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Pathophysiology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

what are the two basic processes in respiratory physiology

A

ventilation
gas exchange

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2
Q

what categories do all lung pathologies fall into

A

hypoventilation
ventilation/perfusion mismatching
impaire diffusion

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3
Q

What factors affect pulmonary ventilation

A

compliance

elasticity

surface tension in the alveoli

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4
Q

high compliance =

A

ease of expansion

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5
Q

low compliance=

A

difficulty in expansion

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6
Q

how does elasticity affect the lungs

A

allow lungs to expand

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7
Q

what controls the surface tension in the alveoli

A

surfactant

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8
Q

low compliance is due to what 4 things

A

scarred lung tissue

excessive fluid in lungs

Deficiency in surfactant -leads to atelectasis

impeded lung expansion

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9
Q

how does smooth muscle tone dramatically affect flow in the lung

A

Para. cholinergic stimulation causes constriction and increased mucus production (M2 and M3)

Sym adrenergic stimulation (β2) causes dilation

Inflammatory mediators like histamine (H1) and leukotrienes

Environmental insults-constriction (irritant receptors)

PCO2 causes inverse effects on tone (high CO2dilation, and vice versa)

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10
Q

what factors affect diffusion in alveoli

A

thickness of membrane

surface are of membrane

diffusion coefficients

partial pressure differences

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11
Q

what conditions lead to respiratory failure

A

Impaired function of the respiratory center

Weakness or paralysis of the respiratory muscles

Chest wall deformities

Airway obstruction

Disease of the airways or lungs

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12
Q

what is a major symptom of respiratory failure

A

dyspnea

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13
Q

what is a major consequence in alteration in blood gas concentration

A

hypoxemia -low O2 in blood

hypercapnia- increased CO2

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14
Q

what are signs and symptoms of pulmonary disease

A

dyspnea
abnormal breath patterns
hypoventilation/hyperventilation
cough
hemoptysis
cyanosis
clubbing of fingernails
abnormal sputum
pain
chest wall pain

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15
Q

what is dyspnea

A

subjective sensation of uncomfortable breathing

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16
Q

what is orthopnea

A

dyspnea when a person is lying down

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17
Q

what are two abnormal breathing patterns

A

-Kussmaul respirations (hyperpnea)

Cheyne stokes respirations

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18
Q

what is Cheyne Stokes

A

neurological origin (Alternating periods of deep and shallow breathing; apnea lasting 15 to 60 seconds, followed by ventilations that increase in volume until a peak is reached, after which ventilation decreases again to apnea

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19
Q

what classifies a cough as chronic

A

> 3 weeks

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20
Q

what is an acute cough

A

2-3 weeks

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21
Q

what is pleural pain

A

Is usually sharp or stabbing in character.

Infection and inflammation of the parietal pleura (pleuritis or pleurisy) can cause pain when the pleura stretch during inspiration and are accompanied by a pleural friction rub

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22
Q

what is the most common pain caused by pulmonary diseases

A

pleural pain

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23
Q

what is chest wall pain

A

may be from the airways

may be from muscle or rib pain

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24
Q

what are conditions caused by pulmonary disease

A

hypercapnia

hypoxemia

pulmonary edema

acute respiratory failure

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25
Q

what is hypercapnia

A

increase CO2 in blood concentration

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26
Q

what causes hypercapnia

A

hypoventilation
V/Q mismatch
resp muscle fatigue

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27
Q

what is hypoxemia

A

reduction in blood O2 levels

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28
Q

what are gradient increases in respiratory diseases

A

low V/Q ratios
anatomic shunts
diffusion block

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29
Q

what are clinical manifestations of hypoxemia

A

impaired function of vital centers

activation of compensatory mechanisms (similar to anemia)

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30
Q

what is a result of excessive deoxy-Hb

A

cyanosis

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31
Q

who are less prone to cyanosis even though they may be hypoxic

A

anemia

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32
Q

how does polycythemia lead to cyanosis without hypoxia

A

they have a higher Hgb level.

decrease of 5 deoxy hemoglobin results in cyanosis but they still have normal level hemoglobin

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33
Q

where do you see central cyanosis

A

tongue lips gums

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34
Q

where do you see peripheral cyanosis

A

extremities
nose
ears

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35
Q

what is the O2 extraction ratio

A

ratio of O2 consumption (by tissues) to delivery (via microcirculation);

average is about 25% (heart is ~60%) meaning a significant safety factor exists at the cellular level as well

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36
Q

what is hypoxia influenced by

A

supply and demand

-Decrease in arterial O2 content
-Decrease in blood flow
-Inability of cells to use O2

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37
Q

what are factors that increase O2 consumption

A

-Surgery, trauma, burns
-Inflammation and sepsis
-Pyrexia
-Seizures
-Agitation/anxiety/pain
-Adrenergic drugs
-Weaning from ventilation

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38
Q

what are factors that decrease O2 consumption

A

-Sedation/analgesics
-Paralysis
-Shock
-Mechanical vent
-Antipyretics
-Starvation

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39
Q

what are the two stages of hypoxia

A

carotid body drive

slow rise in ventilation (ventilation acclimatization)
-chemoreceptor involvement
-kidney involvement

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40
Q

what is cardiovascular acclimatization

A

-Increased pulmonary blood flow (and vasodilation systemically)

-Increased RBC production

-Improved transport of O2 and CO2

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41
Q

define pneumothorax

A

a chest wall injury that results in air in the pleural space, preventing ventilation

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42
Q

what is atelectasis

A

an incomplete expansion of part of the lung – “collapse”

Many causes including obstruction, compression due to pneumothorax, effusion, tumor or loss of surfactant

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43
Q

describe restrictive lung disorders

A

Characterized by reduced compliance-Chest wall is deformed, traumatized, immobilized, or made heavy by fat

Takes much more effort to expand lungs during inspiration resulting in dyspnea

Increased rate of shallow breaths (TV is reduced)

Reduced forced vital capacity; V/Q mismatching; reduces O2 diffusion and causes hypoxemia

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44
Q

what are common types of restrictive lung disorders

A

aspiration
atelectasis
bronchiectasis
pulmonary fibrosis
pulmonary edema
ARDS

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45
Q

what is bronchiectasis

A

Persistent abnormal dilation to the bronchi.

Chronic inflammation of the bronchi leads to destruction of elastic and muscular components of their walls-it generally occurs in conjunction with other respiratory illness/injury

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46
Q

what are the three kinds of bronchial dilations

A

cylindrical

saccular

varicose

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47
Q

what is a cylindrical bronchial dilation

A

cylindrical bronchiectasis) with symmetrically dilated airways, as seen after pneumonia and is reversible

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48
Q

what is saccular bronchial dilations

A

(saccular bronchiectasis),
in which the bronchi become large and balloon like

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49
Q

what is varicose bronchial dilations

A

(varicose bronchiectasis), in which constrictions and dilutions deform the bronchi, creating a bulbous appearance.

In both varicose and saccular the small bronchial divisions are plugged with secretions or obliterated by fibrosis

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50
Q

what are the primary symptoms of bronchiectasis

A

Chronic productive cough

Commonly associated with recurrent lower respiratory infections.

Voluminous amounts of foul-smelling purulent sputum.

Clubbing of the fingers from chronic hypoxemia.

Hemoptysis can occur

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51
Q

how does heart conditions cause pulmonary edema

A
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52
Q

how does injury to capillary endothelium cause pulmonary edema

A
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53
Q

how does blockage of lymphatic vessels cause pulmonary edema

A
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54
Q

describe obstructive pulmonary disease

A

airway obstruction that is worse with expiration

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55
Q

what are common signs of obstructive pulmonary disease

A

dyspnea
wheezing

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56
Q

what are the common obstructive pulmonary disorders

A

asthma
emphysema
chronic bronchitis

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57
Q
A

chronic bronchitis

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58
Q
A

emphysema

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59
Q
A

asthma

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60
Q

what is the extrinsic trigger of asthma

A

produce symptoms in people who are predisposed to asthma (type 1-hypersensitivity reaction against a specific allergen)

-Family history of allergy
-Early onset

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61
Q

what is intrinsic trigger of asthma

A

exert effects through inflammatory response and vagal reflexes;

make airways hyperresponsive to nonallergic stimuli;

also induce bronchospasm

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62
Q

what is the mechanisms of asthma

A

Early-bronchoconstriction w/i 10-20 minutes of exposure; key event is release of chemical mediators from sensitized mast cells

Late-develops 4-8 hours later; involves prolonged inflammation and increased airway responsiveness

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63
Q

asthma chart

A
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64
Q

what is the early response in asthma

A

Antigen exposure to the bronchial mucosa activates dendritic cells (antigen-presenting cells) to present the antigen to CD4+ T cells.

Interleukin 4 (IL-4) stimulates B-cell activation and the production of antigen-specific IgE.

IL-5 stimulates the activation of eosinophils, which contributes to increased bronchial hyperresponsiveness, fibroblast proliferation, epithelial injury, and airway scarring.

IL-8 activates neutrophils that cause a more exaggerated inflammatory response.
IL-13 impairs mucociliary clearance, enhances fibroblast secretion, and contributes to bronchoconstriction.

IL-17 increases neutrophilic inflammation.

IL-22 stimulates airway epithelial cells, causing further innate and adaptive immune responses

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65
Q

what do interleukins do

A

class of glycoproteins produced by leukocytes for regulating immune response

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66
Q

symptoms of asthma

A

episodic wheezing and feelings of chest tightness to an acute, immobilizing attack

expiration becomes prolonged because of airway obstruction

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67
Q

what happens with prolonged asthma attack

A

air becomes trapped in lungs → hyperinflation → more energy needed to overcome tension → dyspnea and fatigue → alveolar ventilation declines which leads to mismatching of ventilation and perfusion → hypoxemia and hypercapnia

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68
Q

what is pathogenesis of COPD

A

Inflammation and fibrosis of the bronchial wall

Hypertrophy of the submucosal glands and hypersecretion of mucus

Loss of elastic lung fibers and alveolar tissue

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69
Q

what are examples of COPD

A

Emphysema (breakdown of elastin and other alveolar wall fibers)

Chronic Bronchitis (inflammation of major and small airways)

The major difference between these is the respiratory responsiveness to hypoxia, although patients often exhibit some degree of both

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70
Q

how is COPD diagnosis

A

diagnosed by two numerical values that are assessed via spirometry: FEV1 and FVC.

FEV1 is Forced Expiratory Volume in 1 second, or the amount of air that can be blown out of the lungs in the first 1 second.

FVC, or Forced Vital Capacity, refers to the total amount of air that a person can exhale.

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71
Q

what is FEV1

A

Forced Expiratory Volume in 1 second, or the amount of air that can be blown out of the lungs in the first 1 second.

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72
Q

what is FVC

A

Forced Vital Capacity, refers to the total amount of air that a person can exhale

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73
Q

COPD chart

A
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74
Q

what are the clinical features of emphysema

A

Proportionate loss of ventilation and perfusion area in the lungs – compensate by overventilating

Marked dyspnea

Prominent use of accessory breathing muscles

Airway collapse on expiration (pursed lip breathing to help this)

Work of breathing is difficult, eating is difficult → weight loss

increased AP diameter (barrel chest)

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75
Q

what are the clinical symptoms
of bronchitis

A

Excessive bronchial secretions and airway obstruction that causes mismatched ventilation and perfusion; cannot compensate by overventilating → hypoxemia and cyanosis

Shortness of breath and progressive decline in exercise tolerance

Cannot maintain normal blood gases → eventually develop pulmonary hypertension and RHF with pulmonary edema

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76
Q

respiratory disease COPD

A
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77
Q

what are the comorbidities of COPD

A
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78
Q

what are the manifestations of PE

A

dyspnea and ↑ respiratory rate;

infarction causes pain associated with breathing (inspiration);

gas exchange problems (hypoxemia)

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79
Q

pulmonary vascular disorders chart

A
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80
Q

describe pulmonary HTN

A

Most is secondary to another disease process (LHF, congenital heart defects, PE, hypoxemia)

Cor pulmonale – RHF resulting from 1° lung disease and prolonged pulmonary hypertension

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81
Q

pulmonary HTN chart

A
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82
Q

what is ARDS

A

Sudden, severe (fulminant) form of respiratory failure characterized by acute lung inflammation and diffuse alveolocapillary injury

Injury to the pulmonary capillary endothelium

Inflammation and platelet activation

Surfactant inactivation
Atelectasis (collapse of lung tissue)

Lung damage often the result of inhalation (e.g. smoke or water), sepsis, infection, trauma (chest

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83
Q

ARDS chart

A
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84
Q

ARDS alveoli

A
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85
Q

what is the clinical progression of ARDs

A

Dyspnea and hypoxemia

Hyperventilation ->Respiratory alkalosis

Decreased tissue perfusion, organ dysfunction, metabolic acidosis (loss of HCO3- production by the kidneys)

Decreased tidal volume and hypoventilation –>Respiratory acidosis

Further hypoxemia

Hypotension, decreased cardiac output, death

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86
Q

describe upper airway of children

A

airways smaller in diameter (increase through childhood) = more obstruction problems

87
Q

children conducting airways are present

A

at birth

88
Q

infants up to 2-3 months are

A

obligatory nose breathers

nasal congestion is serious threat to young infants

89
Q

describe lower airways and parenchyma in children

A

infants and young children continue to form new alveoli for several years after birth

90
Q

what is surfactant

A

a lipid protein mixed produced by alveolar type II cells

91
Q

what does surfactant do

A

maintains alveolar expansion

decreases alveolar surface tension

92
Q

what causes respiratory distress syndrome and hyaline membrane disease in infants

A

surfactant deficiency in premature infants

93
Q

when is surfactant produced

A

20-24weeks gestation

secreted into airways by 30 weeks gestation

94
Q

which infants are more likely to develop respiratory distress syndrome

A

infants of diabetic mothers
infants of c sections (esp elective c section)

bc the labor associated with catecholamine and steroid surge do not occur which decreases pulmonary surfactant release

95
Q

infants have ____ chest wall compliance

A

high

particularly premature infants

96
Q

what kind of breathing do children have

A

paradoxic or diaphragmatic breathing

During inspiration in the young child, air is drawn in by the downward movement of the diaphragm, but the resulting negative pressure causes the “soft” chest wall to be drawn inward

97
Q

the metabolic rate of a child is ____than an adults

A

higher

98
Q

describe oxygen consumption in children

A

oxygen consumption (VO2) is greater per unit of body weight in children than in adults

99
Q

what can cause acute upper airway obstructions in children

A

infections
foreign body
angioedema
sleep apnea
trauma

100
Q

what causes chronic upper airway obstructions in children

A

Congenital malformations of the airway,

cartilaginous weakness,

vocal cord paralysis,

subglottic stenosis

101
Q

what is a major sign of airway obstruction

A

stridor

102
Q

loud gasping snore suggests

A

enlarged tonsils or adenoids

103
Q

stridor during inspiration suggests

A

airway is compromised at the level of the supralaryngeal structures (epiglottis/ arytenoid cartilages), vocal cords and glottic opening

104
Q

expiratory stridor or central wheezes suggest

A

narrowing or collapse of lower trachea or bronchi

105
Q

airway noise heard during inspiration and expiration

A

fixed obstruction at the vocal cords

106
Q

if cough is croupy or low pitched

A

Suspect tracheal pathology

107
Q

what is one of the leading causes of morbidity in the first year of life

A

disorders of the lower airways

108
Q

what are examples of lower airway disorders

A

respiratory distress syndrome of the newborn
bronchopulmonary dysplasia
asthma
cystic fibrosis
infections
ARDS

109
Q

what is the major cause of pulmonary disease in infants

A

bronchopulmonary dysplasia

110
Q

what causes bronchopulmonary dysplasia

A

lung immaturity and inflammation coupled to mechanical ventilation

proper lung development is arrested with poor alveolar formation-> reducing surface area for gas exchange

111
Q

what is Cystic Fibrosis

A

autosomal recessive multisystem disease

CFTR gene

abnormality of chloride transport

112
Q

what happens in Cystic fibrosis

A

Abnormal secretions cause obstructive problems within the respiratory, digestive, and reproductive tracts.

Exocrine or mucus-producing glands secrete abnormally thick mucus as a result of defective epithelial ion transport

113
Q

typical features of CF

A

mucus plugging
chronic inflammation
infection of the small airways

114
Q

how does chronic inflammation impact CF

A

leads to:
hyperplasia of goblet cells
bronchiectasis
PNA
hypoxia
fibrosis

115
Q

what is most often the cause of death in CF

A

respiratory failure

116
Q

what are clinical manifestations of CF

A

persistent cough or wheeze
sputum production
recurrent or severe PNA
clubbing

117
Q

CF flow chart

A
118
Q

what is the most common cause of unexplained infant death in western world

A

SIDS

119
Q

what is the possible genetic contribution to SIDS

A

ion channel/protein association with primary electrical heart disease (long QT syndrome)

120
Q

Respiratory distress syndrome flow chart

A
121
Q

what is the functional unit of the kidney

A

nephron

122
Q

what is the renal blood flow amount

A

1000-1200ml/min

20-25% of cardiac output

123
Q

what is the major function of the kidney

A

regulate volume
regulate osmolality
electrolyte balance
balance acid-base concentrations
help regulate blood pressure

124
Q

what are the secondary functions of the kidney

A

excretion of metabolic waste products

125
Q

what is an endocrine function of the kidney

A

producing erythropoietin
producing 1, 25 dihydroxyvitamin D3

126
Q

where does ultrafiltration occur in the kidney

A

glomerulus

127
Q

where dose selective resorption and secretion of water and filtered substances occur

A

along the tubules

128
Q

Renal disease can be broadly categorized in the following manner:

A

Acute Renal Failure– kidneys abruptly stop working entirely or almost entirely, but may eventually recover normal or nearly normal function

Chronic Renal Failure– progressive loss of function of more and more nephrons that gradually decreases overall kidney function

129
Q

common signs/symptoms of kidney dysfunction

A
130
Q

what acute renal failure

A

Clinical syndrome characterized by rapid decline of glomerular filtration rate (GFR), azotemia, and perturbation of acid-base, fluid, and electrolyte homeostasis

131
Q

what are the 3 categories of acute renal failure

A

pre-renal
post renal
intrinsic

132
Q

ARF picture

A
133
Q

what are contributing factors for UTI

A

host and bacterial factors

134
Q

what conditions predispose to UTIs

A

Obstructions
-Enlarged prostate
-Pregnancy
-Calculi
Diabetes
Catheters

135
Q

what is prerenal ARF

A

renal injury due to hypoperfusion or ischemia to the kidney

136
Q

what is the most common cause of Acute renal failure

A

pre renal

prolonged renal ischemia from decreased renal perfusion

137
Q

pre renal ARF is rapidly reversible upon

A

restoration of renal blood flow and glomerular ultrafiltration pressure

there may be long term consequences though such as loss of capillaries

138
Q

what is post renal ARF caused by

A

acute obstruction of urinary outflow

139
Q

what does post renal ARF lead to

A

hydronephrosis,
severe damage to the renal parenchyma, and
intrinsic ARF if prolonged

140
Q

what is a urinary tract obstruction

A

blockage of urine flow within the urinary tract

141
Q

what is the severity of obstruction based on

A

Location

Completeness

Involvement of one or both upper urinary tracts

Duration

Nature and/or cause

142
Q

what can cause an obstruction in the urinary tract

A

anatomic or functional defect

143
Q

what are upper urinary tract obstruction complications

A

Hydroureter: Dilation of the ureters

Hydronephrosis: Dilation of the renal pelvis and calyces

Ureterohydronephrosis: Dilation of both the ureters and the renal pelvis and calyces

Tubulointerstitial fibrosis: Deposition of excessive amounts of extracellular matrix

Leads to excess cellular destruction and death of nephrons

144
Q

Compensatory hypertrophy and hyperfunction in the kidney:

A

Partially counteracts the negative consequences of unilateral obstruction.

145
Q

what is post obstructive diuresis

A

Is caused by relief of the obstruction in the upper urinary tract

May cause fluid and electrolyte imbalance.

146
Q

what is another name for kidney stones

A

renal calculi

urolithiasis

147
Q

what are kidney stones

A

Masses of crystals, protein, or mineral salts form in the urinary tract and may obstruct the urinary tract.

148
Q

what are kidney stones made of

A

Composition of mineral salts

Calcium oxalate and calcium phosphate: 70% to 80%

Struvite (magnesium, ammonium, phosphate): 15%

Uric acid: 7%

149
Q

what other reasons can predispose someone to kidney stones

A

genetic disorders of amino acid metabolism

Excess urine can cause cystinuria, or xanthine, stone formation in the presence of a low urine pH.

150
Q

what are staghorn calculi

A

large stones that fill the major and minor calyces

151
Q

risk factors of kidney stones

A

-male
-most develop before 50 years of age
-inadequate fluid intake
-geographic locations (temp, humidity, rain fall, dietary patterns)

152
Q

what is the most prevalent risk factor for kidney stones

A

inadequate fluid intake

153
Q

what is the clinical manifestation of kidney stones

A

renal pain (colic)

154
Q

what are causes of lower urinary tract obstruction

A

Prostate enlargement
Urethral stricture
Pelvic organ prolapse
Low bladder wall compliance

155
Q

clinical manifestation of lower urinary tract obstruction

A

Frequent daytime voiding
Nocturia
Urgency; hesitancy
Dysuria
Poor force of stream
(feelings of) incomplete voiding

156
Q

what is overactive bladder syndrome

A

chronic syndrome of detrusor overactivity

157
Q

what are symptoms of overactive bladder

A

syndrome of urgency, with or without urge incontinence;

usually associated with frequency and nocturia

158
Q

what is urge incontinence

A

common in older adults and associated with involuntary contractions of the detrusor muscle and strong desire to void;

loss of bladder wall compliance

159
Q

what is stress incontinence

A

common in women under 60 and men following prostate surgery;

associated with involuntary loss of urine during activities that increase abdominal pressure (coughing, sneezing, etc.)

160
Q

what is overflow incontience

A

overdistension of bladder;

lesions below S1, enlarged prostate

161
Q

what is mixed incontinence

A

common in older women and is a combo of urge and stress

162
Q

what is functional incontinence

A

involuntary loss of urine due to dementia or immobility

163
Q

incontinence picture

A
164
Q

what is the most common cause of intrinsic ARF

A

acute tubular necrosis (ATN)

165
Q

what is acute tubular necrosis (ATN)

A

destruction of tubular epithelial cells

causes include prolonged ischemia or exposure to nephrotoxins

166
Q

tubuloglomerular feedback acts as a

A

positive feedback mechanism

167
Q

urinary indices of ATN include

A

high Na excretion
isoosmotic urine
cells/cellular casts in urine

168
Q

what happens when a backleak exists in intrinsic ARF

A

hypervolemia and hypertension follow

169
Q

what is another cause of intrinsic ARF

A

glomerulonephritis

170
Q

what is the primary injury in glomerulonephritis

A

due to immune responses, ischemia, drugs/toxins, infections

Following infection with group A Streptococcus

Deposition of antigen-Ab complexes(type III hypersensitivity)

Ab against glomerular basement membrane (autoimmune; type II hypersensitivity)

171
Q

secondary injury of intrinsic ARF is

A

is a consequence of systemic disease such as SLE, DM (not generally acute)

172
Q

what is acute nephritic syndrome

A

hematuria, oliguria, mild proteinuria and edema-is commonly seen

173
Q

glomerular injury chart

A
174
Q

what is acute pyelonephritis

A

an intrinsic renal disease

infectious inflammatory response ascending from lower urinary tract

175
Q

what can cause acute pyelonephritis

A

Catheterization and endoscopes

Kidney stones

Pregnancy

Neurogenic bladder

Sexual trauma

176
Q

what can result from acute pyelonephritis

A

abscess formation
tubular necrosis

177
Q

what are common bacteria causes of acute pyelonephritis

A

Gram negative bacteria like E. coli and Pseudomonas are common

178
Q

what are moderate effects of ARF

A

When moderate, the main effects are retention in the blood and ECF of water, waste products of metabolism, and electrolytes

Edema and hypertension
Hyperkalemia
Metabolic acidosis

179
Q

what are severe physiological effects of ARF

A

Most severe cases include anuria;

patients can die within 8-14 days unless kidney function is restored or another means is used to rid the patient of excess water, wastes, etc.

180
Q

what is uremia

A

Syndrome of renal failure

Elevated blood urea and creatinine levels

Fatigue, anorexia, nausea, vomiting, pruritus, and neurologic changes

Retention of toxic wastes, deficiency states, electrolyte disorders, and proinflammatory state

181
Q

what is azotemia

A

Increased serum urea levels and frequently increased creatinine levels

Renal insufficiency or renal failure, causing azotemia

Both azotemia and uremia: Accumulation of nitrogenous waste products in the blood

182
Q

Oliguria chart

A
183
Q

what is the intact nephron hypothesis of chronic renal failure

A

As the disease advances and nephrons are progressively destroyed, the remaining nephrons hypertrophy

Single nephron GFR is increased in the remaining nephrons to maintain fluid and electrolyte balance until more than 90% are destroyed

184
Q

what is the hyperfiltration theory of chronic renal failure

A

Intact nephrons are eventually injured by the increased plasma flow and GFR and the increased glomerular intracapillary hydrostatic pressure

185
Q

what kind of feedback loops is chronic renal failure

A

positive

continuing nephron loss over time

186
Q

what are causes of chronic renal failure

A

Injury to the renal vasculature
-Atherosclerosis
-Fibromuscular hyperplasia
-Nephrosclerosis-results from hypertension

Injury to the glomeruli
-Glomerulonephritis
—Immunologic damage (SLE)

Injury to the interstitium
-Pyelonephritis (this can be acute as well)

Cystic diseases of the kidney
-Autosomal dominant polycystic disease

187
Q

what is a common consequence of chronic renal failure

A

nephrotic syndrome

188
Q

Analgesic nephropathy

A

a form of tubulointerstitial disease caused by the long-term administration of analgesic agents like NSAIDs (multiple types; high doses)

189
Q

characteristics of nephrotic syndrome

A

massive proteinuria (>3.5 g/day),

hypoalbuminemia (and hypoglobulinemia),

generalized edema,

hyperlipidemia

190
Q

what are the main causes of nephrotic syndrome

A

DM

SLE

amyloidosis

GN

191
Q

nephrotic syndrome chart

A
192
Q

physiological effects of CRF

A

Loss of functional nephrons requires the surviving nephrons to excrete more water and solutes

In early renal failure (polyuria) likely to see “salt-wasting”; in later stages (oliguria) you are likely to see salt and fluid retention leading to hypertension

Isothenuria

193
Q

what is the effects on bodily fluids of CRF

A

Generalized edema
Acidosis
Uremia or azotemia
Anemia

194
Q

end stage renal chart

A
195
Q

what are the leading causes of ESRD

A

Diabetes (30-40%)

Hypertension (25%)

Glomerulonephritis (20%)

Chronic pyelonephritis (10-20%)

Polycystic kidney disease (5%)

196
Q

what are the five stages of diabetic neuropathy and ESRD

A

Early functional changes including hypertrophy and hyperfiltration

Early structural changes including thickening of the glomerular capillary basement membrane

Incipient nephropathy with microalbuminuria and hypertension

Established nephropathy with gross proteinuria and decreased GFR

Progressive renal insufficiency with rapidly declining GFR (up to 3%/month)

197
Q

what is critical in slowing the progression of chronic renal failure

A

good glycemic control

198
Q

what is the most common single cause of ESRD

A

DM and CRF

199
Q

what is the role of hyperglycemia in CRF

A

Increased renal blood flow due to osmotic effects systemically

Vasodilation within the kidneys along with increased permeability of microcirculation allowing leakage of solutes into vascular walls and tissues

Glycosylation of glomerular structural components that increases matrix material and increases membrane permeability leading to proteinuria

200
Q

what is the main cause of ESRD and a consequence of chronic renal failure

A

hypertension

201
Q

what leads to nephrosclerosis

A

hypertension

202
Q

Renal lesions that reduce the ability of the kidneys to

A

excrete Na+ and water promote hypertension (due to volume expansion)

203
Q

renal damage that leads to an increase in renin secretion can cause

A

hypertension (vasoconstriction and volume expansion)

204
Q

define urinary tract obstruction

A

interference with the flow of urine at any site along the urinary tract

205
Q

what is obstructive uropathy

A

anatomic changes in the urinary system caused by obstruction

206
Q

what is the severity of an obstruction determined by

A

(1) the location of the obstructive lesion,
(2) the involvement of one or both upper urinary tracts (ureters and renal pelvis),
(3) the completeness of the obstruction,
(4) the duration of the obstruction,
(5) the nature of the obstructive lesion.

207
Q

what are common causes of upper urinary tract obstructions

A

stricture or congenital compression of a calyx or the uretero- pelvic or ureterovesical junction (e.g., stones [calculi]);

ureteral compression from an aberrant vessel, tumor, or abdominal inflammation and scarring (retroperitoneal fibrosis)

ureteral blockage from stones or a malignancy of the renal pel- vis or ureter.

208
Q

what is hydroureter

A

Dilation of the ureter
(accumulation of urine in the ureter)

209
Q

dilation of the renal pelvis and calyces proximal to the blockage results in

A

hydronephrosis

210
Q

what is hydronephrosis

A

enlargement of the renal pelvis and calyces

211
Q

what is uterohydronephrosis

A

dilation of both the ureter and the pelvicalyceal system

212
Q

Tubulointerstitial fibrosis

A

is the deposition of excessive amounts of extracellular matrix (collagen and other proteins).

213
Q

Isothenuria

A

Inability of kidneys to concentrate or dilute urine

214
Q

What host factors predispose to UTI

A

Kidney stones
DM
Immunosuppression
Ureter reflux
Pregnancy
Neurogenic bladder
P blood group antigens
Prostatic hypertrophy
Short urethra in women
Catheters
E. coli contamination from colon

Pathophysiology (3 decks)

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