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Pathophysiology > Patho Unit 7 > Flashcards

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
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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
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3
Q

Coughing

A

A protective reflex that cleans airways with an explosive expiration to remove foreign particles

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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
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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
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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
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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
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8
Q

Hypoventilation

A

Alveolar gas exchange insufficient for metabolic demands

  • Increased PCO2
  • Respiratory Acidosis
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9
Q

Hyperventilation

A

Alveolar gas exchange greater than metabolic demands

  • Decreased PCO2
  • Respiratory Alkalosis
  • Causes: anxiety, head injury, pain, Low PO2
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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%)
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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

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12
Q

Pleuritic Pain

A

Sharp, stabbing pain associated with breathing

- From disorders affecting the pleurae, airways, and chest wall

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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
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14
Q

Perfusion

A

Q = the amount of blood that flows through the lung capillaries each minute

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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)
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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)
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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
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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
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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
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20
Q

Problem with Blood Arriving to be Oxygenated

A
  • Cardiac defects

- Arteriovenous malformations in lung

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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
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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
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23
Q

Pleural Effusion

A

Any abnormal or excess liquid in the alveoli interferes with external respiration - dyspnea
2 types:
- Transudative Effusion
- Exudative Effusion

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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

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25
Q

Exudative Effustion

A

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)
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26
Q

Bronchiectasis

A

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
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27
Q

Bronchiolitis

A

Chronic inflammation of the Bronchioles

  • Fibrous connective tissue replaces functional tissue (such as smooth muscle)
  • Narrowing of the bronchiole lumen
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28
Q

Pulmonary Edema

from Heart Disease

A

1- Valvular Dysfunction, Coronary Artery Disease, Left Ventricular Dysfunction
2- Increased pressure in left atrium
3- Increased pulmonary capillary hydrostatic pressure
4- Pulmonary edema

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29
Q 
Pulmonary Edema
(from Injury to Capillary Endothelium)
A

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

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30
Q

Pulmonary Edema

from Blockage of Lymphatic vessels

A

1- Blockage of Lymphatic Vessels
2- Fluid not removed from interstitial space
3- Fluid accumulates in interstitial space
4- Pulmonary edema

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31
Q

Acute Respiratory Distress Syndrome

ARDS

A

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
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32
Q

ARDS

Step 1

A
  • 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
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33
Q

ARDS

Step 2

A

The damaged alveolar epithelial barrier breaks, allowing flooding of the alveolar space and making it difficult or impossible for oxygen to diffuse into capillaries

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34
Q

ARDS

Step 3

A

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
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35
Q

Type II Alveolar Cells

A

Make surfactant to reduce lung surface tension

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36
Q

ARDS

Step 4

A
  • Protein and enzymes make a jelly-like substance called the hyaline membrane
  • Not much gas exchange can take place
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37
Q

Asthma

A
  • 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)
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38
Q

Chronic Obstructive Pulmonary Disease

COPD

A
  • Chronic Bronchitis and Emphysema
  • Signs and Symptoms: exercise intolerance, dyspnea, wheezing, productive cough, hypoxemia causing polycythemia and cyanosis, pulmonary hypertension, and congestive heart failure
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39
Q

Emphysema

A

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
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40
Q

a1-antitypsinase

A

Blocks Neutrophil Elastase and prevents it from breaking down elastin

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41
Q

Emphysema Signs and Symptoms

A 
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
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42
Q

Chronic Bronchitis

A

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
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43
Q

COPD Treatment

A

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
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44
Q

Pneumonia

A

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
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45
Q

Types of Pneumonia

A

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

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46
Q

Pneumonia Signs and Symptoms

A
  • Productive cough
  • Pleuritic chest pain, chills, malaise
  • Inspiratory crackles
  • Evidence of infiltrates on x-ray is the key diagnostic feature
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47
Q

Pneumonia Treatment

A

Depends on where the disease was acquired, the causative organism, and the severity of the disease

  • Antibiotics
  • Supplemental O2
  • Mechanical ventilation in severe cases
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48
Q

Tuberculosis

A

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
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49
Q

Factors that contribute to Tuberculosis

A
  • 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
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50
Q

Pulmonary Embolism

A

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
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51
Q

Pulmonary Hypertension

A

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)
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52
Q

Cor Pulmonale

A

Pulmonary-Related Heart Disease, right ventricular disease due to pulmonary hypertension
- Manifested by: chest pain, tricuspid murmur, pulmonary valve murmur

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53
Q

Renal Threshold

A

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

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54
Q

Proteinuria

A
  • 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
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55
Q

Blood Urea Nitrogen

BUN

A

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

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56
Q

Creatinine

A

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
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57
Q

Glomerular Filtration Rate

GFR

A

Measures how much blood is filtered through the glomerulus and becomes filtrate

  • Normal > 90 mL/min
  • Decreased in kidney disease
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58
Q

GFR Stages in Kidney Disease

A 
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
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59
Q

Urine

A
  • 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
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60
Q

Urinalysis

A
  • 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
Q

Upper Urinary Tract Obstruction

A 
Kidney
  - Stones
  - Blood vessel compression
  - Tumor
  - Scarring/Fibrosis
Ureter
  - Stones
  - Tumor
62
Q

Lower Urinary Tract Obstruction

A 
Bladder
  - Neurogenic bladder
Urethra
  - Urethral stricture
  - Prostate enlargement (in men)
  - Pelvic organ prolapse 
  - Obstruction of urethra
63
Q

Renal Calculi

Kidney Stones

A

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
Q

Neurogenic Bladder

A

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
Q

Urinary Tract Infection

UTI

A

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
Q

Cystitis

A

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
Q

Pyelonephritis

A

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
Q

Glomerulonephritis

A

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
Q

Glomerulonephritis

common types

A
  • Post-streptococcal (PSGN)
  • Rapidly progressing (crescentic)
  • Membranoproliferative and minimal change disease (MCD)
  • IgA nephropathy (Berger’s disease)
70
Q

Glomerulonephritis

lab findings

A
  • RBCs in urine
  • Proteinuria (3-5 g/day)
  • RBC casts
  • Serum BUN and creatinine levels are increased
71
Q

Nephrotic Syndrome

A

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
Q

Acute Renal Failure

A

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
Q

Acute Renal Failure

Pre-renal/Renal hypoperfusion

A
  • Hypovolemia
  • Shock
  • Cardiac failure
  • Hypotension
74
Q

Acute Renal Failure

Intrarenal

A
  • Renal ischemia
  • Acute tubular necrosis
  • Toxins
  • Glomerulopathies
  • Malignancies
75
Q

Acute Renal Failure

Urinary obstruction

A
  • Tumors
  • Stones
  • Clots
  • Outlet obstructions (benign prostatic hyperplasia or urethral structures)
76
Q

Acute Tubular Necrosis

ATN

A

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
Q

Chronic Renal Failure

A

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
Q

Chronic Renal Failure

Stages

A

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
Q

Systemic Effects of Uremia

A
  • 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
Q

Anorexia

A

A lack of desire to eat

81
Q

Nausea

A
  • Symptoms: subjective

- Signs: increased salivation and tachycardia

82
Q

Vomiting

A

Forceful emptying of the stomach and intestinal contents through the mouth
- Stimuli initiate the vomiting reflex (in the area postrema of the medulla)

83
Q

Retching

A

Strong involuntary effort to vomit

- Deep inspiration, abdominal muscles contract, upper esophageal sphincter remains closed

84
Q

Constipation

A

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
Q

Diarrhea

A

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
Q

Abdominal Pain

A 
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
Q

Dysphagia

A

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
Q

Achalasia

A

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
Q

Peristalsis

A

A traveling wave of contraction

- Controlled by the autonomic nervous system that resides in the bowel wall

90
Q

GI Motility

A

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
Q

Gastroesophageal Reflux Disease

GERD

A

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
Q

Hiatal Hernia

A

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
Q

Pyloric Obstruction

A

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
Q

Motility Disorders

A
  • GERD
  • Hiatal Hernia
  • Pyloric Obstruction
  • Intestinal Obstruction
  • Ileus
95
Q

Intestinal Obstruction

A
  • 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
Q

Ileus

A
  • 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
Q

Gastritis

A

An inflammatory disorder of gastric mucosa and is usually superficial

98
Q

Peptic Ulcer Disease

PUD

A

An ulceration that exposes the submucosa to gastric secretions (acid and pepsin)
- Results in autodigestion

99
Q

Gastritis and PUD

A

Both result in an imbalance in

  • Aggressive factors: acid production, pepsin production, histamine (inflammation)
  • Defensive factors: mucus, bicarbonate, blood flow
100
Q

Acute Gastritis

A

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
Q

Chronic Gastritis

A

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
Q

Peptic Ulcer Disease

A

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
Q

Gastric Ulcers

A

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
Q

Duodenal Ulcers

A
  • 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
Q

Malabsorption Syndromes

A

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
Q

Pancreatic Insufficiency

A

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
Q

Lactase Deficiency

A

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
Q

Bile Salt Deficiency

A

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
Q

Types of Malabsorption Syndromes

A
  • Pancreatic insufficiency
  • Lactase deficiency
  • Bile Salt Deficiency
110
Q

Inflammatory Bowel Disease

IBD

A

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
Q

Ulcerative Colitis

A
  • 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
Q

Crohn’s Disease

A
  • 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
Q

Celiac Disease

A

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
Q

Celiac Crisis

A

Severe malabsorption resulting in diarrhea, dehydration, and protein loss

115
Q

Diverticula

A

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
Q

Diverticulosis

A

Having Diverticula

117
Q

Diverticulitis

A

Inflamed diverticula

118
Q

Appendicitis

A

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
119
Q

Anorexia Nervosa

A

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

120
Q

Bulimia Nervosa

A

Binge and Purge cycle
- Continual vomiting of acidic chyme can cause pitted teeth, pharyngeal and esophageal inflammation, and tracheoesophageal fistulae

121
Q

Bulimia Nervosa Criteria

A
  • 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
122
Q

Anorexia Nervosa Criteria

A
  • 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
123
Q

Obesity

A

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
124
Q

Starvation

A
  • 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
125
Q

Portal Hypertension

A

Hepatic portal vein receives all nutrient-rich, oxygen-poor blood draining from GI tract

  • Pressure 10mmHg (normal: 3mmHg)
  • 3 types: Prehepatic, Intrahepatic, Posthepatic
126
Q

Prehepatic Portal Hypertension

A

A clot, or narrowing of the portal vein

127
Q

Intrahepatic Portal Hypertension

A

Liver disease interferes with blood flow

128
Q

Posthepatic Portal Hypertension

A

Right heart failure

129
Q

Cirrhosis of the Liver

A

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
130
Q

Alcoholic Cirrhosis

A

Oxidative damage to hepatocytes

131
Q

Biliary Cirrhosis

A
  • Primary biliary cirrhosis is an autoimmune disorder

- Secondary biliary cirrhosis is caused by an obstruction

132
Q

Post-Necrotic Cirrhosis

A

It may follow viral hepatitis, dietary deficiencies, and a number of chronic diseases

133
Q

Hepatic Encephalopathy

A

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
134
Q

Hyperbilirubinemia

A

Heme to Bilirubin

- 3 types: Prehepatic, Hepatic, Post-hepatic

135
Q

Prehepatic Hyperbilirubinemia

A

Before conjugation to become water soluble

- Hemolytic jaundice

136
Q

Hepatic Hyperbilirubinemia

A
  • Hepatitis (viral or chemical)

- Cirrhosis

137
Q

Post-hepatic Hyperbilirubinemia

A

After conjugation, it is now water soluble

- Biliary obstruction

138
Q

Ascites

A 
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
Q

Viral Hepatitis Phases

A 
Prodromal Phase
  - From the time of exposure until jaundice appears
Icteric Phase
  - Yellow phase, painful swollen liver
Recovery Phase
  - Jaundice resolution (6-8 weeks)
140
Q

Viral Hepatitis

A

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
Q

Hepatitis Viruses

A
  • 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
Q

Hepatitis A

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

143
Q

Hepatitis B

A

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
Q

Gallbladder Disorders

A

Most problems arise from 1 of 2 disorders

- Cholecystitis and Cholelithiasis

145
Q

Cholecystitis

A

Infection and inflammation of the common bile duct

146
Q

Cholelithiasis

A

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
Q

Cholelithiasis

Signs, Symptoms & Treatment

A 
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
148
Q

Pancreatitis

A

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
Q

Pancreatitis Signs & Symptoms

A
  • 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

Pathophysiology (11 decks)

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