Genitourinary System Disorders Flashcards
(318 cards)
1
Q
What is cryptorchidism?
A
Undescended testes. One or both of the testicles fail to move down into the scrotal sac. Testes develop intra-abdominally in the fetus
2
Q
When do testes usually descend into the scrotum through the inguinal canal?
A
7 to 9 months gestation
3
Q
What are the consequences of cryptorchidism?
A
Infertility, malignancy, testicular torsion (10x increased risk), psychological effects of an empty scrotum.
4
Q
What is hydrocele?
A
Fluid accumulates in the layers around the scrotum.
5
Q
Hematocele
A
blood in the layers around the scrotum
6
Q
Spermatocele
A
a cyst in the epididymis (might contain sperm)
7
Q
Varicocele
A
Enlargement of the veins of the scrotum
8
Q
Testicular torsion
A
Twisting of the spermatic cord that suspends the testis and the spermatic vessels that supply the testis with blood
9
Q
Orchitis
A
An infection of the testes
10
Q
Mumps virus
A
An infection that can spread to testes through the bloodstream or the lymphatics. Can also be caused by rubella, other viruses ad bacterial infections.
11
Q
S/s of mumps virus
A
Sudden onset, painful enlargement of testes (usually one testicle). Urinary symptoms absent. Symptomatic for 7-10 days. Atrophy of testes may occur - impacting spermatogenesis.
12
Q
Testicular cancer prevalence
A
Relatively rare, most common in 15-29 year olds. 5 year survival rate of 97%
13
Q
Testicular cancer tx
A
Surgical removal of testes and spermatic cord plus radiation
14
Q
Risk factors for testicular cancer
A
cryptorchidism, family hx, personal hx
15
Q
Stage I classification for testicular cancer
A
tumor confined to testes, epididymis, or spermatic cord
16
Q
Stage II classification testicular cancer
A
tumor spreads to retroperitoneal lymph nodes below the diaphragm
17
Q
Stage III classification testicular cancer
A
metastases outside the retroperitoneal nodes or above the diaphragm
18
Q
Generally, what is prostatitis?
A
inflammation or swelling of the prostate gland
19
Q
acute bacterial prostatitis etiology
A
ascending urethral infection (E. coli)
20
Q
acute bacterial prostatitis manifestations
A
fever, malaise, frequent/urgent urination, urethral discharge
21
Q
acute bacterial prostatitis tx
A
antibiotics, reduce activity, hydration, pain management
22
Q
chronic bacterial prostatitis
A
recurrent UTI, persistent in prostatic fluid and urine
23
Q
What are the methods for retrieving different genitourinary specimens?
A
1st part of voided urine - urethral specimen. Midstream - bladder specimen. Prostatic expression obtained by prostatic massage, and urine after massage considered prostatic specimen.
24
Q
Chronic bacterial prostatitis manifestations
A
Similar to acute - fever, malaise, frequent/urgent urination, urethral discharge
25
Tx for chronic bacterial prostatitis
Tx difficult: antibacterial drugs less effective in penetrating chronically inflamed prostate
26
Chronic prostatitis/chronic pelvic pain syndrome - inflammatory
Unknown cause. No bacteria, elevated leukocytes and abnormal inflammatory cells
27
Chronic prostatitis/chronic pelvic pain syndrome - noninflammatory prostatitis
symptoms resembling nonbacterial prostatitis. Negative urine cultures (normal leukocyte counts)
28
Benign Prostatic Hyperplasia (what is it)
age related, nonmalignant enlargement of the prostate gland
29
Characterization of BPH
formation of large discrete lesion in the periurethral region of the prostate, rather than peripheral zones (commonly affected by prostate cancer)
30
Static BPH stage
anatomical increase in prostatic size - result sin we urinary system, post void dribbling, frequency of urination, and nocturia
31
Dynamic stage BPH
Functional aspect of BPH - obstruction of urinary flow caused by enlarged prostate. When activated alpha 1 adrenergic receptors leads to smooth muscle constriction around prostate and urethra
32
Pathophysiology of BPH
Disruption in balance between testosterone, estrogen, and DHT (dihydrotestosterone). A relative increase in estrogen (with aging and decreased T) - sensitizes prostate to DHT = growth and enlargement
33
BPH Tx
alpha 1 adrenergic blocking drugs - relieves obstruction, increase urine flow (relaxes smooth muscle). 5 alpha reductase inhibitors (finasteride) - cause atrophy of prostate cells and block androgen effects of DHT. Surgery
34
Prostate Cancer prevalence
3rd to lung and colon/rectal cancer for cancer related deaths in Canadian males
35
Prostate cancer risk factors
Age (85% over age of 65). Diet and ethnicity. Diets low in veg and high in meat and saturated fats. Overweight and obese individuals. Androgens - increased levels
36
Screening for prostate cancer
Digital rectal exam
37
Diagnosis of prostate cancer
Biopsy, Gleason score, tumor markers (KLK3), MRI
38
Prostate cancer tx
Watchful waiting, surgery, radiation therapy, high intensity focused ultrasound, chemo, cryosurgery, hormonal therapy (antiandrogen), combination therapies
39
Prostate tumor grading -T1
primary stage tumors are asymptomatic and discovered on histologic examinations of prostatic tissue specimens
40
Prostate tumor grading system - T2
tumors are palpable on digital exam, but are confined to the prostate gland
41
Prostate tumor grading system - T3
tumors have extended beyond the prostate
42
prostate tumor grading system - T4
tumors have pushed beyond the prostate to involve adjacent structures
43
Vulva cancerous tissue
squamous cell carcinomas
44
Cervix cancer tissue
Squamous cell carcinomas, transformation zone
45
Endometrial cancer
associated with conditions producing excessive estrogen stimulation and endometrial hyperplasia
46
Ovarian Cancer
most common and most lethal cancer
47
Stage of Gynecologic cancer
0 - rarely used, preinvasive lesions; I - cancer is confined to organ it originated in; II - cancer involves some structures surrounding the organ of origination; III - regional spread of cancer with lymph node involvement; IV - distant spread of cancer with metastasis
48
Cervix Composition
undergoes functional changes during each menstrual cycle related to spermatozoa transport
49
Exocervix (visible portion) composition
stratified squamous epithelium (also lines vagina)
50
Endocervical canal composition
columnar epithelium
51
Varying composition of stratified squamous exocervix and mucus secreting endocervix
Periods of high estrogen production - cervix everts/turns outwards, columnar epithelium exposed to low vaginal pH -> metaplasia - gradual transformation from columnar to squamous. This dynamic area = transformation zone
52
transformation zone
critical area for development of cervical cancer. Vulnerable to dysplasia and susceptible to cancerous transformation. Transformation initially reversible, but can transform to carcinoma
53
Pap smear test focused area
transformation zone
54
Screening and Diagnosis of CErvical Cancer
Pap smear, colposcopy, cervicography, LEEP (loop electrosurgical excision procedure)
55
Tx of cervical cancer
Removal of lesion by one of following techniques: biopsy or local cautery; electrocautery, cryosurgery, or carbon dioxide laser therapy used to tx moderate to severe dysplasia limited to exocervix, radiation and surgery, radical hysterectomy, LEEP
56
Cervical cancer and STI
causal link between HPV infection and cervical cancer (increased with HPV subtypes 16, 18, also 31, 33, and 45
57
HPV med prevention
Gardasil or Cervarix vaccine prevents subtypes 16, 18, also 6 and 11
58
HPV subtypes responsible for 70% of cervical cancer
16 and 18
59
Two most common benign strains of HPV responsible for genital warts
6 and 11
60
Disorders of the Uterus - endometritis
cervical barrier is compromised,infection of the endometrium (the inner lining of the uterus
61
Disorders of the Uterus - endometriosis
Functional endometrial tissue is found in ectopic sites. Lesions stimulated by ovarian hormones, bleeding (pain) and pelvic adhesions
62
Disorders of the Uterus - endometrial cancer
most common cancer found in the female pelvis
63
Endometrial cancer types - Type 1
prolonged estrogen stimulation and endometrial hyperplasia. Hormone sensitive, low grade, favorable prognosis, painful bleeding
64
endometrial cancer types - benign
smooth muscle origin
65
endometrial cancer types - submucosal
displace endometrial tissue, more likely to cause bleeding, necrosis, and infection than other types
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endometrial cancer types - subserosal
located beneath the perimetrium of the uterus
67
endometrial cancer types - intramural
embedded in the myometrium
68
Pelvic Inflammatory Disease (what is it)
inflammation of the upper reproductive tract that involves: the uterus (endometritis), fallopian tubes (salpingitis), the ovaries (oophoritis). A polymicrobial infection
69
Predisposing factors for pelvic inflammatory disease
16-24 years of age, nulliparity (never haven given birth), hx of multiple sexual partners, previous hx of PID
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Complications of pelvic inflammatory disease
peritonitis, pelvic abscesses
71
What is an ectopic pregnancy
fertilized ovum implants outside uterus - most commonly in fallopian tube
72
Predisposing factors for ectopic prgenancy
pelvic inflammatory disease, therapeutic abortion, tubal ligation or tubal reversal, previous ectopic pregnancies, use of fertility drugs to induce ovulation
73
Ovarian Cysts
mot common form of ovarian tumor. Frequently cause menstrual and fertility problems. RElated to hypothalamic, pituitary, or adrenal dysfunction
74
Polycystic ovary syndrome (PCOS)
infertility, hyperandrogenism, common source of chronic anovulation, menstrual irregularity
75
Ovarian tumors
may be hormonally active: granulosa - excess estrogen production. Often diagnosed in advanced stage as many symptoms are nonspecific. May present with ascites. links to metastasis
76
Ovarian tumor tx
surgical excision
77
Majority of all ovarian malignancies
epithelial ovarian carcinomas arising from fallopian tube epithelium account for the majority
78
Screening for epithelial ovarian carcinomas
lack of effective screening strategies - emphasis on prevention
79
preventing epithelial ovarian carcinomas
removal of fallopian tubes(salpingectomy) if reproductive needs have been met
80
dysfunction of menstrual cycles - amenorrhea
absence of mensuration
81
dysfunction of menstrual cycles - hypomenorrhea
scanty mensuration
82
dysfunction of menstrual cycles - oligomenorrhea
infrequent menstruation (>35 days apart)
83
dysfunction of menstrual cycles - polymenorrhea
frequent menstruation (<21 days apart)
84
dysfunction of menstrual cycles - menorrhagia
excessive menstruation
85
dysfunction of menstrual cycles - metrorrhagia
bleeding between periods
86
dysfunction of menstrual cycles - menometrorrhagia
heavy bleeding during and between menstrual periods
87
Estrogen deprivation in menstrual cycle
retrogression of previously built up endometrium and bleeding. Bleeding is often irregular in amount and duration
88
Progesterone deprivation in menstrual cycle
abnormal menstrual bleeding (less). Absence allows estrogen to induce thicker endometrial layer with greater blood supply
89
menstrual cycle - dysmenorrhea
pain or discomfort with menstruation
90
primary dysmenorrhea
not associated with physical abnormality or pathology
91
secondary dysmenorrhea
organ condition exacerbated by the menstrual cycle: endometriosis, adenomyosis, pelvic adhesions, IUDS, PID- painful menstruation caused by organ abnormality
92
premenstrual syndrome - physical symptoms
painful and swollen breasts, bloating - abdo pain, headache and backache
93
premenstrual syndrome - psychological symptoms
depression, anxiety, irritability, behavioral changes
94
causes of symptoms of premenstrual syndrome
hyperprolactinemia, estrogen excess, alteration in estrogen - progesterone ratio, aldosterone,
95
disorders of the breast - mastitis
inflammation of the breast
96
disorders of the breast - fibroadenoma
firm rubbery, sharply defined round mass
97
disorders of the breast - fibrocystic
nodular granular breast masses
98
disorders of the breast - breast cancer
mass, puckering, nipple retraction, or unusual discharge
99
breast cancer prevalence
most common female cancer - 2nd leading cause of cancer relate deaths in women
100
breast cancer risk factors
Sex, age; hx of breast cancer or benign breast disease; hormonal influences; obesity; long term use of postmenopausal hormone therapy; alcohol; physical inactivity
101
Breast cancer screening
mammography (every 2 years from 50-74 years)
102
breast cancer known mutations
BRCA1 on chromosome 17 - tumor suppressor, BRCA2 on chromosome 13
103
Breast cancer diagnosis
physical examination, mammography, ultrasonography, percutaneous needle aspiration, stereotactic needle biopsy, excisional biopsy
104
STI portals of entry
mouth, genitalia, urinary meatus, rectum, skin
105
STIs can:
selectively infect the mucocutaneous tissues of the external genitalia, cause vaginitis, or produce genitourinary and systemic effects
106
HPV that results in genital warts
6 and 11
107
HPV that results in cervical dysplasia
16 and 18
108
HPV that results in cervical cancer
16 and 18
109
Neurotropic alpha group herpes viruses
Herpes simplex types 1 and 2, varicella zoster virus
110
Varicella zoster virus
shingles, chicken pox
111
Herpes simplex type 1
cold sores
112
Herpes simplex type 2
genital herpes
113
Lymphotropic beta group herpes viruses
cytomegalovirus, epstein-barr vius, human herpesvirus type 8
114
Pathogenesis of Genital Herpes infections
viruses replicate in the skin and mucous membranes at the site of infection (oropharynx or genitalia, grow in neurons and share biologic property of latency, virus ascends through the peripheral nerves to the sacral dorsal root ganglia
115
Diagnosis of genital herpes
based on symptoms, appearance of lesions, identification of the virus from cultures taken from lesions
116
Candidiasis
yeast like fungi, present in 20-50% of women without causing symptoms,
117
causes of Candidiasis
antibiotic therapy - suppresses the normal protective bacterial flora, high hormone levels owing to pregnancy, use of oral contraceptives - causes an increase in vaginal glycogen stores, diabetes mellitus or HIV infection - compromises immune system
118
Gonorrhea
a pyogenic gram-negative diplococcus that evokes inflammatory reactions characterize by purulent exudates (2nd most commonly reported STI in Canada
119
Gonorrhea hosts
human is the only natural host
120
gonorrhea host tissue
warm secreting epithelia
121
gonorrhea portal of entry
genitourinary tract, eyes, oropharynx, anorectum, or skin
122
Gonorrhea transmission
intercourse. May infect child in birth canal - risk of conjunctivitis and blindness if not treated in child
123
gonorrhea tx
tetracycline, penicillin, ceftriaxone, cefixime, ciprofloxacin, ofloxacin, etc
124
Chlamydia
most prevalent STI in Canada. 75% of females and 50% of males have no symptoms. Obligate intracellular bacterial pathogen. Chlamydia trachomatis - gram - negative bacteria
125
Chlamydia transmission
vaginal, anal, or oral sex. To child in birthing process
126
Chlamydia symptoms - female
mucopurulent vaginal discharge, pelvic pain, dysuria and hematuria, complications in 40% of cases - PIDc
127
Chlamydia symptoms - males
urethritis and purulent urethral discharge, testicular pain, prostatitis and epididymitis
128
chlamydia tx
azithromycin, doxycycline, amoxicillin (penicillin ineffective)
129
Syphilis
bacterial spirochete - Treponeama pallidum. can spread to fetus in utero
130
Syphilis complicaitons- birth
untreated congenital syphilis may result in prematurity, still birth, congenital defects and active infections
131
Primary syphilis
appearance of chancre at the site of exposure
132
secondary syphilis
last 1 week to 6 months. Symptoms of rash (esp palms and soles), fever, sore throat nausea, loss of appetite, and inflamed eyes
133
tertiary syphilis
delayed response of the untreated disease - may be decades later
134
tx of syphilis
penicillin
135
Infection with HIV leads to immunodeficiency - why?
HIV primarily infects and destroys CD4 + T cells and other WBCs (CD8 + T cells, B cells and macrophages) - causing an inability of the immune to fight off infections
136
HIV incorporates itself into host cells to replicate - which cells??
CD4 + T cells
137
HIV in the cell
Usually DNA transcribes into RNA and that forms proteins. HIV takes RNA and reverse transcribe it into DNA of the host
138
HIV complications
results in profound immunosuppression, develops in infections and cancers very readily, may advance to AIDS
139
HIV transmission
semen can contain the virus, virus can be carried in blood, maternal - in utero, lactation, during labor and delivery
140
Tests for HIV and AIDS
ELISA, saliva tests, viral load test, western blot, home tests
141
Diagnosis of AIDS
less than 200 CD4 + T cells per cubic millimeter of blood, CD4+ T cells accounting for less than 14% of all lymphocytes, plus: one or more of a certain list of illnesses
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PrEP
prevents HIV
143
PEP
taken within 72 hours of exposure to HIV
144
ART
tx for HIV positive people to reduce levels in body
145
HIV Tx
ART, cannot be cured
146
Fx of Kidneys/Urinary System
filters blood (to produce urine), excretion of metabolic waste products and toxins, maintains fluid balance (regulates blood volume and BP), regulates solute concentration in body (osmolarity), maintains blood pH
147
Kidney Structure and Location
multi-lobular structure, each lobule is composed of nephrons, the functional units of the kidney, located outside the peritoneal cavity in the back of upper abdomen, one on each side of the vertebral column at the level of the 12th thoracic to the 3rd lumbar vertebrae
148
Nephron Functions - filtration
filtrate of blood pushes across glomerulus into the glomerular capsule (to form urine)
149
Nephron Functions - reabsorption
movement of useful molecules from tubules back into blood (so they aren't excreted in urine)
150
Nephron fx - secretion
transport of undesirable molecules from blood into tubules
151
Peritubular capillaries
located around PCT and DCT
152
vasa recta
locate around loops of nephron
153
Ureters
convey urine from kidney to bladder (1 ureter per kidney), lined in transitional epithelium; layer of smooth muscle
154
urinary bladder
stores urine (500 mL - 1 L)
155
Urethra
drains bladder, controls micturition
156
2 urethral sphincters
internal (smooth muscle) - prevents leakage; external (skeletal muscle) - voluntary control
157
Urine formation - output
output 1-2 L/dayby filtering blood
158
Urine components
95% water, 5% solutes: electrolytes (Na, Cl, Mg, Ca, H, HCO3, PO4, K), urobilin, hormones, nitrogenous wastes: urea (protein breakdown), creatinine (creatine P breakdown), uric acid (nucleotide breakdown)
159
Abnormal components of urine - glycosuria
glucose in urine - diabetes
160
Abnormal components of urine - proteinuria
protein in urine - kidney disease/damage
161
Abnormal components of urine - hematuria
blood cells/hemoglobin in urine - inflammation, infection, kidney stones, trauma
162
Abnormal components of urine - bilirubinuria
bile pigments in urine - liver disease
163
Abnormal components of urine - ketonuria
ketones in urine - starvation, diabetes low carb intake
164
Tests for renal fx
GFR; urinalysis - specific gravity of urine, the high the number - the more dehydrated; blood tests - serum creatinine; blood urea nitrogen; cystoscopy, ultrasonography
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glomerular filtration
hydrostatic pressure in glomerular capillaries forces a filtrate of blood into glomerular capsule
166
filtrate of blood components
water, electrolytes, nutrients (glucose, amino acids), urea, uric acid, creatinine
167
What does filtrate not contain?
blood cells and proteins (too large to pass through)
168
Glomerular Filtration Rate
volume of filtrate formed/minute. GFR affected by BP
169
For filtration to occur...
glomerular hydrostatic pressure (GHP) > capsular hydrostatic pressure (CsHP) + blood colloid osmotic pressure (BCOP)
170
Glomerular Hydrostatic PRessure
pressure exerted by blood in the glomerular capillaries
171
capsular hydrostatic pressure
Pressure exerted by fluid in the capsule surrounding the glomerular capillaries in the renal corpuscle of the kidney.
172
Blood colloid osmotic pressure
pressure exerted by proteins (primarily albumin) in the blood as it flows through glomerular capillaries
173
What would happen if GHP was equal to CsHP + BCOP?
net filtration pressure would be 0 mm Hg = anuria (no urine formation)
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How is glomerular filtration regulated?
by regulating blood pressure and flow
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What is tubular reabsorption?
reabsorption of substances in filtrate back into blood (recovery of useful solutes)
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Where does most of the reabsorption in the nephron occur?
from the PCT (proximal convoluted tubule) because its cuboidal epithelium has microvilli - huge surface area
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What is reabsorbed into the blood by active transport?
Sodium (Na+) - 80% reabsorbed
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What is reabsorbed into the blood by facilitated transport and cotransport with Na+?
Glucose, amino acids, and vitamins (100% reabsorbed)
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What is reabsorbed into the blood in the nephron by diffusion?
Cl-, K+, Mg++, Ca++ (down electrochemical gradients) - 80% reabsorbed
180
What is transported back into the blood by osmosis?
H2O (follows solute)
181
Reabsorption (esp of water, Na+,and Cl-) also occurs along...?
nephron loop, DCT, and collecting duct
182
Which hormone increase the calcium reabsorption from the DCT?
Parathyroid Hormone (PTH)
183
Which hormone increases the reabsorption of Na+ from the DCT?
aldosterone -triggers synthesis of additional Na+/K+ transporters in the membrane of cells
184
What does the reabsorption of HCO3- do?
Maintain blood pH by buffering H+ in blood
185
What is the transport maximum (Tm)?
maximum transport for each substance (carriers get saturated) if renal threshold is exceeded, substances will appear in urine
186
Tm for glucose?
375 mg glucose/min
187
Where does tubular secretion occur?
along length of renal tubule
187
Tubular Secretion
secretion of substances from peritubular blood into tubular filtrate (removal of undesirable solutes). Active transport of waste into filrate
188
In tubular secretion where are H+, NH4+, and some drugs secreted?
PCT
189
In tubular secretion, where is urea excreted?
nephron loop
190
In tubular secretion, where is K+ secreted?
DCT
191
An increase in aldosterone causes an increase in what?
K+ secretion (K+ secretion is coupled to Na+ reabsorption [Na+/K+countertransport)
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What is the fx of ADH?
makes collecting duct more permeable to H2O; water leaves and urine is concentrated
193
Ascending loop of Henle
Thick, impermeable to water. NaCl actively transported out
194
Descending loop of Henle
thin, water permeable
195
Why is NaCl actively transported out of the ascending loop of Henle and not water?
To create a high concentration of solutes in the interstitial space surrounding the nephron that drives passive reabsorption of water into the interstitial space from the collecting ducts and the descending limb (fluid maintenance)
196
Why does water leave the descending loop of HEnle?
due to the medullary gradient by NaCl being actively transported into the interstitial space by the ascending loop
197
Loop diuretics action
exert effect in the thick ascending loop of henle
198
Thiazide diuretics
prevent absorption of NaCl in the distal convoluted tubule
199
aldosterone antagonists (potassium sparing diuretics)
reduce sodium reabsorption and decrease potassium secretion in late distal tubule and cortical collecting tubule site regulated by aldosterone
200
What is erythropoietin?
Hormone excreted by the kidney in response to hypoxia - regulates the differentiation of RBCs in bone marrow
201
What is the fx of vitamin D?
increases calcium reabsorption from the GI tract, excreted by kidneys, helps regulate calcium deposition in bone tissue
202
What occurs when HCO3- combines with H+?
Carbonic acid is formed H2CO3
203
What should the pH be?
7.35-7.45
204
Volatile acid (H2CO3 - carbonic acid)
dissociates in H2O and CO2 and leaves via lungs
205
nonvolatile acid or fixed acids
buffered by body proteins or extracellular buffers and are eliminated via kidneys. Product of metabolism of dietary proteins, oxidation of sulfur containing amino acids, etc, etc
206
How is carbon dioxide transported in circulation?
dissolved as a gas, as a bicarbonate ion, as carbaminohemoglobin
207
This reaction is catalyzed by carbonic anhydrase...
CO2 + H2O -> H2CO3 -> H+ + HCO3-
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How is pH regulated?
1. Chemical buffer systems of the body fluids 2. the lungs (inc/decr ventilation, bicarbonate buffering system) 3. the kidneys which eliminate H+ and both reabsorb and generate HCO3-
209
Where does most of H+ elimination (to maintain pH) and HCO3- reabsorption occur?
PCT - 80-90%
210
LAb tests used in assessing acid-base balance
1. arterial blood gases and pH 2. CO2 content and HCO3- levels 3. base excess or deficit 4. the anion gap
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What is the anion gap?
difference between the negatively charged and positively charged electrolytes. Anion gap high? - blood is more acidic
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Metabolic disorders
alteration in plasma bicarbonate due to changes in ECF acid-alkali levels (e.g. metabolic acidosis could result from renal bicarb wasting)
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respiratory disorders
alterations in PCO2 due to changes in alveolar ventilation rates (e.g. respiratory acidosis would result from impaired CO2 elimination)
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Metabolic Acidosis
A decrease in bicarbonate due to excessive production of metabolic acids, inability of kidneys to excrete acids, bicarbonate loss, increased plasma Cl- concentrations
215
Respiratory compensation for metabolic acidosis
hyperventilation to decrease PCO2
216
Renal compensation of metabolic acidosis
increased H+ excretion and increased HCO3- reabsorption
217
Tx of metabolic acidosis
correct root cause, restore fluid and electrolyte loss, improve O2 delivery to overcome lactic acidosis, use of NaHCO3 under limited circumstances
218
Metabolic alkalosis
increase in bicarbonate caused by excessive gain of bicarbonate or alkali, excessive loss of H+ ions, increased HCO3- retention, volume contraction
219
Respiratory compensation of metabolic alkalosis
hypoventilation to increase PCO2
220
Renal compensation of metabolic alkalosis
decreased H+ excretion and decreased HCO3- reabsorption
221
Tx of metabolic alklalosis
KCL therapy - Cl- replaces HCO3- and K+ corrects potassium deficit allowing kidney to retain H+ while eliminating K+
222
Metabolic alkalosis - vomiting
increase in pH due to primary excess of HCO3- ions caused by loss of H+ ions, net gain in HCO3, loss of Cl- ions in excess of HCO3- ions
223
Respiratory acidosis
increase in the PCO2 due to acute or chronic conditions that impair effective alveolar ventilation and causes and accumulation of PCO2
224
Renal compensation of respiratory acidosis
increased H+ excretion and increased HCO3- reabsorption
225
Tx of respiratory acidosis
improve ventilation
226
Respiratory alkalosis
decrease in PCO2 due to excessive ventilation (anxiety)
227
renal compensation of respiratory alkalosis
decreased H+ excretion and decreased HCO3- reabsorption
228
Tx of respiratory alkalosis
Correct underlying cause, supplemental O2 if hypoxic
229
Most common renal congenital anomalies
anomalies in shape and position - e.g. horseshoe kidney - fusion of two kidneys
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What is dysgenesis?
failure of an organ to develop normally
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What is agenesis?
complete failure of an organ to developW
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What is Potter syndrome?
characteristic facial features of newborns with renal agenesis - eyes widely separated and have epicanthic folds, ears low set, nose borad and flat, chin receding. Causes: cystic renal dysplasia
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Hypoplasia
failure of an organ to reach normal size, normally only affects one kidney
234
Cystic disease of the kidney
fluid filled sacs or segments of a dilated nephron
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What are the causes of cystic disease of the kidney?
1. tubular obstructions that increase intratubular pressure 2. changes in the basement membrane of the renal tubules that predispose to cystic dilation 3. May be congenital, genetic, or result of a secondary pathology 4. replacement of kidney tissue by cysts reduces/removes functional properties
236
Types of Cystic Disease of the Kidney
1. Simple and acquired renal cysts 2. medullary cystic disease 3. polycystic kidney disease (PKD) - single gene disorders
237
What are the polycystic kidney disease - autosomal dominant polycystic kidney disease, manifestations?
pain, gross hematuria, infected cysts, hypertension due to compression of intrarenal blood vessels
238
What are the polycystic kidney disease - autosomal recessive polycystic kidney disease, manifestations?
bilateral flank masses, severe renal failure, impaired lung development, liver fibrosis, portal hypertension
239
Causes of Urinary Tract Obstruction
Developmental defects, calculi (stones), pregnancy, BPH, scar tissue resulting from infection and inflammation, tumors, neurological disorders such as spinal cord injury
240
Manifestations of Urinary Tract Obstruction depend on:
site of obstruction and cause, the rapidity with which the condition developed
241
Common symptoms of Urinary Tract Obstructions
pain, s/s of UTI, manifestations of renal dysfunction
242
What are the damaging effects of Urinary Obstruction?
hydronephrosis - urine filled dilation of renal pelvis and calices associated with progressive atrophy of kidneys due to obstruction of urine outflow
stasis of urine - predisposes to infection and stone formation
development of backpressure - interferes with renal blood flow and destroys kidney tissue (atrophy) while inducing formation of cysts
243
Kidney Stones/Renal Calculi/Nephrolithiasis
crystalline structures that form from components of the urine
244
Requirements for formation of kidney stones/renal calculi/nephrolithiasis?
- a nidus to form
- urinary environment that supports continued crystallization of stone components
- high levels of circulating (for example) can become very concentrated in filtrate, under acidic conditions the filtrate will undergo precipitation of calcium and crystals will form
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Factors influencing the formation of renal calculi
-concentration of stone components in the urine
- the ability of stone components to complex and form stones
- the presence of substances that inhibit stone formation
246
Types of renal calculi
-calcium stones (oxalate or phosphatase)
-uric acid stones
-cystine stones
247
Examples of endogenous renal calculi inhibitors
Citrate (citric acid cycle by-product), magnesium, mucoproteins
248
Prevention of Renal calculi
-dietary restriction (increase fluids, reduce Na+ to reduce Ca++ excretion, reduce animal protein)
-calcium salt supplementation
-thiazide diuretics (by decreasing saturation of calcium salts in urine)
-cellulose phosphatase
249
Tx of Renal Calculi
-pain management
- antibiotic for infection
- removing stones - uteroscopic removal, percutaneous removal, extracorporeal lithotripsy (lasers)
250
Dx of Renal Calculi
-urinalysis
-radiography
-intravenous pyelography
-ultrasonography
251
UTIs prevalence
2nd most common type bacterial infection presenting in clinics after respiratory infections
252
types of UTIs
-asymptomatic bacteriuria
-symptomatic infections
-lower UTIs - cystitis
-upper UTIs - pyelonephritis, more serious (ability to induce renal damage
253
Causes of UTIs (uncomplicated)
bacteria that enter through the urethra
-E. coli (most common cause)
-non E. coli negative rods
-staphylococcus saprophyticus
-gram positive cocci
254
Most common cause of gram-negative septicemia in hospitalized patients
catheter induced infection
255
Causes of UTIs associated with stasis of urine flow
-anatomic obstructions (urinary tract stones, BPH, pregnancy, malformations of the uterovesical junction
-increased pressure resulting in reflux
-functional obstructions (neurogenic bladder, infrequent voiding, detrusor (bladder) muscle instability, constipation
256
Body protective mechanisms against UTIs
-washout phenomenon - flushing out of bacteria through urine
-mucin layer (physical barrier)
-local immune responses
-normal flora of the vaginal periurethral area
-prostate secretions
alterations in pH, diet, and drug interactions can alter this normal production and result in infections
257
Dx of UTIs
-based on symptoms and presence of microorganisms in urine
-xray fils, ultrasonography, and CT and renal scans are used to idenitfy contributing factors
-urine dipstick
258
Tx of UTIs
-based on the pathogen causing the infection (C +S test)
259
Characteristics of acute episode of Cystitis (bladder infection)
-frequency of urination (as often as every 20 mins)
-lower abdominal or back discomfort
-burning pain on urination (dysuria)
cloudy and foul smelling urine on occasion
260
S/s of UTI
-urination urgency
-frequent urination
-painful urination (dysuria)
-hematuria
-cloudy or foul smelling urine
-pelvic discomfort/pressure
-low grade fever
261
Urinary incontinence
involuntary voiding, many different causes
262
Types of Urinary Incontinence
-Neurogenic incontinence - caused by nerve spinal cord or brain damage
-stress incontinence - leakage of urine with sudden pressure on the bladder and urethra
-overflow incontinence - weak bladder muscle or blockage, incomplete emptying
-urge incontinence/overactive bladder - condition where the bladder can no longer urinate normally
- functional incontinence - physical barriers that block access to bathroom
263
Tx for Urinary Incontinence
- behavioral - manage fluid intake before bed
-drugs - alpha adrenergic agonists
-catheters and urine collecting devices
-surgery
264
Immune Mechanisms of Glomerulonephritis
- glomerular antibodies - inflammatory response - interact with antigens present in basement membrane of glomerulus
-circulating antigen-antibody complexes - can stimulate autoantibody reactions against the glomerular membrane or circulating complexes can get stuck in the glomerular filtration pore - immune and inflammatory damage to membrane
265
Characteristics of Glomerulonephritis
-hematuria with red cell casts (clusters of RBCs held together by protein matrix derived from renal tubules
- a diminished GFR
- oliguria
-HTN
266
Causes of Glomerulonephritis
-disease that provoke a proliferative inflammatory response of the endothelial, mesangial, or epithelial cells of the glomeruli
-inflammatory process: damages the capillary wall, permits RBCs to escape into the urine, produce hemodynamic changes that decrease the GFR
267
Cellular changes in glomerular disease - Proliferative
- endothelial
-mesangial
-leukocyte infiltration
-crescent formation
disrupts normal structure - end result of decreased GFR with loss of filtration and subsequent tubule damage
268
Cellular changes in glomerular disease - Basement membrane thickening
deposition of dense non-cellular material on endothelial and epithelial sides of basement membrane or within membrane
disrupts normal structure - end result of decreased GFR with loss of filtration and subsequent tubule damage
269
Cellular changes in glomerular disease - sclerosis
increased extracellular material in mesangial , subendothelial or subepithelial tissue of the glomerulus
disrupts normal structure - end result of decreased GFR with loss of filtration and subsequent tubule damage
270
Cellular changes in glomerular disease - fibrosis
deposition of collagen fibers
disrupts normal structure - end result of decreased GFR with loss of filtration and subsequent tubule damage
271
Diffuse glomerular changes
involving all glomeruli/all parts
272
focal glomerular changes
only some glomeruli affected
273
segmental glomerular changes
only certain segment of glomeruli affected
274
mesangial glomerular changes
only affects mesangial cells
275
Urinary Changes in Glomerulonephritis
-proteinuria
-hematuria
-pyuria (increased WBCs)
-oliguria (low urine output)
-edema
-hypertension
-azotemia (buildup of nitrogenous products in the blood)
276
Types of Glomerular Disease
-acute proliferative glomerulonephritis - immune complex mediated, induces inflammation, cells lost (RBCs and WBCs) and proteins, pyuria, hematuria, oliguria, low GFR HTN, granular casts
-rapidly progressive glomerulonephritis
-nephrotic syndrome - results from increased glomerular permeabilityy and loss of plasma proteins (albumin) in urine
-membranous glomerulonephritis
-chronic glomerulonephritis
277
Nephritic syndrome vs nephrotic syndrome
nephritic syndrome - a disease
nephrotic syndrome - a collection of symptoms
278
Nephritic syndrome(a disease) causes:
-strep throat
-lupus
-hereditary
-goodpasture syndrome
-reactions to meds
-too little K+
-too much Ca ++
-autoimmune diseases
279
Diagnostic Features of Nephritic Syndrome (disease)
hematuria, mild to moderate proteinuria, HTN, oliguria, red casts in urine
280
Clinical features of Nephritic syndrome (disease)
hematuria, edema (less than in nephrotic), oliguria, pruritus
281
Nephrotic Syndrome (collection of symptoms) caused by:
-diseases and conditions that only affect the kidneys (focal segmental glomerulosclerosis)
-less commonly venous thromboembolism, ARF, or serious bacterial infection
282
Diagnostic Features of nephrotic syndrome (collection of symtpoms:
-proteinuria
-hypoalbuminemia
-diagnosed based on these findings
283
Clinical features of nephrotic syndrome
-edema
-hyperlipidemia
-hypercoagulability
frothy urine
284
Tubulointerstitial disorders
-damage to the proximal loop, or distal portion of the nephron
-acute tubular necrosis
285
What is renal tubular acidosis
-proximal tubular disorders that affect bicarbonate reabsorption
-damage to the proximal tubule is due to decreased bicarbonate, thus less H+
-H+ accumulates over and above any buffering that may be present from bicarbonate
286
What is pyelonephritis
-inflammatory reactions will damage the tubular portion of the nephron resulting in decreased functioning
-underlying stimulus is the infective organism
-Tx must be aimed at removing the infective organism in order to lessen the inflammatory damage
287
major groups of renal cancer
- embryonic kidney tumors occurring during childhood
-adult kidney cancers
288
Embryonic kidney tumor occurring during childhood
-Wilms Tumor
-onset - 3-5 years in one or both kidneys
-WT1 mutation on chromosome 11
-distorts the kidney and decreases its function
-surgery and chemo and radiation
-90-95% long term survival for stages 1-3
289
Adult kidney cancers
-renal cell carcinomas
-silent disorder in early stages - symptoms indicate advanced disease
-triad S/s - hematuria, flank pain, prsence of palpable mass
290
Renal failure
kidneys fail to remove metabolic end products from the blood and regulate the fluid, electrolyte, and pH balance of the extracellular fluids
291
Acute renal failure (ARF)
-abrupt in onset
-often reversible if caught early and tx
292
Chronic Kidney disease (CKD)
-end result of irreparable damage to kidneys
-develops slowly, usually over the course of a number of years
293
Underlying causes of renal failure
-renal disease
-systemic disease
-urologic defects of non-renal origin
294
Prerenal causes of ARF/AKI
-hypovolemia
-decreased vascular filling
-HF and cardiogenic shock
-decreased renal perfusion due to vasoactive mediators, drugs, diagnostic agents
results in decreased GFR - lack of flow to the kidney
295
Postrenal causes of AKI/ARF
-bilateral ureteral obstruction
-bladder outlet obstruction
results in decreased GFR - result of backpressure on the kidney
296
Intrinsic or Intrarenal causes of ARF/AKI
acute tubular necrosis (ATN) due to:
- prolonged renal ischemia
- exposure to nephrotoxic drugs, metals, organic solvents
-trauma, burns and mjor surgery are common precursors
-intratubular obstruction resulting from hemoglobinuria (Hgb in urine), myoglobinuria, myeloma light chans or uric acid casts
-acute renal disease
297
Phases of Acute renal failure
-onset or initiating phase - last hrs to days, time from onset of precipitating event until tubular injury occurs
-maintenance phase - chracterized by a marked decrease in GFR
-recovery phase - period during which repair of renal tissue takes places
298
Common Causes of CKD
-HTN
-diabetes mellitus
-polycystic kidney disease
-cancers
-glomerulonephritis
-obstructions of the urinary tract
-diseases of the heart and lungs
-chronic use of pain medication
slow to develop and arising from other disorders, renal tissue slowly damaged and lost insidious onset
299
Stages of CKD progression
-diminished renal reserve
-renal insufficiency
-renal failure
-end stage renal disease (ESRD)
300
Clinical manifestations of CKD
-accumulation of nitrogenous wastes (azotemia)
-alterations in water, electrolyte, and acid base balance
-mineral and skeletal disorders
-HTN and alterations in cardiovascular fx
-gastrointestinal disorders
-neurologic complications
-disorders of skin integrity
-immunologic disorders
301
Factors determining the manifestations of renal failure
-extent of renal function that is present
-coexisting disease conditions
-type of renal replacement therapy that the person is receiving
302
CKD manifestations - accumulation o nitrogenous wastes (azotemia)
-urea starts to accumulate in blood (early sign of kidney failure) - can eventually result in uremia
-nitrogenous waste accumulation can occur in blood without symptoms (azotemia)
-uremia = symptoms associated with decreased clearance of nitrogenous wastes (when approx 2/3 of nephrons destroyed, encephalopathy, peripheral neuropathies, pruritus + serositis
303
CKD manifestations - disorders of water, electrolyte, and acid base balance
-sodium water balance - early sign of kidney damage is polyuria with nearly isotonic urine to plasma, fluid volume expansion, edema, and HTN
-potassium balance - approx 90% of potassium excretion is through kidneys, excretion increases as kidney adapts to a decrease in GFR, hyperkalemia in late stage/renal failure
-acid base balance - kidneys normally regulate blood pH by eliminating hydrogen ions produced in metabolic processes and regenerating bicarb - breakdown can result in metabolic acidosis - can become stabilized with buffering capacity of bone - result in skeletal disorders due to increased bone resorption
304
CKD manifestations - skeletal disorders
-decreased phosphate excretion and increased serum phosphate levels
-serum calcium levels decrease
-PTH is stimulated to increase bone resorption releasing calcium
-PTH increases phosphate excretion
-vit d synthesis is impaired (conversion to active form of vitamin d - calcitriol - occurs at kidney
-combo of these factors result in renal osteodystrophy
305
2 major types of osteodystrophy
-high bone turnover
-low bone turnover
306
Hematologic Disorders Accompanying renal failure - anemia
- kidneys primary site for EPO production
- iron deficiency - dietary restrictions and blood loss with dialysis
- decreased blood viscosityand compensatory HR increase - angina linked to reduced O2 supply
-hypoxic/oxidative stress at kidney may further contribute to CKD progressionH
307
Hematologic Disorders Accompanying Renal Failure - coagulopathies
platelet function is impaired with CKD
308
Cardiovascular disorders accompanying renal failure
-HTN - increased vascular volume, elevated peripheral vascular resistance; decreased renal vasodilator prostaglandins; increased RAAS system
-heart disease - left ventricular hypertrophy and dysfunction; ischemic heart disease
-pericarditis - approx 20% of people receiving chornic dialysis; metabolic toxins either from uremic state or dialysis
309
CKD altered drug reabsorption
due to antacid treatment (contain phosphate, magnesium)
310
CKD altered metabolism
-less protein bound drugs - man ydrugs bind to albumin, unbound drugs free to be metabolized
-alterations in dosage may be required qith CKD
-because of a loss of proteins (hypoalbuminemia)
311
Tx during renal insufficiency stage of renal failure
-tx UTIs promptly
-avoid med with renal damaging potential
-control BP
-control blood glucose
-stop smoking
-dietary management - protein, carbs, fats, calories, potassium, sodium and fluid intake
312
Med management of renal failure - hemodialysis
-artificial kidney - capillary tubes with semipermeable membranes
-typically requires 3 times/week 3-4 hrs
313
Med management of renal failure - peritoneal dialysis
sterile dialyzing solution is injected into peritoneal cavity - metabolic end products and ECF diffuse into dialysis solution, remove after few hours, can be performed at home
314
med management of renal failure - transplantation, sucess depends on
-health of recepient
-degree of histocompatibility
-organ preservation
-immunologic management
-organ rejection primary concern
-recipient must be on immunosuppressant therapy for rest of life
315
CKD children causes
-congenital malformations
-inherited disorders
-acquired diseases
-metabolic syndromesMAnif
316
manifestations of CKD in children
-severe growth impairment
-developmental delay
-delay in sexual maturation
-bone abnormalities
-developmental psychosocial problems
317
CKD in elderly
-normal decrease in GFR with age
-increased detrimental effects of nephrotoxic drugs
-greater incidence of cerbrovascular, cardiovascular, and skeltal system effects
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