Exam 2 Flashcards
(214 cards)
1
Q
what are the two basic processes in respiratory physiology
A
ventilation
gas exchange
2
Q
what categories do all lung pathologies fall into
A
hypoventilation
ventilation/perfusion mismatching
impaire diffusion
3
Q
What factors affect pulmonary ventilation
A
compliance
elasticity
surface tension in the alveoli
4
Q
high compliance =
A
ease of expansion
5
Q
low compliance=
A
difficulty in expansion
6
Q
how does elasticity affect the lungs
A
allow lungs to expand
7
Q
what controls the surface tension in the alveoli
A
surfactant
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
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 CO2dilation, and vice versa)
10
Q
what factors affect diffusion in alveoli
A
thickness of membrane
surface are of membrane
diffusion coefficients
partial pressure differences
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
12
Q
what is a major symptom of respiratory failure
A
dyspnea
13
Q
what is a major consequence in alteration in blood gas concentration
A
hypoxemia -low O2 in blood
hypercapnia- increased CO2
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
15
Q
what is dyspnea
A
subjective sensation of uncomfortable breathing
16
Q
what is orthopnea
A
dyspnea when a person is lying down
17
Q
what are two abnormal breathing patterns
A
-Kussmaul respirations (hyperpnea)
Cheyne stokes respirations
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
19
Q
what classifies a cough as chronic
A
> 3 weeks
20
Q
what is an acute cough
A
2-3 weeks
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
22
Q
what is the most common pain caused by pulmonary diseases
A
pleural pain
23
Q
what is chest wall pain
A
may be from the airways
may be from muscle or rib pain
24
Q
what are conditions caused by pulmonary disease
A
hypercapnia
hypoxemia
pulmonary edema
acute respiratory failure
25
what is hypercapnia
increase CO2 in blood concentration
26
what causes hypercapnia
hypoventilation
V/Q mismatch
resp muscle fatigue
27
what is hypoxemia
reduction in blood O2 levels
28
what are gradient increases in respiratory diseases
low V/Q ratios
anatomic shunts
diffusion block
29
what are clinical manifestations of hypoxemia
impaired function of vital centers
activation of compensatory mechanisms (similar to anemia)
30
what is a result of excessive deoxy-Hb
cyanosis
31
who are less prone to cyanosis even though they may be hypoxic
anemia
32
how does polycythemia lead to cyanosis without hypoxia
they have a higher Hgb level.
decrease of 5 deoxy hemoglobin results in cyanosis but they still have normal level hemoglobin
33
where do you see central cyanosis
tongue lips gums
34
where do you see peripheral cyanosis
extremities
nose
ears
35
what is the O2 extraction ratio
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
36
what is hypoxia influenced by
supply and demand
-Decrease in arterial O2 content
-Decrease in blood flow
-Inability of cells to use O2
37
what are factors that increase O2 consumption
-Surgery, trauma, burns
-Inflammation and sepsis
-Pyrexia
-Seizures
-Agitation/anxiety/pain
-Adrenergic drugs
-Weaning from ventilation
38
what are factors that decrease O2 consumption
-Sedation/analgesics
-Paralysis
-Shock
-Mechanical vent
-Antipyretics
-Starvation
39
what are the two stages of hypoxia
carotid body drive
slow rise in ventilation (ventilation acclimatization)
-chemoreceptor involvement
-kidney involvement
40
what is cardiovascular acclimatization
-Increased pulmonary blood flow (and vasodilation systemically)
-Increased RBC production
-Improved transport of O2 and CO2
41
define pneumothorax
a chest wall injury that results in air in the pleural space, preventing ventilation
42
what is atelectasis
an incomplete expansion of part of the lung – “collapse”
Many causes including obstruction, compression due to pneumothorax, effusion, tumor or loss of surfactant
43
describe restrictive lung disorders
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
44
what are common types of restrictive lung disorders
aspiration
atelectasis
bronchiectasis
pulmonary fibrosis
pulmonary edema
ARDS
45
what is bronchiectasis
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
46
what are the three kinds of bronchial dilations
cylindrical
saccular
varicose
47
what is a cylindrical bronchial dilation
cylindrical bronchiectasis) with symmetrically dilated airways, as seen after pneumonia and is reversible
48
what is saccular bronchial dilations
(saccular bronchiectasis),
in which the bronchi become large and balloon like
49
what is varicose bronchial dilations
(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
50
what are the primary symptoms of bronchiectasis
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
51
how does heart conditions cause pulmonary edema
52
how does injury to capillary endothelium cause pulmonary edema
53
how does blockage of lymphatic vessels cause pulmonary edema
54
describe obstructive pulmonary disease
airway obstruction that is worse with expiration
55
what are common signs of obstructive pulmonary disease
dyspnea
wheezing
56
what are the common obstructive pulmonary disorders
asthma
emphysema
chronic bronchitis
57
chronic bronchitis
58
emphysema
59
asthma
60
what is the extrinsic trigger of asthma
produce symptoms in people who are predisposed to asthma (type 1-hypersensitivity reaction against a specific allergen)
-Family history of allergy
-Early onset
61
what is intrinsic trigger of asthma
exert effects through inflammatory response and vagal reflexes;
make airways hyperresponsive to nonallergic stimuli;
also induce bronchospasm
62
what is the mechanisms of asthma
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
63
asthma chart
64
what is the early response in asthma
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
65
what do interleukins do
class of glycoproteins produced by leukocytes for regulating immune response
66
symptoms of asthma
episodic wheezing and feelings of chest tightness to an acute, immobilizing attack
expiration becomes prolonged because of airway obstruction
67
what happens with prolonged asthma attack
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
68
what is pathogenesis of COPD
Inflammation and fibrosis of the bronchial wall
Hypertrophy of the submucosal glands and hypersecretion of mucus
Loss of elastic lung fibers and alveolar tissue
69
what are examples of COPD
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
70
how is COPD diagnosis
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.
71
what is FEV1
Forced Expiratory Volume in 1 second, or the amount of air that can be blown out of the lungs in the first 1 second.
72
what is FVC
Forced Vital Capacity, refers to the total amount of air that a person can exhale
73
COPD chart
74
what are the clinical features of emphysema
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)
75
what are the clinical symptoms
of bronchitis
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
76
respiratory disease COPD
77
what are the comorbidities of COPD
78
what are the manifestations of PE
dyspnea and ↑ respiratory rate;
infarction causes pain associated with breathing (inspiration);
gas exchange problems (hypoxemia)
79
pulmonary vascular disorders chart
80
describe pulmonary HTN
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
81
pulmonary HTN chart
82
what is ARDS
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
83
ARDS chart
84
ARDS alveoli
85
what is the clinical progression of ARDs
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
86
describe upper airway of children
airways smaller in diameter (increase through childhood) = more obstruction problems
87
children conducting airways are present
at birth
88
infants up to 2-3 months are
obligatory nose breathers
nasal congestion is serious threat to young infants
89
describe lower airways and parenchyma in children
infants and young children continue to form new alveoli for several years after birth
90
what is surfactant
a lipid protein mixed produced by alveolar type II cells
91
what does surfactant do
maintains alveolar expansion
decreases alveolar surface tension
92
what causes respiratory distress syndrome and hyaline membrane disease in infants
surfactant deficiency in premature infants
93
when is surfactant produced
20-24weeks gestation
secreted into airways by 30 weeks gestation
94
which infants are more likely to develop respiratory distress syndrome
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
infants have ____ chest wall compliance
high
particularly premature infants
96
what kind of breathing do children have
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
the metabolic rate of a child is ____than an adults
higher
98
describe oxygen consumption in children
oxygen consumption (VO2) is greater per unit of body weight in children than in adults
99
what can cause acute upper airway obstructions in children
infections
foreign body
angioedema
sleep apnea
trauma
100
what causes chronic upper airway obstructions in children
Congenital malformations of the airway,
cartilaginous weakness,
vocal cord paralysis,
subglottic stenosis
101
what is a major sign of airway obstruction
stridor
102
loud gasping snore suggests
enlarged tonsils or adenoids
103
stridor during inspiration suggests
airway is compromised at the level of the supralaryngeal structures (epiglottis/ arytenoid cartilages), vocal cords and glottic opening
104
expiratory stridor or central wheezes suggest
narrowing or collapse of lower trachea or bronchi
105
airway noise heard during inspiration and expiration
fixed obstruction at the vocal cords
106
if cough is croupy or low pitched
Suspect tracheal pathology
107
what is one of the leading causes of morbidity in the first year of life
disorders of the lower airways
108
what are examples of lower airway disorders
respiratory distress syndrome of the newborn
bronchopulmonary dysplasia
asthma
cystic fibrosis
infections
ARDS
109
what is the major cause of pulmonary disease in infants
bronchopulmonary dysplasia
110
what causes bronchopulmonary dysplasia
lung immaturity and inflammation coupled to mechanical ventilation
proper lung development is arrested with poor alveolar formation-> reducing surface area for gas exchange
111
what is Cystic Fibrosis
autosomal recessive multisystem disease
CFTR gene
abnormality of chloride transport
112
what happens in Cystic fibrosis
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
typical features of CF
mucus plugging
chronic inflammation
infection of the small airways
114
how does chronic inflammation impact CF
leads to:
hyperplasia of goblet cells
bronchiectasis
PNA
hypoxia
fibrosis
115
what is most often the cause of death in CF
respiratory failure
116
what are clinical manifestations of CF
persistent cough or wheeze
sputum production
recurrent or severe PNA
clubbing
117
CF flow chart
118
what is the most common cause of unexplained infant death in western world
SIDS
119
what is the possible genetic contribution to SIDS
ion channel/protein association with primary electrical heart disease (long QT syndrome)
120
Respiratory distress syndrome flow chart
121
what is the functional unit of the kidney
nephron
122
what is the renal blood flow amount
1000-1200ml/min
20-25% of cardiac output
123
what is the major function of the kidney
regulate volume
regulate osmolality
electrolyte balance
balance acid-base concentrations
help regulate blood pressure
124
what are the secondary functions of the kidney
excretion of metabolic waste products
125
what is an endocrine function of the kidney
producing erythropoietin
producing 1, 25 dihydroxyvitamin D3
126
where does ultrafiltration occur in the kidney
glomerulus
127
where dose selective resorption and secretion of water and filtered substances occur
along the tubules
128
Renal disease can be broadly categorized in the following manner:
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
common signs/symptoms of kidney dysfunction
130
what acute renal failure
Clinical syndrome characterized by rapid decline of glomerular filtration rate (GFR), azotemia, and perturbation of acid-base, fluid, and electrolyte homeostasis
131
what are the 3 categories of acute renal failure
pre-renal
post renal
intrinsic
132
ARF picture
133
what are contributing factors for UTI
host and bacterial factors
134
what conditions predispose to UTIs
Obstructions
-Enlarged prostate
-Pregnancy
-Calculi
Diabetes
Catheters
135
what is prerenal ARF
renal injury due to hypoperfusion or ischemia to the kidney
136
what is the most common cause of Acute renal failure
pre renal
prolonged renal ischemia from decreased renal perfusion
137
pre renal ARF is rapidly reversible upon
restoration of renal blood flow and glomerular ultrafiltration pressure
there may be long term consequences though such as loss of capillaries
138
what is post renal ARF caused by
acute obstruction of urinary outflow
139
what does post renal ARF lead to
hydronephrosis,
severe damage to the renal parenchyma, and
intrinsic ARF if prolonged
140
what is a urinary tract obstruction
blockage of urine flow within the urinary tract
141
what is the severity of obstruction based on
Location
Completeness
Involvement of one or both upper urinary tracts
Duration
Nature and/or cause
142
what can cause an obstruction in the urinary tract
anatomic or functional defect
143
what are upper urinary tract obstruction complications
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
Compensatory hypertrophy and hyperfunction in the kidney:
Partially counteracts the negative consequences of unilateral obstruction.
145
what is post obstructive diuresis
Is caused by relief of the obstruction in the upper urinary tract
May cause fluid and electrolyte imbalance.
146
what is another name for kidney stones
renal calculi
urolithiasis
147
what are kidney stones
Masses of crystals, protein, or mineral salts form in the urinary tract and may obstruct the urinary tract.
148
what are kidney stones made of
Composition of mineral salts
Calcium oxalate and calcium phosphate: 70% to 80%
Struvite (magnesium, ammonium, phosphate): 15%
Uric acid: 7%
149
what other reasons can predispose someone to kidney stones
genetic disorders of amino acid metabolism
Excess urine can cause cystinuria, or xanthine, stone formation in the presence of a low urine pH.
150
what are staghorn calculi
large stones that fill the major and minor calyces
151
risk factors of kidney stones
-male
-most develop before 50 years of age
-inadequate fluid intake
-geographic locations (temp, humidity, rain fall, dietary patterns)
152
what is the most prevalent risk factor for kidney stones
inadequate fluid intake
153
what is the clinical manifestation of kidney stones
renal pain (colic)
154
what are causes of lower urinary tract obstruction
Prostate enlargement
Urethral stricture
Pelvic organ prolapse
Low bladder wall compliance
155
clinical manifestation of lower urinary tract obstruction
Frequent daytime voiding
Nocturia
Urgency; hesitancy
Dysuria
Poor force of stream
(feelings of) incomplete voiding
156
what is overactive bladder syndrome
chronic syndrome of detrusor overactivity
157
what are symptoms of overactive bladder
syndrome of urgency, with or without urge incontinence;
usually associated with frequency and nocturia
158
what is urge incontinence
common in older adults and associated with involuntary contractions of the detrusor muscle and strong desire to void;
loss of bladder wall compliance
159
what is stress incontinence
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
what is overflow incontience
overdistension of bladder;
lesions below S1, enlarged prostate
161
what is mixed incontinence
common in older women and is a combo of urge and stress
162
what is functional incontinence
involuntary loss of urine due to dementia or immobility
163
incontinence picture
164
what is the most common cause of intrinsic ARF
acute tubular necrosis (ATN)
165
what is acute tubular necrosis (ATN)
destruction of tubular epithelial cells
causes include prolonged ischemia or exposure to nephrotoxins
166
tubuloglomerular feedback acts as a
positive feedback mechanism
167
urinary indices of ATN include
high Na excretion
isoosmotic urine
cells/cellular casts in urine
168
what happens when a backleak exists in intrinsic ARF
hypervolemia and hypertension follow
169
what is another cause of intrinsic ARF
glomerulonephritis
170
what is the primary injury in glomerulonephritis
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
secondary injury of intrinsic ARF is
is a consequence of systemic disease such as SLE, DM (not generally acute)
172
what is acute nephritic syndrome
hematuria, oliguria, mild proteinuria and edema-is commonly seen
173
glomerular injury chart
174
what is acute pyelonephritis
an intrinsic renal disease
infectious inflammatory response ascending from lower urinary tract
175
what can cause acute pyelonephritis
Catheterization and endoscopes
Kidney stones
Pregnancy
Neurogenic bladder
Sexual trauma
176
what can result from acute pyelonephritis
abscess formation
tubular necrosis
177
what are common bacteria causes of acute pyelonephritis
Gram negative bacteria like E. coli and Pseudomonas are common
178
what are moderate effects of ARF
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
what are severe physiological effects of ARF
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
what is uremia
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
what is azotemia
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
Oliguria chart
183
what is the intact nephron hypothesis of chronic renal failure
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
what is the hyperfiltration theory of chronic renal failure
Intact nephrons are eventually injured by the increased plasma flow and GFR and the increased glomerular intracapillary hydrostatic pressure
185
what kind of feedback loops is chronic renal failure
positive
continuing nephron loss over time
186
what are causes of chronic renal failure
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
what is a common consequence of chronic renal failure
nephrotic syndrome
188
Analgesic nephropathy
a form of tubulointerstitial disease caused by the long-term administration of analgesic agents like NSAIDs (multiple types; high doses)
189
characteristics of nephrotic syndrome
massive proteinuria (>3.5 g/day),
hypoalbuminemia (and hypoglobulinemia),
generalized edema,
hyperlipidemia
190
what are the main causes of nephrotic syndrome
DM
SLE
amyloidosis
GN
191
nephrotic syndrome chart
192
physiological effects of CRF
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
what is the effects on bodily fluids of CRF
Generalized edema
Acidosis
Uremia or azotemia
Anemia
194
end stage renal chart
195
what are the leading causes of ESRD
Diabetes (30-40%)
Hypertension (25%)
Glomerulonephritis (20%)
Chronic pyelonephritis (10-20%)
Polycystic kidney disease (5%)
196
what are the five stages of diabetic neuropathy and ESRD
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
what is critical in slowing the progression of chronic renal failure
good glycemic control
198
what is the most common single cause of ESRD
DM and CRF
199
what is the role of hyperglycemia in CRF
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
what is the main cause of ESRD and a consequence of chronic renal failure
hypertension
201
what leads to nephrosclerosis
hypertension
202
Renal lesions that reduce the ability of the kidneys to
excrete Na+ and water promote hypertension (due to volume expansion)
203
renal damage that leads to an increase in renin secretion can cause
hypertension (vasoconstriction and volume expansion)
204
define urinary tract obstruction
interference with the flow of urine at any site along the urinary tract
205
what is obstructive uropathy
anatomic changes in the urinary system caused by obstruction
206
what is the severity of an obstruction determined by
(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
what are common causes of upper urinary tract obstructions
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
what is hydroureter
Dilation of the ureter
(accumulation of urine in the ureter)
209
dilation of the renal pelvis and calyces proximal to the blockage results in
hydronephrosis
210
what is hydronephrosis
enlargement of the renal pelvis and calyces
211
what is uterohydronephrosis
dilation of both the ureter and the pelvicalyceal system
212
Tubulointerstitial fibrosis
is the deposition of excessive amounts of extracellular matrix (collagen and other proteins).
213
Isothenuria
Inability of kidneys to concentrate or dilute urine
214
What host factors predispose to UTI
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
