Cardiovascular/CAD/PAD/Pulmonnary Flashcards
Flash cards for exam 3
Blood flows from the RA thru the __ valve
Tricuspid
Blood flows from the LA thru the __ valve
Mitral
Blood flows from the RV thru the __ valve
Pulmonary
Blood flows from the LV thru the __ valve
Aortic
Heart valves in order of flow:
Tricuspid
Pulmonary
Mitral
Aortic
Average stroke volume:
70mL/Beat
Cardiac output is determined by:
SV X BPM
Ability of the heart muscle to pump effectively!
Cantractility
Volume of blood in ventricles before contraction
Preload
Pulmonary vascular Resistance
RV afterload
Systemic vascular resistance
LV afterload
RV afterload can cause
right sided heart failure
LV after load can be too high due to:
HTN or atherosclerosis/arteriosclerosis
RV afterload can be caused by
atherosclerosis/arteriosclerosis of pulmonary vessels; stiff, noncompliant lung tissue
Normal preload value:
~4-6 L/min
Blood flow back to the heart
venous return
Most venous disorders occur in:
the legs
CVI
chronic venous insufficiency
DVT
deep vein thrombosis
CVI & DVT are usually related to problems pertaining to:
maintaining forward flow
AKA “valve incompetence”
Venous insufficiency
Pooling of blood due to venous insufficiency
venous congestion
Factors contributing to venous congestion
Gravity (standing for long periods)
Valve incompetence
Worn out, “floppy” valves in leg veins
Venous insufficiency
Blood pooling due to worn out, floppy leg vein valves
Venous stasis
Venous stasis causes an increase in:
hydrostatic pressure
Increased hydrostatic pressure can result in:
fluid shifting into the legs > edema
Mini concept map for Venous stasis ulcers
Venous stasis > increased hydro. pressure > fluid shift into tissue > edema > improperly functioning skin cells due to pressure > skin breaks easily > venous stasis ulcers
Another possible sequela to Venous insufficiency caused by increased hydrostatic pressure
Varicose veins
Contributing factors to CVI
Aging Genetics Obesity Pregnancy Job functions (standing) Immobility
Pathologic clot that forms in walls of veins, especially in veins of thighs & calves
deep vein thrombosis
Inflamed tissue around a DVT
thrombophlebitis
S/S of DVT
SHEP
Usually occurs unilaterally
May be extreme or discrete
May have no S/S
Risk factors of DVT are called:
Virchow’s Triad
Virchow’s triad consists of:
Injury to venous endothelium
Stasis of blood flow (due to immobility or venous insufficiency)
States of hyper-coagulability (dehydration, individual tendencies to clot easily)
Individual tendency to clot easily is called
coagulopathy
Potentially deadly sequela of DVT
Pulmonary embolism
Mini concept map of PE
DVT > thrombus or part breaks loose & travels > embolus > embolus travels to/thru the heart > embolism lodges into pulmonary arterioles
Oxygenated blood blocked from entering the pulmonary capillaries due to an embolism can cause:
SOB, chest pain
Hemoptysis as a S/S of PE is caused by:
inflammation of alveolar tissue causing leakage of blood/fluids into the alveolar space
S/S of PE include:
SOB, chest pain, shock, hemoptysis, death
Treatment/prevention of PE includes:
Encouraging mobility & hydration
Elevating feet & legs
Monitor skin for breakdown & stasis ulcers
Anticoagulants
Ability of arteries to work efficiently is determined by
vasomotor tone
State of the lumen
__ can be determined by vasomotor tone
BP
Normal, healthy arterial lumens should be
smooth and patent (free of any sort of blockage)
Delivery of O2 & nutrients to tissue beds via the arterial system
perfusion
Good perfusion results in:
adequate delivery of O2 & nutrients
Normal pulses & BP
Normal cap refill
Normal organ function
Strength & quality of pulses are indicative of:
state of the lumen & vasomotor tone
AKA “arterial disease”
arterial insufficiency
Common to all arterial disorders is:
ischemia
Arterial dz is almost always due to
athero/arteriosclerosis
Atherosclerosis=
stiffening of arteries & buildup of fat & other substances in arterial walls
Chronic dz of arterial system usually related to aging, where arterial walls become thick & hard
arteriosclerosis
Etiology of arteriosclerosis is caused by vessel damage from:
HTN smoking diabetes infection high cholesterol aging genetics free radicals
Mini concept map of arteriosclerosis
tunica intima microscopically damage > collagen fibers enter vessel wall > stiffening of vessel wall > decreased elasticity & arterial compliance
Atherosclerosis develops from:
atherous involvement of arteriosclerosis
“fatty deposits”
Athero
Atherosclerotic walls have deposits of:
collagen as well as LDLs
Fatty deposits in arterial walls cause:
irritation
inflammatory & coagulation responses
Formation of a fibrous capsule with a fatty middle section
Plaque
Formation of plaque is caused by:
stiff arteries, fat deposits, and inflammatory & clotting responses
Sequela of plaque growing & protruding into the lumen
Ischemia
Buildup of blockage in/along arterial walls results in:
loss of vasomotor tone and non-patent lumen
If arterial pathology exists in one area…
it is usually occurring system-wide
Narrowed, stiff, atheromatous arteries often result in:
compromised perfusion > ischemia
Characteristics of ischemic pain:
increased with exacerbation
decreases with rest
present in tissue distal to the plaque or narrowed arteries
S/S of ischemia seen in the periphery
diminished/absent pulses
delayed cap refill
pale, cool skin/mucous membranes
delayed healing
Specific S/S of ischemia in the heart
Altered function
decreased cardiac output
Specific S/S of ischemia in the brain
Altered LOC
Specific S/S of ischemia in the kidneys
Decreased urine output
Non-modifiable risk factors of arterial dz
Family HX (tendency to atherosclerosis &hypercholesterolemia) Advanced age > stiffer arteries
Modifiable risk factors for arterial dz
Diet, obesity, sedentary lifestyle
Alcohol consumption
DM2
Cigarettes/nicotine
Characteristic of DM2, increased circulating LDLs
lipodystrophy
Nicotine is a powerful ___
vasoconstrictor
Cardiovascular dz can be described as ___
atherosclerosis of coronary arteries
Venous insufficiency is often due to ___ and results in ___
bad valves in leg veins; venous congestion & peripheral edema
Arterial insufficiency is almost always due to ___ and results in ___
atherosclerosis; ischemia
PAD =
Peripheral artery disease
PAD is a dz of ___
any arterial vessels outside the heart, but most commonly refers to arterial problems of the legs
PAD usually manifests as __ due to __
problems of ischemia; narrowed peripheral arteries
S/S of PAD
Intermittent claudication Cool, pale feet Diminished pulses & delayed cap refill No hair growth on legs (shiny skin) Ischemic skin ulcers
5 Ps of PAD
Pain Pallor Paresthesias Pulselessness Poikilothermia
Poikilothermia =
cold, pale feet
Arterial thrombi form where __
flow is sluggish, and/or where there is narrowing/injury to vessel walls
Veinous thrombi block blood flow ___, causing ___
to the heart; congestion distal to the blockage
Arterial blockage results in ___
ischemia to distal tissue
If narrowing/injury/atherosclerosis occurs at an arterial bifurcation:
a thrombus might form
Emoboli of a bifurcation thrombus would travel to:
distal arteries &arterioles
Hypertension is ___
consistent elevation of systemic arterial BP over 140/90
2 categories of HTN
primary & secondary
Secondary HTN is caused by ___
altered hemodynamics associated with a dz process
Primary HTN, AKA ___, is caused by ___
Essential HTN; a complex set of factors
__% of hypertensives have primary HTN
92-95
Non-modifiable Risk factors of HTN
Family HX (inherited tendency) advanced agin
Modifiable risk factors of HTN
Diet, obesity, sedentary lifestyle
Heavy alcohol consumption
DM2
Cigarette smoking/nicotine intake
Certain conditions usually present in HTN to come degree:
Atherosclerosis
Overactivity of SNS & RAAS
Atherosclerosis contributes to HTN due to __
decreased elasticity of vessels
__ is consistently released by intracardiac nerve fibers, causing over stimulation of ___ to increase __ & __
Epinephrine
beta receptors
HR & contractility
Mini concept map of increased HR & contractility due to SNS overactivity
greater cardiac output & ejection pressure > pathologically larger volume of blood & pressure > sustained increase in BP
RAAS is usually a ___ triggered by ___
compensatory mechanism; drop in BP
For unknown reasons the RAAS sometimes becomes ___ causing ___
chronically activated; chronically high BP & blood volume
Vicious cycle of chronic HTN
arterial walls stimulated to strengthen via hypertrophy & hyperplasia > decreased lumen size > HTNn increases even more
Chronic HTN damages the __
tunica intima
S/S of HTN are often __
secondary to years of vascular damage
3 systems most often affected by HTN
Neuro
Renal
Cardiovascular
Neurological effects of HTN on the brain
Strokes due to ischemia from narrowed vessels
Effects of HTN on the eyes
ischemia & infarcts of parts of retina, vision changes
Effects of HTN on the renal system
High pressures & vessel damage can cause spilling of blood & protein into urine > eventually kidney failure
Effects of HTN on the cardiovascular system
increased workload ejecting blood against narrowed, stiff arteries;
Multiple problems including MI
Local dilation or out pouching of arterial vessel walls
Aneurysms
Pathology of aneurysms
Atherosclerosis & HTN cause weakness in arterial walls which can cause bulges in certain areas;
Minute injuries to intimal lining accumulate & allow blood to seep into muscle & tissue layers of arteries, which increase the size & chances of rupture
Areas of typical aneurysms
brain & aorta
The aorta is susceptible to aneurysms due to:
constant stress, especially from higher pressure of HTN
S/S of AAA
pulsatile, palpable mass inn abdomen; abdominal pain
S/S of thoracic aortic aneurysm
S/S usually resemble that of MI (chest pain, diminished pulses unilaterally)
Educational aspects of nursing implications for managing HTN
managing stress, smoking cessation, moderation of alcohol intake
Dietary aspects of managing HTN
low LDL intake; high intake of HDL & omega-3 fats
Desired daily intake of HDL:
40 mg/dL
Medicinal approaches for overactivity of SNS
beta & Ca channel blockers
Medicinal approaches for overactivity or RAAS
ACE inhibitors or angiotensin receptor blockers
Symbolizes ventricular repolarization on an EKG
T wave
Symbolizes ventricular depolarization on an EKG
QRS complex
Consistent, regular pattern or PQRST
sinus rhythm
Good CO is linked with ___
S/S of good perfusion
S/S of good perfusion
normal BP, pulses, cap refill, mentation, and skin color/ and warmth
SV is affected by:
contractility
preload
afterload
CO can improve or deteriorate based on:
changes in HR/rhythm; changes in SV
Definition: how well cardiomyocytes responds to electrical impulses
contractility
The effect of different factors on contractility
Inotropic
Some thing that enhances contractility
Positive inotropic effect
Something that decreases contractility
Negative inotropic effect
Amount or volume of blood in the ventricles before contraction
Preload
Any form of resistance to ejection of blood from any heart chamber
afterload
Normal after load exists when the receiving arteries have:
good vasomotor tone; smooth, patent lumens
Normal RV after load is called:
pulmonary vascular resistance
Normal LV after load is called:
systemic vascular resistance
HR >100BPM
tachycardia
Describe the neurohormonal effect on the SNS during physical exertion or stress:
Epinephrine binds to beta receptors, causing HR to increase
Hypopolarization causes cardiomyocytes to ___
contract more quickly
The PNS effect on HR involves the release of ___ by the ___
acetylcholine; vagus nerve
Interference in impulse conduction due to ischemic or infarcted cardiac tissue causes:
dysrhythmias
Chaotic electrical impulses in the atria that cause atrial “quivering”
Afib
Percentage of elderly that have Afib
~3%
Afib can cause a small, but sometimes significant ___
decrease in CO
Arterial thrombi in the LA that break loose can cause:
stroke
Arterial thrombi in the RA that break loose can cause:
PE
Increased preload, pathologically, relates to:
increased blood volume/fluid volume overload
Decreased preload, pathologically, relates to:
decreased blood volume/fluid volume deficit
Fluid volume deficit eventually leads to:
decreased BP & CO
Pathologically increased after load in the RV can be caused by:
atherosclerosis of pulmonary arteries, or chronic disorders such as bronchitis
Pathologically increased after load in the LV can be caused by:
Atherosclerosis of the aorta & systemic arteries; peripheral vasoconstriction; HTN; pathologically high blood volume
Pathologically decreased afterload in the LV is usually due to:
massive peripheral vasodilation/shock
A disorder in which the coronary arteries are narrowed or occluded
Coronary artery disease
Risk for CAD increases with high serum levels of:
hemocysteine
Risk of CAD is linked with ___ due to inflammatory process of plaque formation
elevated CRP
Cardiac cell ischemia has a ___ effect, leading to ___
negative inotropic; decreased CO
If not reversed, CAD can lead to:
cell death/necrosis
Most common symptom of CAD
angina
Ischemic pain in the heart muscle tissue
Angina
Classification of CAD is based on:
degree of coronary artery occlusion & ischemia
2 categories of CAD, based on symptoms
Stable Angina; Acute coronary syndrome
___ is established thru arteriogenesis to compensate for slow development of plaque
Collateral circulation
Acute coronary syndrome manifests as __ or __
Unstable angina or MI
Necrosis of myocardial cells
MI
2 enzymes that indicate MI upon lab testing
Creatine kinase; troponin
2 internal compensatory mechanisms of CAD patients
Collateral circulation; hypertrophy of cardiac muscle cells
A heart murmur is caused by ___ or ___
cardiac valve stenosis (valvular prolapse/ insufficiency)
or
regurgitation (back flow)
Right sided heart valves
Tricuspid, Pulmonary
Left sided heart valves
mitral, aortic
Valve malfunction may be caused by autoimmune disorders, such as:
rheumatic fever
Stenosis impedes blood flow because of:
narrowed or constricted valve orifices
A state of incompetent, floppy valves is called:
valvular prolapse
valve insufficiency
regurgitation
General term used to describe types of cardiac dysfunction secondary to failure of the heart to effectively propel blood forward
Heart failure
3 aspects of the pathology of HF
weakened contractility (pump problem) increased afterload (resistance) Increased preload (fluid volume overload)
One sequela of HF pertaining to the kidneys is:
Diminished CO stimulates the kidneys to secrete Renin as part of the RAAS, causing retention of fluids, making the problem worse instead of better
4 sequela of venous insufficiency
localized edema
local skin breakdown
Local skin discoloration
Varicose veins
Renin stimulates:
secretion of angiotensin I
Angiotensin 2 stimulates:
peripheral vasoconstriction, secretion of Aldosterone from Adrenal glands
Effects of Aldosterone:
causes distal convoluted tubules to reabsorb Na > increases tonicity > water is shifted from tissues into blood > increased UO
Increased systemic tonicity triggers release of __ which aids in fluid retention
ADH
Most common type of hypertension
Primary/Essential
Factors contributing to left heart failure
Weekend LV w/ decreased contractility
and/or
High afterload
High afterload can be due to:
HTN and/or
pathologically increased arterial vasoconstriction and/or
narrowed/blocked systemic arteries
Common sequela of LHF
Fluid overload overwhelms the LV, causing fluid to backup in the lungs > pulmonary edema
Weakened LV contractility can be caused by:
Ischemia/MI and/or Electrolyte imbalance and/or HR/rhythm problems And/Or High afterload
Sequela of RHF
RV overwhelmed by fluid overload (high preload) > fluid buildup in systemic veins > peripheral edema
RAAS complication of RHF
Aldosterone secreted by adrenal glands causes retention of Na+ > H2O retention > further increased preload
General S/S of decreased CO
Fatigue, weakness mentation changes hypotension dyspnea delayed cap refill Oliguria
S/S of pulmonary Edema (fluid backup)
Fluid congestion in lungs Crackles on auscultation Pink, frothy sputum Orthopnea Increased RR Decreased SpO2
S/S of peripheral Edema
JVD
Pedal edema
Liver congestion/enlargement
Ascites (abdominal edema)
Definition: when RHF is caused by pathologically increased pulmonary vascular resistance
Cor pulmonale
Lung congestion is caused by ___
But
Lung congestion causes __
LHF; RHF
Fluid volume overload triggers the __
NPS
NPS causes the kidneys to ___, > ___
excrete more Na+ > water follows
In volume overload, the ventricles secrete ___ and the atria secrete ___
BNP; ANP
The gold-standard for confirmation/quantification of level of HF is ___
serum level BNP
Healthy male serum BNP level:
50pg/mL
S/S of cariogenic shock are generally related to ___
decreased perfusion + compensatory responnses
Normal ABG values pH: pO2: sO2: pCo2: HCO3:
7.35-7.45 80-100mmHg 97-100% 34-45mmHg 22-26mEq/mL
If pCO2 is abnormal, the pH imbalance is ___ in nature
if HCO3 is abnormal, the pH imbalance is ___ in nature
respiratory
metabolic
Respiratory acidosis is a state of ___
low pH caused by inhibition of normal breathing pattern
Decreased RR causes:
hypercapnia (retention of CO2
Respiratory acidosis is typically caused by some degree of __
hypoventilation
Typical ABG findings of respiratory acidosis
low pH
low pO2
high pCO2
normal HCO3
Increased depth or rate of breathing causes:
CO2 blow off > alkalosis
The kidneys attempt to compensate for respiratory alkalosis by:
decreasing HCO3 production
or
increasing excretion os HCO3
State of low pH caused by accumulation of acids in the body
metabolic acidosis
HCO3 levels will be ___ in metabolic acidosis
low
Normal breathing should be ___
passive
Subjective feeling of not getting enough air
dyspnea
DOE
dyspnea on exertion
dyspnea upon lying down
orthopnea
Usually related to increased preload when lying down + compromised LV unable to pump effectively
Orthopnea
Waking suddenly and feeling SOB
paroxysmal nocturnal dyspnea (PND)
RR < 12/min
hypoventilation
RR > 20/min
tachypnea/hyperventilation
Shallow breathing
hypopnea
increased depth of breathing
hyperpnea
absence of breathing
apnea
Purulent sputum usually indicates ___
infection
Accessory muscle use during exhalation due to difficulty breathing =
respiratory distress
When a PT can no longer breathe adequately on their own
respiratory failure
Restrictive lung dz generally refers to dz processes related to ___
difficulty w/ inhalation
V/Q ratio means:
liters of air breathed in per minute/# liters of blood available for gas exchange in one minute
Normal V/Q ratio:
0.8 (4/5)
Low VQ disorders are caused by
inability to get the normal amount of air from the atmosphere to the blood
High VQ disorders are caused by:
difficulty w/ perfusion
In low VQ disorders, low V=
less ventilation (can’t get air from atmosphere to blood)
Low VQ disorders include restrictions in the: (4)
chest wall
airway
Pleura
lung tissue
Chest wall restrictions can include:
physical deformity or neuromuscular weakness
airway restrictions can include:
foreign bodies, tumors
inflammation
Most dz that cause inflammation of the larynx and bronchi are caused by:
viruses
Inflammation of the larynx, trachea, and bronchi typically seen inn young children
croup
Pleural restrictions include:
pleural effusion, pneumothorax
irritation/inflammation of the pleural space that causes fluid buildup
pleural effusion
S/S of pleural effusion
chills, fever (infection related)
pleuritic pain w/ movement
shallow respirations
Presence of air in pleural space caused bay rupture in pleura
pneumothorax
Pneumothorax disrupts the ___
normal negative pressure environment
Pneumothorax caused by outside trauma
open pneumothorax
Pneumothorax caused by internal trauma
closed pneumo
Lung tissue restriction is caused by __
pneumonia
Pneumonia is an infection of the ___
lower respiratory tract
Pneumonia can be caused by:
viruses
bacteria
parasites
fungi
3 types of pneumonia
Community acquired
Hospital acquired (nosocomial)
Aspiration
Organisms that cause CAP are usually ___
less virulent
Nosocomial pneumonia is typically caused by __
virulent microbes like pseudomonas
Inhalation of foreign substance into lungs that results in inflammation of lung tissue
aspiration pneumonia
Aspiration pneumonia usually effects:
ppl with debilitations or depressed/absent gag, cough, or swallowing reflexes
Collapse of portions of lung tissue
atelectasis
Atelectasis is caused by:
accumulation of inflammatory/infectious debris that accumulates in alveoli
Excess water in alveoli
pulmonary edema
Noncardiogenic pulmonary edema is caused by:
injury to capillary endothelium from external sources
Pathology of pulmonary edema:
capillary endothelium injured by external source > increased capillary permeability, disruption of surfactant production > fluids/proteins shift from capillaries into alveoli
S/S of pulmonary edema
pink, frothy sputum
inspiratory crackles
hypoxemia
Dyspnea
Lung cancer arises from __
respiratory epithelium
Pathology of lung cancer
carcinogens from smoking cause genetic abnormalities in bronchial cells > carcinoma in situ > invasive carcinoma
High VQ disorders involve restriction of:
blood vessels in the lungs
Most common cause of High VQ ratio
pulmonary embolism
Virchow’s triad:
endothelial injury Hypercoagulability Venous stasis (DVT)
High VQ ratio in PE is caused by:
lower O2 saturation of blood returning to the LV
Obstructive pulmonary dz results in:
difficulty w/ exhalation
S/S of obstructive pulmonary disorders
Accessory muscle use
Prolonged expiratory phase
Dyspnea
Common types of obstructive pulmonary dz
Asthma
Bronchitis and Emphysema
Cystic fibrosis
Chronic inflammatory disorder caused by bronchial hypersensitivity to stimuli
Asthma
Pathology of asthma
Inhaled irritants > inflammatory mediators > vasodilation and swelling
spasm and constriction of bronchi
Collective term for emphysema and chronic bronchitis
COPD
S/S of COPD
prolonged expiration
accessory muscle use
chronically low PF made worse by exacerbation
Basic pathology of emphysema
Inhalation of irritants > airway inflammation > alveolocapillary membrane and walls between clusters destroyed > alveoli stiff and hyper inflated > loss of elastic recoil > air becomes trapped in alveoli and exhalation becomes harder
Emphysemics live in a chronic state of ___
hyperventilation > respiratory alkalosis
Hypersecretion of mucous and chronic productive cough for > 3 months for > 2 consecutive years
chronic bronchitis
Hypoxemia in chronic bronchitis is caused by:
mucous plugs in bronchial walls
PTs with chronic bronchitis are typically in a state of chronic ___ due to ___
hypercapnia (>45); inability to exchange gases
Enlargement of the prostate gland tissues
Benign prostatic hyperplasia
S/S of BPH
Varying degrees of urinary flow obstruction
Urgency, delayed start of flow
Decreased flow
Urine retention
TX for BPH
TURP
Transurethral resection of prostate
Malignant neoplasm of the prostate
prostate cancer
Risk factors for Prostate cancer
Age >50
family Hx
diet high in saturated fat
high T levels
Cancer most common in males age 15-35
testicular cancer
Inflammation of the
a. prostate
b. urethra
prostatitis
urethritis
Female flow related problems of the uterus
dysmenorrhea, amenorrhea, endometriosis
More painful, higher than normal volume of bleeding than normal menstruation
dysmenorrhea
Absence of menses (can be sign of start of menopause)
amenorrhea
Presence of functioning endometrium outside of the uterus
Endometriosis
pathology of Endometriosis
sloughed off endometrium travels to the abdominal cavity thru the Fallopian tube > tissue reacts to menstrual hormones by proliferating & bleeding as if still in the uterus
S/S of endometriosis
dyspareunia,dysmenorrhea, pelvic pain
1 cause of cancer deaths in females
ovarian cancer
early S/S of ovarian cancer
bloating, mild abdominal pain, constipation
S/S of abdominal metastasis ovarian cancer
abdominal pain, ascites, dyspepsia, committing, alterations in BMs
Infection of the female reproductive tract
pelvic inflammatory disease
PID can cause:
infertility
UTIs are most commonly caused by __
E. coli
UTI involving the urinary bladder
cystitis
UTI involving only the kidneys
pyelonephritis
STI that causes urethritis in males, PID in females
Chalmydia
STI that is easily treated in early stages, but left untreated may become systemic and evolve
Syphilis
Not an STI:
HSV1 - HSV2
HSV1
STI that invades the genital area and spreads to the perineum and anus
HSV2 “genital herpes”
Anything that interferes with flow of urine from the kidneys to the urethral meatus
Obstructive disorders of the urological system
Enlargement of and pressure on the renal pelvis due to pathologic accumulation of fluid
hydronephrosis
Hydronephrosis is caused by:
retrograde flow of urine that cannot get past an obstruction
Hydronephrosis can lead to:
infection and fibrosis within the kidney; decline in nephron function
Types of urological obstructions (not gender specific)
Tumors
scarring from past problems
Neurogenic problems (paralysis)
Kidney stones
Presence of kidney stones
lithiasis
Risk factors for lithiasis
male gender Gout Dehydration Dietary factors Hypercalcemia caused by dz state
Kidney stones form when urine becomes super saturated with:
calcium, uric acid, and other ions
Volume of fluid filtered from the glomerular capillaries into the Bowmans capsule per minute
Glomerular filtration Rate (GFR)
Clinically speaking, decreased GFR = ___
decreased UO
Decreases in GFR increases the risk of ___
accumulation of wastes and water in the body
Abbrupt (<48 hrs) oliguria and/or jump in serum creatinine
acute kidney injury
2 possible outcomes of AKI
full recovery if caught and corrected early
Some degree of residual kidney problem if not caught early enough
3 categories of AKI based on location
Prerenal AKI
Intrarenal AKI
Postrenal AKI
Intrarenal AKI can lead to ___
acute tubular necrosis (ATN)
S/S of prerenal AKI
S/S of decreased preload:
dry mucous membranes, dry mouth
and oliguria
Causative factors of Prerenal AKI
decreased arterial blood flow to kidneys due to arterial vasoconstriction or trauma to aorta/renal arteries
and
hypotension/hypovolemia
Occurs when a blockage occurs between the kidneys and the urethral meatus
post renal AKI
Factors that can cause Postrenal AKI
obstruction from BPH
Uterine prolapse
Ureteral obstruction/calculi
Intrarenal AKI can occur when:
post- or prerenal AKI are not fixed
Acutely diminished kidney function due to direct kidney tissue injury
Pathology of infrarenal AKI
ischemia to nephron blood supply > tubule cells slough off and block urine flow > retrograde flow > hydronephrosis > ischemia, necrosis, malfunction
Causative agents of ATN
direct trauma to nephrons by:
ischemia, hydronephrosis, nephrotoxic drugs, poison/toxins, renal infections
S/S of intrarenal AKI
acute oliguria
high serum creatinine
Casts in urine
Slow, negative effect on renal function from a slow, insidious problem or genetic disorder
Chronic kidney dz (CKD)
Congenital Disorders that can cause CKD
PKD
Acquired dz that can cause CKD
unresolved AKI
Atherosclerosis
diabetes mellitus
HTN
Autoimmune dz that can cause CKD
glomerulonephritis
2 divisions of CKD
fluid/solute balance impairment
Metabolic function impairment
Pathology of glomerulonephritis
inflammatory process > glomerular capillaries become leaky > substances allowed into urine that aren’t supposed to be (RBCs, protein)
post infectious glomerulonephritis is caused by
autoantibodies attached to the glomerular membrane, causing inflammation & leakiness
high BUN and serum creatinine
Azotemia
___ is almost always associated with renal dysfunction
high serum creatinine
serum creatinine levels are high in renal dysfunction due to:
inability of impaired kidneys to excrete the normal amount into urine
Azotemia + other S/S is called ___
uremia
Precipitation of urea on skin, causing itching
pruritis
Hyperkalemia/hypernatremia in CKD is due to:
unresponsiveness of DCT to aldosterone
Sequela of Na+ and H2O retention in CKD
peripheral/pulmonary edema, HTN
Neurological changes from toxic levels of urea in the blood
Uremic encephalopathy
Inability to activate vitamin D in CKD is caused by
hypocalcemia
because CKD PTs will usually be hypocalcemic, they will also be:
hyperphosphatemic
pH imbalance seen in CKD
metabolic acidosis
Dietary restriction for CKD patients should include
restrictions of Na, K, and H2O intake
Dietary supplements that should be given to CKD patients:
vitamin D and calcium, phosphate-binding antacids, erythropoeietin
Medications given to CKD patients should include
antihypertensives and non-potassium sparing diuretics
___ is converted from ammonia by the liver
urea nitrogen
Pathology of hyperkalemia/hypernatremia in CKD
DCT unresponsive to aldosterone > pathologic retention of solutes > increase in serum K+ and Na+
