Content Summary and Exam 3 Blueprint
Circulatory Disorders (20-22 questions)
NOTE: THERE IS NO WAY TO UNDERSTAND THESE DISORDERS IF YOU DO NOT HAVE A THOROUGH
UNDERSTANDING OF THE BASIC FLOW OF THE CIRCULATORY SYSTEM (that means forwards & backwards!):
Right atriumtricuspid valve right ventriclepulmonic valvepulmonary artery
pulmonary arteriolespulmonary capillaries [gas exchange with alveoli occurs here]
pulmonary venules pulmonary veinsleft atriummitral valveleft ventricle aortic
valve aorta
part of this freshly oxygenated blood goes into coronary arteries, which
branch off the aorta just beyond the aortic valve.
part goes up to brain via carotids
rest goes to tissue beds of remainder of body
arterioles capillaries [gas exchange with tissue occurs here] venules
veinsinferior vena cava (from body) or superior vena cava (from head) right atrium
Peripheral vascular disorders: arterial & venous
Arterial
1.
2.
healthy arteries:
 normal muscle tone = flexible, compliant, patent normal state of resistance
 good arteries = good perfusion (delivery of O2 & nutrients to tissues) = no ischemia
o some ways to measure good perfusion: cap refill < 2-3 seconds; skin pink, warm; pulses
normal; organ-specific: good urine output, good mentation (note: other important factor in good
perfusion – good cardiac output)
bad arteries (with arterial problems, think ischemia)
 two basic categories of problems:
o alteration in tone: too constricted (inflexible, brittle, non-compliant, inelastic) or too dilated (no
tone, too slack)
o altered lumen: non-patent—blockage of some sort
 arteriosclerosis & atherosclerosis biggest causes of bad arteries… & if found in one set of arteries in body,
will usually be in others as well—ie, usually systemic disease processes.
 arteriosclerosis
o arteries stiffen, thicken, due to damage from HTN, diabetes, hyperlipidemia
o elasticity & compliance decrease= abnormal tone & resistance.
 atherosclerosis
o fatty deposits settle into micro-injuries in arteriosclerotic vessels inflammatory process
triggered combination of fat, collagen, clots, etc = plaques that can narrow artery lumens
further
o increased risk and severity the higher the LDLs in the bloodstream & the lower the HDLs
 LDLs—high in cholesterol; primary component in plaques
 HDLs—high in protein; scavenge extra LDLs in circulation and take them to liver to be
broken down & gotten rid of; ideally want HDLs to be high, at least >40, & the total
cholesterol-to-HDL ratio to be <4.
 narrowing / hardening / plaques can block flow to tissues = bad perfusion= ischemia; sequela / S&S:
o ischemic pain—worse with exertion, eases with rest
 in leg arteries intermittent claudication

in heart angina
o poor perfusion in peripheral arteries: diminished pulses, delayed cap refill; pale cool skin; delayed
healing
o heart: hypoxic cardiomyocytes decreased contractilitydecreased cardiac output
o brain: altered mentation
o kidneys: decreased urine output
1
3.
HTN
 consistent elevation of BP > 130’s/80’s.
 most hypertensives have primary HTN, AKA “essential” HTN, rather than secondary HTN (caused by
some other disease factor like adrenal tumor).
 risk factors—see notes
 patho: usually there is atherosclerosis and/or overdrive of sympathetic nervous system (SNS) and/or
overdrive of RAAS
o SNS overdrive:
 epinephrine levels are consistently elevated stimulates beta receptors in heart
tachycardia &/or increased contractility of heart
 causes greater ejection pressures greater driving pressure over time will cause
sustained increase in BP.
o RAAS overdrive
 normal effects of RAAS are increased blood volume from vasoconstriction & retention of
Na+ & H2O when needed for low blood pressure and/or low blood volume
 but with overdrive state, RAAS always “in gear” sustained vasoconstriction & larger
blood volume higher BP
 sequela of these overdrive situations:
o higher pressures on arteries damage them & make atherosclerosis worse and /or
o arterial walls respond by “shoring up”—hypertrophy makes things worse by narrowing arterial
lumens even more.
 S&S of HTN take long time to show up; will usually affect 3 organ systems the most:
o neurologic: strokes; retinal changes from damage arterioles in retina.
o renal system: hematuria, proteinuria; renal failure
o circulatory system: increased workload on heart (increased resistance to LV ejection) MI, HF;
peripheral arterial dz (PAD).
 treatment is aimed at different parts of the overdrive situations—ACE inhibitors, diuretics, beta-blockers
4.
peripheral arterial insufficiency, AKA peripheral arterial disease (PAD)
 arterial disease outside the heart—seen most often in ischemic S&S in the legs
 S&S – intermittent claudication, diminished pulses, skin ulcers, no hair on legs, cool pale mottled skin.
5.
aneurysms
 outpouching of arterial walls due to:
o stiff, noncompliant arteries, as in atherosclerosis plus
o HTN (usually).
 can be found in brain, aorta (abdominal & thoracic), other arteries like femoral.
 S&S usually include pain (if large and/or if ruptures), sometimes diminished pulses & ischemia to distal
tissues
6.
arterial thrombi & emboli
 clots that from in pockets of sluggish arterial flow and/or where there are areas of arterial injury
 examples include atrial fibrillation & thrombus of femoral artery
 atrial fibrillation (chaotic electrical impulses cause quivering of atria instead of concerted, organized
ejection of blood into ventricles) causes pockets of blood in the atria to sometimes not flow
appropriately platelets, fibrin, etc, can collect thrombus on atrial wall
o if happens in left atrium, clots can become emboli can flow to brain & other parts arterial
system
o if happens in right atrium, emboli would go to lungs
 other areas of thrombi femoral artery would cause ischemia to distal tissue
5.
summary of arterial disorders
 think problems with decreased perfusionleads to ischemia, usually due to:
o
arteries that are pathologically dilated or constricted
o non-patent lumen (clot, plaque, etc)
 all have commonalities of ischemic pain, certain risk factors, and treatment modalities (see notes)
2
Venous
1.
2.
3.
venous insufficiency (with most venous problems, think peripheral venous congestion edema)
 seen in older people, pregnant women, standing up for long time, genetics
 valves in leg veins “floppy”—allows gravity to overcome normal upward flow of venous blood
 backflow congestion & stasis of blood in lower legs & feet increased hydrostatic pressure edema
 complications include venous stasis ulcers and “breeding ground” for thrombi
venous thrombi & emboli—
 venous thromboembolism—VTE-- encompasses both the states of DVT (deep vein thrombosis) and PE
(pulmonary embolism)
o Virchow’s triad—3 classic risk factors (predispose a person to VTE):
 venous stasis (ex—venous insufficiency, immobility)
 injury to lining of vein (ex—surgery, etc)
 hypercoagulability (ex—dehydration)
o DVT—thrombus in the deep veins that can develop in presence of certain risk factors
 S&S of DVT are those of thrombophlebitislocal inflammatory state pain, erythema,
warmth of area
o PE-- venous thrombi can get loose & become venous emboli… can go to lungs (pulm
embolus)SOB, chest pain, hemoptysis
summary of venous disorders
 think problems with venous backflow/ congestionperiph edema
 also, stasis & immobility = sluggish blood flow
 tx relates to patho:
o encourage mobility
o encourage hydration
o put up feet
o watch for skin problems related to tightness from edema
o give anticoagulants to prevent thrombus—coumadin, heparin, aspirin (same ones are given for
preventing arterial thrombi too, as in tx for coronary artery dz, atrial fibrillation, etc.)
Cardiovascular disorders
1.
changes that can affect CO: HR X SV (SEE CONCEPT MAP: FACTORS INFLUENCING CARDIAC FUNCTION)



rate & rhythm properties
o normal heart rate (HR) & rhythm called normal sinus rhythm (NSR)—anything outside NSR norm
has potential to affect cardiac output (CO).
o HR norm = 60-100; higher = tachycardia, lower = bradycardia
o normal rhythm = regular, NSR; irregular rhythms include atrial fibrillation, ventricular fib
neurohormonal influences: epinephrine & norepinephrine (sympathetic) increase HR & contractility;
acetylcholine (parasympathetic) via vagus nerve decreases HR.
electrolyte disturbances
o hypokalemia hyperpolarization bradycardia, decreased contractility, weakness
o hyperkalemia hypopolarization irritable myocardium till later patient picture looks like
hypokalemia.

contractility—how toned, how well heart ejecting blood.
o diminished contractilitylow SV low CO diminished perfusion
o negative inotropic effect—anything that decreases contractility; positive inotropic effect—
anything that increases contractility; ex—certain meds like digoxin are positive inotropes

preload = blood coming back to heart = volume-related issues
o low preload fluid volume deficit usually S&S dehydration; also low amt of blood sent to left
heart = low SV CO
o high preload fluid volume overload S&S fluid overload; also high amt of blood sent to left =
can cause too much workload on left ventricle.
3

afterload = resistance to flow
o can be normal resistance, low, or high – ultimately affects SV, CO, perfusion
o can affect right heart or left
o
o
2.
afterload alterations to LEFT VENTRICLE:
 pathologically high afterload, AKA high SVR(systemic vascular resistance)—systemic
arterial resistance to flow leaving left ventricle (ejection of blood):
 can be due to systemic arterial probs such as brittle arteries, high blood volume,
chronic HTN, other systemic arterial vasoconstriction situations
 S&S are related to decreased perfusion (because high resistance to ejection
results in not enough pressure & volume going to tissues): delayed cap refill,
cold extremities, diminished pulses, eventually could result in low BP
 pathologically low afterload usually associated with arterial vasodilation: heat, meds,
endotoxins, inflammatory mediators.
 S&S—initially CO is high due to less resistance, but eventually there is pooling of
blood in periphery  less blood back to heart low CO low BP

afterload alterations to RIGHT VENTRICLE:
 pathologically high afterload—ie, any resistance to flow leaving right ventricle; often
referred to as pulmonary vascular resistance – PVR-- because the resistance is coming
from the vasculature & general status of the lungs; caused by pathologically increased
pulmonary arterial vasoconstriction and/or lung problems such as chronic bronchitis
coronary artery disease (CAD)
 caused by same problems as with any other arterial disease (atherosclerotic process, HTN, etc), but
coronaries are the ones affected
 also linked to high homocysteine levels (free radical-type behavior) and CRP (inflammatory component).
 angina—ischemic pain in the heart muscle, so usually follows typical ischemic pattern of increasing with
exercise, decreasing with rest.
o classic S&S-- chest pain, left arm, jaw, back pain
o but not all S&S are classic, due to the many sensory nerve pathways that lead to brain from
heart area
 other S&S of cardiac ischemia
o SOB, nausea, diaphoresis
o dysrhythmias, other EKG changes
o coronary-specific S&S:
 LCA blockage LV affected low CO  can have S&S decreased perfusion
 RCA blockage RV affected; also SA node bradycardia, for ex.; eventually can also
result in low CO.

ischemic pattern is a spectrum from mild to severe; the more severe, the more likely to have infarction
(cell death due to ischemia)—see diagram on pg 21 of notes; classification of CAD usually falls in one of
two subcategories according to that spectrum:
o on milder end of spectrum is first category: stable angina
 pain pattern very stable & predictable, usually rated on low end of pain scale – ex--“3 out
of 10”
 stability usually due slow plaque development, thereby allowing development of collateral
circulation over time
o on more severe end is second category: acute coronary syndrome (ACS)
 usually occurs with sudden blockage or worsening of preexisting plaque
 2 subdivisions of ACS—unstable angina (ischemia worsening) & MI (cells beginning to
die)
4



3.
S&S of ACS
 pain on higher end of pain scale (6 to 10 out of 10) plus some or all of S&S
noted above
 blood work—high CK & troponin
tx for CAD
o anything that opens up coronaries more and decreases workload of heart (ex—decrease high
afterload & preload) ; depending on severity of CAD:
 O2, NTG, other vasodilators, anti-hypertensive meds, anticoagulants (coumadin, heparin,
aspirin), other anti-platelet meds…why would these be given?
 for MI, also may give clot-busting med.
sequela of CAD-related situations can be hypertrophy of cardiac muscle cardiomegaly
heart failure (HF) [SEE HF CONCEPT MAP in notes]
 basic definition / characteristic: failure of heart to eject all of blood in normal forward fashion
 this is due to one or more of these factors:
o pump problem (ex—MI weakens the heart & decreases contractility)
o increased afterload—increased resistance (such as narrowed, atherosclerotic arteries) has
decreased ability of heart to easily eject blood.
o increased preload—fluid volume overload has increased work load of heart
 two general sequelae:
o decreased CO, therefore resulting in inadequate tissue perfusion (inability to deliver what is
needed by body)
 because of this, the RAAS kicks in (“thinking” it is helping, but is really hurting the
situation!), and there is yet more systemic arterial vasoconstriction (increased afterload)
AND body hanging on to water (increased preload)
AND
o problems with fluid back-up (into the lungs when the left ventricle fails; into the venous system
when the right ventricle fails)
 **NOTE: it is these characteristics of hanging on to fluid & the back-up of fluid that give heart failure its
often-used label of “congestive”—heart failure almost always has fluid overload as a main component.**

left HF
o etiological mechanisms:
 can’t pump: process such as MI weakens left heart muscles (example: MI from a
blockage of the LCA damage to left heart myocardium can’t eject blood
forwardlow CO kidneys perceive a low blood volume/ pressure RAAS triggered
end result is increased systemic arterial vasoconstriction & increased blood volume [fluid
overload, ie increased preload] worsens workload on heart HF)
and/or
 high afterload (systemic vascular resistance-- SVR): high BP and/or chronically
constricted, inflexible arteries as in atherosclerosis (ex: aorta is narrowed & stiff from
atherosclerosis so LV can’t eject blood into it very well back-up of fluid into lungs)
and/or
 high preload – too much blood volume = too much workload on the heart  can’t eject
all blood forward
o
S&S --poor perfusion due to inability to fully eject blood from LV to tissues & cardiogenic
pulmonary edema from back-up lung crackles, dyspnea, orthopnea, PND (paroxysmal
nocturnal dyspnea)
o
o
diagnosis—(both LHF & RHF)-- BNP level—the higher the BNP the more HF there is.
tx (both LHF & RHF)—vasodilators to decrease afterload, diuretics to decrease preload, decrease
HR, increase contractility (positive inotrope)
5

4.
right HF
o etiological mechanisms:
 can’t pump: process such as MI weakens right heart muscles & can’t pump forward
and/or
 high afterload (resistance):
o increased pulmonary resistance (ex—from lung dz’s like chronic bronchitis) -– in
this case the RHF is called cor pulmonale
and/or
 high preload – too much blood volume = too much workload on the heart  can’t eject
all blood forward
o S&S—peripheral venous congestion (jugular venous distension, hepatic congestion & ascites,
peripheral edema) due to fluid back-up from right side of heart into periphery.
valvular disorders
 can have problems with opening properly (stenosis) or closing properly (insufficiency, AKA prolapse, AKA
incompetence,)
 etiology varied:
o ischemia from blocked coronary
o endocarditis
o rheumatic fever
 S&S depends on the valve affected, but commonality is usually a murmur
 stenosis-- valve gets stiff, blood-flow opening is then smaller and can block forward flow of blood
 valve insufficiency--valve is “floppy”
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Pulmonary Disorders (12-15 questions)
1.
ABGs (SEE “ABGs interpretation summary” document)
 basic tip: if PCO2 is out of normal range, the problem is respiratory; if HCO3 is out of normal range, the
problem is metabolic
ROME—Respiratory Opposite, Metabolic Equal
 respiratory acidosis
o pH low, pCO2 high
o usually caused by some degree of hypoventilationCO2 retention (hypercapnea) means more
carbonic acid tips scale toward acidosis (CO2, H2CO3, H+ = too much acid gang)
o many possible situations can be associated with hypoventilation: unconscious, head injury
impairing respiratory centers, neuromuscular disorders, pneumonia, flail chest, etc.
o kidneys try to compensate (“buffering”) by holding on to HCO3 or making more HCO3
 respiratory alkalosis
o pH high, pCO2 low
o cause: hyperventilation states too much CO2 blown off (not enough acid gang)
o kidneys compensate excrete more HCO3 in urine or hold on to more H+
 metabolic acidosis
o pH low, HCO3 low
o cause: metabolic accumulation of acid gang, as in ketoacidosis & lactic acidosis; or state of low
HCO3.
o lungs compensate blow off CO2 by hyperventilating
 metabolic alkalosis
o pH high, HCO3 high
o cause: metabolic accumulation of HCO3
o lungs compensate hypoventilation (thus holding on to more CO2 to increase acid gang)
ABG norms (memorize all these ranges):
pH: 7.35- 7.45; HCO3 (bicarb): 22-28; PCO2: 35-45; PO2: 80-100; SO2 97-100%
6
2.
terminology / concepts related to respiratory problems: see notes – know all terms such as dyspnea, hypo /
hyperventilation, kussmaul, V/Q ratio, etc.
3.
restrictive lung diseases (problem with inhalation)

can’t get air in to blood (V) OR can’t get blood to alveoli to be oxygenated (Q), so can have:
o
hypoxemia (low pO2 & SO2)
o S&S related to various degrees of dyspnea
o central cyanosis
o finger clubbing, if the hypoxemia is a chronic problem over long period of time
o V/Q mismatch
 normal V—4L air /minute inhaled; Q—5L blood/ minute come to alveoli; V/Q ratio is 0.8
 mismatch usually means some disease has caused either the V or Q to be low, resulting
in a ratio that is either higher or lower than normal
 significance is that mismatch causes or worsens hypoxemia & can have cyanosis.

broad categories of restrictive problems: those that result in low V/Q & those that result in high VQ

restrictive problems that result in low V/Q (usually result in low ventilation (V) so mathematically the
V/Q ratio is low)
o
chest wall restrictions:


o
airway restrictions



o
mechanical—deformities like kyphosis, flail chest, obesity
neuromuscular—myasthenia, polio, other paralytic diseases
foreign bodies, tumors of trachea & bronchi
croup (laryngotracheobronchitis)
 fever, barking cough, stridor
 treated by cool mist to decrease swelling & sometimes steroids
epiglottitis (this subject is “FYI” & not on test):
 usually viral infection that causes edema of epiglottis airway narrows
 S&S—fever, drooling, inspiratory stridor
pleural restrictions:

pleural effusion
 pleura get irritated (like in lung cancer) edemafluid into pleural space
 S&S—pleuritic pain (pleurisy), shallow breathing to avoid pain of deep breaths

pneumothorax—“collapsed lung”





disruption of normal lung integrity resulting in loss of normal negative pressure
in thorax that is key to the normal process of inhalation
traumatic pneumothorax—penetrating trauma from outside or penetrating
trauma from inside puncture to lung air into thorax positive pressure
collapses lung
spontaneous pneumothorax  rupture of weakened or diseased alveoliair leak
and collects between the pleural spaces  loss of negative intrathoracic pressure
 lung collapses
tension pneumothorax  when the collection of “trapped” air CAN affect the
uninjured lung AND reduce the cardiac output
tx—reestablish negative pressure by inserting chest tube other end goes to
water seal end result is one-way valve—air can escape thorax and can’t get
back in lung can re-expand into the thoracic space that was pathologically
occupied by air.
7
o
tissue restrictions
 pneumonia--lung infection;
 3 types-- community acquired (CAP), nosocomial, and/or aspiration.
o CAP—“walking pneumonia”
o nosocomial--usually more virulent type—gram neg organisms, etc.
o
aspiration pneumonia
can occur as result of aspirating food, fluid, vomitus, etc, when
person has suppressed gag or cough or swallow reflex (elderly
pts, debilitated, unconscious pts, etc)
 doesn’t usually occur when people are alert & have intact
reflexes
patho of pneumonia in general: microorganism inhaled inflammatory
reaction debris (called infiltrates) collects in parts of lung blocks off
bronchioles and/or bronchi atelectasis (collapse of small portions of lung
consolidation (parts of lung become stiff, no air exchange there)
one lobe—lobar pneumonia; more diffuse—bronchopneumonia
S&S—hypoxemia, crackles on auscultation and/or area of diminished sound (air
cant’ get through areas of consolidation), cough, dyspnea, fever, abnormal chest
xray
(note: atelectasis not just seen in pneumonia—can also happen in any situation
where pt is breathing shallow—post surgery, immobility, etc)






tuberculosis (TB)
 patho --inhaled microorganism like pneumonia but likes apices of lungs & forms
tubercles
 also can invade other body systems—bone, liver, spleen, meninges—then is
called miliary TB
 S&S very similar to pneumonia but more subtle & chronic, not as acute
 other S&S—fatigue, weight loss, night sweats, hemoptysis
 dx—skin test, chest xray
 tx—multiple antibx for 6 months or more

noncardiogenic pulmonary edema
not
on
test




S&S of cardiogenic and non-cardiogenic pulmonary edema are the same as both
are caused by fluid in alveoli decreased gas exchange hypoxemia, dyspnea,
crackles, pink frothy sputum coughed up.
etiology of cardiogenic and non-cardiogenic pulmonary edema differs (the
“story”): inhalation of noxious/harmful substance increased capillary
permeability  movement of fluid and plasma proteins  “fluid/water” damage
to alveolar cells  loss of surfactant  atelectasis  collapsed alveoli no longer
available for gas exchange
lung cancer


caused by smoking most of time; poor prognosis
2 main types:
o NSCLC—non-small cell lung cancer—prognosis not as bad as small cell
o SCLC—small cell—produce ectopic ADH SIADH often how this kind
of cancer is discovered – patient has S&S of SIADH.
restrictive problems that result in high V/Q (can’t get blood to air due to less perfusion than normal)
o patho-- perfusion defect—something that interferes with blood getting to alveoli to get
oxygenated ( results in low perfusion, therefore mathematically is a high VQ ratio, since Q =
perfusion).
o pulmonary embolus is typical perfusion defect problem
 risk factors—DVT, anything contributing to Virchow’s triad
8


4.
embolus lodges in smaller pulmonary arterioles blood doesn’t get to alveoli can
cause infarct of parts of lung tissue plus general hypoxemia
S&S—SOB, chest pain, sometimes hemoptysis
obstructive diseases (exhalation problems)
 commonalities of all obstructive diseases (apply to all specific obstructive dz’s mentioned below):
o usually can get air in ok (till late in the dz), but elastic recoil of lungs poorprevents easy
exhalation & often patients must use accessory muscles (intercostal, sternal, supraclavicular
retractions)
o expiratory phase is prolonged in an effort to give more time to get air out
o peak flow test (PF) is lower than normal
o tx—bronchodilators & steroids (to maximize lumen diameter of airways so air can escape more
easily)
o ABGs
 varied degree of hypoxemia (low SO2 & PO2) due to decreased gas exchange across
diseased airway lining or narrowed bronchi.
 in asthma & emphysema, usually mild respiratory alkalosis because most pts have mild
chronic hyperventilation to compensate for hypoxemia
 if condition worsens pt tirescannot keep up the hyperventilation PLUS CO2
cannot diffuse across diseased airway lining to be blown off retain CO2
hypercapnea respiratory acidosis dangerous situation!
 in chronic bronchitis, don’t usually see alkalosis—more likely to be in chronic respiratory
acidosis.

asthma
o

genetic predisposition to having hyper-responsiveness of airways to environmental allergens
inflammatory response edema of bronchial lining + bronchial constriction & spasmnarrowed
airways wheezing upon exhalation.
COPD—chronic obstructive pulmonary disease
o
o
2 subcategories—chronic bronchitis & emphysema—both mostly caused by smoking
emphysema



o
cigarette smoke irritants  chronically inflamed airways eventual destruction of
alveolocapillary membrane stiff, hyperinflated alveoli air trapping large,
hyperinflated, stiff lungs
some types also have alpha1-antitrypsin deficiency—contributes to loss of elastic recoil
characteristic S&S
 pink puffer—hyperventilates to get more air, so stays pink
 thin  hyperventilating takes up energy
 barrel chest to accommodate big lungs
 retractions, pursed lip breathing, tripod position
 chronic respiratory alkalosis
chronic bronchitis


cigarette smoke irritants inflammation bronchial edema thick mucus &
bronchospasm airways obstruction can’t get air out
characteristic S&S—blue bloater
 in general doesn’t hyperventilate-- hyperventilating doesn’t help get air in past
thick mucous, so stays cyanotic (“blue”)
 only recourse is to not expend energy usually slightly overweight “bloater”
 another reason for “bloater” nickname is they tend to have cor pulmonale due
to right ventricle fighting against lungs that are full of mucous & obstruction
 tends to retain CO2 (hypercapnea) due to inability of CO2 to diffuse out through
thick mucous therefore is usually in respiratory acidosis.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
9
GU & Renal Disorders (12-15 questions)
GU problems
1. male
 testicular cancer:
o younger men; usually painless mass
o cryptorchidism—undescended testicles—increases risk
o high cure rate when caught early (self-exam!)
 prostate problems:
o BPH—proliferation of prostate tissue seen in most men over 50
 biggest problem is compressing urethra S&S urgency, weak flow, slow to start flow, urinary
retention
 if urine backs up hydronephrosis, postrenal ARF
o cancer—diet high in saturated fat, high testosterone, family history and African American race; S&S
similar to BPH
 dx of both BPH & prostate cancer-- high PSA (prostate-specific antigen), enlarged prostate
on rectal exam
 infections—urethritis, prostatitis; most often caused by STI such as Chlamydia & gonorrhea.
2. female
 uterus
o dysmenorrhea—painful, heavy periods
o amenorrhea—no periods; associated with hormonal disturbances; hallmark of menopause
o endometriosis—ectopic endometrium in pelvis, abdomen which responds to monthly hormonal cycle;
pain, dyspareunia, can lead to infertility
 ovarian cancer—vague S&S—bloat, vague abdominal discomfort, constipation—so often not diagnosed till
has metastasized to areas such as liver.
 infections
o PID—pelvic inflammatory disease; infection of uterus, fallopian tubes (salpingitis) and/or ovaries
(oopheritis); most frequent causative organism—chlamydia; S&S—vaginal discharge, pelvic pain that
worsens with movement
o urologic infections—often generally called UTIs-- cystitis, pyelonephritis
 most common in women due to short urethra & proximity of urethral meatus to anus &
vaginal os
 S&S dysuria, frequency, pyuria, hematuria, sometimes costovertebral angle pain, fever.
3.
non-gender-specific disorders
 STI’s
o chlamydia, gonorrhea
o syphilis --chancres in primary stage; if not treated, other S&S show up in later stages, such a
neurosyphilis
o herpes simplex virus (HSV): HSV1—cold sore; HSV2—genital herpes… both stay permanently in
the body, “hiding out” in nerve tracts and breaking out periodically.
 obstructive disorders of urinary tract
o main serious sequela of any urinary obstructive disorder is hydronephrosis  can lead to malfunction
of nephrons & subsequent renal failure
o can be caused by variety of problems—adhesions, BPH uterine prolapse, neurogenic probs (page 6 of
notes); one of most common cause is lithiasis (state of having stones):
 kidney stones also called renal calculi or lithiasis; also nephrolithiasis; sometimes called by
area they have moved to: ureteral calculi / lithiasis, urethral calculi / lithiasis.
 stones can be caused by dehydration, problems with hyperuricemia (gout), hypercalcemic
disorders such as multiple myeloma
 classic S&S—sudden onset colicky pain, hematuria
 tx—lithotripsy if stone is too large to pass
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Renal problems (see prep, notes for A&P info, including importance of GFR, and AKI concept map)
AKI—Acute Kidney Injury-- abrupt (occurs over <48hrs) decrease in urine output (ie, GFR) and/or in serum
creatinine, so typical patient has acute oliguria and/or acute jump in serum creatinine. Usually classified as pre-renal,
post-renal, intra-renal (see drawing on page 10 of notes)
o prerenal--usually a problem of blood flow to kidneys—either a vessel problem like renal artery
blockage or decreased cardiac output from a volume deficit due to bleeding or dehydration, heart
failure, sepsis. Prerenal AKI can ultimately result in intrarenal AKI if the illness/problem is not fixed
quickly.
o intrarenal--something has caused acute tubular necrosis (ATN): ischemia to nephron blood
supply cells (casts) slough off into tubular canal & block urine flow retrograde pressure
hydronephrosis ischemia, necrosis, malfunction
 the cause of ATN is most often a direct “trauma” to nephrons, such as from
nephrotoxic drugs, hydronephrosis, toxic microbes, toxins, poisons, etc.
 S&S include casts seen on UA due to sloughing of dead cells
o postrenal—obstruction causes backup of urine into kidney (hydronephrosis) that interferes with
tubular function—can result in intrarenal AKI if not fixed
CKD—chronic kidney dz
1.
basically a spectrum of severity of decline in ability of kidneys to 1) maintain fluid balance & 2) maintain
metabolic functions.
2.
causes: congenital issues such as PKD; acquired nonrenal dzs such as HTN, diabetes, atherosclerosis;
autoimmune renal dzs such as:
 glomerulonephritis—inflammation of glomerulus
o inflammatory process causes glomerular membrane to become “leaky”—allows substances into urine
that are supposed to be kept in blood, such as protein & RBCs
o most often caused by autoimmune disorders such as
o post-infectious GN: post-strep autoimmune disorder—autoantibody attach to glomerular
membrane  inflammation, leaky membrane
o S&S --hematuria, hyperproteinuria, oliguria (due to less GFR)
3.
general patho & S&S of CKD
 see page 14-16 of notes for various concept maps & chart— most CKD patients end up with fluid
overload (edema, etc), and electrolyte probs such as hyperkalemia (be sure you can link S&S with the
“why”—ie, the patho)
o S&S—all body systems affected
 oliguria or anuria with often a low specific gravity because the kidneys are unable to concentrate
urine
 azotemia—high BUN & creat
 BUN high because kidneys can’t get rid of the urea nitrogen that is a breakdown product of
protein (BUN when high by itself & creatinine normal may not indicate renal problem – may
just indicate dehydration)
 a high creatinine (breakdown product of creatine kinase) is more specific to renal problems;
creatinine clearance will be low.
 uremia-- azotemia + other S&S listed below
 fluid & lyte imbalances from malfunction of absorption and/or excretion
 Na & H20 are retained peripheral edema, pulmonary edema (SOB, crackles), HTN
 hyperkalemia from unresponsiveness of DCT to effects of aldosterone
 hypocalcemia from lack of ability to activate vitamin D can’t absorb calcium in gut S&S
hypocalcemia (hypopolarization + Chvostek’s, etc—see Endocrine I chart for more)
 hyperphosphatemia—since pt is usually hypocalcemic, they are also hyperphosphatemic (Ca+
& PO4+ always balance each other)
 metabolic acidosis—can’t manufacture HCO3
 urea precipitates on skin pruritis
 neurologic changes from urea irritating brain tissue
 fatigue from anemia due to less production of erythropoietin
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
treatment (tx)
 when CKD reaches < 10% functioning nephrons, usually have to go on dialysis—this
is the point of end-stage-renal failure
 other tx based on patho above:
 restrict K, Na, & H2O in diet
 give phosphate-binding antacids
 give calcium & vitamin D supplements
 give erythropoietin
 antihypertensive meds & non-potassium sparing diuretics
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