First Aid - GI - Pathology - Part 2

Acute mesenteric ischemia presentation

Abdominal pain out of proportion to physical exam findings due to bowel necrosis.

May see “Currant jelly” stools

Acute mesenteric ischemia etiology

• Thrombosis

• Embolism

Acute mesenteric ischemia risk factors

• AFib

• Peripheral Artery Disease

• Recent MI

• CHF

What is Angiodysplasia

It refers to tortuous dilation of blood vessels, leading to hematochezia

Where along the GI tract is angiodysplasia more common

Right-sided colon

Which age groups is angiodysplasia more common in

Older patients

How can you diagnose angiodysplasia

With Angiography

Angiodysplasia risk factors

• End-stage renal disease

• von Willebrand disease

• Aortic Stenosis

What is chronic mesenteric ischemia

It’s aka “Intestinal Angina”, and it works similarly to stable angina

It represents atherosclerosis of the Celiac Artery, or SMA (most common), or IMA → Intestinal hypoperfusion

Chronic mesenteric ischemia presentation

Postprandial epigastric pain → Food aversion & Weight loss

How does colonic ischemia present

Presents as Crampy abdominal pain followed by HematocheziaC

Colonic ischemia frequently affects which areas of the colon

Watershed areas: Splenic Flexure & Rectosigmoid junction

Colonic ischemia seen in which age groups

Typically in older adults

Colonic ischemia on imaging

Thumbprint sign

Ileus vs Pseudo-obstruction

Ileus refers to a functional/ non-mechanical obstruction of the small bowel. If large bowel it's called a pseudo-obstruction instead

Ileus symptoms and presentation

• Symptoms: Constipation, and Decreased flatus

• Presentation: Distended/tympanic abdomen with decreased bowel sounds

Ileus risk factors

• Abdominal surgeries

• Opiates

• Hypokalemia

• Sepsis

Ileus Imaging

No transition zone on imaging

Ileus treatment

• Bowel rest

• Electrolyte correction

• Cholinergic drugs

Necrotizing enterocolitis is seen in which groups and why

Premature, formula-fed infants with immature immune system

(In preterm babies, Gut barrier and Gut immune system not fully matured -> easier for bacteria to invade)

What can necrotizing enterocolitis lead to

• Pneumatosis intestinalis (Pneumatosis Intestinalis = Gas in the Bowel wall. Bacterial gas can enter the wall and accumulate in the submucosa/subserosa. So on imaging you can see little bubbles/linear streaks of gas within the bowel wall.

• Pneumoperitoneum

• Portal venous gas

Proctitis common causes

• Infection (N gonorrhea, Chlamydia, Campylobacter, Shigella, Salmonella, HSV, CMV),

• IBD

• Radiation.

Proctitis symptoms

• Tenesmus

• Rectal bleeding

• Rectal pain

Proctoscopy findings in proctitis

Proctoscopy reveals inflamed rectal mucosa (ulcers/vesicles in the case of HSV). Rectal swabs are used to detect other infectious etiologies.

Small bowel obstruction risk factors/etiologies

• Intraperitoneal adhesions (fibrous band of scar tissue)

• Tumors

• Hernias
  
  

• Meconium plug in newborns → meconium ileus).

Small bowel obstruction symptoms/presentation

Abrupt onset of abdominal pain, nausea, vomiting, abdominal distension

A 25-year-old man presents with acute abdominal pain, nausea, and bilious emesis. His only medical history is of a reported “lump” in his groin area that has been present since birth. The abdominal pain is crampy, severe, initially intermittent, and now persistent. He is passing less gas and has not had a bowel movement in a few days. On exam he is tachycardic and mildly hypotensive. Abdominal auscultation reveals “tinkling”high-pitched bowel sounds. His abdomen is distended, tympanic to percussion, and tender to palpation. There is a nonreducible and extremely tender inguinal mass with overlying normal appearing skin. Evaluation/Tests: Upright chest/abdominal X-ray shows dilated loops of small bowel with multiple horizontal lines that are radiolucent above and radiopaque below.

Small-bowel obstruction secondary to incarcerated hernia

Short bowel obstruction X-Ray findings

Air-fluid levels

SBO management

• Gastrointestinal decompression

• Volume resuscitation

• Bowel rest

SIBO Risk factors

• Altered pH (e.g. achlorhydria, PPI use)

• Anatomical (e.g. small bowel obstruction, adhesions, fistula, gastric bypass surgery, blind loop)

• Dysmotility (e.g. gastroparesis)

• Immune mediated (IgA deficiency, HIV)

SIBO Symptoms/presentation

• Bloating

• Flatulence

• Abdominal pain

• Chronic watery diarrhea

• Malabsorption (vitamin B12) in severe cases.

SIBO diagnosis

• CHO breath test

• Small bowel culture

Hamartomatous polyps Description + Transformation risk

Solitary lesions do not have significant risk of transformation. Growths of normal colonic tissue with distorted architecture. Associated with Peutz-Jeghers syndrome and juvenile polyposis.

Hamartomatous polyps are usually pedunculated. They can cause painless rectal bleeding if they auto-amputate, this can rarely cause Iron-deficiency Anemia

Polyp stuff

Lynch syndrome

Hereditary nonpolyposis colorectal cancer (HNPCC).

It’s caused by an autosomal Dominant mutation in mismatch repair genes (MLH1/MSH2), Which causes Microsatellite Instability: 80% CRC progression

In Lynch syndrome, which part of the colon is always involved

Proximal Colon

Lynch syndrome is associated with which non-GI cancers

Endometrial

Ovarian

Skin

---

Lynch has many CEOS (C for colon)

Risk factors for CRC

• Adenomatous and serrated polyps

• familial cancer syndromes

• IBD

• Tobacco use

• Diet of processed meat with low fiber

Right sided vs left-sided/Sigmoid CRC

Ascending—exophytic mass, iron deficiency anemia, weight loss.

Descending—infiltrating mass, partial obstruction (pencil-thin stools), colicky pain, hematochezia.

What should you do if a patient presents with S.bovis Endocarditis

Colonoscopy to check for colorectal cancer

What’s a condition that raises CRC suspicion in men over 50 and Postmenopausal women

Iron-deficiency anemia

CRC common X-Ray finding

Apple core lesion

CRC screening stuff

Why NSAIDs in CRC

Because CRCs have elevated COX-2 activity for some reason

Molecular pathogenesis in CRC

Chromosome instability pathway: APC → Risky → KRAS → Adenoma → p53 → Carcinoma

Microsatellite instability pathway: MLH1 or MSH mutations

Cirrhosis etiologies

• alcohol

• nonalcoholic steatohepatitis

• chronic viral hepatitis

• autoimmune hepatitis

• biliary disease

• genetic/metabolic disorders.

Portal hypertension etiologies

• Cirrhosis (most common)

• schistosomiasis

• portal vein thrombosis.

Ascites test

Serum-to-ascites albumin gradient (SAAG) analysis of ascitic fluid sample determines between etiologies of ascites.

SAAG ≥ 1.1 = portal hypertension.

Cirrhosis manifestations

Hepatic encephalopathy cause and treatment in cirrhosis

Cause: bacterial NH3

Treat: Lactulose, antibiotics (Rifamixin), Low protein diet

Cirrhosis hemodynamics stuff

What’s Budd-chiari

Thrombosis of the hepatic veins (hepatic outflow tract)

Budd-chiari symptoms

Centrilobular congestion and necrosis → congestive liver disease:

• hepatomegaly

• ascites

• varices

• abdominal pain

  • liver failure
    
    ***Absence of JVD unlike in Right heart failure where backup into liver is a consequence of the RHF itself***

Budd-chiari risk factors

• hypercoagulable states

• polycythemia vera

• postpartum state,

• HCC

(In HCC my have compression of centrilobular veins)

Portal vein thrombosis risk factors

• Cirrhosis

• Malignancy

• Pancreatitis

• Sepsis

Complications in Portal vein thrombosis

May lead to bowel ischemia if thrombosis extends to superior mesenteric vein

Which liver zone will be affected first in Buddchiari

Zone 3

What is SBP

SBP aka Primary bacterial peritonitis is a common and potentially fatal bacterial infection in patients with cirrhosis and ascites

Spontaneous bacterial peritonitis pathogenesis

Cirrhosis → portal HTN + intestinal barrier dysfunction → ascites + bacterial translocation from gut → ↓ hepatic complement/opsonization & impaired immunity → bacterial seeding/proliferation in ascitic fluid → peritoneal inflammation.

SBP Symptoms

Often asymptomatic, but can cause:

• Fevers

• chills

• abdominal pain

• Ileus

• Worsening encephalopathy

Which bacteria typically cause SBP

Commonly caused by gram ⊝ organisms (eg, E coli, Klebsiella) or less commonly gram ⊕ Streptococcus

How is SBP diagnosed

Paracentesis with ascitic fluid absolute neutrophil count (ANC) > 250 cells/mm³

Empiric first-line treatment for SBP

Ceftriaxone

Reye etiology & pathophysiology

Aspirin in viral infection in children (Especially VZV & Influenza)

Aspirin-associated mitochondrial injury → ↓ oxidative phosphorylation + ↓ fatty-acid β-oxidation → microvesicular hepatic steatosis and impaired urea-cycle function → hyperammonemia + hypoglycemia → astrocyte dysfunction/swelling → cerebral edema → encephalopathy

Findings in reye syndrome

• High ICP

• Mitochondrial abnormalities

• Microvesicular fatty liver changes

• Hyperammonemia

• Hypoglycemia

• Vomiting

• Hepatomegaly

• Cardiac failure

• Renal failure

• Coma

High morbidity & mortality

AFLD

Excess NADH production → decreased fatty acid oxidation and increased lipogenesis

Microvesicular vs Macrovesicular fatty liver changes

• Microvesicular: many small lipid droplets → usually mitochondrial dysfunction / ↓ β-oxidation. Think Reye, valproate, acute fatty liver of pregnancy.

• Macrovesicular: large lipid droplet displaces nucleus peripherally → excess triglyceride accumulation/storage. Think alcohol, obesity/MASLD, insulin

Memory: Micro = Mitochondria. Macro = Massive fat storage.

When does Alcoholic hepatitis tend to present

Occurs after heavy binge drinking on top of long history of alcohol consumption

Alcoholic hepatitis findings

• Swollen and necrotic hepatocytes with neutrophilic infiltration.

• Mallory bodies B (intracytoplasmic eosinophilic inclusions of damaged keratin filaments)

Alcoholic cirrhosis

Final and usually irreversible form of AFLD

Regenerative nodules surrounded by fibrous bands in response to chronic liver injury → portal hypertension and end-stage liver disease

MASLD

Autoimmune hepatitis populations

More common in females

Autoimmune hepatitis presentation

It’s a chronic inflammatory liver disease

It presents with:

• fatigue

• nausea

• pruritus.

Autoimmune hepatitis labs & serologies

Serology: ⊕ for anti-smooth muscle or anti-liver/kidney microsomal-1 antibodies

Labs: Very high ALT and AST.

Autoimmune hepatitis histology

Portal and periportal lymphoplasmacytic infiltrate.

What’s a hepatic hemangioma

Most common benign liver tumor (Venous malformation, full of blood vessels)

Hepatic hemangioma typical age of onset

30-50

Hepatic hemangioma constraindication

Do NOT biopsy, risk of hemorrhage

What’s a hepatic focal nodular hyperplasia

Second most common benign liver tumor

hepatic focal nodular hyperplasia typical age onset

35-50

hepatic focal nodular hyperplasia etiology

Hyperplastic reaction of hepatocytes to an aberrant dystrophic artery

Common sign in hepatic focal nodular hyperplasia

Central stellate scar

hepatic focal nodular hyperplasia symproms

Usually asymptomatic, detected incidentally

Hepatic adenoma

Rare, benign tumor, often related to oral contraceptive or anabolic steroid use

Hepatic adenoma progression

May regress spontaneously or rupture, causing abdominal pain and shock

HCC epidemiology

Most common primary liver tumor in adults

HCC associations

HBV with or without cirrhosis + all other causes of cirrhosis:

• HCV

• AFLD

• MASLD/MASH

• Autoimmune liver disease

• Hemochromatosis

• Wilson disease

• α1-antitrypsin deficiency

• Aflatoxin exposure (Aspergillus)

HCC findings

• Anorexia

• Jaundice

• Tender hepatomegaly

• Decompensation of previously stable cirrhosis → Ascites (Ya3ni if there’s some functional tissue it destroys it)

• Portal vein thrombosis

How does HCC metastasize

Hematogenously

HCC diagnosis

Ultrasound (screening) or contrast CT/MRI (confirmation); biopsy if diagnosis is uncertain

HCC monitoring

Monitor recurrence with serum AFP

Hepatic angiosarcoma

Rare malignant tumor of endothelial origin He

Hepatic angiosarcoma risk factors

Exposure to Arsenic or Vinyl chloride

Metastatic liver disease

Most common malignant liver tumors overall

Originate from:

• GI cancers

• Breast cancers

• Lung cancers

A1AT liver involvement

Misfolded protein aggregates in hepatocyte ER leading to Cirrhosis with PAS ⊕ globules in liver

A1AT typical presentation

Young patient with liver damage & dyspnea (panacinar emphysema) without a history of smoking

Diastase test on A1AT liver

Biliary Atresia

Fibro-obliterative destruction of bile ducts → cholestasis

Biliary atresia epidemiology

Most common reason for pediatric liver transplantation

Biliary atresia accompanying findings

Associated with absent/abnormal gallbladder