Last Test GI, Neuro, Skin Flashcards
What is the function of cholecystokinin?
Secreted from I cells in Jejunum in response to fat substances, stimulates gallbladder to release bile (breaks down fat) and pancreas to secrete digestive enzymes. Stimulates gallbladder and pancreas
Which cells in the stomach produce intrinsic factor necessary for B12 absorption?
Parietal Cells
All of the following statements are correct regarding pancreatic secretions EXCEPT: Amylase digests polysaccharides Trypsin digests proteins Lipase digests lipids Bile digests carbohydrates
Bile does not digest carbohydrates, Bile digests fats
What is the main function of the large intestine
Water and electrolytes are primarily absorbed
Normal hepatic function does not include:
Production of bile for carbohydrate digestion
PNS (peripheral) control in the GI tract increases or decreases GI motility and secretions?
Increases motility/secretions
Cleft Lip and Palate Risk Factors - Cause When can it be detected on a U/S
Genetic, maternal medications, alcohol, smoking, vitamin deficiencies Can be detected on U/S at 12 weeks
Cleft Lip vs Cleft Palate Clinical Manifestations
Lip: Opening in maxillary process & upper lip (doesn’t fuse) Palate: Failure of hard & soft palate to fuse
Esophageal Atresia Diagnosis
Cannot detect congenital on U/S although a clue would be polyhydramnios X-ray to diagnose
Esophageal Atresia Clinical Manifestations
Will be detected immediately after birth - drooling, vomiting, scaphoid abdomen, distended abdomen with TEF due to air
Esophageal Atresia Patho
Congenital malformation of the esophagus Two separate esophageal sections not connected Associated with tracheoesophageal fistula
Pyloric Stenosis Patho
Narrowing and obstruction of the pyloric sphincter (stiff muscle fibers) Risk factors: Macrolides in pregnancy (Zithromax/Biaxin). Olive sized mass in babies
Pyloric Stenosis Clinical Manifestations
Noted at birth Hard olive-shaped mass in abdomen palpated. Projectile vomiting after meals, very hungry. Failure to gain weight, dehydration In adults causes, delayed gastric emptying can cause vomiting
Dysphasia Mechanical Obstruction
Mechanical – esophageal stenosis; esophageal diverticula, esophagitis, tumor Extrinsic - tumor, goiter, mass Intrinsic - inside the esophagus
Dysphasia Neurological Disorders
Neurological – CVA, Parkinson, Alzheimer, MS, ALS, Muscular, Muscular dystrophy Any disease that changes muscle fx
Dysphasia Functional
Functional – Sensation with no structural cause Feels like “I can’t swallow” without any cause
Dysphasia Iatrogenic
Iatrogenic – Radiation, muscle relaxants, sedatives, NSAIDs, neck surgery
Vomiting Pathology
Vomiting Reverse peristalsis with obstruction Stimulation of infection or chemicals ICP, Pain, Migraines Should have nausea first Gastric, Duodual Ulcer, Varicies – Blood Obstruction – Bile Undigested food – Pyloric stenosis, Obstruction, Gastroparesis
Hiatal Hernia Pathogenesis & Risk Factors & Clinical Manifestations
Defect in diaphragm allowing a portion of the stomach to come up above diaphragm into the thorax. Risks: older age, smoking, obesity, increased abdomen pressure (heavy lifting, straining) Clinical Manifestations: Reflux inflammation of esophagus - heartburn, belching, chest pain, dysphagia. Worse sx with positioning, fullness after eating, epigastric pain
GERD Pathogenesis Risk factors & Clinical Manifestations
Pathophysiology -Abnormal Lower Esophageal Sphincter relaxation, Gastroparesis Risk Factor Obesity, smoking, alcohol, caffeine; hiatal hernia Medications – beta blockers, sedatives, calcium channel blockers, anticholinergics Clinical manifestations Heartburn, regurgitation of food, nausea Dry cough, laryngitis, pharyngitis Lump sensation in the throat; dysphagia Diag with Bravo pH test
Barrett Esophagus
Cells adapt to inflammation by becoming another type of cell Normal healthy tissue is replaced by COLUMNAR TISSUE. HIgh risk of CA - esophageal strictures
Two types of abdominal pain
Visceral Pain: diffuse poorly localized, gnawing, burning r/t inflammation Somatic Pain: Sharp, pinpoint pain
Esophagitis Clinical Manifestations
Difficult swallowing Painful swallowing Chest pain, particularly behind the breastbone, that occurs with eating Swallowed food becoming stuck in the esophagus (food impaction) Heartburn Acid regurgitation
Gastric Reflux Clinical Manifestations
A burning sensation in your chest (heartburn), usually after eating, which might be worse at night. Chest pain. Difficulty swallowing. Regurgitation of food or sour liquid. Sensation of a lump in your throat. Burping
Acute Gastritis Patho and Clinical Manifestations
Inflammation of the stomach’s mucosal lining with neutrophil infiltration Pathophysiology Infections - bacterial (H. pylori, E Coli) or viral Ingestion of irritating substances Alcohol, Aspirin, NSAIDs Excess HCL acid secretion Bile reflux into the stomach Manifestations Nausea Epigastric pain
Chronic Gastritis Patho and Clinical Manifestations
Pathophysiology Presence of lymphocytes, plasma cells, and macrophages Progresses from superficial inflammation to deeper mucosal gland dysfunction Gastric atrophy – glandular loss (shrinks) Clinical Manifestations: Dull , epigastric pain, nausea, sensation of fullness, anorexia, hematemesis
Type A Chronic Gastritis
Gastritis affecting the fundus and body Autoimmune, destroys parietal cells (HCL acid, intrinsic factor. This can cause a B12 deficiency
Type B Chronic Gastritis
Gastritis affecting the Antrum of the stomach. H-pylori embeds in the mucosal layer Alcohol smoking and NSAID use
What is the best way to test for H-pylori
Breath and Stool Blood tests are IgG and test only for past infection
Gastric and Duodenal Ulcers Patho Clinical Manifestations
Stomach and duodenal lesions extending through muscularis mucosae due to imbalance of destruction and protection Epigastric or RUQ pain, nausea GI hemmorhage, perforation
Gastric Ulcers
Gastric >50 yo, Increases with age; increased NSAID use ***Pain on empty stomach that worsens with eating Epigastric pain
Duodenal Ulcer
Duodenal Younger age, excess acid, H. Pylori ***Pain relieved by eating and occurs 2-3 hours later RUQ pain
Zollinger-Ellison Syndrome
Younger 20-50 years old Excessive gastrin secretion – gastric acid Diarrhea due to excess acid
Gastroparesis Pathology
Paralysis of the stomach Parasympathetic nervous system stimulates the vagus nerve PNS dysfunction causes decreased motility of the stomach
Gastroparesis Clinical Manifestations
Vomiting due to Delayed emptying Nausea Fullness Causesd by diabetic neuropathy and narcotics
Biliary Tree
Cystic duct from gallbladder communicates with hepatic duct to make the common bile duct which empties into the duodenum
Cystic duct (only affects the gallbladder) from gallbladder communicates with hepatic duct to make the common bile duct which empties into the duodenum Sphincter of Oddi is low and probably will affect the gallbladder and the liver
Cholelithiasis Pathogenesis
Pathogenesis: Supersaturation of bile with hypomobility and cholesterol causing precipitation of cholesterol Hypomotility (stasis of bile) allowing stone growth
Risk factors for Cholelithiasis
Risk factors: Fair-skinned, women Obesity, rapid weight loss Oral contraceptives
Cholelithiasis Clinical Manifestations
Clinical manifestations Small stones - asymptomatic Large/multiple stones – Biliary Colic Sharp RUQ/epigastric pain radiating to right shoulder Precipitated by a meal Nausea, vomiting Diaphoresis
Diagnostic Tests for Cholelithiasis
HIDA Scan – GB function ERCP – invasive, scope passed into duct MRCP – noninvasive MRI
Acute Cholelithiasis Clinical manifestations
Acute cholecystitis Gallbladder inflammation from obstruction Severe, steady pain > 4 hours Nausea and vomiting Fever, Leukocytosis Positive Murphy’s sign
Acute Cholangitis
Acute cholangitis Gallstones in the common bile duct Charcot Triad – fever, pain, jaundice Elevated liver tests Can progress to acute pancreatitis
Murphy’s Sign
Used to diagnose cholelithiasis While palpating the liver have take in and hold a deep breath. If pain occurs on inspiration, when the inflamed gallbladder comes into contact with the examiner’s hand, Murphy’s sign is positive.
Hepatitis Pathogenesis
Pathogenesis - Inflammation of the liver Infections – usually viral Alcohol Medications Autoimmune disease – SLE, Scleroderma May be acute, chronic, or fulminant
Jaundice Pathogenesis
Green-yellow staining of tissues by bilirubin Pathogenesis: Impaired bilirubin metabolism Damaged RBCs release hemoglobin Heme and globin separate into free unconjugated bilirubin Liver conjugates into water soluble bilirubin which is released into plasma In correct process, we go from unconjugated to conjugated bilirubin
Pre Hepatic Causes - Jaundice
Hemolysis, ineffective erythropoiesis, resorption of large hematomas
Hepatic causes - Jaundice
Dysfunction of liver cells: increased levels of unconjugated bilirubin
Post Hepatic causes - Jaundice
Mechanical obstruction in bile duct causes conjugated hyperbilirubinemia
Gilbert Syndrome Pathogenesis
Benign Syndrome High Bilirubin Normal Bilirubin 0.1-1 patients with this have Bilirubin 2-3 range Genetic and no associated jaundice
Hepatitis A (HAV) Pathology
RNA virus spread by fecal-oral route (enteric) 2- to 7-week incubation period Clinical Manifestations (last 2 weeks) Abrupt onset Jaundice (not everyone gets it), RUQ pain, malaise, anorexia, nausea, low-grade fever, children may not experience jaundice Followed by jaundice lasting approximately 2 weeks Self-limited course
Hepatitis A (HAV) Testing and Prevention
Serologic testing Anti-HAV IgM (acute infection) Anti-HAV IgG (previous infection) Prevention Careful handwashing Segregation Cleaning of laundry and personal items Immunization – 2 doses 6-12 months apart ***Exposure – passive human immunoglobulin within 2 weeks of being exposed***
Hepatitis B (HBV) Patho and Risk Factors
Partially double-stranded DNA virus Parenteral contact with infected blood or blood products, sexual contact Risk Factor Health care settings (3%); transfusions and dialysis (1%); acupuncture, tattooing, residence in an institution
Hepatitis B (HBV) Course of disease with clinical manifestations
Incubation period of 2-5 months (avg 90 days) Prodromal period Asymptomatic or rashes, arthralgia, arthritis, angioedema, serum sickness, glomerulonephritis, jaundice Positive for Hepatitis B DNA for more than 6 months classified as chronically infected
Hepatitis (HBV) Serologic Testing Surface antigen (HBsAg)
Surface antigen (HBsAg): first to appear; 1-9 weeks; actively contagious. Becomes negative once recovered HBsAg (antigen) resolves and not detected after 6 months May be transiently + 1-2 weeks after vaccine
Hepatitis (HBV) Serologic Testing Surface antibody (HbsAb - anti HBs)
Surface antibody (HbsAb – anti-HBs), becomes + after HBsAg disappears. Indicates recovery with immunity *** (+ after 3 doses of vaccine)***
Hepatitis (HBV) Serologic Testing Core Antibody (HBcAb - anti-HBc)
Core antibody (HBcAb – anti-HBc): seroconversion at 3-5 weeks and ****remains positive indefinitely implying past infection***
Hepatitis (HBV) Serologic Testing Hepatitis B e antigen (HBeAg)
Hepatitis B e antigen (HBeAg): active viral replication and ***highly infective ***
Hepatitis (HBV) Serologic Testing Hepatitis B e antibody (HBeAb) anti Hbe
Hepatitis B e antibody (HBeAb) – minimal replication and decreased infectivity - chronic
Hepatitis B Titers
•Acute:
HBsAg – (surface antigen) – appears first
HBcAb IgM (core Ab) – seroconverts early
HBsAb – (surface Ab) recovered and/or
has immunity from vaccine (anti-HBs)
HBeAg - very infective
HBeAb - minimally infective
Total anti-HBc – positive indefinitely
•Chronic:
HBsAg - remains positive 6 months after infection
HBsAb (anti-HBs) NEGATIVE - never becomes positive
Total anti-HBc – positive indefinitely (IgG)
Hepatitis B DNA remains positive
HBsAg (antigen) resolves and not detected after 6 months Surface AB (anti-HBs) detected - recovered long term Total Anti HBc - always present if there once was an infection HBeAg - contagious initially anti-Hbe - means less or not contagious due to resolving
Hep B
Small window period where only the Total and IgM anti-HBc is detected as the disease moves from acutely infected into the resolved phase In the resolved phase, the IgM anti-HBc will go away and the anti-HBs (AB) will appear
Acute Hepatitis B Titers
Acute: HBsAg – (surface antigen) – appears first HBcAb IgM (core Ab) – seroconverts early HBsAb – (surface Ab) recovered and/or has immunity from vaccine (anti-HBs) HBeAg - very infective HBeAb - minimally infective Total anti-HBc – positive indefinitely
Hepatitis Titers Chronic
Chronic: HBsAg - remains positive 6 months after infection HBsAb (anti-HBs) NEGATIVE - never becomes positive Total anti-HBc – positive indefinitely (IgG) Hepatitis B DNA remains positive
Hepatitis B Diagnostic Testing
+ test for HBeAG or HBsAg or HBV DNA on 2 samples 6 months apart –or– test for HBeAg, HBsAg, HBV DNA and - for IgM anti HBC
Hepatitis C (HCV) Pathology
Single-stranded RNA virus Spread blood contact High risk - IV drug use or blood transfusions prior to 1990 Insidious onset usually Have 6 types Type 1: most common in the United States but has a lower response rate to treatment Types 2 and 3: common in N. America Types 4 to 6: common overseas
Acute HCV infection vs. Chronic HCV infection
Acute HCV infection Usually asymptomatic – mild viral symptoms Brief elevated liver enzymes Chronic HCV infection Usually asymptomatic until advanced liver disease intervenes Permanent liver enzyme elevation ***Most common cause of end-stage liver disease with cirrhosis*** ***Test Anti-HCV to detect HCV RNA by PCR to measure levels of viral load
Hep D and E
Hepatitis D is a incomplete virus that requires the helper function of HBV to replicate Hepatitis E is not found in the US high mortality for pregnant women
Viral Hepatitis Phases
Asymptomatic incubation phase (infectious) Prodromal phase 2 weeks after exposure Low grade fever, fatigue (feels like flu), headache Nausea, vomiting, abdominal pain Icteric phase Jaundice Pruritus Clay colored stools, dark urine (bilirubin goes into urine not stool) Hepatomegaly Recovery phase 6-8 weeks after exposure
Viral hepatitis
Inflammation of the liver parenchyma Caused by many viruses Cytomegalovirus, Epstein–Barr “Viral hepatitis” Hepatitis A - “infectious hepatitis” Hepatitis B - “serum hepatitis” Hepatitis C Hepatitis D (Delta) – defective RNA virus Hepatitis E
Alcoholic Hepatitis Pathogenesis
Pathogenesis Active inflammation of the centrilobular region of the liver Liver cells show pathologic changes of hepatocyte necrosis with neutrophilic infiltration (Mallory bodies). Causes Alcoholics binge in larger quantities than usual.
How to diagnose Alcoholic Hepatitis
Diagnosis AST (SGOT) markedly > ALT (SGPT) Mortality rate 33%
Cirrhosis Pathogenesis
Damage to the liver resulting in decreased liver function Chronic, progressive, irreversible, diffuse Results in fibrosis, nodular scarring Most frequent causes Hepatitis C infection and chronic alcohol abuse Hepatic venous obstruction due to RHF Hemochromatosis NAFLD due to rising obesity
Identify the pathogenesis of NASH Non-Alcoholic Steato Hepatitis
Highly linked to obesity Spectrum of liver diseases which originate from nonalcoholic fatty liver disease (NAFLD) and progresses to fibrosis and cirrhosis. Liver has excessive buildup of triglycerides in the hepatocytes without consumption of alcohol or idiopathic liver disease and viral infection Fat deposition in the liver along with inflammation which can progress to liver failure
Clinical manifestations of NASH
Manifestations Early disease is asymptomatic Intermittent upper quadrant pain, weakness, fatigue, anorexia Diag: U/S shows echogenicity (fatty)
Hepatic Encephalopathy
Clinical Manifestations
Clinical manifestations
- •Ammonia level correlates positively with the level of encephalopathy
- •Dementia
- •Psychotic symptoms
- •Spastic myelopathy
- •Asterixis “liver flap” (classic sign)
- •Spastic jerking of hands held in forced extension
- •Mild confusion and lethargy to stupor and coma (Grade 1 to 4)
Hemochromocytosis
Pathogenesis
Autosomal recessive disorder prominent in Europeans
Activity of mutant gene (HFE) this allows excessive and uncontrolled iron absorption.
Fe deposits in the liver, pancreas, and heart, can lead to liver failure
High level of iron in plasma and serum
Grading of Hepatic Encephalopathy
0 - AOx3, NO Asterixis
1 - mild confusion. Can detect Asterixis
2 - Lethargy with inappropriate behavior. Obvious Asterixis
3 - Somnolent with incomprehensible speech and marked confusion
4 - COMA
Complications of
Portal Hypertension
Sluggish blood flow resulting in increased pressure in portal circulation
- Congested venous drainage of the GI tract
- Clinical manifestations
- Anorexia
- Varices (esophageal, gastric, hemorrhoidal) can rupture; cause uncontrolled bleeding
Ascites
Complications of
Esophageal Varices
Complication of portal HTN from hepatitis
Engorgement from portal vein refluxes into esophageal vasculature
- Variceal bleeding
- 30% will have hemorrhage within 2 years
- Mortality 50%
The greatest risk of rebleed occurs in first 72 hours
Pancreatitis
Etiology
Causes:
- Cholelithiasis - #1 cause
- Alcohol abuse
- Biliary dysfunction
- Hypertriglyceridemia = >600
- Pancreatic tumor
Pathogenesis of
Acute Pancreatitis
Manifestations
- Steady, boring pain in epigastric area or LUQ worse after eating
- Increases in intensity
- Severe tenderness on palpation
- Radiates or penetrates to back
- Nausea and vomiting
- Abdominal distention
- Hypoactive bowel sounds
- Low-grade fever
Medical emergency with 15% mortality due to pseudocyst/abscess rupture and peritonitis
Acute Pancreatitis
Labs
Labs
- Amylase – rises within 12 hours; lasts 5 days
- Lipase – rises within 8 hours; lasts 14 days
- C reactive protein – (CRP) immune
- CMP – LFT changes, bilirubin
- CBC - infectious
- Triglyceride level
- CT or MRI ABD
Chronic Pancreatitis
Pathogenesis
Higher incidence in alcohol abuse
Pathogenesis
- Presence of chronic inflammatory lesions in the pancreas
- Key element: necrosis of exocrine parenchyma followed by fibrosis
- Leads to calcification—obstructed flow of pancreatic juices
- Persistence of symptoms secondary to pancreatic dysfunction over weeks and months
Chronic Pancreatitis
Clinical Manifestations
Clinical manifestations
- Bouts of acute pancreatitis with progressive endocrine and exocrine pancreatic dysfunction
- Diabetes: progressive loss of pancreatic islets
- Malabsorption: fat and vitamins A, D, E, and K
- Weight loss: poor intake related to pain
- Insidious onset of steady, boring epigastric pain radiating to back (first symptom)
- Nausea
After about 5 years of continual pain: decrease in symptoms (pain “burns out”)
CT best for diagnosis
Small and Large Intestine
Small Intestine - 5-6 meters long
Absorbs most of the nutrients
Duodenum, Jejunum, Ileum
Ileocecal valve – separate ileum from colon
COLON – 1.5 meters long
Ascending , Transverse, Descending
Sigmoid to rectum
Acute vs Chronic Diarrhea
Acute - < 14 days
Chronic - > 4 weeks
Acute onset
- Infectious cause – viral, bacterial, parasitic
- Giardia, Salmonella, C Diff, Shigella
- Medications
- Anxiety
Chronic occurrence
- Crohn disease
- Ulcerative colitis
- Celiac disease
Diarrhea Characteristics/Causes in
Small Intestine
ABD pain -RLQ pain with small intestine
Small intestine – large, watery, provoked by eating
Melena black tarry stools - upper GI, small bowel or right colon
Diarrhea Characteristics/Causes in
Large Intestine
Clinical Manifestations
- ABD pain - LLQ pain with large intestine
- Large intestine – small and frequent, more often bloody and mucous with stool
- Hematochezia - Bright red blood from lower colon (diverticulitis, hemmhoroids)
- Colonoscopy can only show large intestine; cannot pass ileocecal valve
Constipation - Etilolgy
decreased fluid intake or excessing absorption
slow motility
medications
decreased fiber diet
spinal cord injury
Bristol Stool Chart
Clinical manifestations of
Appendicitis
Manifestations
- Intensifying pain near the umbilicus initially then localization to RLQ (McBurney Point), worse with movement
- Anorexia
- Nausea
- Vomiting
- Fever, chills, leukocytosis
Pathophysiology of Appendicitis
- Inflammation of the vermiform appendix
- Occurs as a result of obstruction
Pathophysiology
of
Peritonitis
Inflammation of the peritoneum
Pathogenesis
- Chemical irritation – rupture GB or spleen
- Direct organism invasion – appendicitis, abscess
Clinical Manifestations
of
Peritonitis
Classic manifestation
- Abdominal rigidity
- Rebound tenderness
- Nausea and vomiting
- Fever, Leukocytosis
Pathophysiology
of
Celiac Disease
Pathogenesis
- Inflammation and atrophy of the intestinal villi reduces surface area
- Defect in intestinal enzyme needed to digest gliadin
- Decreased brush border enzymes
- Impaired nutrient absorption
Etiology
of
Celiac Disease
- Inherited, autoimmune, malabsorption disorder - intolerance of gluten-containing foods
- More common in females and Caucasians; children
Clinical manifestations
of
Celiac Disease
Clinical Manifestations
- Abdominal pain, bloating, gas
- Diarrhea, odor
- Steatorrhea
- Weight loss
- Vitamin Deficiencies – fatigue, hair loss
How to diagnose
Celiac Disease
Intestinal Biopsy
Anti-tissue transglutaminase antibody - anti-ttG - tTG-IgA
Gliadin Antibodies - IgA and IgG
Stool fat absorption test
Persistent Celiac dysfunction increases risk for intestinal malignancy
Dumping Syndrome
- Dumping of stomach contents into small intestine because of impaired gastric emptying - common after gastrectomy and gastric surgery
- Loss of pyloric sphincter regulation
- Common after gastrectomy and gastric surgery for the control of obesity, ulcers or cancer
- Large volume of food dumped rapidly into the small intestine without chemical breakdown from the stomach
- Diarrhea and abdominal pain
- Rebound hypoglycemia - because body releases 2nd phase insulin release but so rapid glucose doesn’t get absorbed
Short Bowel Syndrome
Short-Bowel Syndrome
- Develops after surgical removal of large portions of small intestine
- Rapid transit time and reduced surface area for absorption (if ileocecal valve removed)
- Diminished ability to absorb nutrients
- Severe diarrhea and significant malabsorption; electrolyte imbalances
Removal of large intestine = DIARRHEA
Removal of small intestine = MALABSORPTION
Inflammatory Bowel Disease
Pathogenesis
INFLAMMATION
Chronic inflammation of the GI tract
- Crohn’s Disease
- Ulcerative Colitis
- Discovered at young age
- Abnormal immune response to intestinal microbiota
- Alterations in epithelial barrier and immune cells
- Abnormal secretion of immune related mediators
Crohn Disease
Pathogenesis
INFLAMMATION
Onset adolescent to young adult
Pathogenesis
- Slow progressive T cell Inflammation through all the layers of the intestinal wall; lymphatic structures become blocked with development of deep linear ulcers; area then becomes fibrotic - cobblestoning
- Deep fissures may develop into fistulas
- Lumen becomes narrowed, potentially obstructed
- Affects ileum, terminal ileum (most common), and proximal colon. Can affect multiple areas along the entire GI tract with normal areas in between the diseased portions.
Proximal
Ascending Colon
Terminal Ileum
Last section of the small bowel
Crohn’s Disease
Clinical Manifestations
& Complications
INFLAMMATION
Clinical Manifestations:
- Constant abdominal pain in the RLQ
- Occasionally there is a palpable mass in the RLQ
- Hematochezia (less than UC)
- Diarrhea
- Weight loss
Complications
- Vitamin deficiencies, anemia, malnutrition
- Electrolyte imbalances
- Fistulas, bowel obstructions,
Ulcerative Colitis
Pathogenesis
Progressive chronic inflammatory disease of the mucosa of the rectum and colon
Onset in 20-30 years of age
INFLAMMATION - BLEEDING
Pathogenesis
- Begins as T cell inflammation of the colon lining resulting in damage and necrosis; abscess formation in crypts; abscesses develop into large ulcerations develop in epithelium
- Colon lining bleeds due to damage
- Exacerbations and remissions
Ulcerative Colitis
Clinical Manifestations
INFLAMMATION - BLEEDING - ANEMIA
Clinical Manifestations:
- Hematochezia
- Melena
- Loose stools/diarrhea
- Abdominal cramping
- Fluid and electrolyte imbalances
- Anemia
- Weight loss
Crohn’s vs. Ulcerative Colitis
Irritable Bowel Syndrome
Pathophysiology
NOT INFLAMMATORY
FUNCTIONAL
Chronic GI function disorder - assoc with stress
HARD TO FIND TRIGGER - R/O ALL OTHER DISORDERS - FOOD ELIMINATION - FOOD DIARY
Pathogenesis
- Bowel pattern alterations and abdominal pain with no structural or biochemical abnormalities
- Increased intestinal motility and contractions
Irritable Bowel Syndrome
Clinical Manifestations
NOT INFLAMMATORY
FUNCTIONAL
Clinical manifestations
- Abdominal distension, fullness, flatus, and bloating relieved with defecation
- Mucous in stool - nonbloody
- Chronic and frequent constipation/diarrhea
- Food intolerance may be present
Irritable Bowel Syndrome
Diagnosis
NOT INFLAMMATORY
FUNCTIONAL
- Based on clinical presentation and exclusion of other GI disorders
- Colonoscopy
- IBS –D - irritable bowel with diarrhea
- IBS – C - irritable bowel with constipation
Diverticular Disease
Diverticulosis vs Diverticulitis
Diverticulosis - Presence of diverticula (herniations) in the colon
More common in the descending & sigmoid colon (left side) can be right
Increases >60 yo
Low fiber, high fat diet increases risk
Asymptomatic
Diverticulitis - Pocketed food in diverticula cause inflammation and necrosis - acute infection
LLQ pain, fever, abd. distension, occasional blood in stool
Diagnosis and Complications
Diverticulitis
Acute Diverticulitis - no colonoscopy
Bowel perforation
Peritonitis
Diverticulum in throat
Zankurs
- Asymptomatic unless large
- Gurgling in the throat, dysphagia
- Risk for aspiration
Diverticulum in small intestine
Meckles
- Mostly asymptomatic
- Risk for ulceration and bleeding due to retained acid in the diverticulum
Oral Cancer
Pathogenesis
Squamous cell carcinomas of tongue and mouth floor
Influence of tobacco and alcohol (75%)
Men more than women
Pathogenesis
- HPV lesions
- Leukoplakia or erythroplakia (premalignant lesions)
- Progress to nodular or ulcerative lesions
Esophageal Cancer
Pathogenesis
Squamous or Adenocarcinoma
Men more than women (3x)
Risk factors
Genetic, chronic severe reflux, smoking, alcohol
Pathogenesis
- Chronic irritation of the distal esophagus leads to cellular dysplasia
- Barrette esophagus to adenocarcinoma
- EGD if GERD >5 years
Gastric Carcinoma
Adenocarcinoma
Risk
- Preserved and smoked foods
- H. Pylori untreated
- Smoking and alcohol
- Genetics
Pathogenesis
- Localized tissue inflammation advances to dysplastic cells
Liver Cancer
- Commonly a secondary tumor that has metastasized (breast, lung, GI)
- Can be a primary site - hepatocellular
Pathogenesis
- Chronic cirrhosis, HBV, or HCV lead to hepatocellular carcinoma (primary)
Pancreatic Cancer
Pathogenesis
- Aggressive malignancy,
- ductal adenocarcinoma arising from exocrine cell
- Can quickly spread to nearby structures
Clinical Manifestations - usually delayed
- Upper abdominal pain
- Indigestion, nausea
- Early satiety, anorexia
- Jaundice, steatorrhea, clay colored stools
Colon Polyps
Major precursor lesion in development of colon cancer
Celular types
Cellular type
- Hyperplastic - benign (will never become malignant)
- Adenomatous - malignant potential (initially benign but if not removed can become malignant and advance to adenocarcinoma)
Colon Polyps
Structural Types
- Sessile polyp: raised protuberance with a broad base, harder to remove. A sessile polyp that is adenomatous type is even a bigger concern
- Pedunculated polyp: attached to bowel wall by a stalk that is narrower than the body of the polyp
Colon Cancer Screening Guidelines
2nd to Lung Cancer as cause of cancer risks
- Colon cancer screening guidelines; for the individual at average risk, colonoscopy every 10 years starting at age 45- new guideline starts age 45
- Family history colon cancer - Start colonoscopy 5 years earlier than age at diagnosis
- Important hereditary condition
- Familial adenomatous polyposis (FAP)
- At least three close relatives with colorectal cancer, colorectal cancer involving at least two generations, and one or more cases of colorectal cancer occurring before age 50 years
Colon Cancer
Risk Factors
Risk factors
- Increases after age 40
- High-fat, low-fiber diet
- Polyps
- Chronic irritation or inflammation
- Hereditary
Colon Cancer
Clinical manifestations
Clinical manifestations
- Change in bowel habits or new onset constipation
- Right side: black, tarry stools
- Left side: intermittent abdominal cramping and fullness; narrowed or pencil-shaped stools; blood or mucus in stool
- Rectum: urgent need to defecate on awakening; alternating constipation and diarrhea; sensation of rectal fullness; dull ache in rectum/sacral region
Alpha 1 - antitrypsin deficiency
- Autosomal recessive condition found mainly in children and young adults
- α1-antitrypsin is an enzyme inhibitor found in many tissues.
- Normally prevents elastase and collagenase from damaging tissues
- Genetically controlled by a gene with many allelic variations
A1-antitrypsin deficiency
Pathogenesis
•Defective α1-antitrypsin protein accumulates in liver; produces diagnostic granules
large amounts of abnormal alpha-1 antitrypsin protein (AAT) are made in the liver; nearly 85 percent of this protein gets stuck in the liver. If the liver cannot break down the abnormal protein, the liver gradually gets damaged and scarred.es.
A1-antitrypsin deficiency
Clinical Manifestations
Clinical manifestations
- Centrilobular emphysema
- Pancreatic insufficiency
- Cirrhosis symptoms
When would peripheral neurons regenerate
•Peripheral neurons may regenerate if Schwann cells provide a pathway for growth.•Injury in PNS results in degeneration of the distal segment
Neural stem cells in the ventricles and hippocampus can proliferate to produce
•Neural stem cells in the ventricles and hippocampus can proliferate to produce glial or neuronal cells depending on specific cues.
Touch, pressure, and vibration travel up the
__________ side of the cord until the medulla
Pain, itch, and temperature usually cross over and travel to the brain on the __________ side
- Touch, pressure, and vibration travel up the ipsilateral side of the cord until the medulla
- Pain, itch, and temperature usually cross over and travel to the brain on the contralateral side.
Intensity of the stimulus is reflected in the rate of action potentials generated
Two Sensory pathways
•Two major tracts
- Dorsal column–medial lemniscal tract: fine touch, vibration, and proprioception•
- Anterolateral tract: pain, temperature, and itch
•Sensory information from both tracts is transmitted from the thalamus to the same areas of the somatosensory cortex by way of the internal capsule.
Motor Function requires interaction among the
•Requires interaction among the basal ganglia, cerebellum, and cortex•
Transmitted from the primary motor cortex down the corticospinal tract
- Controls distal muscles of the arms, wrists, fingers, lower legs, feet, and toes
- These are the muscles capable of fine-motor control
What is the point of decussation?
•Decussates in the medullary pyramids and travels down the spinal cord to control muscles on the contralateral side of the body
What are geriatric considerations for aging r/t neuro
Geriatric considerations
- Decreased cerebral blood flow, number of neurons, synthesis and metabolism of neurotransmitters, degeneration of myelin sheath and astrocytes, white and grey matter
- Excessive degeneration of neurons – Alzheimer’s or senile dementia
- Cerebral Atrophy
- Dendrites shrink - slow cognition
- Degeneration of myelin sheath - decreased reaction time.
- Decreased neurotransmitters - tremors
Hydrocephalus
Pathology
Risk Factors
Clinical manifestations
Pathogenesis
•Excess CSF accumulation resulting in dilation of ventricles and compression of the brain and blood vessels due to ICP
Risk Factors
- Premature birth, CNS tumors, CNS infections, cerebral hemorrhage, head injury
- Congenital – primary cause – myelomeningocele
- 60% fatality rate if untreated
Clinical Manifestations
- Infants with unfused cranial sutures
- Unusually large head, bulging fontanelle, vomiting, dilated scalp veins, lethargy, etc.
Clinical manifestations of
Hydrocephalus in adults
Presents like Dementia or Alztimers - Slow process
- Gait dysfunction, cognitive impairment, and urinary incontinence
- Gait – wide stance and small steps
- Cognitive – difficulty conceptualizing – slower psychomotor, decreased attention, apathy
- Urinary – Urgency and incontinence
What is Spina Bifida
A Neural Tube defect where vertebrae does not fuse allowing the meninges and spinal cord herniation
Related to Folate Deficiency in pregnancy
Spina Bifida
Clinical Manifestations
Diagnose with Alpha Fetal Protein elevation in amniotic fluid
Clinical manifestations
Spina bifida occulta – mildest, common
- No protrusion of the cord, no symptoms
- Sacral dimple , tuft of hair
Meningocele – rare
- Meninges protrusion – sac on the back
- No impairment
Myelomeningocele – open; most severe
- Meninges, spinal cord, and nerves protrude
- Paralysis, bowel and bladder dysfunction, seizures
Cerebral Palsy
CP
Pathogenesis
&
Risk Factors
Pathogenesis
- Permanent, nonprogressive motor movement and muscle coordination
- Cognition and communication dysfunction
- Results from brain abnormalities or damage to cerebellum in prenatal period (childbirth)
•Risk factors
- Male, African American, Low socioeconomic
- Prematurity, LBW, breech births, multiple fetuses, hypoxia, hypoglycemia
- Maternal smoking and alcohol use
- Rubella or varicella during pregnancy
Cerebral Palsy
Clinical Manifestations
Classified according to movement disorder involved (area of brain affected)
- Neurobehavioral signs - irritability
- Developmental reflexes – exaggerated Moro reflex
- Motor tone - varies from stiff to flaccid; delayed milestones
- Spastic subtype - hyperreflexia; impaired fine motor skills
- Dyskinetic subtype – irregular, unpredictable contractions of muscles
- Ataxic subtype - uncoordinated movements, slow speech
What are some complications of
Cerebral Palsy
Complications
- Balance and coordination
- Communication delays
- Cognitive difficulties
- Seizures
- Vision and hearing deficits
What are 2 infectious
Neurologic
Disorders
Meninges - Meningitis
Brain parenchyma - Encephalitis
Meningitis Pathogenesis
- Inflammation of the meninges with inflammatory exudate causing obstructive hydrocephalus
- Bacteria - Streptococcus pneumoniae; Neisseria meningitides; Haemophilus influenzae
- Viral - West Nile, Influenza, HIV, herpes (aseptic)
- Fungal or parasitic
- Transmission modes – respiratory secretions, saliva, fecal-oral, insect bite, skull fracture
When would you administer the Meningoccal Vaccine
•Meningococcal vaccine - age 11-12 and booster at 16; Meningococcal B vaccine
HIB vaccine for infants
Kernig’s Sign
Kernig’s sign
Flex knee and hip at 90 degrees and straightening the knee will cause lumbar pain
Hematomas
- Classified by location
- Epidural – Dura and skull involves arteries fast
- Subdural – Dura and Arachnoid can take weeks esp with elderly
- Intracerebral – into brain tissue
- Subarachnoid – Arachnoid and pia mater worst HA of life back of head, aneurysm, arteriovenous maliformation
Visual Fields
Types of
Multiple Sclerosis
Progressing-Relapsing MS
Second Progressive MS
Primary-Progressive MS
Relapsing-Remitting MS
Parkinson’s Disease
Pathogenesis
Pathogenesis
- May be idiopathic, acquired or drugs
- Dopamine deficiency in the basal ganglia (substantia nigra) associated with motor impairment
- Lewy Bodies – clumped proteins in neurons
•
Parkinson
Parkinson Stooped Posture Progression
AML
Clinical Manifestations & Diagnosis
•Clinical manifestations
- Spinal cord injury leads to Footdrop, weakness and eventual wasting (atrophy) of upper or lower extremities; dysarthria or dysphagia, respiratory dysfunction leads to death
•Diagnosis:
- History and examination; no definitive test
- MRI Brain; Lumbar puncture
- Electromyogram
- No definitive test
Kyphosis
Humphed Posturing
•Kyphosis - thoracic spine curved outward (hump)
Scheuermann - juvenile development during adolescent growth spurt; pain with activity
Adult – degeneration of vertebrae, osteoporosis, fracture; back pain, spine stiffness
Lordosis
Concave
•Lordosis – exaggerated concave lumbar spine
- Develops in adolescent with poor posture; worsens with pregnancy and obesity; low back pain
DeQuervain’s Tendonitis
•De Quervain’s Tendonitis - thumb radial head to tip of thumb – cant open jar
Bursitis
Pathogenesis
Pathogenesis
- Inflammation of fluid-filled, pocket of connective tissue between muscles or between muscle, tendon, and bone due to trauma or overuse
- Bursea contain synovium to cushion the structures
Olecranon, trochanter, patellar
de Quervain tendinopathy
de Quervain tendinopathy
- •Inflammation of wrist tendons on radial side
- •Manifestation - swelling and pain on distal radial side and with movement of the thumb
- •Diagnosis – examination
- Finkelstein test
Tinel Test for Carpal Tunnel Syndrome
Phalen Test for Carpal Tunnel Syndrome
Dupuytren’s Contracture
•Dupuytren’s contracture
- Thickening and contracture of the palmar fascia due to fibroblast proliferation and abnormal collagen deposition
- Manifestation – limited extension of the finger
Osteoporosis Grading
DEXA SCAN REPORT
Osteoarthritis
Clinical Manifestations
•Manifestations
- Localized joint pain and crepitus with movement
- Bony enlargement, morning stiffness lasting < 30 minutes or after inactivity
- Heberden and Bouchard nodes (buttons on distal joints)
Diagnosis of Rheumatoid Arthritis
Diagnosis
- History and examination
- X-rays, MRI
- Rheumatoid Factor (RF) elevation
- Anti- CCP elevation –more specific test
- ESR and CRP elevation
- Synovial fluid aspiration
Systemic Lupus Erythematous
SLE
- Chronic multisystem, inflammatory, autoimmune disease characterized by periods of exacerbations and remission
- Considered an atypical inflammatory reaction to the body’s own tissues, cells, and protein
- Overactive B-lymphocytes → overproduction of autoantibodies and ↑ reactivity of T-lymphocytes
Peak incidence 15 to 40 yr olds
Affects collagen tissue
Renal impairment, heart disease and infection
Atopic Dermatitis
•Chronic inflammatory condition – eczema
Etiology - Inherited tendency; family hx of eczema, asthma
•More common in children
Pathogenesis - immune system malfunction
- Manifestations
- Xerosis and pruritus
- Face, scalp, extensor surfaces (knees, elbows)
- Diagnosis
- History and physical exam
- Elevated IGE level
Seborrheic Dermatitis
- Papulosquamous skin disease manifested by various degrees of scaling and erythema in areas of high oil gland concentration
- Cradle cap (infants) and dandruff (adults)
- Facial area
Psoriasis
Chronic inflammatory condition
Etiology - Inherited condition; immune system involvement; Adult condition
Pathogenesis - Inflammation promotes hyperproliferation of the skin
- Triggers – cold weather, stress, alcohol
- Manifestations – Chronic plaque presentation
- Papules and plaques with overlying silvery scale
•Lesions on knees, elbows, lower back, scalp, nails
•Joint pain with psoriatic arthritis
Exacerbation and remission
Bacterial Infection
Folliculitis
Furuncles
Impetigo (non-bullous and bullous)
•Folliculitis – hair follicles
- •Tender pustules in areas of hair
•Furuncles – boils
- •Firm, erythematous, painful nodule with purulent exudate
•Impetigo (non-bullous and bullous)
- •Caused by staphylococci or streptococci bacteria
- •Characterized by vesicles, pustules, and yellowish crusts
Pityriasis Rosea
•Occurs after a viral infection
•Benign, uncommunicable
- Starts with a herald patch – solitary, salmon colored well demarcated patch on chest, neck, or back
- 2-14 days later develop scaly papules and plaques in a Christmas tree pattern on the posterior trunk
Scabies
(Mite)
- Sarcoptes scabiei is a mite.
- Begins with eggs laid in the stratum corneum, hatch into larvae within 3 to 4 days
- Contracted after close contact with an infested individual
- Small erythematous papules with overlying dry scale or crust; linear burrows
- Finger webs; wrists, groin
Lyme Disease
- Tick bite that carries spirochete Borrelia burgdorferi from deer and mice
- Affects skin, nervous, heart, and musculoskeletal system
- Stage I: single or multiple erythematous papules that itch or sting; flulike symptoms
- Stage II: meningitis, cranial nerve palsies, and peripheral neuropathy
- Stage III: oligoarticular arthritis
First Degree Burn
First-Degree: Superficial Burns
- Involve only superficial tissue destruction of outermost layers of the epidermis
- Manifestations: local discomfort, erythema, headache, chills, N/V
- NO BLISTER
- Typically self-limiting, healing in 3 to 6 days
Second Degree Burn
Second-Degree: Superficial Partial-Thickness Burns
- Involve the epidermis to the level of the dermis and appear red to pale ivory
- Moist thin-walled blisters often form
- Pain is a major clinical feature.
- Injuries typically heal in 7 to 21 days in the absence of wound infection.
Hair typically reappears in 7 to 10 days.
Third Degree Burn
Third Degree: Full-Thickness Burns
- Involve epidermis, dermis, and underlying subcutaneous tissue
- Appear white, cherry red. or black, with deep blisters; painless areas
- Wound has dry, hard, leathery texture.
- Treatment: often requires skin grafting
Forth Degree Full Thickness with Deeper Structures
Fourth-Degree: Full-Thickness with Deeper Structures
- Full-thickness injuries that extend beyond the dermis to involve muscle, bone, or both
- Often occur in victims of high-voltage electrical injury or those with prolonged exposure to intense heat
Basal Cell Carcinoma
- Basal cell carcinoma – most common
- Abnormal cell growth in lowest epidermis layer
- Dry macular area; pearly nodule
Low metastatic potential
Squamous Cell Carcinoma
- Squamous cell carcinoma
- Changes in squamous cells in the middle epidermis layer – rapid growth
- Smooth nodule or hyperkeratotic lesion
- Can metastasize
