping
Ulcerative Colitis: Dx?
Hx & Px (exclude other conditions)
Sigmoidoscopy, colonoscopy, biopsy
Labs to exclude GI infection
Ulcerative Colitis: Tx?
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
Herniation
- Organ protrusion through retaining structure
- Usually in abdominal cavity
Herniation Patho?
-Weakened retaining structure (eg: muscles)
Etiology:
- Acquired or Congenital
- Increased intra-abdominal pressure (pregnancy, obesity)
Hernias: Types?
1) Hiatal:
- axial/sliding (95%)
- parasophageal/nonaxial (rolling)
2) Inguinal
- direct (through the abdominal wall)
- indirect (through the inguinal canal)
Hiatal Hernia: Patho?
- Hiatus enlarges
- part of stomach protrudes into thoracic cavity
Axial/Sliding (95%): description + manifestations?
- 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)
Paraesophageal/Nonaxial (rolling): description + manifestations?
- 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)
Hiatal Hernia: Tx?
- 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
Inguinal Hernia: Types + Tx?
- 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)
Direct Hernia
projection through abdm wall
Indirect Hernia
projection through inguinal canal
Peptic Ulcer Disease: describe?
- Ulcerative disorder of the lining of the stomach (20%) or duodenum (80%)
- Affects mucosa (can penetrate) > can lead to peritonitis
- Spontaneous remissions and exacerbations
Peptic Ulcer: Et/Risk Factors?
Aggressive components that facilitate the formation of ulcers or compromises the protection of the lining
- Aspirin & NSAIDs use
- Helicobacter pylori
- HCl & biliary acid
- Chronic gastritis
- Smoking, alcohol & caffeine
Peptic Ulcer: Patho?
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?
Peptic Ulcer: manifestations?
- abdominal pain
- burning
- cramping
- N+V
Complications:
Perforation > Peritonitis > Life Threatening!
Hemorrhage
Obstruction d/t edema, spasm & scar tissue contraction
Peptic Ulcer: Dx?
- Hx
- Serology
- Stool sample
- UBT (Urea Breath Test)
- Barium Swallow (contrast)
- Endoscopy
Peptic Ulcer: Tx?
Aim to eradicate bacteria
- Antiacids to manage manifestations
- Triple regimen
>PPI (H2RA) + Amoxyl + Biaxin
>PPI (H2RA) + Flagyl + Biaxin
> continued PPI to assist ulcer healing - Sx if complications
Hepatitis
Inflammation of the Liver
Hepatitis: Etiology?
- Microbes (viruses mostly; fungi, bacteria, parasites)
- Autoimmunity
- Drugs (hepatotoxicity)
Viral Hepatitis
ABC - most common forms
DE
FG (not severe)
Viral Hepatitis: differences?
Virus & transmission mode
Incubation period
Severity
Carrier state
Hepatitis A
mild, acute form
orofecal transmission route
HAV antibodies measured & IgM
28 days - 1 month incubation period
Hepatitis B
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
Hepatitis C
worst form
80% chronic > cirrhosis & hepatocellular CA? via infected blood - IV use - high risk sex practices antibodies & viral testes for Dx
Hepatitis: Patho?
2 mechanisms cause decrease liver fx:
> IR: inflammation & necrosis
> viral injury > necrosis
Damage to vasculature & ducts
~4 months to heal
Hepatitis: Manifestations?
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
Viral Hepatitis Tx
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
Autoimmune Hepatitis Et
Complex trait
~Environmental triggers viral & chemical agents
~HLA genes and MHC on Chr. 6
Autoimmune Hepatitis Type 1
More common
~80% in women
ANA & anti smooth muscle antibodies
Usually have other autoimmune conditions associated
Autoimmune Hepatitis Type 2
2-14 yo
Antibodies against cytosol & microsomes
Autoimmune Hepatitis Manifestations and Dx
Mnfts vary, usually asymptomatic to those of Liver Failure
Dx Exclude other liver disease - viral hepatitis Increase of gamma globulins ANA tests Biopsy
Autoimmune Hepatitis Tx
Immunosuppressants
Transplant if non responsive to immunotherapy
Cirrhosis
Cirr - yellow- jaundice
Final stage of chronic liver disease Life threatening Leading cause of death Aka Liver Failure Complication
Cirrhosis Et
Alcoholism 60-70% Hepatitis Biliary disease - low prevalence when compared to ETOH Metabolic disorders - Wilson disease Drugs Cryptogenic Etiology - aka unknown
Cirrhosis Patho
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!
Cirrhosis Manifestations
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
Cirrhosis Tx
Think- Goal is to facilitate regeneration and reduce liver workload
- diet modification - smaller meals
- refrain from ETOH
- prevent complications
Portal HTN
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
Ascites
Fluid accumulation in Peritoneal Cavity
Et+patho
- Cirrhosis
- Portal HTN
- Fluid retention d/t increased hydrostatic pressure
Ascites Mnfts
Dyspnea
Abdominal distension
Ascites Tx
Small Volume
- diuretics
- Na Restriction
- Fluids and lytes
Large Volume exceeds 5L
- paracentesis
- volume expander - albumin - to prevent further fluid leaving vasculature
Liver Failure
Acute or Chronic
Loss of Functional capacity - 80%
~50% mortality
Liver Failure Et
Several
- toxic liver damage
- fulminant hepatitis
- cirrhosis
Colorectal CA: Et
Unknown
Incidence increases with:
-age
-family hx (crohn’s or ulcerative colitis)
-diet (fat intake, refined sugar intake, fibre intake)
Colorectal CA: Mnfts
Usually present for a long time before producing s+s
Bleeding
Change of bowel patterns (diarrhea or constipation); sense of urgency or incomplete emptying
Colorectal CA: Stages
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!
Colorectal CA: screening and Dx
Early Dx improves prognosis
Detection methods: -digital rectal examination -fecal occult blood test X-Ray Colonoscopy and sigmoidoscopy
Colorectal CA: Tx
Sx - removal
Preoperatively radiation therapy
Postoperative adjuvant chemotherapy
Liver Failure
Acute or chronic
Loss of functional capacity - greater than 80% to present failure s+s
~50%
Liver Failure: Et
Several
~toxic liver damage
~Fulminant hepatitis
~Cirrhosis
Liver Failure: Patho
Hepatic Insufficiency - multiorgan failure 1-Hematology 2-Metabolism 3-Hepatorenal syndrome 4-Encephalopathy
Liver Failure: Tx
Address underlying cause and reverse cause
Purgative - potent laxative to clear toxins eg. Ammonia
Non absorbable Antibiotics - replace normal flora
Transplant if non responsive
Cholelithiasis: Et
Bile stasis
Altered bile composition ~Eg high cholesterol dec bile salts
Genetics
Cholelithiasis: Patho
Debris - nuclei for stone formation
Precipitation of bile content - stone
Cholelithiasis: Types
Cholesterol stones 80%
Pigment stones 20%
Mixed - bilirubin, Ca salts, Phosp
Cholelithiasis: manifestations
Colic - intermittent and radiating pain
Nausea and vomitting
Cholelithiasis: Dx
Hx
Px
US
Nuclear scans
Cholelithiasis: Tx
Pain management Dissolving agents - Actigal drug - less invasive Sx if required US to blast the stones Retrograde endoscopy Tx complications such as Pancreatitis
Acute Pancreatitis:
inflammation of the Pancreas due to Auto Digestion
Acute Pancreatitis: Et
Alcohol abuse
Cholelithiasis
Idiopathic
Other: trauma, drugs…
Liver CA: Primary?
- Hepatocarcinoma
(most common >80%);
mnfts often masked by underlying liver damage;
poor prognosis - Cholangiocarcinoma
arises from epithelial of bile duct
Liver CA: Secondary?
Metastasis from colon, lung and breast
Liver CA: Primary > Et?
- Chronic Liver disease > eg. Hep C
- Toxins (arsenic)
Liver CA: Tx
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
Pancreatic CA: Et?
Unclear
Risk Factors:
- Smoking
- Age (>50yo)
- DM, Chronic Pancreatitis, Poor diet
Pancreatic CA: mnfts?
Very aggressive Very fast Jaundice (unclear why?) Wt loss Abdominal pain
Pancreatic CA: Dx
US
CT
Mets at Dx- usually too late when found
Pancreatic CA: Tx
Pain management
Primary approach -Sx resection then palliative care
Cleft Lip
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
Cleft palate
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
Hirschsprung disease
~1 in 5000 live births
RET gene in Chr 10- genetics problem
Areas of colon lack parasympathetic ganglia - NO PERISTALSIS
Tx: Resection Sx
Intussusception
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
