How can we help?

You can also find more resources in our Help Center.

169 terms

Emma Pathophysiology

This set includes various questions regarding Pathophysiology in Nursing
STUDY
PLAY
an adaptive cell response that could be a precursor to cancer is
dysplasia
the most frequent source of free radicals in the body is
oxygen
the best way to rid the body of free radicals is antioxidants
free radicals are cell particles which have an impaired electron
impaired wound healing may be due to
lack of vitamin C, hypoxia, corticosteroid therapy, lack of vitamin A
a benign tumour of glandular tissue is called
adenoma
neoplasia results when
cell differentiation and growth characteristics become altered
what features apply to malignant but not benign tumours
grows at the periphery and infiltrates surrounding tissue
what are the steps of metastasis is the correct order
-break loose from the primary tumour
-invade surrounding extracellular matrix
-gain access to and survive in the bloodstream
-emerge from blood and invade surrounding tissue
which of the following is NOT one of the american cancer society's 7 early warning signs of cancer
IS:
-a nagging cough
-a sore throat that does not heal
-a change in a wart or mole

ISN'T:
-a sudden decrease in hearing
oncogenesis is best described as
genetic mechanism whereby normal cells are transformed into cancer cells
the human immunovirus (HIV) is transmitted in all of the following ways except
IS:
-perinatally
-sexual contact
-blood contact

ISN'T:
-casual contact
seroconversion i.e. when HIV antibodies can be detected in the blood following exposure typically takes
3 months
which one of the following statements is true (about HIV)
FALSE:
-an HIV-infected person can transmit the virus to others before seroconversion

TRUE:
-an HIV-infected person can not transmit the virus to others before seroconversion
-an HIV-mother will not infect her infant with HIV through breastfeeding
-in healthcare workers the occupational risk of HIV infection is greater than for Hepatitis B infection
the most common opportunistic infection occuring in persons with AIDS is
pneumocystis carinii
a deficiency is B lymphocytes will cause reduced levels of
antibodies
which one of the following is NOT part of the acute inflammatory response
IS:
-chemotaxis by mast cells
-phagocytosis by neurophils
-activation of complement

ISN'T:
-formation of granulomas
_________ are the predominant phagocytic cell early in the immune response
neutrophils
which of the following hypersensitivity reactions does not involve antibody
type IV (4)
odema due to increased capillary pressure can occur with
heart failure
accumulation of fluid in the abdominal cavity is termed
ascites
dehydration of the elderly commonly occurs for all of the following reasons EXCEPT
IS:
-a decrease in the ability to sense thirst
-decreased sensory ability following stroke
-confusion and loss of short term memory

ISN'T:
inceased sensation with electrolyte imbalance
increased levels of antidiuretic hormone are associated with
nausea
raised levels of aldosterone could lead to
hypokalaemia and hypernatremia
decreased fluid intake and dehydration is likely to manifest as
weight loss
decreased intestinal absorption of vitamin D, eg. following surgical resection of part of the intestine, can result in
hypocalcemic tetany
hyperparathyroidism leads to
elevated serum calcium levels
the major protein buffers in the vascular compartment are
albumin and plasma globulins
which acid-base imbalance would have a deficiency of bicarbonate
metabolic acidosis
prolonged tissue hypoxia following caridac arrest and resuscitation would be expected to cause
metabolic acidosis
prolonged bladder outflow obstruction from prostatic hypertrophy can result in
-urinary stasis
-stone formation
-dilation of ureters
-hydronephrosis
what is the correct order for the progressive stages of renal failure
(ESRF: end stage renal failure)

-diminished renal reserve
-renal insufficiency
-renal failure
-ESRF
arterial pressure increases if
peripheral resistance increases
a __________ aneurysm develops when an inner arterial layer tears and blood forces it's way between arterial wall layers
dissecting
if a thrombus in the L) common iliac vein became dislodged which arteriole system would it enter first
lungs
the pain associated with angina is due to
ischaemia of the myocardium
loss of the sympathetic nerve supply to the heart would result in
decrease in heart rate
the symptoms of weakness and east fatigability in persons with congestive heart failure (CHF) are probably a consequence of
low cardiac output
which one of the following arrhythmias is usually fatal without prompt treatment
ventricular fibrillation
what correctly depicts the functional difference between the L) and R) heart of a person with chronic obstructive respiratory (pulmonary) diease
the R) heart works against greater resistance than the L) heart
the pathological changes associated with chronic bronchitis include
hypertrophy of the bronchial glands
in bronchial asthma when there is exacerbation
medium and small sized bronchi are plugged with mucus
a rise in the carbonic acid levels of blood will affect respiration in which way
the respiratory rate increases and the breathing becomes stronger and deeper
the primary ventilatory problem associated with obstructive lung disease such as exacerbation of COR/COPD or asthma is
delay of the airflow out of the lungs
a person who has COR pulmonale will have
right heart hypertrophy
a person who has respiratory insufficiency could be expected to have
pH below normal
the pulmonary oedema associated with adult respiratory distress syndrome (ARDS) is caused by
increased membrane permeability
which condition is commonly associated with haemoptysis
pulmonary tuberculosis
in early hypovolaemic shock a reduction in the circulating blood volume would give risk to
narrowing of the pulse pressure
in disseminated intravascular coagulation (DIC) there is
sluggish tissue flow causing agglutination and microclot formation
vascular disease of the lower limb - cool to touch and with pain relieved by dependant position - is most likely due to
artherosclerosis
why are venous thrombi more common than arterial thrombi
aterial flow and pressure are lower in veins
risk factors for venous thrombosis
-ageing
-inactivity
-dehydration
-hypercoagulability
-increased hematocrit
-constrictive clothing
what are the clinical manifestations of venous thrombosis
-pain
-tenderness
-redness and swelling over the area of the thrombus
-some people have no symptoms
the major complication of deep vein thrombosis (DVT) is
pulmonary embolus
what is an allergen
antigens that induce exaggerated immune responses
when discussing allergic reactions to bee stings, what are the underlying mechanisms that trigger Type 1 immune responses in the body
type 1 responses mediated via IgE antibodies that bind to mast cells (or other immune cells) triggering the release of histamine and other inflammatory mediators
examples of clinical manifestations that may occur in allergic reactions are
GI:
-vomiting
-abdominal pain
-diarrhea
SKIN:
-urticartia
-itching
-angioedema
-conjunctivitis
RESPIRATORY:
-bronchospasm
-rhinitis (irritation and inflammation of the mucous membrane inside of the nose)
-asthma
-laryngeal oedema
CV:
-hypotension
-tachycardia
-arrhythmia
-vasodilation
how may emphysema occur in persons who are not exposed to cigarette smoke
inherited deficiency of alpha/antitrypsin
an enzyme that inhibits proteolytic destruction of lung tissue
persons with CORD/COPD should not receive oxygen therapy via tightly fitting face masks, what is the physiological reason for this
normally central chemoreceptors near the respiratory centres in the medulla are stimulated by increased PaCO2 (which reduces pH or raised carbonic acid)
chronic hypercapnia desensitizes central chemoreceptors and persons affected rely on peripheral chemoreceptors that respond to hypoxia
high levels on inspired oxgen inhibit peripheral chemoreceptors
what is idiopathic
of unknown cause
CVA stands for
cerebrovascular accident (stroke)
what are free radicals
cell particles which have an unpaired electron
unpaired electrons can attach to other
cells causing instability and agitation to other cells
define necrosis
changes that follow cell death in living tissue
progressive degradation of enzymes on the lethally injured cell
appearance of necrosis is the result of enzyme disgestion and denaturation of proteins
oxidative stress
characterised by an imbalance between the levels of damaging reactive free radicals and the antioxidant defense mechanisms present within cells
apoptosis
a process of programmed cell death of single cells scattered in a population of healthy cells
what is cancer
cancer is an abnormal multiplication of cells
classification of cancer includes
-cell type
-degree of differentiation
-malignant/benign
-location
-spread
carcinogenesis is
the transformation of a normal cell into a cancer cell
angiogenesis is
formation/production of new blood cells
carcinogens are
agents that bind to DNA => cell mutations acts as initiators/promoters eg.:
-industrial agents
-aniline dyes
-heavy metals
-asbestos
-benezenes
-soot
-cigarette smoke
-charcoal
-aflotoxins
-x-ray
-ultra violet rays
-microwave
-gamma rays
what is hyperplasia
cells in a tissue overgrow resulting in a defined mass (tumour/neoplasm)
is benign (eg. moles)
has a slow growth rate
expands in the same tissue
often in response to hormonal stimulation
what is dysplasia
an abnormal change in the size, shape, and organisation of cells in a tissue
often an early step towards cancer
microscopic characteristics of cancer cells
behave differently from normal cells

deranged cell growth of a specific tissue
variation in size, shape and loss of cell orientation with alteration in nucleus
potentially reversible if not too severe
BUT: can go on to become cancer
grades of change: 1, 2, 3 can go on to become carcinoma in situ (CIS)

in cervical cancer:
cells become increasingly displasic => low grade changes CIN1 => CIN2 can go on to become high grade => CIN3 => CIS
peripheral vascular disease (PVD) includes
-aneurysm
-primary varicose veins
-venous thrombosis (thromboembolus)
what are the 3 types of myocardial ischaemia
-stable
-variant
-silent
myocardial ischaemia : stable
due to atheroma
comes on with increased muscle contraction resulting in lactic acid
pain may be referred
associated with a stable plaque
myocardial ischaemia : variant
coronary artery spasm
comes on at rest
? due to sympathetic activity or decreased prostaglandins
myocardial ischaemia : silent
no angina pain
may have dyspnea and fatigue
more common in women
what is myocardial ischaemia
the lack of/little blood supply to the myocardium, the heart muscle
lack of O2 to muscles and tissues of heart, specific area only
what is coronary heart disease
the narrowing or blockage of the coronary arteries that supply blood and oxygen to the heart
usually caused by atheroscelrosis
telemetry is cardiac monitoring
urinary tract obstruction
an interference with the flow of urine at any site along the urinary tract
the obstruction can be caused by an anatomic or functional defect
lower urinary tract symptoms:
-tumours
-strictures
-calculi
-benign prostate hypertrophy
upper urinary tract symptoms:
-stones
-tumours
-enlarged lymph nodes
-polycystic kidney disease
severity is based on:
-location
-completeness
-duration
-involving one of both upper urinary tracts
glomerular disorders
mostly result of immune dysregulation
results in sudden on insideous onset of hypertension, oedema and an elevated blood urea nitrogen (BUN)
decreased glomerular filtration rate
elevated plasma creatinine, urea and reduced creatinine clearance
glomerular damage
PROLIFERATIVE: number of cells increase
SCLEROTIC: amount of extracellular matrix increases
MEMBRANOUS: thickness of glomerular capillary wall increases
all can decrease the efficiency of filtration
allow blood cells, lipids, or proteins to pass into the urine
what is the definition of obesity
excess body fat caused by the energy intake exceeding the energy output of the body over an extended period of time
obesity complications
insulin resistance in type 2 diabetes: high fasting sugars and increased triglycerides
CV disease: dyslipidaemias, hypertension, CHD, CH, stroke etc
cancer: bowel, breast, ovary
gallstones: fatty, liver and in females
arthritis: esp. weight bearing joints
dyspnea: SOBOE then at rest, excess weight need more oxygen and lung expansion is decreased
snoring
obstructive sleep apnea due to decreased airways and decreased lung expansion which can lead to deacreased PO2 and hypoxaemia
excessive sleepiness
irritability
psychosocial problems
infertility
what are the four cardinal signs of acute inflammation
redness (rubor)
heat (callor)
swelling (tumor)
pain (dolor)
+ loss of function (functio luefa)
inflammation response
begins with a flood of inflammatory chemicals released into the extracellular fluid
includes kinins, prostaglandins, complement and cytokines which are released by injured tissue, phagocytes, lymphocytes and mast cells
causes local small blood vessels to dilate resulting in hyperemia
inflammation response : vascular permeability
chemicals liberated by the inflammatory response increases the permeability of local capillaries
exudate (fluid containing proteins, clotting factors, and antibodies)
seeps into tissue spaces causing local oedema (swelling) which contributes to the sensation of pain
IgE : trigger immune response, stops the response of histamine
inflammatory response : oedema
the surge of protein-rich fluids into tissue space (oedema):
-helps to dilute harmful substances
-brings in large quantities of oxygen and nutrients needed for repair
-allows entry of clotting proteins, which prevents the spread of bacteria
inflammatory response : phagocytic mobilisation
occurs in four main stages:
leukocytosis : neutrophils released from bone marrow in response to leukocytosis - inducing factors released by injured cells
margination : neutrophils cling to walls of capillaries in the injured area
diapedesis : neutrophils squeeze through capillary walls and begin phagocytosis
chemotaxis : inflammatory chemicals attract neutrophils to the injury site
inflammation versus infection
inflammation involves non-specific immune responses to cell injury
it happens the same regardless of the cause
infection : from invasion of micro-organisms, causes cell injury and inflammation
can have inflammation with/without infection, infection is from pathogens
atrophy is
shrinking in cell size resulting in decreased size of a body part
causes include:
-disuse
-deneruation
-ischaemia
-poor nutrition
-often reversible
hypertrophy is
an increase in cell size resulting in increased size of a body part
may be physiological
eg. with resistance training
may be pathological
eg. heart ventricle muscle with heart failure
metaplasia is
fully differentiated adult cell converts to another cell type in response to stimulus
eg. in smokers airways chronic irritation => ciliated epithelium replaced by more robust stratified squamous epithelium

when a cell changes from one type to another
not definite cancer
tuberculosis is
infectious disease due to myocobacterium tuberculosis (human or bovine form)
spread via droplets, infects lungs and occasionally GI tract
inhaled bugs multiply, affecting alveoli in upper lobes, some escape to lymph nodes and set up immune responses
inflammation occurs within hours, neutrophils surround organisms
after a few days macrophages surround organisms
asthma is
a chronic inflammatory disease of airways involving mast cells, eosinophils, T cells, neutrophils, macrophages and epithelial cells (+++)
it causes recurrent episodes of wheezing and coughing often during the night
often reversible : spontaneously or with treatment
inflammation causes bronchial hyper-responsiveness to a variety of stimuli
asthma pathophysiology
triggered by allergens or irritants exposed to hyper-responsive airways
IgE and mast cell degranulation release
inflammatory mediators and chemotaxis attracts WBC
resulting inflammation causes bronchial smooth muscle spasm, increased vascular permeability and mucus, vascular congestion, oedema, thick sputum, eventually thickening airway walls
atelectasis is
collapse of lung tissue (alveoli)
two types : compression and obstruction (absorption)
compression : pressure on part of a lung eg. from tumor, fluid, air in pleura or abdominal distention
obstruction (absorption) : eg. from a mucus plug, inhaled anaesthetics => absorption of distal alveolar air and collapse
risk increases with pain, ineffective airways clearance post-operatively
bronchiectasis is
irreversible dilation and destruction of bronchial walls
caused by:
-repeated respiratory infections (common)
-tumor obstruction
-apsirated FB (?)
-congenital (rare)
COPD
chronic obstructive pulmonary disease
chronic bronchitis - inflammation and irritation of airways
emphysema - destruction of the alveoli and surrounding capillaries with a reduction in areas for gas exchange
chronic bronchitis
associated with irritants in airways - smoking
middle aged men most commonly affected
excessive mucus production of irritated airways mucosa causes recurrent infections
chronic productive cough for 3 consistent months of the year, (3/12) for at least 2 consecutive years
pulmonary hypertension and right heart failure follow with peripheral edema
narrowed airways collapse causing air trapping => hypoventilation => hypercapnia
emphysema
enlargement and destruction of airspaces distal to terminal bronchioles (+++)
pan-lobular : affects peripheral alveoli
centrilobular : affects respiratory bronchioles with initial preservation of alveolar ducts and sacs
emphysema causes alveolar air trapping dyspnea, altered V/Q, increased ventilatory effort
cystic fibrosis
a heredity autosomal recessive disease
thick tenacious mucus in resp tract
have chronic respiratory disease, from hyperplasia of goblet cells, viscid mucus plugs => bronchial obstruction => inflammation, repeated infections, bronchiectasis, hypoxaemia and clubbing => pulmonary hypertension => eventually rheumatic heart failure at a young age
diagnosis: Guthrie test, increased sodium chloride (NaCI) in sweat, early treatment essential to avoid death in childhood
cardinal signs of respiratory disease
cough : responds to irritants (increased sputum)
sputum : clear, purulent
dyspnea : graded 0-4
orthopnea : SOB lying flat
hypoxaemia
decreased O2 transported in blood
eg. pneumonia
airway obstruction
shallowing breathing eg. abdominal ascites
hypoxia
reduction in tissue oxygenation
caused by: an increased altitude
sudden blood loss
acute circulatory or respiratory problems
severe hypoxia : PO2 < 60 mmHg
hypercapnia
increased CO2 in arterial blood
caused by decreased drive to breathe or inability to respond to ventilatory stimulation eg. airway obstruction
respiratory depression, decreased nervous stimulation of respiratory muscle, damage to brain stem, increased work of breathing
circulatory shock
a clinical syndrome characterised by decreased cardiac output, failure of the circulation, inadequate tissue perfusion and hypoxic cellular damage that results in impaired cell functioning which can go on to cell death, organ dysfunction and stimulation of inflammatory responses
types of shock
hypovolaemic : loss of at least 15% of circulating blood volume
obstructive : (cardiogenic) reduced cardiac output
distributive : loss of vasomotor tone
peripheral pooling
septic (endotoxins)
failure of cells to take up oxygen
arterial varicose veins
caused by:
incompetent valves meaning blood won't get to the limbs
this can also cause ulcers and itching etc
manage by:
increased exercise, increases circulation and increases the ulcer status
venous varicose veins
caused by:
incompetent valves meaning blood can't get away from the limb back to the heart
manage by:
elevating legs to encourage blood flow
prinzmetal
a type of MI (myocardial infarction)
variant angina
causing spasms
doesn't require immediate attention
occurs at rest
often is what patient may show with MI
what is PO2
partial pressure of oxygen
what is ischaemia
lack of blood supply, causing no O2 getting through body, causing hypoxia
anaplasia is
definite cancer
inflammatory responses vascular and cellular
IMMEDIATELY: haemostasis vascular constriction and clotting contain wound: form surface scab
then: increased capillary permeability => leakage of plasma and blood components to exit vessels
followed by cellular effects of WBC and phagocytosis
initially phagocytosis by neutrophils, then macrophages: remove debris, bugs, etc. WBC release growth factors (GFs) => angiogenesis (new capillaries) and attract fibroblasts
is non-specific
increased WBC, neutrophils in WBC
neutrophils are main WBC in inflammation, have a phagocytic response
carcinogenesis
risk/contribute factors increased risk of cancer: - oncogenic viruses, chronic inflammation, chemical and environmental carcinogens, heredity, altered immunity
some diseases can have a carcinogenic effect on the tissues
increased risk = oncogenic viruses
oncogenesis
2 week process: needs something to trigger it and something to promote it
hormones can induce cell mutations of act as promoters
eg: cervix cancer resulting from HPV virus that is then promoted by hormones leading to cancer
oncogenic viruses
virus DNA replaces the cells normal DNA and then multiplies
carcinogens
agents that bind to DNA causing cell mutations that act as initiators/promoters and take over
solar ionising radiation and physical agents
damage DNA - mutate proto-oncogene or inactivate tumour suppressor gene
sunlight with UV radiation
EMF controversial
chronic irritation could promote it eg. jagged teeth, pipe, can cause oral cancers eg. leukoplakia
alters normal DNA, becomes dysplasic, later turning cancerous
metastases: steps
angiogenesis and tumour growth, attachment to basement membrane, invasion and enzymatic breakdown of membrane, increased motility and detachment, dissemenation in blood, lymph etc, survival from immune cells, mechanical entrapment or adhesion, extravasation, growth at 2o site?
4 types of hypersensitivities are
Type I: E mediated
Type II: bacteria in wound
Type III: immune complex-mediated: virus
Type IV: anaphylaxis (IgE)
for hypersensitivity to occur you need an antigen to trigger the response
antibodies are soluble proteins secreted by activated B cells and plasma cells in response to an antigen

classes of antibodies include:
IgB: B cells
IgM: plasma cells
IgA: epithelial
IgE: mast cells, basophils
hypersensitivity reactions: type I
IgE binds to mast cells causing release of histamine and other inflammatory substances
response is immediate, usually localised and subsides in 30 mins
manifestations seen is skin, respiratory tract, GI tract eg. ASTHMA, hay fever
systemic responses are rare when allergens enter blood - anaphylaxis
hypersensitivity reactions: type II
mediated via IgG or IgM
onset 1-3 hours, lasts 10-15 hours
antibodies bind to tissue specific antigens
this triggers complement or phagocytosis by macrophages (or neutrophils) or non-specific cell destruction by cytotoxic T cells or receptor blockage
eg. some drug and transfusion reactions
hypersensitivity reactions: type III
IgM or IgG mediated
soluble antigens widely distributed - antigen antibody complexes
complement activated: attracts neutrophils, attempt phagocytosis, immune complexes too big => inflammation persisting in a particular area causing tissue damage; eg mushroom growers or pigeon breeders alveolitis
hypersensitivity reactions: type IV
delayed hypersensitivity; 1-3 days
mediated by sensitised T cells
involves cytotoxic Ts, T helpers, macrophages (release cytokines directly attack target cells)
eg. allergic contact dermatitis, latex allergy, plant allergies, mantoux test, can be transferred by transfusion
antihistamines don't work, steroids do on cytokines
lipoproteins
cholesterol/triglycerides carried in plasma by fat-transporting proteins (apoproteins)
5 types, classified by densities
carry varying amounts of triglycerides, cholesterol, phospholipids
apoproteins control interactions of lipoproteins
chylomicrons: transport dietary lipids from the intestines to other locations in the body
LDLs: BAD
HDLs: GOOD : carry excess cholesterol from the arteries to the liver to be made into bile
atheroclerosis
deposits of fat and fibrin on endothelium of arteries that hardens over time eventually => decreasing lumen size
affected arteries = medium and large arteries eg. aorta and its branches, coronary and cerebral arteries
insidious: 20-40+ years => symtpoms
endothelium: allows for exchange and extra fat absorption
reversible at fatty streak stage, early stages (usually seen in children)
hyperlipidaemia
elevated cholesterol levels increase risk of atherosclerosis
dyslipidaemias: high LDLs, high total cholesterol, low HDLs
increased cholesterol from genetics, nutrition, disease, lifestyle
peripheral vascular disease
any condition that impairs peripheral circulation, aterial or venous
aterial: atherosclerosis: occlusion from thrombus/embolus, commonest lower limbs: aorto-iliac, femoro-popliteal, popliteal-iliac arteries
narrow lumen => ischaemia, pain at rest, intermittent claudication, decreased foot pulses, cool, elevate limb => pallor
acute coronary syndromes
term for unstable agnina, MI without ST elevation, MI with ST elevation
plaque starts to fissure, clot begins to form, breaks up, still have flow to myocardium
unstable angina: presents 3 ways:
prolonged symptoms at rest
severe new onset stable angina
worsening stable angina
pre-infarction state: clot can grow=> obstruction
where is the most common site of an MI
left ventricle
clinical manifestations of MI
prolonged O2 deficit => ischaemic death of heart muscle at same time end products of anaerobic metabolism accumulate
chest pain may be referred
sympathetic effects: nausea and vomiting, pallor, diaphoresis, tachycardia, anxiety, restlessness, sense of impending doom
DP drops/unchanged
up to 50% silent infarcts
diagnosis confirmed with enzyme changes
CK (creatinine kyamine) energy transfer enzyme, 4-6 hours, peaks 18-24 hours
troponin I: relaxing protein, released in hours, peaks 1-2 days
ECG
HIV pathophysiology
HIV retrovirus (genetic info is in RNA) - slow virus: long delay from infection to symptoms
targets cells with CD4+ receptors in immune nervous systems (T helpers, macrophages, dendritic cells) (+++)
viral envelope has protein spikes: GP120 that interact with receptors of target cells, cause a conformation change and allow the viral core into the host cell
there may be a long time between the exposure and expression of symptoms
HIV inside the host cell
the HIV uses reverse transcriptase to convert its RNA to 2 stranded DNA
a 2nd enzyme helps this DNA into host cell DNA
infected cells may remain dormant
once activated, this DNA reprograms host cell DNA to make viral protein: assembled and coated in cytoplasm, then bud off as new virions and finally host cell dies
HIV transmission of infection
directly through infected body fluids
unprotected sexual intercourse
healthcare workers (needle sticks)
sharing needles
blood transfusions/products
maternal
cadaver
clinical manifestations of HIV (+++)
early stage: symptoms similar to flu eg:
night sweats
lymphadenopathy
fatigue
malaise
without treatment, immunity declines
progresses from HIV to AIDS (read how this happens)
CRF definition
chronic renal failure: permanent loss of nephrons and renal function
erythropoietin definition
hormone produced by kidneys and regulates production of red blood cells
filtrate definition
liquid entering the nephron
filtration definition
movement of liquid through a membrane (like a sieve), allows only small molecules and liquids to pass through
movement is from higher to lower pressure
GFR definition
glomerular filtration rate: amount of filtrate produced each minute
glomerulus definition
filtration system of the nephron, composed of capillaries surrounded by a thin double-walled capsule, called Bowman's capsule
renal physiology
-control the fluid/electrolyte balance for the body
-remove metabolic wastes from the blood and excrete them to the outside
-regulate red blood cell production
-regulate blood pressure
-important in calcium ion absorption
-control volume, composition and pH of the blood
glomerular disorders
glomerular disease mostly the result of immune dysregulation
results in a sudden or insidious onset of hypertension, edema, and an elevated blood urea nitrogen (BUN)
decreased glomerular filtration rate - elevated plasma creatinine, urea and reduced creatinine clearance
nephritic syndromes
glomerular disorders that INITIATE THE INFLAMMATORY RESPONSE within the glomeruli and initially DECREASES permeability of the membrane
nephrotic syndromes
glomerular disorders that affect the glomerular capillary membrane and INCREASE permeability to plasma proteins
glomerular damage
proliferative: number of cells increase
sclerotic: amount of extracellular matrix increases
membranous: thickness of glomerular capillary wall increases
all can decrease the efficiency of filtration
allow blood cells, lipids or proteins to pass into the urine
when there is glomerular damage, blood is passed into the urine (haematuria)
further causes of obstructive shock include
heart prevented from pumping
see renal heart failure and increased cardiovascular pressure (CVP)
PE- pulmonary edema
tension pneumothorax
compensatory mechanisms of shock
body attempts to restore tissue perfusion and oxygenation in early stages of shock with neuro-endocrine and smooth muscle responses
for clinical assessment and treatment shock is divided into 3 stages:
compensated
progressive
decompensated/irreversible
in reality, shock is a continuum
sympathetic effects of shock
sympathetic stimulation increases venous return by constricting arterioles and venules causeing decreased capillary flow and more interstitial fluid returned to the body resulting in an increased preload
blood vessels shut down in skin, kidneys and gastro-intestinal tract to shunt blood to heart and brain
gastro-intestinal tract result in haemorrhage after compensatory phase of shock
progression of shock
as shock state progresses, life saving interventions are required
compensatory mechanisms fail to maintain adequate tissue perfusion causing hypoxic cell injury, free radical damage, inflammatory responses and lactic acidosis
metabolic acidosis can cause organ dysfunction with arrhythmias, which along with myocardial depressant factors can cause decreased CO and worsening shock
will a patient with severe anaemia have cyanosis
no
respiratory and cardiac problems cause cyanosis
GI ulceration in shock
GI ulceration is a result of shock
sympathetic activity diverts blood flow away from the gut
GI cells vulnerable to decreased perfusion which decreases mucosal protective barriers
ulcers can occur in hours which can cause severe haemorrhage
heart failure
systolic dysfunction- difficulty ejecting blood and/or
diastolic dysfunction- problems with ventricular filling eg high filling pressure or pulmonary congestion
compensatory mechanisms- maintain perfusion and cardiac output but as compensation fails, symptoms develop at rest
COPD patients can go into heart failure due to resistance in the pulmonary circulation
right side may become hypertrophic because the blood backs up venous pressure making it work harder which can cause heart failure
compensatory mechanisms of heart failure
remember CO=HR x SV
increased heart failure (sympathetic activity)
damaged chamber dilates (to increase stroke volume, but this leaves more blood in the ventricles after contraction)
myocardium hypertrophies (attempts to increase pumping capacity but this increases afterload causing increased resistance (muscle has to work harder)
neural humoral responses in heart failure
sympathetic activity triggering the blood supply to the vital organs therefore could lead to haemorrhage in the gut
left ventricular failure
commonest site of myocardial infarctions as it works harder than the right side
less blood ejected into aorta and coronary arteries
blood dams up and raises pressure in pulmonary circulation: causing congestion and respiratory effects including:
cyanosis
cough
SOBOE
orthopnea
paroxymal nocturnal dyspnea
blood tinged sputum
kidney stones
also known as renal calculi
incidence is common
usual site is the kidneys (nephrolithiasis)
precipitating factors include:
UTIs especially with IDCs
diabetes
fluid depletion (concentrates solutes)
urinary stasis eg from inactivity eg bed rest or wheel chair
hypercalciuria
family history, ageing
gout (high uric acid levels)
kidney stone formation
masses of crystals, protein or other substances form within the urinary tract
supersaturation of one or more salts
-presence of salt in a higher concentration than the volume able to dissolve the salt
precipitation of a salt from liquid to solid state
growth into a stone via crystallisation or aggregation
stone types
80% calcium stones (oxalate or phosphate)
15% struvites : magnesium (ammonium phosphate) form large staghorn calculi in renal pelvis
7% uric acid
can have many small stones or bigger ones
over 3mm => symptom management, over 7mm => intervention is required
primary/essential hypertension
arises from genetic and environmental factors causing neural and hormonal effects
inflammation and insulin resistance may contribute
secondary hypertension
due to underlying disease commonly kidney disease or some drugs that increase peripheral resistance or cardiac output
exercise and hypertension
diet and exercise are both modifiable factors in hypertension
when someone with hypertension continually exercises, at first their heart rate will rise, but after some time of constant exercise it will begin to decrease
how hypertension affects vessel walls
prolonged pressure injuries endothelium and stimulates inflammatory responses causing altered permeability to Na, Ca, proteins etc and smooth muscle contraction
prolonged vasoconstriction and high pressure damages vessel walls (arteries, arterioles) causing thickening and strengthening
smooth muscle hypertrophies and eventually decreases lumen size and increases blood pressure
sustained hypertension damages organs including
myocardium
coronary arteries
kidneys
brain
eyes
aorta
arteries of lower extremities
AIDS associated cancers
karposi's sarcoma
non hodgkins lymphoma
uterine, cervical carcinomas
haemoptysis
is blood in the sputum, commonly seen in tuberculosis
major complication of DVT
pulmonary embolus
chronic alteration
chronic and continuous irritation ie. grinding teeth on lip all the time can lead to dysplasia which can lead to cancer