Module 4 Flashcards
GI, Liver, Biliary, Neuro
Primary cause of GERD
Backup of chyme (acid, pepsin) into the esophagus
Causes of esophagitis
GERD, infections, medications (NSAIDS), allergies
Cell changes in Barrett’s esophagus
Squamous cell epithelial -> metaplastic columnar; is a precursor to adenocarcinoma
Risk factors for esophageal cancer
Males, > 60 years old, smoking/alcohol, dietary, East Asia/Africa
Types of esophageal cancer
Squamous Cell: in upper/middle esophagus, associated with tobacco/alcohol
Adenocarcinoma: lower esophagus, associated with GERD and Barrett’s esophagus
Cause of peptic ulcer disease
Stomach/duodenal lesions in the muscularis musocae, caused by NSAID and H pylori
How do NSAIDs cause mucosal injury in gastritis?
They block COX enzyme (produces prostaglandins - protect the stomach lining by stimulating mucus and bicarb production); they increase gastric acid secretion
How does autoimmune gastritis affect the hematological system?
Autoantibodies attack the parietal cells (help with nutrient absorption)
-Vitamin B12 and Fe deficiency
Major risk factor for developing intestinal gastric cancer
Environmental factors (H PYLORI, smoking/alcohol, toxins
Major risk factor for developing diffuse gastric cancer
Genetic mutations (family hx, hereditary diffuse gastric cancer [HDGC], pernicious anemia
Gastric subtype associated with H pylori
Involved in both acute and chronic, but chronic is only type B (from environmental factors)
Patho of Crohns
Autoimmune: The immune system attacks the GI tract, leading to chronic inflammation. Triggers macrophages and dendritic cells involves T-helper cells (Th1 and Th17), and releases pro-inflammatory cytokines (TNF-α). Has periods of flare-ups and remission.
Intestinal strutcure of Crohns
Transmural Inflammation: patchy areas on inflammation which affects all layers of the tissue. COBBLESTONE appearance (GRANULOMAS), SKIP LESIONS, and ulcers.
Where is Crohns located?
Any part of GI tract
Lab results for Crohns
↑ CRP and ESR. CBC often shows anemia, leukocytosis, and thrombocytosis
Patho of UC
Risk factors (genetics, environmental, immune response, and DYSBIOSIS) leads to inflamed colonic mucosa.
Innate: macrophages engulf pathogens and release pro-inflammatory cytokines (TNF-α, IL-1β) and neutrophils form CRYPT ABCESSES
Adaptive: Th2 dominated response release IL-5 and IL-13, and T-reg cells are impaired which leads to inflammation.
Intestinal Structure of UC
Mucosal and submucosal inflammation, starts in rectum and extends proximally. Has continuous inflammation and bloody stool is common.
Location of UC
Limited to colon and rectum
Lab results for UC
↑ CRP and ESR. CBC often shows anemia, leukocytosis, and thrombocytosis.
↑ fecal calprotectin and lactoferin
p-ANCA antibody + in UC
Patho of IBS
Gut-brain axis dysregulation; increased cortisol levels and CRH receptor expression in GI tract are observed in IBS
Acute Pancreatitis
Premature activation of pancreatic enzymes which leads to autodigestion and pancreatic tissues. This activates trypsin, and local inflammation leads to SIRS.
Risk factors for acute pancreatitis
GALLSTONES, alcohol, hyperlipidemia, hypercalcemia, and medications
Chronic Pancreatitis
Progressive inflammatory condition with irreversible structural damage which leads to fibrosis, is associated with recurrent episodes of acute pancreatitis and ongoing injury.
Risk factors for pancreatic cancer
Chronic pancreatitis, smoking, obesity, family hx, genetics (KRAS), and long-term diabetes
Patho and transmission of Hep A
Acute; fecal-oral
Diagnostic Tests for Hep A
+ HAV IgM
Patho and Transmission of Hep B
Acute and chronic, chronic leads to cirrhosis/liver cancer; blood, sexual, perinatal
Diagnostic Tests for Hep B
+ HBsAg
+ IgM & Anti-HBs
+ HBV DNA
Patho and Transmission of Hep C
Asymptomatic when early, can develop chronic and develop cirrhosis/liver cancer; blood, IV drug use
Diagnostic Tests of Hep C
+ Anti-HCV antibodies
+ IgG & HCV RNA
Patho and transmission of Hep D
Chronic infection and worsens HBV, increases liver disease and cirrhosis; requires co-infection with HBV replicate; blood
Diagnostic Tests of Hep D
+ Anti-HDV antibodies
+ IgG & HDV RNA
Patho and transmission of Hep E
acute infection; fecal-oral (contaminated water)
Diagnostic Tests for Hep E
+ HEV IgM
+ HEV RNA
Which immunoglobulin is associated with recent/active infection?
IgM
Which immunoglobulin is associated with past infection/immunity?
IgG
Patho of cirrhosis
repeated injury to liver triggers fibrosis/scarring
Stage 1 of Cirrhosis
Fatty liver (steatosis), is reversible with lifestyle changes
Stage 2 of Cirrhosis
Inflammation fibrosis, start of permanent damage
Stage 3 of Cirrhosis
advanced fibrosis with regenerative NODULES, significant liver impairment
Stage 4 of Cirrhosis
ESLD, severe scarring and liver failure
Complications Associated with Cirrhosis: Portal HTN
↑ pressure in portal vein from scarring, blood is redirected into other vessels and forces fluid into peritoneal cavity
Complications Associated with Cirrhosis: Hypoalbuminemia
↓ albumin leads to reduced oncotic pressure where fluid can leak and cause third-spacing
Complications Associated with Cirrhosis: Splanchnic Vasodilation
dysfunctional liver triggers release of vasodilatory substances, causing increased blood flow to portal circulation worsening portal HTN
Complications Associated with Cirrhosis: ↑ lymph production and leakage
portal HTN increases exess lymph production, the damaged liver cannot drain excess fluid and leaks into peritoneal cavity and causes ascites
Complications Associated with Cirrhosis: Activation of RAAS
from relative hypovolemia caused by splanchnic vasodilation, causes Na and H2O retention further worsening ascites
Complications Associated with Cirrhosis: Systemic Inflammation
in advanced diseases; has a possibility of ↑ inflammatory mediators and bacteria and leaks to more leakage of fluid in the abdomen
Complications Associated with Cirrhosis: Hepatic Encephalopathy
toxins (AMMONIA, urea) accumulate and impair brain fxn
Complications Associated with Cirrhosis: esophageal and gastric varices formation
↑ portal pressure causes collateral circulation backup into venous system
Lab findings associated with cirrhosis
↑ AST, ALT, ALP, GGT, Bilirubin
↑ PT/INR time (reduced production of clotting factors)
↓ albumin, platelets, Na
Patho of MASLD
Accumulation of fats (steatosis) exceeding 5% of liver cells WITHOUT ALCOHOL CONSUMPTION.
Complications of MASLD
Insulin resistance, lipotoxicity, oxidative stress (ROS production damages mitochondria), and inflammation (Kupffer cells release cytokines like TNF-α, IL-6, and IL-1β), genetic susceptibility
Patho of MASH
Worsened form of MASLD, liver shows both steatosis and inflammation along with liver injury
Complications of MASH
Cell death (apoptosis and necrosis release DAMPS)
BALLOONING DEGENERATION (hepatocytes lose normal shape, become swollen and round)
MALLORY-DENK BODIES (shows ongoing inflammation)
Fibrosis Initiation (stellate cells produce collagen, replacing healthy liver tissue with scar tissue)
Risk Factors for MASLD / MASH
Obesity, T2DM, metabolic syndrome, sedentary lifestyle, poor diet, genetics
DYSBIOSIS: imbalanced gut microbiome which affects bile acid metabolism and promotes inflammation
Dopamine: roles and disorders
Excitatory and inhibitory; inhibits unnecessary movements and release of prolactin, stimulates the secretion of growth hormone.
DEC LEVEL: Parkinson’s addiction
INC LEVEL: ticks, Schizophrenia
Serotonin: roles and disorders
Excitatory/INHIBITORY; regulates temp, perception of pain, emotions, and sleep cycle
DEC LEVEL: anx/dep, insomnia
Norepinephrine: roles
Excitatory; increases alertness and wakefulness, stimulates various processes of the body
Acetylcholine: roles
Excitatory except in heart; regulates sleep cycle, essential for muscle function
GABA: roles
Inhibitory; reduces neuronal excitability throughout nervous system
Causes of bacterial meningitis in adults
STREPTOCOCCUS PNEUMONIAE; Neissseria meningitis
Causes of viral meningitis in adults
Enteroviruses (Coxsackie, echoviruses), arboviruses (west nile, zika), mumps, HSV, varicella
Causes of bacterial meningitis in neonates
GBS, E coli, listeria
Causes of bacterial meningitis in older children
Streptococcus pneumoniae
Causes of viral meningitis in neonates
HSV-2
Causes of viral meningitis in older children
Varicella
Patho of viral meningitis
Virus enters through bloodstream or reactivation; generally milder with gradual onset but still significant
Patho of bacterial meningitis
Bacterial invasion occurs through bloodstream directly into CNS from infections, trauma, or sinusitis
Severe and often life-threatening, rapid onset of symptoms with high morbidity and mortality rates
Patho of Guillian-Barre Syndrome
Autoimmune disease triggered by infections which cause nerve blocks
Clinical features of Guilian-Barre Syndrome
Rapid onset, symmetrical muscle weakness, ascending paralysis, decreased/absent reflexes
Severe Cases: respiratory muscle involvement needing mechanical ventilation
Ischemic Stroke
Obstruction of bloodflow from thrombus/embolus, reversible if reperfusion occurs quickly
Causes of ischemic stroke
Atherosclerosis, HTN, DM, hyperlipidemia
Embolic Stroke
Type of ischemia stroke
Clot or debris travels from another part of the body and lodges in brain artery
Causes of embolic stroke
A fib, carotid artery disease, endocarditis, valve disorders
Thrombotic Stroke
Type of ischemic stroke
From blood clot that forms directly in artery which gradually narrows the artery
Causes of thrombotic stroke
Athersclerosis leading to stenosis, or hypercoagulable states
Patho of multiple sclerosis
Chronic autoimmune disease that affects CNS.
Immune-mediated attack on CNS: T-cells attack myelin, B cells produce antibodies that target myeline. Cytokines (TNF-α, IFN-γ, and IL-17) are released causing further inflammation
Demyelination: loss of myelin sheath slows/blocks nerve signal conduction, forms sclerotic plaques in white matter
Axonal Damage: secondary from chronic inflammation and demyelination, causing progressive disability
Hallmark of ALS
Progressive degeneration of motor neurons in brain and spinal cord. Leads to muscle weakness, paralysis, and respiratory failure.
Loss of neurons results in the inability to send signals to muscle causing atrophy
Hallmark of Myasthenia Gravis
Autoimmune destruction of acetylcholine receptors or related proteins at neuromuscular junction. Antibodies block/destroy ACH receptors, preventing muscle contraction.
Primary mechanism of Bell’s Palsy
Sudden, unilateral paralysis from dysfunction of cranial nerve VII (facial nerve). Linked to viral infection, but exact cause unknown.
Primary mechanism Trigeminal neuralgia
Chronic pain affecting trigeminal nerve (cranial nerve V). Involves vascular compression of trigeminal nerve root. Leads to demyelination of nerve fibers, leading to sudden and sharp facial pain.
Primary mechanism of migraines
Involves cortical spreading depression (neuronal depolarization then suppression which spreads across cerebral cortex). Leads to inflammatory and vascular changes. Releases vasoactive peptides (CGRP).
Plays a key role in vasodilation, neurogenic inflammation, and pain sensation.
Trigger for migriane with aura
Cortical spreading disease.
Aura symptoms include flashing lights, visual disturbances, tingling, numbness.
Others include stress, hormonal fluctuations, dietary factors, changes in weather/barometric pressure
Primary mechanism of tension-type HA
Involve peri-cranial muscle tension and heightened pain pathway
Do not involve CSD or activation of trigeminovascular system.
Prolonged muscle contraction and stress leads to pain, can progress to chronic HAs but lacks severe neurological symptoms seen in migraines
