Patho Unit 7 Flashcards
Understand: - Alterations of Pulmonary Function (Ch 26) - Structure and Function of the Renal and Urologic Systems (Ch 28) - Alterations of Renal and Urinary Tract Function (Ch 29) - Alterations of Digestive Function (Ch 34)
1
Q
Pulmonary Disease
Signs and Symptoms
A
- Dyspnea
- Coughing
- Abnormal sputum
- Hemoptysis
- Cyanosis
- Clubbing
- Pleuritic pain
2
Q
Dyspnea
A
- Also known as shortness of breath
- Breathlessness, labored breathing
- Caused by increased airway resistance
- Symptom: breathing is uncomfortable
- Signs: flared nostrils and use of accessory muscles
3
Q
Coughing
A
A protective reflex that cleans airways with an explosive expiration to remove foreign particles
4
Q
Abnormal Sputum
A
- Sputums is mucus mixed with substances in lower respiratory tract (the passengers on the MUCOCILIARY ESCALATOR)
- Changes in color, consistency, odor, and amount provide information about a disease and disease progression
5
Q
Hemoptysis
A
Coughing up blood or bloody secretions
- Usually bright red (mixing air and red blood cells keeps them oxygenated)
- Localized infection or inflammation has damaged the bronchi or alveolar-capillary membrane
6
Q
Kussmaul Respiration
Hyperpnea
A
Decrease in blood pH (increase in plasma H+) causes hyperventilation Results in: - Increased respiratory rate - Large increase in Tidal Volume - No expiratory pause
7
Q
Cheyne-Stokes Respiration
A
- Breathing fluctuates
- Periods of apnea or hypopnea alternating with periods of hyperpnea
- Occurs in about half of patients with congestive heart failure or neurological disease including stroke
- More common during sleep
8
Q
Hypoventilation
A
Alveolar gas exchange insufficient for metabolic demands
- Increased PCO2
- Respiratory Acidosis
9
Q
Hyperventilation
A
Alveolar gas exchange greater than metabolic demands
- Decreased PCO2
- Respiratory Alkalosis
- Causes: anxiety, head injury, pain, Low PO2
10
Q
Cyanosis
A
Bluish coloration of mucous membranes and the skin caused by increased amounts of deoxygenated hemoglobin
- O2 saturation is a measured of how many oxygen binding sites on hemoglobin are occupied
- In cyanosis O2 saturation is < 85% in arterial blood (normal 97-99%)
11
Q
Clubbing
A
Increased connective tissue and vasculature in fingers/toes because of chronic anoxia
- Mechanisms unclear: probably due to some sort of chemical signaling
12
Q
Pleuritic Pain
A
Sharp, stabbing pain associated with breathing
- From disorders affecting the pleurae, airways, and chest wall
13
Q
Pulmonary Ventilation
A
V = the amount of air (in Liters) entering the lungs per minute Va = the amount of air (in Liters) entering the alveoli per minute
14
Q
Perfusion
A
Q = the amount of blood that flows through the lung capillaries each minute
15
Q
Ventilation-Perfusion Coupling
A
Va/Q, the matching of pulmonary blood flow to oxygen, forces or shunts blood to areas of higher oxygen
- In healthy individuals Va = 4.5L/min, Q = 5.0L/min, ideally it equals ~1
- Under hypoxic conditions, pulmonary blood vessels constrict
- If no air enters the lungs Va/Q=0, blood flows but no gas exchange takes place
- If air enters lungs but blood doesn’t flow Va/Q=∞, blood is not oxygenated and cannot release CO2 (ex: Pulmonary Embolism)
16
Q
Hypercapnia
A
Blood CO2 too high
- Depression of respiratory center by drugs
- Diseases of the Medulla (respiratory centers of brainstem affected by infection or trauma)
- Problem with Phrenic Nerve innervation (polio, amyotrophic lateral sclerosis, spinal cord injury)
- Diseases of the Neuromuscular Junction (myasthenia gravis, muscular dystrophy)
- Thoracic cage trauma or congenital deformity
- Large airway obstruction (tumors, apnea)
- Physiologic dead space (emphysema)
17
Q
Hypoxemia
A
Blood O2 too low
- Problem with O2 delivery to the alveoli (reduced PO2/reduced Va)
- Problem with O2 moving across the alveolar-capillary membrane (Va/Q mismatch, blockage in A-C membrane)
- Problem with blood arriving to be oxygenated
18
Q
Problem with O2 Delivery to Alveoli
A
Reduced PO2: - High altitude - Low O2 content in air - Suffocation Reduced Ventilation of Alveoli: - Brain damage - Chest wall restriction - Airway obstruction - COPD - emphysema, chronic asthma
19
Q
Problem with O2 Moving Across the A-C Membrane
A
Va/Q Mismatch: - Asthma - Bronchitis - Pneumonia - Acute respiratory distress syndrome - Atelectases - Pulmonary embolism Blockage in A-C Membrane - Edema - Fibrosis - Emphysema
20
Q
Problem with Blood Arriving to be Oxygenated
A
- Cardiac defects
- Arteriovenous malformations in lung
21
Q
Pneumothorax
A
- If air can leak into the Pleural Cavity, then Thoracic Cavity can’t develop a pressure difference
- Surface tension takes over and causes the A-C Membrane to collapse in on itself
- The entire lung collapses and Pneumothorax results
- This is a special case of Atelectasis
22
Q
Atelectasis
A
Any abnormal structure in the alveoli of the lung
- What happens when “the grapes” (alveoli) are smashed
- Interferes with gas exchange
23
Q
Pleural Effusion
A
Any abnormal or excess liquid in the alveoli interferes with external respiration - dyspnea
2 types:
- Transudative Effusion
- Exudative Effusion
24
Q
Transudative Effusion
A
Increase in hydrostatic pressure or decrease in oncotic pressure in capillary
- This is the mechanism of Pulmonary Edema in, for example, congestive heart failure
25
Exudative Effustion
Increase in capillary permeability that allows blood cells and/or plasma proteins to leak into alveoli
- Empyema: pus
- Hemothorax: blood
- Chylothorax: chyle (lymph and fats)
26
Bronchiectasis
Remodeling of the bronchi due to chronic inflammation
- Bronchial smooth muscle replaced with connective tissue
- This increases the width of the bronchi, but mucus narrows the lumen and makes it difficult to pass air through the conduction portion of the airways
27
Bronchiolitis
Chronic inflammation of the Bronchioles
- Fibrous connective tissue replaces functional tissue (such as smooth muscle)
- Narrowing of the bronchiole lumen
28
Pulmonary Edema
| from Heart Disease
1- Valvular Dysfunction, Coronary Artery Disease, Left Ventricular Dysfunction
2- Increased pressure in left atrium
3- Increased pulmonary capillary hydrostatic pressure
4- Pulmonary edema
29
```
Pulmonary Edema
(from Injury to Capillary Endothelium)
```
1- Injury to Capillary Endothelium
2- Increased capillary permeability and decreased surfactant production
3- Fluids and proteins leak into interstitial space and into alveoli
4- Pulmonary edema
30
Pulmonary Edema
| from Blockage of Lymphatic vessels
1- Blockage of Lymphatic Vessels
2- Fluid not removed from interstitial space
3- Fluid accumulates in interstitial space
4- Pulmonary edema
31
Acute Respiratory Distress Syndrome
| ARDS
The most severe manifestation of acute lung injury in adults (also occurs in children)
- All disorders that result in ARDs acutely injure the A-C membrane, causing severe pulmonary edema and markedly reduced compliance (elastic properties) of the lung
- Requires treatment with mechanical ventilation
32
ARDS
| Step 1
- Neutrophils release a battery of inflammatory mediators (proteolytic enzymes, O2 free radicals, and pro-inflammatory cytokines)
- This leads to pulmonary vasoconstriction, vascular occlusion an pulmonary hypertension
33
ARDS
| Step 2
The damaged alveolar epithelial barrier breaks, allowing flooding of the alveolar space and making it difficult or impossible for oxygen to diffuse into capillaries
34
ARDS
| Step 3
Edema overwhelms type II alveolar cells (septal cells)
- They cannot make enough surfactant to compensate for the huge amounts of liquid
- Surface tension of liquid causes the alveoli to collapse
35
Type II Alveolar Cells
Make surfactant to reduce lung surface tension
36
ARDS
| Step 4
- Protein and enzymes make a jelly-like substance called the hyaline membrane
- Not much gas exchange can take place
37
Asthma
- Obstructive Pulmonary Disease
- More common in young people
- Manifestations: dyspnea, prolonged expiration with expiratory with wheezing, early nonproductive cough, tachycardia, tachypnea, and acidosis
- Treatment: inhaled bronchodilators, anti-inflammatories (glucocorticoids and leudotriene receptor blockers)
38
Chronic Obstructive Pulmonary Disease
| COPD
- Chronic Bronchitis and Emphysema
- Signs and Symptoms: exercise intolerance, dyspnea, wheezing, productive cough, hypoxemia causing polycythemia and cyanosis, pulmonary hypertension, and congestive heart failure
39
Emphysema
Enlargement and destruction of alveoli, loss of elasticity, and trapping of air
- Cigarette smoking always results in emphysema, the smoke inhibits the enzyme a1-antitypsinase
- Without it elastase breaks down elastic connective tissue of the alveolar wall
- It is replaced with non-elastic, fibrous connective tissue (alveolar remodeling)
- Patients with a mutation causing a deficiency of a1-antitypsinase have a syndrome where this occurs spontaneously
40
a1-antitypsinase
Blocks Neutrophil Elastase and prevents it from breaking down elastin
41
Emphysema Signs and Symptoms
```
Inspiration remains intact but the ability to expire is reduced
- Loss of elastin makes lungs less elastic
- Lungs become over inflated
- Chest muscles forced to work harder
Signs and Symptoms:
- Dyspnea
- Late developing cough
- Tachypnea
- Prolonged expiration
- Pulmonary hypertension
- Barrel chest
```
42
Chronic Bronchitis
Obstruction is caused by inflammation and thickening of the respiratory mucus membranes, ciliary impairment, accumulation of mucus and pus
- No lung remodeling, unless emphysema is also present
- Caused by: cigarette smoking, air pollutants, infections
43
COPD Treatment
Treatment is virtually the same for emphysema and chronic bronchitis
- Stop smoking
- Antibiotics: because of susceptibility to infection
- Bronchodilators
- Anti-inflammatory drugs: glucocorticoids
- O2 administration
44
Pneumonia
Acute infection of the lower respiratory tract, in most individuals susceptibility, not exposure is the overriding factor
- Caused by rickettsiae, mycoplasma and other bacteria; fungi and viruses are also implicated
- Organisms reach the lungs by inspiration or aspiration of oropharyngeal secretions or via the circulation
- Normal lung defenses become inadequate or compromised
45
Types of Pneumonia
Community Acquired
- Streptococcus pneumoniae
- Mycoplasma pneumoniae (walking pneumonia)
Hospital Acquired
- Staphylococcus aureus and Klebsiella pneumoniae
- Occurs in patients with COPD or patients with a viral respiratory illness
Immunocompromised Individuals
- Fungal pneumonia Pneumocystis jiroveci
- Often seen in AIDS patients
46
Pneumonia Signs and Symptoms
- Productive cough
- Pleuritic chest pain, chills, malaise
- Inspiratory crackles
- Evidence of infiltrates on x-ray is the key diagnostic feature
47
Pneumonia Treatment
Depends on where the disease was acquired, the causative organism, and the severity of the disease
- Antibiotics
- Supplemental O2
- Mechanical ventilation in severe cases
48
Tuberculosis
Infection caused by Mycobacterium tuberculosis, an acid-fast bacillus that affects the lungs
- Transmitted in airborne droplets
- Once in the lungs, the bacteria multiply and cause non-specific lung inflammation and can migrate to the lymphatics
- Neutrophils and Macrophages wall off the colonies and form granulomas (tubercles)
- Cells within the tubercles die and form caseous necrosis
49
Factors that contribute to Tuberculosis
- Emigration, crowded institutional settings, substance abuse and poor access to medical care also contribute
- Incidence is increasing due to drug-resistant strains and possibly related to HIV infections
50
Pulmonary Embolism
Caused by an embolus obstructing the pulmonary artery
- Signs and symptoms: tachypnea, dyspnea, pleuritic chest pain, systemic hypotension, shock
- Risk factors: obesity, sedentary life style, birth control, smoking
- Treatment: avoiding venous stasis, anticoagulant and fibrinolytic agents
51
Pulmonary Hypertension
Causes and elevated blood pressure in the pulmonary arteries
- Caused by: elevation of pulmonary arterial pressure due to increased left atrial pressure (as in congestive heart failure) or lung disease
- Manifested by: fatigue chest pain, dyspnea, with exercise, abnormal chest x-ray and abnormal electrocardiogram (showing ventricular hypertrophy)
52
Cor Pulmonale
Pulmonary-Related Heart Disease, right ventricular disease due to pulmonary hypertension
- Manifested by: chest pain, tricuspid murmur, pulmonary valve murmur
53
Renal Threshold
If the filtrate concentration of a substance cannot be reabsorbed fast enough, then the renal threshold of that substance will be reached and the substance will spill into the urine
54
Proteinuria
- In theory albumin should be filtered because of its size, but in reality some protein leaks through
- The tubular system has a limited capacity for protein reabsorption and is easily overwhelmed
- More protein leakage than can be reabsorbed results in proteinuria
- This usually indicates microscopic damage to the glomeruli
55
Blood Urea Nitrogen
| BUN
Metabolism of the amino groups in proteins produces urea, ammonia, and related nitrogen-containing compounds; these are collectively called blood urea nitrogen
- In kidney failure, these compounds are not cleared by the kidney (usually because of decreased GFR) and build up in the blood
56
Creatinine
A waste product of muscle metabolism, levels are directly related to muscle mass
- Muscles use creatine phosphate as an energy source
- Creatinine is a by-product
- Creatinine clearance rate can be measured directly by taking blood and urine at intervals or approximately by measuring blood creatinine then using an equation based on levels, height, weight and age
57
Glomerular Filtration Rate
| GFR
Measures how much blood is filtered through the glomerulus and becomes filtrate
- Normal > 90 mL/min
- Decreased in kidney disease
58
GFR Stages in Kidney Disease
```
1- 90 mL/min, kidney damage with normal GFR
2- 60-89 mL/min
3- 30-59 mL/min
4- 15-29 mL/min
5- <15 mL/min, kidney failure
```
59
Urine
- Volume 1-2 L/day
- Color: variable shades of yellow
- Turbidity: clear
- Odor: variable
- pH: 5 - 6.5, varies widely due to diet and disease, can be 4.5 - 8
- Specific gravity: 1.005 - 1.025
- Chemicals: water, urea, and small amounts of uric acid, creatinine, ketones, Na+, K+, bicarbonate
60
Urinalysis
- Biochemical dipstick: absorbent pads specific to certain analytes, detects possible presence of blood, bilirubin, glucose, albumin, bacteria, and WBCs
- Microscopic: visualization of urinary sediment
61
Upper Urinary Tract Obstruction
```
Kidney
- Stones
- Blood vessel compression
- Tumor
- Scarring/Fibrosis
Ureter
- Stones
- Tumor
```
62
Lower Urinary Tract Obstruction
```
Bladder
- Neurogenic bladder
Urethra
- Urethral stricture
- Prostate enlargement (in men)
- Pelvic organ prolapse
- Obstruction of urethra
```
63
Renal Calculi
| Kidney Stones
Caused by underlying disorders (infections, obstructions) increased dietary intake of specific chemicals (Ca++ and PO4), high or low pH levels, and dehydration
- Symptoms: flank pain radiating to the groin area, nausea, vomiting, and abdominal pain
- Lab findings: high urine specific gravity, hematuria, possible crystals on microscopic exam
- Diagnosis: Intravenous Pyelogram (IVP)
- Treatment: high fluid intake, stone extraction, stone framentation (laser or ultrasonic lithotripsy)
- Can cause renal failure and predisposition to infections
64
Neurogenic Bladder
An obstructive uropathy caused by an interruption of the nerve supply to the bladder; can be caused by CNS or spinal cord damage
- Loss of upper motor neuron function in the primary neuron between the cortex and sacrum results in a patient's loss of voluntary voiding control
- Loss of lower motor neurons in the peripheral nerves from the sacrum causes the patient to lose both voluntary and involuntary urination due to disruption of the sacral reflex
65
Urinary Tract Infection
| UTI
An infection anywhere in the urinary tract
- E. coli is the main pathogen (other gram-negative bacteria are also seen)
- Common in females, uncommon in males (except for STDs which are equal in both sexes)
- Caused by: surgery, catheters, diabetes, ptosis, prostatic hyperplasia, STDs
- Symptoms: dysuria (burning, urgency, and frequency), incontinence, low back or flank pain
66
Cystitis
May be an infectious or non-infectious inflammation
- Obstruction, prostatitis, microorganisms
- Signs & symptoms: painful, burning urination, frequency, urgency, hematuria, foul smelling and cloudy urine
- Lab findings: WBC w/wo bacteria
67
Pyelonephritis
Infection is the usual etiology, but not always
- Ascending microorganisms, urinary obstruction, condition that causes urinary reflux, or urine retention
- Signs & symptoms: fever, chills, back pain, dysuria, frequency
- Lab findings: WBCs and WBC casts, w/wo bacteriuria
68
Glomerulonephritis
Diseases of the glomerulus that are cased by immune responses, toxins, vascular disorders and other systemic diseases
- Hallmark is Hematuria
- Damage occurs from activation of inflammatory process
- There can be antibodies to the glomerulus or antigen/antibody complexes that localize in the glomerular membrane wall
- Inflammatory response changes the permeability of glomerular membrane
69
Glomerulonephritis
| common types
- Post-streptococcal (PSGN)
- Rapidly progressing (crescentic)
- Membranoproliferative and minimal change disease (MCD)
- IgA nephropathy (Berger's disease)
70
Glomerulonephritis
| lab findings
- RBCs in urine
- Proteinuria (3-5 g/day)
- RBC casts
- Serum BUN and creatinine levels are increased
71
Nephrotic Syndrome
A group of symptoms including protein in the urine (from an increase in glomerular permeability), low blood protein, high cholesterol, and edema, urine may also contain fat (lipiduria)
- Often the result of a different primary disease: toxemia of pregnancy, diabetes, systemic lupus erythromatosus (SLE), or glomerulonephritis
- Loss of blood products reduces blood oncotic pressure, allows water to leave the capillaries, and encourages edema
- Hyperlipidemia results from the liver's response to hypoalbuminemia
- As the liver tries to restore albumin, it also synthesizes lipoproteins
72
Acute Renal Failure
Renal failure is a rapid deterioration of renal function with an accompanying elevation of BUN and plasma creatinine (Uremia)
Phases:
- Oliguria: begins ~1 day after hypotensive event and may last 1-3 weeks
- Diuresis
- Recovery
73
Acute Renal Failure
| Pre-renal/Renal hypoperfusion
- Hypovolemia
- Shock
- Cardiac failure
- Hypotension
74
Acute Renal Failure
| Intrarenal
- Renal ischemia
- Acute tubular necrosis
- Toxins
- Glomerulopathies
- Malignancies
75
Acute Renal Failure
| Urinary obstruction
- Tumors
- Stones
- Clots
- Outlet obstructions (benign prostatic hyperplasia or urethral structures)
76
Acute Tubular Necrosis
| ATN
The most common cause of acute renal failure
- Associated with sepsis, burns, trauma, or severe episode of hypotension ( acute decreases in renal perfusion)
- Ischemia generates oxygen and radicals and inflammatory mediators that cause swelling, injury, and necrosis of renal cells
- One theory states that sloughed cells and cellular debris obstruct the tubules
77
Chronic Renal Failure
Usually results in a progressive an irreversible loss of nephron mass (renal atrophy)
- Results in uremia: the decline of renal function and the accumulation and retention of toxic wastes in the blood
- Demonstrates: anemia, metabolic acidosis, elevated blood creatinine (uremia), hypertension (electrolyte imbalance), cardiovascular disturbances (elevated K+)
78
Chronic Renal Failure
| Stages
1- Lack of "reserve capacity", no problem unless kidneys challenged
2- Renal insufficiency, patient a symptomatic, changes in calcitrol and PTH may be seen
3- Chronic renal failure, moderate to severe symptoms
4- End stage, kidney support needed
79
Systemic Effects of Uremia
- Skeletal: bone reabsorption
- Cardiopulmonary: hypertension
- Neurologic: encephalopathy (uremic toxins)
- Endocrine: decreased growth hormone
- Hematologic: reduced erythropoietin
- GI: retention of urochromes, urea, and acids
- Immune: cell-mediated immunity suppression
- Reproduction: sexual dysfunction, amenorrhea, infertility, decreased libido
80
Anorexia
A lack of desire to eat
81
Nausea
- Symptoms: subjective
| - Signs: increased salivation and tachycardia
82
Vomiting
Forceful emptying of the stomach and intestinal contents through the mouth
- Stimuli initiate the vomiting reflex (in the area postrema of the medulla)
83
Retching
Strong involuntary effort to vomit
| - Deep inspiration, abdominal muscles contract, upper esophageal sphincter remains closed
84
Constipation
Difficult or infrequent defecation
- Anything that reduces motility can cause constipation
- Output should average 150 mL/day, less is constipation
- 2 of the following: straining, lumpy or hard stools, sensation of incomplete evacuation, manual maneuvers used to defecate, sensation of blockage, fewer than 3 bowel movements /week
85
Diarrhea
Increased frequency of defecation and an increase in the fluidity and volume of the feces
- Osmotic: non-absorbable substance draws water into the lumen (laxatives)
- Secretory: excess mucosal secretion due to bacterial toxins or neoplasms
- Motility: diarrhea due to surgical resection
86
Abdominal Pain
```
Parietal Pain
- From parietal peritoneum
- Usually well-localized and sharp because these nerves travel with skin nerves from the same area
Visceral Pain
- Distension, inflammation, ischemia
- Poorly localized, dull pain
Referred Pain
- If intense, is referred to the back, between scapulae
```
87
Dysphagia
Difficulty swallowing due to an obstruction or a disorder that affects esophageal motility (includes voluntary and involuntary processes)
- Normally Lower Esophageal Sphincter maintains a "zone of high pressure" to keep it higher than the pressure in the stomach
- Too much or too little LES tone is harmful
- Usually signaled by regurgitation of undigested food and an unpleasant taste
88
Achalasia
Loss of cells in the autonomic ganglia in the wall of the esophagus
- Results in a dilated esophagus with absent peristalsis and a lower esophageal sphincter that doesn't open
89
Peristalsis
A traveling wave of contraction
| - Controlled by the autonomic nervous system that resides in the bowel wall
90
GI Motility
Increased motility means faster transit time from mouth to anus and therefore less absorption of water and nutrients
Factors that increase bowel motility
- Chyme volume (more volume, more motility)
- Chemical composition
- Osmolarity (substances such as sugar alcohols aren't absorbed and draw water from blood stream)
- Laxatives act by increasing GI motility
91
Gastroesophageal Reflux Disease
| GERD
Two possible signs (one or both):
- Transient relaxations of the lower esophageal sphincter
- Decreased acid clearance from peristalsis failure
Caused by:
- High intraabdominal pressure
- Sliding hiatal hernia acts as a fluid trap for acid
- Ulcers (delay in gastric emptying)
- Drugs
92
Hiatal Hernia
The protrusion of the upper stomach though the diaphragm into the thorax
- Weak diaphragm muscles/short esophagus
- Can lead to dysphagia, heartburn, reflux, and frequent epigastric pain
- Treatment: decrease meal size, remain upright after eating, Nissen fundoplication (making a muscular collar or ring from the stomach)
93
Pyloric Obstruction
Obstruction in the pyloric region, between the body of the stomach and duodenum, also called Gastric Outlet Obstruction
- Newborns: smooth muscle hyperplasia (pyloric stenosis)
- Adults: ulcers or tumors
94
Motility Disorders
- GERD
- Hiatal Hernia
- Pyloric Obstruction
- Intestinal Obstruction
- Ileus
95
Intestinal Obstruction
- Volvulus or torsion: twisting
- Intussusception: telescoping
- Foreign bodies
- Herniation: passing through a muscle layer when it isn't supposed to
- Tumor growth
- Formation of strictures
- Physiological causes: electrolyte imbalances, drugs
96
Ileus
- Paralytic ileus is a failure of bowel motility after surgery (anesthetics, inflammation, opioids, and sympathetic stimulation contribute to ileus)
- Loss of blood supply to a bowel segment (peristalsis stops at this point)
- Loss of neurons in enteric ganglia (also stops peristalsis in a bowel segment)
97
Gastritis
An inflammatory disorder of gastric mucosa and is usually superficial
98
Peptic Ulcer Disease
| PUD
An ulceration that exposes the submucosa to gastric secretions (acid and pepsin)
- Results in autodigestion
99
Gastritis and PUD
Both result in an imbalance in
- Aggressive factors: acid production, pepsin production, histamine (inflammation)
- Defensive factors: mucus, bicarbonate, blood flow
100
Acute Gastritis
Inflammation of the gastric mucosa over a wide area
- Symptoms: vague abdominal discomfort, epigastric tenderness
- Conditions which promote gastritis: uremia, trauma, stress
- Drugs which can promote gastritis: NSAIDs, ethanol, histamine, digitalis
101
Chronic Gastritis
Usually due to the thinning or breakdown of the stomach wall
- Occurs in older adults
- Can result in loss of chief and parietal cells
- Causes diminished secretion of pepsinogen, hydrochloric acid and intrinsic factor
- Intrinsic factor needed to absorb B12, pernicious anemia can result
102
Peptic Ulcer Disease
A discrete mucosal defect in the portions of the GI tract exposed to acid and pepsin secretion and leading to autodigestion (gastric or duodenal ulcers)
- Can be superficial or deep
- H. pylori bacteria cause more than 90% of duodenal ulcers and up to 80% of gastric ulcers
- Risks: smoking, persistent NSAID usage, stress or alcohol
- Prevalence percentage about matches age in years
103
Gastric Ulcers
Ulcers of the stomach
- Usually occur in the antral region
- The primary defect is an increased permeability of the mucosa to H+ ions
- Reflux of bile through a defective pyloric sphincter can also be a cause
- Clinical presentation: pain relieved by food, GI bleeding if not treated
104
Duodenal Ulcers
- More common than gastric ulcers
- More common in men, 2:1
- More common at ages 22-50
Contributing factors:
- Increased acid
- Decreased HCO3- and mucus
- A larger number of acid-secreting cells
- High gastrin levels
- Rapid gastric emptying (abnormal acid-bicarbonate balance)
- H. pylori, NSAIDs, toxins, and enzymes
105
Malabsorption Syndromes
Anything that interferes with digestion, absorption or transport of nutrients in the stomach or small intestines
- Can be caused by a variety of intestinal diseases, vascular problems, or resection of gastric or intestinal tissue
- Maldigestion ---> malabsorption
106
Pancreatic Insufficiency
Insufficient enzyme production by exocrine pancreas
- Lypase, amylase, trypsin, or chymotrypsin
- Causes: pancreatitis, pancreatic carcinoma, pancreatic resection, cystic fibrosis
- Fat maldigestion is the main problem, causes fatty stools and weight loss
107
Lactase Deficiency
Lactase is the enzyme which breaks lactose into galactose and glucose
- Bacteria are happy to take over the job of lactose fermentation
- Results in gas (cramping, pain, flatulence), and osmotic diarrhea
108
Bile Salt Deficiency
Bile salts are needed to emulsify and absorb fats
- Caused by liver disease and bile obstruction
- Poor intestinal absorption causes fatty stools, diarrhea, malabsorption of fat-soluble vitamins (A, D, K, E)
109
Types of Malabsorption Syndromes
- Pancreatic insufficiency
- Lactase deficiency
- Bile Salt Deficiency
110
Inflammatory Bowel Disease
| IBD
The signs and symptoms of Ulcerative Colitis and Crohn's Disease are very similar:
- Abdominal pain
- Bloody/mucus-filled diarrhea
Patients demonstrate an increased risk of colon cancer
- Anything that increases inflammation increases cancer risk
111
Ulcerative Colitis
- Typically limited to the lower 1/3 of the colon (Sigmoid colon and rectum)
- Ulcerations tend to be limited to the mucosa
- Lesions can be erosions, or polyps
- Polyps can resemble precancerous polyps
- Treatment: broad-spectrum antibiotics, steroids, salicylates, and surgery
112
Crohn's Disease
- Tends to run in families
- Age peak: 10-30 years
- Equal gender distribution
- Typically affects the distal ileum, but can cause inflammation anywhere in the GI tract
- "Skip lesions": inflammation of some areas but not others
- Malabsorption of B12 and folic acid leads to anemia
- Treatment is similar to Ulcerative Colitis
113
Celiac Disease
In these patients, gluten acts as a toxin causing loss of villous epithelium in the intestinal tract
- It occurs mainly in whites, and appears to be caused by a combination of dietary, genetic, and immunologic factors
- Children with this disease present with failure to thrive
- Patients also exhibit malabsorption leading to rickets, bleeding, or anemia
- Treated with restrictive diet and vitamin D, iron and folic acid supplements
114
Celiac Crisis
Severe malabsorption resulting in diarrhea, dehydration, and protein loss
115
Diverticula
Herniations of mucosa throughout the muscle layers of the colon wall, especially the sigmoid colon
- Occurs in elderly who consume a diet lacking sufficient fiber and bulk,resulting in weakening of the colonic wall
- Signs & symptoms: constipation alternating with diarrhea, distention and flatulence, may progress to bowel obstruction and/or perforation
- Treatment: antibiotics, fiber, exercise
116
Diverticulosis
Having Diverticula
117
Diverticulitis
Inflamed diverticula
118
Appendicitis
Inflammation of the vermiform appendix (projection from the cecum)
- Possible causes include obstruction and infection
- Symptoms: diffuse epigastric pain, eventually becomes peri-umbilical, then localizes to the right lower quadrant (McBurney's Point)
- Like diverticulitis, the most serious complication is peritonitis
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Anorexia Nervosa
A disorder of body image leads to starvation
- BMI less than 18
- Patients can lose 25-30% of their ideal body weight due to fat and muscle depletion
- Electrolyte imbalance may lead to cardiac failure
Criteria:
- Refusal to maintain body weight (<85%)
- Intense fear of gaining weight/becoming fat
- Undue influence of weight or shape on self-evaluation
- Denial of seriousness of low body weight
- Absence of at least 3 consecutive menstrual cycles
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Bulimia Nervosa
Binge and Purge cycle
- Continual vomiting of acidic chyme can cause pitted teeth, pharyngeal and esophageal inflammation, and tracheoesophageal fistulae
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Bulimia Nervosa Criteria
- Eating in a discrete period of time, an amount of food that is definitely larger than most people would eat
- A sense of lack of control over eating
- Recurrent inappropriate compensatory behavior in order to prevent weight gain, such as self-induced vomiting, misuse of laxatives, diuretics, enemas or other medications, fasting or excessive exercise
- Binging and inappropriate compensation occur, on average 2x/week for 3 months
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Anorexia Nervosa Criteria
- Refusal to maintain body weight (<85% of what expected)
- Intense fear of gaining weight/becoming fat
- Undue influence of weight or shape on self-evaluation
- Denial of seriousness of low body weight
- Absence of at least 3 consecutive menstrual cycles
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Obesity
BMI >120% of normal
- Increased risk of cardiovascular disease, cancer, diabetes, breast, cervical, endometrial, prostatic, colon, rectal, and liver cancer
- Causes: excess caloric intake metabolic problems, number and size of adipose cells, genetics, diabetes, or psychological
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Starvation
- Glycogen stores are depleted (glycogenolysis) and the body tries to produce glucose from non-carbohydrate molecule (gluconeogenesis)
- Once the body has used glucose stores (long-term), it will use fat stores, and finally protein
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Portal Hypertension
Hepatic portal vein receives all nutrient-rich, oxygen-poor blood draining from GI tract
- Pressure 10mmHg (normal: 3mmHg)
- 3 types: Prehepatic, Intrahepatic, Posthepatic
126
Prehepatic Portal Hypertension
A clot, or narrowing of the portal vein
127
Intrahepatic Portal Hypertension
Liver disease interferes with blood flow
128
Posthepatic Portal Hypertension
Right heart failure
129
Cirrhosis of the Liver
An irreversible inflammatory disease that disrupts liver structure
- 3 types: Alcoholic, Biliary, Post-Necrotic
- Decreased hepatic function due to nodular and fibrotic tissue synthesis (hepatic fibrosis)
- Biliary channels become obstructed and cause portal hypertension
- Due to hypertension, blood can be shunted away from liver and hypoxic necrosis develops
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Alcoholic Cirrhosis
Oxidative damage to hepatocytes
131
Biliary Cirrhosis
- Primary biliary cirrhosis is an autoimmune disorder
| - Secondary biliary cirrhosis is caused by an obstruction
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Post-Necrotic Cirrhosis
It may follow viral hepatitis, dietary deficiencies, and a number of chronic diseases
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Hepatic Encephalopathy
Liver fails to adequately filter toxins, which then affect brain function (ammonia)
- Increased permeability of the blood-brain barrier
- Astrocytes are most affected, they clean up the brain and die from ammonia toxicity
- Ammonia metabolized to glutamate, an excitatory transmitter which can lead to excitotoxicity
- Many other blood chemicals involved
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Hyperbilirubinemia
Heme to Bilirubin
| - 3 types: Prehepatic, Hepatic, Post-hepatic
135
Prehepatic Hyperbilirubinemia
Before conjugation to become water soluble
| - Hemolytic jaundice
136
Hepatic Hyperbilirubinemia
- Hepatitis (viral or chemical)
| - Cirrhosis
137
Post-hepatic Hyperbilirubinemia
After conjugation, it is now water soluble
| - Biliary obstruction
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Ascites
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Fluid accumulates in peritoneal cavity
Caused by:
- Cirrhosis of the liver
- Heart failure
- Constrictive pericarditis
- Abdominal cancer
- Nephrotic syndrome
- Malnutrition
Pathophysiology:
- Portal hypertension
- Vasodilation
- Hepatocyte failure
- Sodium retention
```
139
Viral Hepatitis Phases
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Prodromal Phase
- From the time of exposure until jaundice appears
Icteric Phase
- Yellow phase, painful swollen liver
Recovery Phase
- Jaundice resolution (6-8 weeks)
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Viral Hepatitis
Infections that attack the liver
- Lab tests: liver enzyme levels (ALT, AST), prolonged bleeding times and low serum albumin levels
- Immunology tests: acute disease/recent infection-IgM, exposure/immunity-IgG, direct tests for the virus
141
Hepatitis Viruses
- A, B, C, D, E, F
- Non A-E: diagnosed by exclusion of A-E
- Other viruses can also cause hepatitis (CMV and EBV)
142
Hepatitis A
Pathology:
- Incubation period: prodromal period is 14-45 days
- Viral replication occurs in the liver
- Virus is excreted through the biliary system into the feces (fecal/oral transmission)
Signs & Symptoms:
- Nausea, vomiting, loss of appetite, malaise, jaundice, diarrhea
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Hepatitis B
Healthcare workers, IV drug users, Prisoners, and Homosexuals at risk
Pathology:
- After initial inoculation (directly into the blood or through mucus membranes) the virus travels to the liver where it replicates in hepatocytes
Prevention:
- "Universal Precautions" for healthcare workers
- Condoms, needle exchange, and methadone programs for IV drug users
- HBV vaccine, 3-dose series
144
Gallbladder Disorders
Most problems arise from 1 of 2 disorders
| - Cholecystitis and Cholelithiasis
145
Cholecystitis
Infection and inflammation of the common bile duct
146
Cholelithiasis
Gallstone formation
- 2 types: Cholesterol (bile duct is saturated with cholesterol) and Pigmented (associated with cirrhosis)
- Risks: obesity, middle-age, female, and diseases of the gallbladder, pancreas, or ileum
- Theories: an enzyme defect in bile salt formation, increased cholesterol synthesis, decreased secretion of bile acids to emulsify fats, combinations of all of the above
147
Cholelithiasis
| Signs, Symptoms & Treatment
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Signs & Symptoms:
- Heartburn/epigastric discomfort
- RUQ abdominal pain (biliary colic)
- Intolerance eating fatty food
- Jaundice
- Leukocytosis
Treatment:
- Laparoscopic cholecystectomy
- Alternative - administration of stone-dissolving medicines
```
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Pancreatitis
Inflammation of the pancreas
- Caused by inflammation or injury to the pancreatic ducts and cells causing a leakage of pancreatic enzymes
- Gallstones can cause obstruction of the pancreatic ducts which damages the tissue
- Leaking enzymes cause autodigestion of pancreas and surrounding tissue
- Toxic enzymes can also be released into the bloodstream and injure other vital organs
149
Pancreatitis Signs & Symptoms
- Epigastric pain radiating to the back
- Fever and leukocytosis
- Hypotension and hypovolemia (enzymes increase vascular permeability)
- Leakage of digestive enzymes into the blood, and serum amylase level rises (normally, there is little amylase in the serum)
- Increased serum lipase levels
